Archive for the ‘Heart physiology’ Category

The longevity of the long distance runner, part 3: Cardiac Outcomes

January 10, 2016

After examining the anecdotal evidence provided by elderly marathoners and then grappling with some of the basic science underlying longevity in recent posts, it is time to attempt to draw some practical conclusions about what can be done to optimise longevity as a runner.   While the unfolding science of the molecular mechanisms by which our bodies respond to wear and tear offers intriguing prospects of identifying strategies for promoting heathy aging, there are at this stage more questions than answers. However we each live only once and if we want to optimise our chances of running fluently in old age, we must make the most of the evidence that is currently available. Despite the uncertainties, the evolving science provides a framework for weighing up the value of the lessons that might be drawn from the anecdotes.

But it is necessary to be aware of the pitfalls if we are too simplistic in our interpretation of the science. For example, at first sight the fact that catabolic hormones such as cortisol promote the break-down of body tissues to provide fuel for energy generation in stressful situations, suggests that avoiding sustained elevation of cortisol is likely to promote longevity. Indeed this conclusion might be valid in some circumstances, but it is not a universal rule. The strategy that is most successful for promoting longevity in animals is a calorie restricted diet. This works for creatures as diverse as worms, fish, rodents and dogs, and there is some evidence for health benefits in primates. The mechanisms by which it achieves its benefits include an increase in resistance to oxidative damage to tissues by virtue of more resilient mitochondrial membranes. However calorie restriction is stressful and promotes long term elevation of cortisol. It appears that animals actually need at a least a moderate level of ongoing stress to encourage heathy adaptation. The goal is achieving balance between stressful stimuli and adaptive responses.   The balance point depends on individual circumstances, and is likely to shift as we grow older.

The nature of training

The basic principle of athletic training is stressing the body in order to encourage it to grow stronger. One of the key mechanisms by which this is achieved is inflammation, a process by which damage to tissues generates a cascade of responses mediated by chemical messenger molecules that circulate in the blood stream, triggering repair and strengthening but also leaving a trail of debris.

There is abundant evidence that running increases life expectancy. In a 21 year follow-up study of elderly runners Chakravarty and colleagues at Stanford University found that continuing to run into the seventh and eighth decades has continuing benefits for both life expectancy and reduction of disability. Death rates were less in runners than in controls not only for cardiovascular causes, but also other causes, including cancer, neurological disorders and infections. Nonetheless, unsurprisingly, Chakravarty reported that although the increase in disability with age was substantially less in runners than in non-runners, the runners did nonetheless suffer increasing disability over the follow-up period. This is of course what would be expected if the processes by which training strengthens the body also leave a trail of debris.

If our goal is to increase not only life expectancy but also to achieve healthy aging and longevity as runners, we need to look more closely at the mechanisms by which running damages tissues. Ensuring longevity as a runner requires training in a manner that ensures that the accumulation of debris is minimised.

Healthy aging is a process affecting all parts of the body. Nonetheless, for the runner, the cardiovascular system, musculoskeletal system, nervous systems and endocrine systems are of special importance. There is a large body of evidence about how these systems age and about both the beneficial and the damaging effects of running on these systems.   I will examine the evidence regarding cardiovascular system in this post, and draw some tentative conclusions about how we might train to achieve healthy aging of the heart. In my next post I will examine the evidence regarding the musculo skeletal system, for which much more detailed information about cellular mechanism is available due to the feasibility of tissue biopsy. This will allow us to extend and consolidate the conclusions regarding optimal training for maximizing longevity as a runner.    In the final posts in this series I will turn my attention to the nervous and endocrine systems, and speculate about the way in which optimal training might impact upon health aging of those crucial systems.

Cardiovascular changes

Running produces both short term and long term changes in the cardiovascular system, some beneficial, some potentially harmful. I have discussed many of these changes in several previous blog posts (e.g. ‘The athletes heart’; ‘Inflammation, heart-rhythms, training-effects and overtraining’; ‘Endurance training and heart health, revisited’) and will present a brief overview here.

In the medium term (over time scale of weeks) regular training leads to an increase in blood volume. This increases venous return to the heart. The stretching of the heart muscle leads to more forceful contraction and a greater stroke volume. The cardiac output for a given heart rate is increased. Resting heart rate decreases and the heart rate required to run at a particular sub-maximal pace decreases.

In the longer term, the heart muscle is remodelled, with an increase in overall volume and in thickness of the ventricular walls. This condition is known as ‘athletes heart’. The mechanism is mediated by the intra-cellular signalling pathway that engages an enzyme known as Akt, which promotes growth of both muscle cells and capillaries. This is usually regarded as a benign physiological adaptation. The enlargement of the heart that accompanies pathological conditions such as high blood pressure or obstruction of the heart valves is also mediated by the Akt signalling pathway, but in contrast to the benign enlargement of the athlete’s heart, the Akt signalling is accompanied by inhibition of a growth factor required for the development of capillaries. Thus, in the athlete’s heart the enlargement is accompanied by adequate development of a blood supply to the heart muscle, whereas in pathological conditions the blood supply is usually inadequate.

However, in some athletes the enlargement might have adverse effects. There is compelling evidence that endurance runners with a long history of substantial training have an increased risk of disturbances of heart rhythm, including both ‘supra-ventricular’ disturbances such as atrial fibrillation, and potentially more lethal ventricular disturbances. The cause of these rhythm disturbances is not fully established but it is probable that the re-modelling of the heart muscle in a way that alters electrical conduction pathways plays a role.  It is likely that residual fibrosis at sites where damaged muscle has been repaired also plays a role by producing local irritability of the cardiac muscle cells leading them to fire spontaneously.

During intense prolonged exercise the strength of ventricular contraction, especially that of the right ventricle, is diminished, a condition known as Exercise-Induced Right Ventricular Dysfunction. If the exercise is sufficiently intense and prolonged, cardiac enzymes can be detected in the bloodstream, indicating a least temporary structural damage to heart muscle.

In a study of forty highly trained athletes competing in events ranging from marathon to iron-man triathlon, LaGerche and colleagues from Melbourne found transient weakening of the right ventricle immediately after the event. This was more severe the longer the duration of the event. The transient weakness returned near to normal within a week. However in 5 of the athletes, there was evidence of long term fibrosis of the ventricular septum, indicating chronic damage. Those with evidence suggesting long term damage had an average age of 43 and had been competing for an average of 20 years. Those without evidence of chronic damage had an average age of 35 and had been competing for an average of 8 years.   The evidence suggests that duration of endurance competition is a strong predictor of chronic damage.

Although an enlarged athlete’s heart usually has a much better blood supply than the enlarged heart associated with high blood pressure or obstruction of the heart valves, there is disconcerting but controversial evidence of excessive calcification of the arteries in at least some athletes, especially in males in who run marathons over period of many years. The mechanism is uncertain, though sustained inflammation is a plausible mechanism.

Effects of the amount and type of training

Although an overwhelming mass of evidence demonstrates that runners have a longer life expectancy and in particular, a lower risk of death from heart attack or heart failure than sedentary individuals, several large epidemiological studies raise the possibility that adverse health effects (especially cardiac events) tend to be a little more frequent in those who engage in a large amount of exercise than in those who exercise moderately. The US Aerobic Longitudinal Study examined the associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, aged 18 to 100 years (mean age 44 years) over an average period of 15 years and found a marked decreased in both cardiac and all-cause mortality in runners compared with non-runners, but the reduction in mortality was a little less in those training 6 or more times per week compared with those training 1-5 times per week. The Copenhagen City Heart Study followed 1,098 healthy joggers and 3,950 healthy non-joggers for a period of 12 years and found that 1 to 2.4 hours of jogging per week was associated with the lowest mortality. These ‘moderate’ joggers had a mortality hazard ratio of 0.29 compared with sedentary non-joggers.

But closer look at the evidence reveals a potentially informative detail. In a study of heart health of over a million women, Miranda Armstrong and her co-investigators from Oxford  found that among obese women, those who did a large amount of exercise suffered more heart problems than those who did a moderate amount. However, in contrast, among the women who had a Body Mass Index less than 25, those doing a large amount of exercise had fewer heart problems than those doing a moderate amount of exercise.   This suggests that if there is a risk in doing a large amount of exercise, it is mainly confined to those for whom the exercise is excessively stressful due to other risk factors that shift the balance towards harm rather than benefit.

Although the evidence from the large epidemiological studies remains a topic of debate because of issues such as possible bias in participant selection and the relatively small numbers of individuals in the category who take a very large amount of exercise, I think the balance of evidence does indicate that at least some individuals who take a large amount of exercise do have an increased risk of death, including death form cardiac events, within a given time period.   In my opinion, the important question is what determines which individuals will be harmed by a large amount of exercise, and whether there are ways in which we can minimise the risk of harm.

There is evidence that adequate prior training can protect against damage.   Neilan and colleagues studied non-elite marathoners runners completing the Boston Marathon and reported that right ventricle weakness was more pronounced in those who had trained less than 35 miles per week compared with those who had trained more than 45 miles per week.   The logical conclusion from studies such as the Oxford study of obese female runners and Neilan’s study of marathoners is that running in a manner that exceeds the individual’s current ability to cope with the stress increases the risk of damage.   This in turn suggests that building up gradually in a manner that ensures that training sessions are never excessively stressful is likely to be the safest approach.

Furthermore, it is likely that lack of adequate prior training or obesity are not the only factors that impair the ability to cope with the stress of demanding training and racing. Following a very demanding marathon or ultra-marathon, the evidence of damage remains detectable for a period of weeks. It is plausible that demanding training when the heart is in a weakened state will compound the damage. It is widely accepted in practice that recovery following intense racing or heavy training is crucial, but unfortunately there is relatively little scientific evidence addressing the question of whether or not the adverse cardiac effects of intense exercise resolve during a recovery period, or conversely, whether the adverse effects are compounded by repeated bouts of exercise.   We must therefore turn to evidence from studies of rats.

Benito and colleagues exercised rats on a treadmill for 60 minutes at a quite vigorous pace of 60 cm/s (achieved after 2 weeks of progressive training) 5 days per week for a total of 4 weeks, 8 weeks or 16 weeks. For a rat, 16 weeks of life is roughly equivalent to 10 years for a human. During the first 8 weeks there was relatively little evidence of damage, but prominent signs of damage emerged between 8 and 16 weeks. After the 16 weeks of exercise, the rats exhibited hypertrophy of the left ventricle and also the reduced function of the right ventricle, similar to the findings reported in humans. Furthermore the rats had marked deposits of collagen in the right ventricle, and messenger RNA and protein expression characteristic of fibrosis in both atria and the right ventricle. The exercised rats had an increased susceptibility to induction of ventricular arrhythmias. A sub-group of the rats were examined after an 8 week recovery period following the 16 weeks of exercise. Although the increased weight of the heart had not fully returned to normal level, all of the fibrotic changes that had been observed after 16 weeks of exercise had returned to the normal level observed in sedentary control rats. Thus, at least in rats, the adverse potentially arrhythmigenic changes produced by intense exercise over a 16 week period appear to be reversible after an adequate recovery period.    Thus the best available scientific evidence does support the accepted principle that recovery following intense racing or heavy training is crucial.


Proposed cardiac outcomes of long-term training. The size of the ellipses indicates cardiac fitness at each stage; colour indicates balance between recovery (blue) and stress (red)

In summary, the evidence regarding the cardiovascular effects of running suggests the following guidelines for healthy aging and longevity as a runner:

  • Continuing to run regularly, at least into the seventh and eight decades decreases risk of death and disability.
  • Training volume should be built up gradually.
  • Adequate recovery after demanding events, such as a marathon (or indeed, even after heavy training sessions) is likely to be crucial.

My next post will examine the evidence regarding the effects of training on the musculoskeletal system, and will both consolidate and extend these conclusions.

Endurance Training and Heart Health, Revisited

February 25, 2015

The perennial question of the benefits and risks of running has been back in the news in the past few weeks. First there was the recent publication of another paper adding to the previously reported findings from the Copenhagen heart study. The main conclusion from this long-term study of mortality among runners is that moderate amounts of running increase the probability of a longer life. However, the newspapers seized on the statement that large amounts of running were not statistically safer than a sedentary life-style. That in itself was a trivial conclusion despite its sensational appeal to newspaper editors. The number of people in the sample doing a large amount of exercise was too small to produce statistically robust evidence of either benefit or harm. While mortality rate was higher in those doing a lot of running compared with those doing a modest amount, it was nonetheless lower than in sedentary individuals, but the decrease was not statistically significant. I suspect that the somewhat sensational reporting was at least partly due to the fact that James O’Keefe joined the scientists who conducted the study, to write the paper. I have previously remarked that in my eyes, O’Keefe appears more like a snake-oil merchant than a scientist.

The other publication, a study of adverse cardiac events in over a million British women by Armstrong and colleagues from Oxford, is more measured in its reporting. It too shows that moderate amounts of exercise are beneficial, but those doing a larger amount of exercise had less good outcome than those doing a modest amount (e.g. half and hour three times per week). Nonetheless, even those exercising daily had a better outcome than sedentary individuals.

A third large epidemiological study, the Aerobic Longitudinal Study of 55,137 American adults also revealed that moderate exercise is associated with a substantial reduction in mortality, but yet again those doing a large amount of exercise tended to have higher mortality that those doing moderate exercise. Thus three large epidemiological studies have all demonstrated that moderate exercise is associated with major health benefits, but these benefits are reduced, though not entirely abolished, in those doing a large amount of exercise.  The evidence suggests that in at least some individuals a large amount of exercise is associated with harmful effects on health. This finding is not surprising in light of the very strong evidence from many studies that at least a minority of individuals who do very large amounts of exercise suffer heart damage.

Evidence of heart rhythm disturbances

The best documented adverse effect of extensive amount of endurance training and racing is disturbance of cardiac rhythm, especially atrial fibrillation. A review by Mont and colleagues revealed that long-term endurance athletes have a to 2-10 fold increase in risk of atrial fibrillation.   There is also an increased frequency of potentially more dangerous rhythm disturbances arising in the ventricles. Ventricular rhythm abnormalities are quite common in elderly endurance athletes, and also occur in a substantial minority of young athletes. For example, Verdile and colleagues observed ventricular rhythm abnormality in 367 (7.3%) of 5011 highly trained young athletes with average age 24 without other evidence of heart disease. Six of these individuals underwent successful surgical ablation of the aberrant heart tissue, while 7 with frequent or complex rhythm disturbances who declined surgery were prohibited from competitive sport.   However no adverse cardiac event occurred in any of the 367 young athletes during a follow-up period of average duration 7 years, indicating that at least in young athletes with no other evidence of cardiac abnormality, the arrhythmias are usually benign.

What are the implications for individuals who want to exercise vigorously?

Is there an upper limit to the amount of exercise that is healthy, and if so, what is it? Or can the likelihood of adverse effects on health be reduced by adjusting the way in which we train? There is a twist in the tail of the Oxford study of a million women that throws some light on this. A sub-group analysis revealed that among those who were obese, the women taking a large amount of exercise had a somewhat higher risk of cardiac events than those who exercised only three times a week. However, among those with BMI below 25, those who exercise frequently have a lower risk than those who exercise only three times week.   This suggests that it is not the amount of exercise in itself that does the damage, it is more likely that it is the amount of stress generated by the exercise that matters.    Emerging evidence about the mechanism by which excessive exercise might produce harmful health effects in runners throws a little more light on the issue.

What are the possible mechanisms of damage?

What determines who among endurance athletes is at greatest risk of damage? The mechanism of the damage remains uncertain, but a growing body of evidence provides some clues. Exercise remodels the heart.  The walls of the ventricles become thicker and the cavities become dilated. This is the typical athletes heart. Some athletes also exhibit fibrosis of the muscle. Fibrosis arises when damaged muscle is repaired with a scaffold of fibrous material.  This is a part of the normal mechanism by which inflammation repairs damaged body tissues but can become disruptive if the fibrous deposits become permanent. Fibrosis of heart muscle is likely to disrupt the normal conduction pathways via which electrical signals initiate heart muscle contraction. Although not directly proven, fibrous deposits are a prime suspect for rhythm disturbances.

What causes the damage that sets the scene for fibrosis? Some thought provoking clues come for studies of the effects of strenuous exercise on the right ventricle. The right ventricle has to pump blood through the lungs, and the capillaries in the lungs do not open up as much during exercise as the capillaries in the muscles. Hence, the right ventricle faces a relatively harder task than the left in having to push the increased volume of blood required with less benefit from an accommodating vascular system.  As a result there is demonstrable weakening of the right ventricle that persist for several days after very strenuous exercise. This weakening is associated with markers of transient heart muscle damage, such as increase in levels of cardiac enzymes in the blood stream. For a well trained athlete, the weakening is only appreciable after extremely strenuous exercise. For example, the weakening is only slight after a marathon, though more marked after an ironman, and still detectable a week later. For recreational runners, the damage can be appreciable after a marathon. But perhaps the crucial observation is that the amount of weakening appears to depends on how thoroughly the runners prepared for the marathon. In a study of runners in the Boston marathon in 2004 and 2005, Neilan and colleagues found that appreciable weakening of the right ventricle in those who had done less than 35 miles per week in the preceding moths, but no appreciable weakening in those who had done more than 45 miles per week.

What might convert transient damage into long term damage? In general when body tissues suffer transient damage the repair process includes the construction of a temporary framework of collagen fibres. If there is repeated trauma before full recovery there is greater risk that the temporary fibrous framework will be become permanent. Although there is little direct evidence that this happens in the heart, perhaps the most plausible explanation for the fibrosis observed in the heart muscle of endurance athletes is repeated trauma without opportunity for adequate recovery. Overall the evidence suggests simply that moderate exercise is beneficial for virtually everybody, but if you want to do a lot of exercise you need to build up gradually to avoid over-stressing the body.  Furthermore, it is plausible that demanding training or racing while incompletely recovered from previous strenuous training or racing creates an especially high risk of converting transient damage into long term fibrosis that might act as a precipitant of disturbance of heart rhythm.


Moderate exercise has major health benefits for virtually every one, but a large volume of endurance training diminishes the benefit for some individuals. There is no evidence indicating a fixed upper limit on the amount of exercise that is healthy.   On the other hand, the evidence suggests, but does not prove, that the risks of extensive training are likely to be low if you if you increase training load gradually and avoid demanding training or racing when inadequately recovered.

It is probably no coincidence that what appears to be the safest strategy for avoiding long term damage is similar to the widely accepted recommendation for training to improve performance: increase training load gradually and recover well after strenuous training or racing.

Hyper and hypokalaemia in athletes

June 8, 2014

Potassium ions are of key importance for health and for athletic performance. The level of potassium in the blood must be regulated within fairly narrow limits: at concentrations above 12 mM there is a very high risk of sudden cardiac arrest*.  Steady state levels above 6.5 mM are considered dangerous in clinical practice, while levels below 3.5 mM are associated with slow repolarization of heart muscle and risk of various disturbances of cardiac rhythm, and also with risk of additional serious disorders such as high blood pressure and stroke (reviewed by Sica and colleagues). Low blood levels are also associated with fatigue of skeletal muscles, but so too is the loss of the normal gradient of potassium ions across muscle cell membranes that arises when potassium moves out of muscle cells into the extracelular fluid.

*[As summarised in the discussion with Michael below, the highest published potassium level in  a person who subsequently survived is 14 mM (possibly arising from muscle damage sustained during cardiac resuscitation.)  However survival after potassium exceeds 10 mM is very rare. ]

Potassium is lost from the body via the kidneys and in sweat. But more important than the maintenance of total body levels is the distribution between the inside of cells and the extra-cellular fluids (including blood plasma). While typical concentration outside of cells is around 4.5 mM, the concentration inside nerve and muscle cells is in the vicinity of 150 mM. About 98% of the body’s potassium is contained within cells. This gradient in ion concentration across the cell membrane is essential for conduction of neural impulses and for muscular contraction. Normal neural conduction and muscle contraction entail flow of potassium though ion channels in the cell membrane, thereby depleting intracellular levels and causing extracellular concentration to rise appreciably. This reduction in the gradient across the membrane contributes to fatigue. Extracellular levels of potassium are regulated by the renin-angiotensin-aldosterone hormonal system, which promotes potassium loss when levels are high.   Thus, higher extra-cellular levels promote potassium loss for the body. Molecular pumps that move potassium (K+) ions back into calls in exchange for sodium (Na+ ) ions minimise loss of potassium form cells during exercise and reducing fatigue, but continue to pump after exercise stops, resulting in a net fall of potassium below the pre-exercise levels.

The first concern of the athlete the development of effective Na/K pumping, and the second concern is ensuring that dietary intake is adequate so that total body store is not depleted. In long endurance races and even more catastrophic issue arises: damage to muscle cells during prolonged exercise can release potassium together with protein myoglobin, which damages the kidneys, and can result in potassium rising to dangerous levels. This is one of the causes of the rare sudden deaths that occur in the late stages of a marathon.   Thus, it is worthwhile understanding how training can promote effective Na/K pumping and the role of both electrolyte replacement and diet in maintaining the appropriate total body level of potassium.


The role of potassium in skeletal muscle contraction

The contraction of skeletal muscles is elicited by a rapid influx of Na+ and an equivalent efflux of K+ ions across cell membranes.  Skeletal muscles contain the largest pool of K+ in the body. During intense exercise, the Na/K-pumps cannot readily return K+ into the muscle cells. Therefore, the working muscles undergo a net loss of K+, while the K+ concentration in the arterial blood plasma can double in less than 1 minute. Even larger increases in K+ in interstitial tissues surrounding the muscle cells. This results in degradation in the electrical potential gradient across membranes, thereby resulting in loss of excitability and force. During continuous stimulation of isolated muscles, there is a strong correlation between the rise in extracellular K+ and the rate of force decline. These events present a major challenge for the Na/K-pumps.   Excitation of the muscle itself, together with the stimulating effects of adrenaline and insulin, increases the Na/K-pumping rate. If all available pumps are engaged, the rate of pumping can increase up to 20-fold above the resting transport rate within 10 seconds. Thus in working muscles, the Na/K-pumps play a dynamic regulatory role in the maintenance of excitability and force. Down-regulation of pump capacity reduces contractile endurance in isolated muscles. The Na/K-pump capacity is a limiting factor for contractile force and endurance, especially when their capacity is reduced as a result of de-training.

The pumping capacity of Na/K-pumps is influenced by hormones, such as thyroid hormone, adrenal steroids including cortisol, insulin, and by fasting and potassium-deficiency (as reviewed by Torben Clausen from University of Aarhus in Denmark). Thus, an adequate intake of dietary potassium is important. Good sources are leafy greens, dried apricots, yoghurt, salmon, mushrooms, and bananas. Perhaps even more importantly, physical inactivity degrades pumping capacity while training enhances it. High intensity interval training is especially effective in enhancing Na/K pump capacity. For example, Bangsbo and colleagues form Copenhagen reported that six to twelve 30-s sprint runs 3-4 times/week for 9 weeks produced a 68% increase in Na/K-pump units (p<0,05) and a significant reduction of blood plasma K+ level, compared with observations in a control group who continued with endurance training (approximately 55 km/Km). The intense sprint training was associated with significant improvement in performance. In those doing the intense sprints, 3-km time was reduced by 18 seconds from 10 min 24 sec to 10 min 6sec while 10-km time improved from 37 min18 sec to 36 min18 sec.


The effect of potassium on the heart

Unlike the situation in skeletal muscle, under normal circumstances, in the heart the rise in intracellular Na+ concretion associated with activation of the muscle activate the Na/K pump adequately to completely compensate for the increased K+ release (evidence reviewed by Sejersted).  Thus, whereas the K+ shifts during intense exercise can contribute substantially to fatigue in skeletal muscle in the heart, the K(+) balance is normally controlled much more effectively. This might not be the case during abnormal circumstances such as ischemia.

If there is serious elevation of blood levels of potassium due to muscle damage (see the section on rhabdomyolysis below) or due to dietary excess in the presence of a disorder of the renin-angiotension –aldosterone mechanism that normally regulates potassium, there is a risk of serious reduction of the electrical gradient across the heart muscle membrane essential for conduction of the excitation signal thought the heart muscle. The consequence can be cardiac arrest, which is usually fatal.

Conversely, when blood levels of potassium are low, due to serious loss and failure of dietary replacement, the re-establishment of the electrical gradient is slower. This delayed re-polarization is, manifest as an increase in the interval between the Q wave and the T wave in the electro cardiogram. The delayed re-polarization can lead to rhythm disturbances due to alteration of the conduction pathways. The most serious of these is the rare but potentially fatal rhythm disturbance known as Torsade de Pointes. However, because of the normally tight regulation of sodium and potassium ion level by the renin-angiotensin aldosterone system, this is very unlikely in otherwise healthy individuals.


Regulation of potassium levels by the renin-angiotensin-aldosterone system

Renin is an enzyme secreted by the kidneys that acts on a substance called angiotensinogen that is produced in the liver. Renin splits angiotensinogen releasing the peptide angiotensin, which has various actions in the body directed towards retaining sodium, conserving blood volume and maintaining blood pressure. One of the important actions of angiotensin is stimulation of release of the steroid hormone, aldosterone, from the adrenal glands. Aldosterone acts on the kidney to promote retention of sodium and excretion of potassium. During exercise, aldosterone production is increased, thereby decreasing urine production and conserving fluid volume, while promoting excretion of potassium. This helps reduce the accumulation of potassium in blood due to efflux from active skeletal muscle, but contributes to the fall in potassium levels after exercise ceases. Maintenance of blood volume by moderate fluid intake is likely to minimise excessive engagement of the renin-angiotensin-aldosterone system.

On one occasion when I made an overly ambitious attempt to find a novel route across a mountain ridge for my return journey during a long run in the Sierra Nevada in southern Spain on a hot dry day with an inadequate supply of water, I became quite dehydrated. I was somewhat alarmed to experience an increase in ectopic heart beats. I suspect that the dehydration had led to excessive activity of the renin-angiotensin-aldosterone system, depletion of potassium and consequent disturbance of heart rhythm. I am now much more careful about hydration during long runs.

For runs greater than 20 Km, I generally prepare a drink containing 4 tablespoons of sugar and one quarter of a teaspoon of salt in four cups of water, together with lemon juice to make it palatable. I do not add any potassium salts to this mixture, as any added potassium might promote excessive activation of the renin-angiotensin-aldosterone system, thereby defeating the purpose. I adjust rate of intake to keep just ahead of appreciable thirst. Typically I find that consuming a mouthful of this drink per Km keeps me adequately hydrated.



Rhabdomyolysis is a condition produced by the breakdown of muscle, resulting in the release of the protein myoglobin, along with potassium in to the blood stream. The myoglobin damages the kidney with multiple adverse consequences including failure of potassium excretion.   In extreme cases the increase in blood potassium can produce fatal cardiac arrest.   In slightly less extreme cases, the kidney failure is nonetheless a serious medical emergency. Severe rhabdomyolysis arises rarely as a result of the muscle damage sustained during endurance events. However, some evidence indicates that mild degrees are not uncommon in males. For example a study by Maxwell and Bloor that tested for evidence of muscle damage after a 14 mile run at 8 min/mile pace in three groups of well-conditioned male athletes who had undergone training regimes differing in volume of running for a period of one months, found that the 14 mile run produced evidence of substantial muscle damage, including increases in serum myoglobin ranging from of 52-405%. The increases were most marked in those who had trained less for 8 miles/day on alternate days. Rhabdomyolysis is much less in females, possible because oestrogen stabilises muscle membranes.

 It should also be noted that exercise induced rhabdomyolysis does not always lead to increased levels of potassium. In a series cases of exercise indices rhabdomyolysis reported by Sinert and colleagues there were no cases of hyperkalaemia.



Efficient regulation of potassium is essential for both good athletic performance and for health. One key issue for endurance athletes is maintaining the capacity of the Na/K-pumps that return potassium excreted by muscle cells as result of muscular activation back into the muscle cells. Inadequate pumping results in fatigue. Training, especially high intensity interval training, enhances the activity of the Na/K pumps. Potassium is lost from the body during exercise and dietary replacement of potassium is necessary though this is not generally an issue provide diet is reasonably well balanced.   However, sustained potassium depletion has adverse effects including heart rhythm disturbances, increased blood pressure and risk of stroke.

The renin-angiotensin-aldosterone system acts to maintain fluid volume during exercise, but promotes potassium loss. It is important to avoid serious dehydration to minimise the risk of excessive activation of the renin-angiotensin-aldosterone system.

In rare instances, muscle damage during endurance events results in life-threatening rhabdomyolysis. This can lead to a dangerous excess of potassium in the blood.  More common is moderate muscle damage that leads to accumulation of myoglobin.  However, training reduces this risk.

Minimising the risks: chronic inflammation

May 24, 2014

In my recent post I summarised the evidence indicating that running, at least in amounts up to 50 minutes of vigorous activity per day, is likely to increase your life expectancy, but nonetheless some endurance runners suffer serious ill-health attributable at least in part to their running. There is unequivocal evidence indicating transient heart muscle damage after endurance event such as a marathon; and unequivocal evidence that endurance athletes are at increased long-term risk of heart rhythm disturbance, such as atrial fibrillation. There is quite strong evidence that many years of marathon training increases the risk of fibrosis of the heart muscle and calcification of the coronary arteries. While the beneficial effects appears to outweigh the adverse effects for the majority, at least some endurance athletes suffer serious adverse effects. On the other hand, the evidence that the benefits appear to outweigh the adverse effects in the majority suggests that is sensible to try to identify what causes the serious adverse effects and take steps to minimise them, thereby increasing the likelihood of being among those who derive more benefit than harm.

Although the mechanisms of cardiac damage are not well established, there is a great deal of evidence regarding plausible mechanisms. We are not detached observers who can afford the luxury of waiting until the mechanisms are established beyond doubt, like climate change deniers who prefer to wait until the outcome is certain before acting. Rather, we are each an experiment of one, and we must make our decision for action or inaction based on the current evidence.

Inflammation and myocardial fibrosis

Perhaps the most plausible mechanism for adverse cardiac effects is a mechanism based on inflammation. Prolonged mechanical stress on heart muscle produces damage, which in turn elicits an increase in cytokines, the chemical messengers that circulate in the blood and trigger the events of inflammation which lead to laying down of fibrous tissue. This is the body’s mechanism for repairing damage and increasing the strength of tissues. But the initial deposition of fibrous tissue is slap-dash and unless redundant fibres are removed, the future function of the relevant body tissue is likely to be impaired. In the long term calcium is deposited at the site of damage, making the tissues stiff and inflexible.

In the case of tissues such as the plantar fascia, the misaligned fibres cause the pain of plantar fasciitis and the deposited calcium gives rise to the heel spurs visible on x-ray. In the case of the heart muscle, misplaced fibrous tissue has the potential to interfere with the electrical conduction pathways producing disturbance of rhythm. In the case of the lining of blood vessels such as the coronary arteries, the process is a bit more complex. The accumulation of cholesterol at the sites of damage to the lining of the artery plays a key role in triggering the inflammatory response. The Wellcome Trust have produced an excellent video depicting the sequence of events.

Minimising the risks

From what we understand of the mechanism, there are three key things we can do to minimise the risk of damage:

1)      Allow adequate recovery after heavy training and racing. Studies in animals and humans demonstrate that much of the fibrosis, though perhaps not all, resolves during an adequate recovery period.

2)      Build up training gradually. The tissue trauma that initiates the inflammatory process is less if the tissues have been strengthened by gradual adaptation. This is illustrated by the fact that DOMS is more marked if you suddenly increase training volume.

3)      Consume a diet that minimises chronic inflammation. Current evidence indicates that a Mediterranean diet, in which the pro-inflammatory omega 6 fats prevalent in the Western diet are balanced by omega 3 fats from fish and/or nuts and green leafy vegetables, is a heart-healthy diet.


It is noteworthy that these three strategies not only have the potential to reduce the risk of serious long term adverse effects on the heart, but are also likely to maximises the long term improvement in running performance.

In future posts I will discuss the more complex issue of cortisol and also the exacerbation of rhythm disturbances by excess potassium that is released from damaged muscle cells

The big debates of the past decade: 5) Is running good for your health?

May 19, 2014

Is running good for your health? Once the answer seemed simple.  However, the sadly premature deaths of several charismatic advocates of endurance running, Jim Fixx, John (Hadd) Walsh and Caballero Blanco, have provided grounds for questioning the claim that a large volume of running is healthy.

The past decade has seen a vigorous debate driven by enthusiasts who claim that the evidence indicates that any more than about 2.5 hours of moderate intensity exercise per week is harmful.   The high priest preaching warnings about the risks is James O’Keefe, a cardiologist from Kansas City, who summarised his views in a review in the respected Mayo Clinic Proceedings and also popularised them in an evangelistic TED talk.   I have discussed O’Keefe’s views previously in a post in Jan 2013. Though I consider that he himself comes across as something of an evangelist, the evidence that he assembles does indeed confirm beyond reasonable doubt that endurance athletes are not immune from either coronary heart disease or from potentially fatal disturbances of cardiac rhythm.

My own belief is that the overall balance between health benefit and harm of running is inclined towards greater benefit than harm, at least up to upper limit of running done by the majority of recreational runners. I reviewed the evidence in my post in Jan 2013, and will not present the details again here. Instead, I will provide an update on the evidence that has been assembled since Jan 2013.

However, my main interest is not on the statistical evidence for or against harm, but rather on what research of the past decade has revealed about likely mechanisms by which running might be expected to cause harm, with the ultimate goal of developing strategies for minimising the risk of harm. Even if the balance of evidence suggests that running is of greater benefit than harm to health, the undeniable evidence that at least some runners do suffer harm suggests to me that the sensible approach is to take what steps we can to minimise the risk of unnecessary harm.

Life expectancy

The picture is moderately clear: life expectancy increases with increasing amount of exercise, but the rate of increase levels off at higher levels. For example, in the study by Wen and colleagues, the reduction in mortality rate (that is the number of deaths that occurred compared with the number expected during the follow-up period) was observed to increase with increasing amount of exercise, but levelled off at a mortality reduction of around 45%  for 50 minutes or more of vigorous exercise per day.   Although there was little evidence of an actual decrease in life expectancy with very large amounts of exercise, the number of individuals exercising at extreme levels is small, so it is difficult to draw statically robust conclusions.

Perhaps the most thought provoking evidence comes from the Copenhagen Heart Risk study, a longitudinal study of nearly 18000 people followed over a period of up to 35 years. As in other relevant studies, the main conclusion regarding the effects of exercise is that jogging reduces mortality. The age-adjusted increase in survival with jogging was 6.2 years in men and 5.6 years in women. However the investigators reported a U-shaped relationship, with best outcome in those who jogged less than 2.5 hours a week at a slow pace. But the numbers in the relevant groups were very small. In those reporting that they jogged slowly, there were 3 deaths in 178 people, whereas among the fast group there were 5 deaths among 201.   These numbers are too small to justify robust conclusions.

In contrast , a study of mortality in a cohort of 49 219 men and 24 403 women who participated in any of the Vasaloppet long-distance ski races in Sweden (90Km for men; 90 and 30Km for women) during 1989–1998,revealed substantially reduced standardised mortality rate (SMR) from all major causes of death including heart disease and cancer. Overall, 410 deaths occurred up to Dec 1999, compared with 851 expected, yielding an SMR of 0.48.   It is reasonable to assume that the majority of competitors in these races had undertaken extensive training.

More recently, a study by Dr Jodi Zilinki and colleagues at Massachusetts General Hospital, reported at this year’s American College of Cardiology meeting in Washington, found evidence of decreased cardiac risk factors following marathon training in 45 recreational runners aged 35-65 who had not achieved Boston Qualifying time for the 2013 event but had nonetheless obtained places to raise money for charity. Half had run at least three marathons in their lifetime. Prior to an 18 week training program, over half had at least one risk factor for heart disease, such as high cholesterol, high blood pressure or a family history of heart disease. During training, potentially harmful low density lipoprotein (LDL) cholesterol decreased by 5% while triglycerides decreased by 15%. Thus for the majority of recreational runners, it appears that marathon training is likely to be good for their health

Specific cardiovascular risks


With regard to cardiovascular risks, the most compelling evidence indicates increased risk of disturbance of heart rhythm, such as atrial fibrillation, in middle-aged male endurance athletes. This is revealed by many studies (which I reviewed in a post in Jan 2012), though the question of whether or not this results in greater mortality is not clearly established. It is possible that other health benefits of running might outweigh the risks associated with arrhythmia. For example, the reduced blood pressure, lower levels of harmful low density lipoprotein cholesterol associated with endurance training would be expected to confer protection.

Coronary artery disease

Perhaps the most worrying issue is the possibility of increased coronary artery disease.   There have been a many of reports of clogged coronary arteries revealed by coronary angiography in endurance athletes. The most substantial of these was a study of 50 men who had competed in the Twin Cities (Minneapolis-St Paul) Marathon for twenty five consecutive years. The proportion of individuals with atheroma was similar in the two groups (atheroma in 60% on marathon runners, and 52% percent of controls), while the extent of the atheroma was significantly greater in the runners. This finding was initially reported at the American College of Cardiology meeting in Atlanta, Georgia in 2010. However, only an abstract was published at that time.

The definitive publication by Robert Schwartz and colleagues appeared in 2014 in a relatively obscure journal, Missouri Medicine. The list of co-authors includes James O’Keefe, who is an Editorial Board Member of Missouri Medicine Preventive Medicine.  I mention the details about publication because when a paper as potentially important as this appears belatedly in a relatively low profile journal, the first question that occurs to me is: why was this not published in a more authoritative journal.   Was it was rejected by other journals?

I am not a cardiologist, though I do frequently provide peer review of scientific and medical manuscripts submitted to high-profile journals. If I had been asked to review this manuscript, my greatest concern would have been for the procedure used to match runners and controls. In any study in which participants of interest are compared with a control group it is important that the two groups are matched on factors that might have an independent effect on outcome. For example, it is usually necessary to match for age, sex and social class. It is often desirable to match for other factors relevant to the condition of interest, such as family history of heart disease. However it is usually undesirable to match for factors that reflect the mechanism by which the ‘treatment’ (in this case, running multiple marathons) might achieve its benefit or harm. For example, because exercise tends to decrease the levels of harmful lipids in the blood, it might be misleading to match the groups on these variables. Such matching would be expected to produce a control group who happen to exhibit below-average risk of cardiovascular disease for incidental reasons related to their genes or environment.   But this is precisely what Schwartz and colleagues did. In effect, they determined the effect of marathon running after allowing for some of the anticipated benefits of marathon running.  Thus the statistical comparison of the two groups is biased and must be interpreted with extreme caution.

Nonetheless, whatever one makes of the statistical comparison, the number of marathon runners with atheroma in their coronary arteries and the extent of their atheroma was alarmingly high.  If I had been the referee reviewing this manuscript, I would have recommended publication subject to a critical discussion of the possible bias introduced by the matching procedure. I think it would be unwise to brush aside these findings simply because of some flaws in the science – there are very few medical studies that are totally free of all possible bias.  In evaluating medical evidence it is necessary to weigh up the whole picture, including the plausibility of the findings on the basis of what we know of human physiology.

Plausible mechanism for cardiovascular damage

I consider that there are at least three plausible mechanisms by which prolonged or intense endurance exercise might lead to cardiovascular damage. These are elevation of cortisol, chronic inflammation and acute release of potassium due to breakdown of muscle cell membranes.

Cortisol is a key hormone that mediates the body’s acute response to stress, but if elevation of cortisol is sustained, it damages most tissues of the body.   Skoluda and colleagues have presented evidence that endurance athletes tend to have sustained elevation of cortisol.

Inflammation is the process by which the body repairs itself following acute damage. It is probable that acute inflammation plays a central role in the repair and strengthening of the body after vigorous training. Thus, it is a key mediator of training effects. However inflammation that becomes chronic is harmful and probably plays a large part in the over-training syndrome. Furthermore, chronic inflammation promotes the formation of coronary atheroma.

The imbalance of concentration of potassium ions across cell membranes plays a central role in nerve conduction and muscle contraction, in both skeletal muscle and in the heart. Potassium concentration within cells is normally high while levels in extra-cellular tissues including blood are low. Damage to muscle cell membranes during vigorous exercise releases potassium into the extracellular tissues. The mechanism for pumping potassium back into muscle cells and also the action of the kidneys can normally cope with this tendency towards excess extra-cellular potassium. But under some rare circumstances, potassium can rise to high levels causing fatal cardiac arrest.

The important thing about all three of these mechanisms is that there are things we can adjust about our training and our lifestyle, including diet, that have the potential to ameliorate all of these risks. Thus, even though for most of us, the health risks of endurance training and racing are small and likely to be outweighed by the benefits, we can shift the balance even further in the direction of benefit by adjusting our training and lifestyle. In future posts I will present my conclusions regarding the best strategies for achieving this.

The five big debates of the past 10 years

February 6, 2014

The past decade has seen a continued growth of distance running as a mass participation sport.   The major city marathons continue to attract many thousands of entrants with aspirations ranging from sub 2:30 to simply completing the distance in whatever time it takes.  Perhaps more dramatically, parkrun has grown from a local weekly gathering of a few club runners in south-west London to an event that attracts many tens of thousands of individuals at hundreds of local parks, not only in the UK but world-wide, on Saturday mornings to run 5Km in times ranging from 15 min to 45 min before getting on with their usual weekend activities. Over this same period, the ubiquity of internet communication has allowed the exchange of ideas about running in a manner unimaginable in the days when distance running was a minority sport pursued by small numbers of wiry, tough-minded individuals whose main access to training lore was word- of-mouth communication.

Not surprisingly, within this hugely expanded and diverse but inter-connected community there have been lively debates about many aspects of running, with diverse gurus proposing answers to the challenges of avoiding injury and getting fit enough to achieve one’s goals.   Pendulums have swung wildly between extremes.  My impression is that the fire in most of the debates has lost much of its heat as the claims of gurus have been scrutinised in the light of evidence.   However, definitive answers have remained elusive.   What have we learned that us useful from this turbulent ten years?

There have been 5 major topics of debate:

1) Does running style matter and if so, is there a style that minimises risk of injury while maximising efficiency?

2) Are minimalist running shoes preferable to the heavily engineered shoes promoted by the major companies?

3) What is the optimal balance between high volume and high intensity training in producing fitness for distance running?

4) Is a paleo-diet preferable to a high carbohydrate diet?

5) Does a large amount of distance running actually damage health, and in particular, does it increase the risk of heart disease.

In all five topics, debate still simmers.  I have scrutinised the scientific evidence related to all five of these question in my blog over the past seven years, and I hope I will still be examining interesting fresh evidence for many years to come.   However whatever answers might emerge from future science, in our quest to determine the answers that will help us reach out running goals we are each an experiment of one and now is the point in time when we must act. I think that the evidence that has emerged in the past decade has allowed me to make better-informed choices in all five of these areas of debate than would have been possible ten years ago.   In my next few posts, I will summarise what I consider to be the clear conclusions for the past decade of debate, what issue remain uncertain, and what decisions I have made with regard to my own training and racing.

For me personally, the greatest challenge as I approach my eighth decade is minimising the rate of inexorable deterioration of muscle power, cardiac output and neuro-muscular coordination that age brings.  Therefore my approach to these debates is coloured by the added complications of aging.  Nonetheless, my goal is not only to continue to run for as many  years as possible, but also to perform at the highest level my aging body will allow during these years.  I hope that the conclusions I have reached will be of interest to any runner aiming in to achieve their best possible performance, whatever their age.

Micah True and cardiac risks: what might mountaineers tell us about balancing risks and safety?

May 30, 2012

Ed Reyna, an 81 year old distance runner from California, recently sent me a very interesting article from the New York Times about Micah True, the American runner who had been inspired by the Tarahumara people of the Copper Canyon region in Mexico.  He had turned away from the soul-destroying pressure of contemporary Western society and become a champion of the traditional simple life-style of the Tarahumara, and their legendary long distance running.

Micah True had in turn become an inspiration for thousands when Chris McDougall gave him a central role in Born to Run.  I have not yet made time to read Born to Run, mainly because I have not found the time to read any book for many years, but also in part, it is because I am naturally sceptical about gurus.  On the basis of the way he presents himself in the video interviews I have seen, I am sceptical of McDougall’s writings.  I am sure he believes his message about the virtue of minimalist running, but True’s own account suggests that McDougal dramatised the story of the Tarahumara (or Raramuri – ‘the light footed ones’, as they call themselves) and of Micah True (or Caballo Blanco, as he was happy to call himself), for the sake of producing a popular book   However, whatever one might make of the authenticity of Chris McDougall’s writing, or indeed of True’s own somewhat idiosyncratic character, I think there is little doubt about the authenticity of True’s sincere belief in the spiritual richness of running, and the shallowness of modern materialism.

The NY Times article described the search for True’s body after he went missing while running in the Gila wilderness of New Mexico in March.  In a manner that I suspect True might have appreciated, his body was found by three friends who became frustrated by the orthodox procedures of the official search, and headed off late in the afternoon along the course of a stream that ran though a rugged and remote canyon, on the basis of a hunch that True would have been likely to have chosen such a route.   They found him lying with his feet in the stream and several superficial scratches and bruises suggesting that he might have suffered an injury and then died of exposure to the night-time chill.  However, the autopsy concluded that he died as a result of cardiomyopathy.

The autopsy

The autopsy report by the Chief Medical Investigator from University of New Mexico Health Sciences Centre describes the superficial scratches and bruises, but there was no evidence of substantial external trauma.  I was intrigued also to read of the congenital deformation of True’s toes.  The second and third toe had a flexion deformity and the third lay over the fourth.  I know that deformity well because I have it myself.  I was intrigued because of the light it throws on my favourite anecdote about True.    Apparently one day when he was running along a dusty road in an old pair of trainers he came face to face with a van load of paparazzi.  Noting the contrast between the imagined huarache-shod high priest of minimalist running evoked by Chris McDougall, and the real-life True shod in tatty trainers, the response of the paparazzi was “Look, he’s wearing shoes. What a phoney”.    Although I understand that that he did often run in sandals, in my imagination, tatty old trainers suit True perfectly.  He used to joke that women would faint if they saw his ugly feet.  More pragmatically, I think it is very likely that the flexion deformity of his toes was associated with downward protruding metatarsal heads, and he almost certainly found it more comfortable to have a moderate amount of padding beneath them.

However, the serious part of the autopsy was the description of the heart.  It was described as large and globular.  The wall of the left ventricle was 15 mm thick at a point halfway from apex to base.  Apart from some mild atherosclerosis partially obstructing several blood vessels, there was no other evidence of disease that might have accounted for an enlarged heart.  Not surprisingly, the Chief Medical Investigator concluded death was due to idiopathic  cardiomyopathy– meaning pathology of the heart muscle arising from no  obvious cause.  In particular, there was no appreciable fibrosis of the heart muscle, as would be expected if True had suffered from ischaemic heart disease in the past.

Was the cardiomyopathy idiopathic?

However, the term idiopathic might not be strictly accurate.  There is a very obvious reason why True should have had a large heart with thick ventricular walls.   A runner’s heart experiences both volume loading and pressure loading.  The 4 to 6 fold increase in cardiac output during running relative to rest ensures that a large volume of blood is returned to the heart at the end of each contraction.  The large volume of blood stretches the heart muscle, creating an eccentric load which causes it to contract more forcefully, and leading to the adaptive formation of new sacromeres (contractile elements) in series with the existing sarcomeres.  Thus the diameter of the heart grows larger.  In addition, the more forceful contraction creates a larger pulse pressure so the heart muscle contracts against a heavier resistance.  This subsequent concentric loading causes adaptive hypertrophy in which fibres are added in parallel with the existing sarcomeres.  This thickens the wall of the ventricles.    The overall result is a large heart with think ventricular walls, that pumps more powerfully and more efficiently.   But this raises two questions concerning True’s heart

Might the degree of cardiac hypertrophy recorded at the autopsy be accounted for by True’s extensive running?  The Medical Investigator reported that the thickness of the ventricular walls was 15 mm.  The average value in the male population is approximately 10mm.  It is conventionally regarded that 13 mm is the limit that distinguishes the normal range from cardiomyopathy.    Perhaps the most definitive study of ventricular wall thickness in athletes is the study of 947 elite athletes from various sports, published by Pelliccia and colleagues in the New England Journal of Medicine in 1991.    While the majority of the athletes had a wall thickness less than 13 mm, wall thicknesses greater than or equal to 13 mm were identified in 16 of the 947 athletes (1.7 percent), and the thickest was 16 mm.    Fifteen of the 16 were rowers or canoeists, and 1 was a cyclist.  Pelliccia included runners along with jumpers in the category of track athletes, and this group had a wall thickness that was on average 1.5 mm less than the rowers.  Part of this difference might be accounted for by the fact that  96% of the rowers were male whereas only 75% of the track athletes were male.  Perhaps even more importantly, the largest sub-group among the track athletes were sprinters, while only 12% were distance runners (covering a range of events from 3000m to marathon).  Almost certainly there were very few marathon runners, so the data for track athletes tells us little about long distance runners.  With regard to cardiac loading during training, long distance runners are probably more similar to cyclists than to sprinters.  The average wall thickness in cyclists was approximately midway between that of track athletes and rowers.

Granted that True ran for exceptionally long periods of time (up to 6 hours, often in arduous circumstances) I think it is quite likely that running was a major factor contributing to the thickness of the wall of his left ventricle, though of course, factors such as the genetic predisposition of his heart muscle to respond to training, and other aspects of his life-style including nutrition, probably contributed as well.   In their study of elite athletes, Pellicia and colleagues noted that all athletes with wall thickness greater than or equal to 13 mm also had enlarged left ventricular end-diastolic cavities.  Thus, if we accept that running probably contributed to the thickening of True’s ventricular wall, it is also probable that running contributed to the large diameter of True’s heart.

How might enlargement of the heart cause death?

But even if we accept that running made a substantial contribution to the enlargement of his heart, we are left with the question of whether or not it contributed to his death.  In an athlete’s large heart, the thickened walls are usually also well supplied with capillaries, and in most respects, the enlarged heart is strong and healthy. The absence of appreciable fibrosis suggests that his coronary arteries and capillaries provided this enlarged heart with an adequate supply of oxygen.  However,   we are left with the teasing question of the likelihood that an athlete’s enlarged heart will suffer rhythm disturbances, especially disturbance arising in the ventricles that might precipitate fatal ventricular fibrillation.  As reviewed in several of my previous posts, there us abundant evidence that many years of high volume training does produce a high rate of rhythm disturbances, mainly arising in the atrium, but a minority arising in the ventricles.  It is probable that the remodelling that occurs as the heart enlarges alters the electrical conduction pathways.

However, despite the evidence for frequent rhythm disturbances in athletes with a long history of high volume training, there is very little evidence to suggest that this leads to a higher overall mortality.  In my opinion, the balance of evidence suggest that the benefits of a strong heart outweigh any risk of rhythm disturbance under most circumstances.  But are there identifiable circumstances where the risk of rhythm disturbances outweighs the protection afforded by a strong heart?

Various nutritional and biochemical disturbances, such as elevated levels of calcium and potassium or low magnesium can increase the risk of rhythm disturbances.  Similarly decreased oxygen supply increases the risk. In a review of the literature, published in Sports Health: A Multidisciplinary Approach in  2010 (vol. 2 pp 301-306) Day and Thompson found a substantial body of evidence indicating that transient biochemical and functional abnormalities of the heart occur commonly following completion of a marathon.  There can be regions of transient ischaemia.  It is well established that the level of cardiac enzyme, toponin, in the blood stream is elevated for many days after a marathon.  While there is little reason to assume that this will lead to permanent damage to the heart, it is probable that this represents local cardiac tissue damage that might indeed be part of the stimulus to adaptive hypertrophy, but nonetheless, creates a period of vulnerability after a very long run.   Much of the evidence indicates that even well trained athletes can suffer such disturbances.

According to Chris McDougall, True had done a six hour run the day before he died.  I am very cautious about attaching much weight to such anecdotes and accept that the Medical Examiner’s  conclusion that the cause of death was ‘idiopathic  cardiomyopathy’  was a prudent conclusion in the absence of more detailed evidence.  Nonetheless, while I wish to avoid jumping to any strong conclusions about the cause of True’s death, I think that many of the features of the sad event  provide a salutary reminder of the accumulating evidence that a long history of high volume training does create a risk.  Overall this risk is largely offset by the benefits of a strong heart.   On the other hand, there are identifiable circumstances when the risk of rhythm disturbance is probably higher.  I believe it is worthwhile to try to understand these circumstances, and to develop practical procedures for monitoring cardiac stress level.

The ethics and aesthetics of mountaineering

This creates an interesting challenge that I believe that True’s life and death brings into focus.  Do we destroy the spirit of running if we make it too technical?  Years ago I was a climber – both a rock climber and also an alpine mountaineer.  When I first started climbing, we tied onto the rope with a loop around the waist secured with a bowline knot.    Some climbers used devices such as pitons or even bolts hammered into the rock face, but in my mind, there was one over-riding ethical principle in climbing and that was to leave the rock-face or mountain in a condition as near as possible to the condition in which you found it.  I was much happier with an odd collection of metal chocks and nuts threaded on wire or cord loops, that could be jammed in cracks or hung around projecting rock to provide the belay points that provide protection in case of a fall.  On snow and ice, I carried an ice axe with a stout wooden shaft.

Around 40 years ago, there was a revolution in climbing gear.  Ropes, karabiners, ice axes and much other gear became high tech items incorporating the latest developments in materials science and mechanical design.   It seemed to me that provided one was using the gear purely for safety and that one respected the principle of leaving the mountain as you found it, it was simply sensible to take advantage of the high technology.

However there was much debate in the climbing community, and a decade or so later the concept of minimalist free climbing became popular.  I remember watching spell-bound as an athletic young man moved freely, unencumbered by any gear apart from a thin pair of shorts, lightweight boots, and a pouch of resin at his waist, up and across the face of the Cow and Calf Rocks one sunny afternoon on Ilkley Moor in Yorkshire.  The sheer athleticism was a delight to the eyes.  Nonetheless, despite the fact that the Rocks are not all that high, the risk was also appreciable.  I did contemplate wryly the ethics of the resin, which the young man used to enhance the grip of his fingers on tiny nooks and crannies, and which in turn left horrible white smudges on the rock, but this was a small peccadillo in an awe inspiring display of physical and mental technique, strength and agility.   However, for the remainder of my climbing days, I continued to be happy to lug a sac of alloy chocks, synthetic tape slings and high tech karabiners with me when I went into the mountains. As long as I left a minimal mark on the mountains, I was quite content to tip the balance between risk and safety in the direction of safety.  In fact, developing the skills to maximise safety on rock or ice, and navigation skills in the wilderness, was an important part of my enjoyment of mountaineering.

What might runners learn from mountaineers?

In long distance running, the risk is less overt than in mountaineering, but the evidence indicates that the risk is real.  In most cases, the risk is small and is outweighed by the health benefits.  But just as the rock-climber faces a spectrum of choice between the simplicity of unencumbered free climbing to elaborate protection afforded by high tech gear, the long distance runner must find his/her niche along the spectrum that extends for the simplicity of the Raramuri in their huarachi’s, to high tech shoes and gadgets such as a heart rate monitor.  True was pragmatic enough to wear shoes – ranging from tatty trainers to highly commercialised ‘pseudo-minimalist’ shoes produced by Hi-Tec and Vibram, but I doubt that he ever wore a heart rate monitor.   I have experimented less with high technology shoes than True, but in my own philosophy of running, a heart rate monitor fills a niche not unlike that filled by alloy chocks, synthetic slings and high tech karabiners in a climber’s kit.

In general, I am eager to explore any technology that might help me to run with minimal risk to health.  On the other hand, I am very dubious about technology whose purpose is to enhance performance, and I am equally sceptical of the commercialization of minimalism.   I am amused rather than dismayed by Nike’s slick promotional video of its troupe of elite athletes running nude through the wilderness in an imaginative re-creation of South Dakota’s Bear Butte National Park.  It appears to me to be a clever ruse to reinforce the notion than running in Nike Frees captures the essence of running naturally.  I am even more sceptical of Nike’s Oregon project, which goes to the opposite extreme.   Nike’s elite athletes eat and sleep in buildings with reduced air pressure to mimic the effects of living at high altitude, while training at sea level.

The mechanism of healthy adaptation and of damage

Central to the emerging scientific understanding of the benefits and risks of training is the proposal that inflammation plays a crucial role in the short term beneficial adaptations to training, but that chronic inflammation might indeed be responsible not only for the generalised bodily and mental malfunction known as the over-training syndrome, but also might contribute to focal problems in lungs and heart.   The role of exercise as a trigger of asthma is well known.  However, the majority of recent studies suggest that regular mild to moderate exercise is has a beneficial effect on lung function.  Nonetheless, the possibility that very prolonged aerobic exercise might play a causal role in asthma has not been excluded.   Similarly, there is no doubt that regular mild to moderate exercise is beneficial for the heart, but, as discussed  above, the evidence indicates that beneficial adaptations can turn risk after prolonged arduous exercise, at least in some circumstances.

There is an emerging body of evidence regarding the various complex molecular signalling processes in the body that might mediate adaptive acute inflammation and also  mal-adaptive chronic inflammation.   Current understanding provides only tentative pointers towards the best way of minimising risk – but at the current state of knowledge, it appears that the most informative things to measure are heart rate and rhythm.

 What is worth measuring?

As an elderly runner with both functional and structural evidence of a heart that is strong but also large, I use a heart rate monitor with the capability to measure R-R intervals  to monitor several aspects of the electrical activity of my heart.  I keep an eye on the frequency of missed beats (which are likely to be ventricular ectopics that failed to generate the sharp R wave that the monitor is designed to detect).   I have abundant evidence that recordings made using my HRM during exercise are fairly unreliable, and I would not base any firm diagnosis on the information the device provides.  However, I consider that I understand its vagaries well enough to use it as a screen for possible problems.  Fortunately I only experience missed beats very rarely, but if these increase in frequency, I will seek an expert medical opinion.  The other aspects of cardiac function that I monitor with my HRM are intended to provide an estimate of the day to day stress on my heart.    I record resting rate and heart rate variability (HRV) regularly and in addition perform an orthostatic test on the days following exceptionally heavy training.  I record heart rate during the cool down after almost all training sessions, and have found that the stable value reached after a few minutes of the cool-down is a quite reliable guide to the amount of stress experienced during the session.

There is of course no way of entirely abolishing the risks of any activity we undertake.   I strongly believe that running generally increases the likelihood of both a higher quality and a longer life.  But I continue to try to increase my understanding of the circumstances that exacerbate the risk and also of the best way to minimize the risk.

The athlete’s heart

January 1, 2012

The human heart is an enigma, and the athlete’s heart especially so. It is no accident that the heart is the body part that acts as the final defender keeping mortality at bay while serving as the icon for our aspirations and passions.  It is no accident because this mundane but crucial pump beats autonomously, but is also modulated by subtle, ethereal influences.  It is governed by the non-conscious autonomic nervous system – the exciting sympathetic division often dominating in the duel with the soothing parasympathetic division – and also by a multitude of hormones: adrenaline and the adrenal steroids; insulin and growth hormone; and also the sex steroids, oestrogen and testosterone, which might explain the greater vulnerability of the male runner’s heart – a topic we shall return to later.   Oxytocin, the hormone released in response to human touch that fosters not only the bond between a mother and her infant but also the bonds between lovers, can reduce the inflammatory processes that appear to contribute to the over-training syndrome, and even prevent cell death in an injured heart – at least in rats[1].

Perhaps to the non-runner, the enigma is why runners are so devoted to their sport.  It is of course relatively easy to comprehend the mind of the elite athlete striving for Olympic glory, but a surprising passion is found  across the entire spectrum for those whose ambition is to run 10 Km in an hour to those aiming to run a half-marathon in that time.  In the internet era, running has become a major social event.  On web-sites such as Fetch Everyone, hundreds of runners not only record hundreds of thousands of training miles, diverse races and numerous hard-won PB’s,  but also engage in a wide range of chatter, most of it mutually supportive but sometimes it is bitchy and at other times ribald.   The austere amateur spirit that permeated athletics when it was largely the preserve a small group of dedicated, almost monastic, individuals in the 1950’s has given way to something of a carnival.  Though of course the ribald graffiti occasionally uncovered on medieval monastic cell walls suggest that monasticism has always been only a thin veil over seething passion.

John Hadd

But to runners the enigma of the heart is more profound.   Sadly, this was illustrated by the recent death of John ‘Hadd’ Walsh.  He was the founder and a guiding spirit of the Malta marathon in the 26 years since its inception, but by virtue of his generous spirit, thoughtful analysis of heart physiology, and pugnacious writing, his influence extended far beyond the island of Malta and shaped the training programs of runners worldwide.    He was devoted to his wife, the marathon runner, Carol Galea.   He was 8 years her senior, and declared that he would train with a dedication sufficient to ensure that he lived to be 108, so they would not be separated prematurely.  Tragically, his promise was not fulfilled as he died, apparently of a totally unanticipated heart attack, during an early morning run at age 56 [2].  Though a personal tragedy, his death, along with the occasional reports of other untimely deaths of athletes and coaches, might merely be taken as confirmation of the widespread acceptance that running does indeed place an immediate stress upon the heart, but overall, the health benefits of running far outweigh the risks [3].

However the picture is a little more complex.   While at least some premature cardiac deaths among athletes are due to previously unidentified congenital defects, or to unsuspected coronary artery disease in those who take up running in middle age, the challenging question is: does endurance training actually produce persisting damage to the heart?

Two of the greats

The evidence is extensive and controversial, but before dipping into the vast body of scientific evidence, it is illuminating to look at the cases of two other athletes.  The first, Wally Hayward, a legendary figure in the history of the Comrades Marathon, did almost make it to his hundredth birthday.    Hayward first won that gruelling hilly 90 Km ultra-marathon between Durban to Pietermaritzburg  in 1930 at age 21; he was the winner again on four occasions in the 1950’s; and became the oldest person to complete the race when he staggered across the finishing line at age 80 in 1989.    He died in 2006 a few months before his 98th birthday.   At age 70, at a stage when he had engaged in regular training for 52 years, he underwent extensive physiological testing [4]. A treadmill exercise test revealed no ischaemic ECG abnormalities and an excellent functional capacity (VO2max = 58.6 ml/kg/min).  His overall fitness was exceptional for a 70 year-old.  The only two abnormalities reported were frequent premature atrial contractions (PACs) and moderately increased thickness of the left ventricular wall.

The second case is that of Emil Zatopek, world record holder at 5000m and 10,000m in the 1950’s and winner of gold medals in the 5000 m, 10,000m and marathon in the Helsinki Olympics in 1952.   Unlike Wally Hayward, he retired from competitive running at age 35, after 17 years of training that had included a hitherto unheard of combination of intensity and volume.   He continued to be active in the Communist Party in his native Czechoslovakia, but due to his support for the democratic wing of the party during the Prague Spring in 1968, he was banished to work in a uranium mine.  At age 71, three years after his after his rehabilitation as a national hero by Vaclav Havel in 1990, he underwent extensive medical and physiological testing at the Institute of Sports Medicine in Prague [5].   Perhaps as a legacy of the privations of the uranium mine his muscles were flabby and he was a pale shadow of his former self, though it is noteworthy that his joints were remarkable free of the degenerative changes common in his age group.   Of particular interest in the current context, his heart showed some ischaemic changes and he had both atrial fibrillation and ectopic ventricular contractions.

Ventricular hypertrophy and PACs

General conclusions should not be drawn from anecdotes of exceptional athletes.  Nonetheless, the two abnormalities reported in Wally Hayward, hypertrophy of the muscular wall of the left ventricule and frequent premature atrial contractions are both well documented features of the elderly athlete’s heart.  For example, in a study comparing 11 elderly male athletes (mean age 73) with a life-long history of strenuous exercise with matched controls (mean age 74), Jensen-Urstad and colleagues [6] found that 9 of the 11 athletes had more than 100 premature atrial contractions in24 hours compared with 4 of the controls, while 8 of the athletes had multiform ventricular ectopics (indicating multiple maverick electrical sources in the ventricles) compared with 2 of the controls.

Of course ventricular hypertrophy in athletes is only to be expected.  It contributes to the powerful contraction of the well-trained heart.  Unlike the hypertrophy associated with pathological conditions in non-athletes, in which there is decreased blood supply to the heart muscle via myocardial capillaries,  the hypertrophy in athletes is usually accompanied by normal or increased capillary density [7].

Cardiac damage and remodelling

Nonetheless it is probable that the remodelling of cardiac muscle produced by endurance training involves some breakdown of muscle cells, similar to that which can readily be observed in skeletal muscle following intense training.  For example, following demanding endurance events, increased levels of the cardiac enzyme troponin are found in the blood stream, implying damage to heart muscle cells.  Immediately after the 2004 Otztal Radmarathon, troponin levels in the cyclists’ blood were increased 10 fold relative to baseline, and returned to baseline one week later [8].

In skeletal muscle, the muscle cells damaged by training are rebuilt stronger than before.  The persistence of collagen fibres that formed a scaffold during repair is of little importance provided the fibres become well aligned along the direction of pull of the muscle.  On the other hand, heart muscle is different.  Cardiac muscle performs not only physical work of contraction, but the muscle cells themselves from part of the conducting system that initiates and transmits the electrical signal that triggers contraction.   If the heart is to pump efficiently, this electrical signal must be transmitted across the myocardium from the sinoatrial node in the right atrium via the atrioventriclar node to the ventricles, in a well coordinated manner.  It is plausible that misplaced collagen fibres might upset the orderly transmission of the signal and perhaps even cause maverick muscle cells to take over the pace-maker role, generating ectopic beats.  As reported by Jensen-Urstad [6], premature atrial beats and also multiple maverick ventricular sources are substantially more frequent in elderly athletes than in age-matched non-athletes.

Atrial fibrillation

Premature atrial contractions are of little functional importance, but the crucial issue is whether they can lead to the chaotic ill-coordinated contraction that is atrial fibrillation.  In a large population-based study of men and women aged 55-75 in Denmark, Binici and colleagues found that a frequency of premature ectopic atrial contractions greater than 30 /hour, or runs of more than 20 consecutive atrial ectopic beats, was associated with an almost three fold increased risk of hospital admission for atrial fibrillation in the follow-up period of approximately 6 years [9].  There is also worrying evidence of a similar risk in endurance athletes.    The anecdotal account of Emil Zatopek’s atrial fibrillation is consistent with the findings of several large, well designed scientific studies.  For example in an 11 year follow-up study of 252 marathon runners, with mean age 39 at recruitment, the risk of symptomatic atrial fibrillation, based on an observed annual onset rate of 0.48 per 100,  was 8.8 times greater than in a comparison sample of 305 sedentary men, after adjusting or other risk factors such as high blood pressure [10].

Although far less serious than ventricular fibrillation (which is usually lethal) atrial fibrillation has some life-threatening consequences.  It predisposes to the formation of blood clots in the atrium which can subsequently be released into the blood stream, causing a myocardial infarction if they lodge in the coronary arêtes or a stroke if they lodge in the brain.   However, despite the quite compelling evidence for an increased incidence of atrial fibrillation in middle-aged and elderly runners, the balance of evidence does not indicate that the commonly observed heart rhythm abnormalities lead to an increase rate of serious adverse cardiovascular events in middle-aged athletes.   For example, in a 5 year follow-up of 117 middle-aged and elderly cross-country skiers, Lie and Erikssen [11] found that while persisting abnormalities of heart rhythm and also ventricular hypertrophy were common, only 2 developed angina and none suffered a myocardial infarction.  They concluded that the ECG abnormalities were mainly related to physiological adaptation to training and that training seems to protect against coronary heart disease.

Coronary obstruction

So far, we have focussed mainly on possible disturbances of heart rhythm.  In contrast, we have noted that capillary blood supply to the myocardium is often enhanced in athletes, and coronary disease might in fact be reduced.   However, perhaps the most disconcerting study of all is a recently reported investigation of calcified plaques furring-up the coronary blood vessels of elderly men who have participated in multiple marathons.  Schwartz and colleagues found that the prevalence of calcified plaques in the coronary arteries of men who had run in the Twin Cities Marathon annually for at least 25 years was almost twice as high as in age matched sedentary comparison subjects [12].  Enigmatically, the same research group carried out a similar study in female marathoners, with the opposite result: namely, the female runners had far fewer calcified plaques than the matched comparison subjects, though it is noteworthy that the female runners had run at least one marathon annually for only a period of 10 years.   The results of both of these studies should be treated with extreme caution until they have been replicated.  Despite the evidence that the male heart is generally more vulnerable to injury than the female heart, the diametrically opposite findings in the two sexes raise doubt about the generalizability of the findings.  Furthermore, it should be noted that the finding in males might reflect the consequences of running a larger number of marathons.

At least for the time being, the majority of the evidence suggests that despite the fairly high likelihood that long term endurance training will lead to an increased number of premature atrial contractions, the overall effect of endurance training is to increase life expectancy.    In future posts I will examine the evidence in greater detail, and also describe my discoveries about my own heart rhythm since acquiring a heart rate monitor that records the time intervals between consecutive beats.   More formal investigations have demonstrated that my heart is functioning well.  Nonetheless, in light of the growing evidence that elderly endurance athletes face a significant risk of atrial fibrillation, my current opinion is that monitoring heart rate beat by beat is indeed a sensible way of screening for possible increases in frequency of premature atrial contraction.  It would of course be foolish to make any definitive diagnosis based on one’s own observations using equipment that is demonstrably fallible.  It would be similarly foolish to curtail an activity that I enjoy passionately, when even the risk of atrial fibrillation is less daunting than the risk of a sedentary life style.


[1] Jankowski M, Bissonauth V, Gao L, Gangal M, Wang D, Danalache B, Wang Y, Stoyanova E, Cloutier G, Blaise G, Gutkowska J. 2010 Anti-inflammatory effect of oxytocin in rat myocardial infarction. Basic Res Cardiol. 105(2):205-18.

[2] Times of Malta, Saturday, September 17, 2011. Malta marathon founder dies  []

[3] Thompson PD, et al. (2007) Exercise and acute cardiovascular events placing the risks into perspective: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism and the Council on Clinical Cardiology. Circulation. 115(17):2358-68.

[4] Maud PJ, Pollock ML, Foster C, Anholm JD, Guten G, Al-Nouri M, Hellman C, Schmidt DH. (1981) Fifty years of training and competition in the marathon: Wally Hayward, age 70–a physiological profile. S Afr Med J. 31;59(5):153-7.

[5] Novotný V, Brandejský P, BaráckováM, Boudová L, Vilikus Z, Streda A, Novotný A.(1994) Medical and anthropological study of a world and Olympic champion, long-distance runner, 35 years after the end his racing career. Sbornik Lekarsky (Journal of Czech Physicians and the Czech Medical Society) 95(2):139-55.

[6] K Jensen-Urstad,F Bouvier,B Saltin,M Jensen-Urstad (1998) High prevalence of arrhythmias in elderly male athletes with a lifelong history of regular strenuous exercise.Heart 79:161–164

[7] Hudlicka O, Brown M, Egginton S. (1992) Angiogenesis in skeletal and cardiac muscle.  Physiol Rev. 72(2):369-417.

[8] Neumayr G, Pfister R, Mitterbauer G, Eibl G, Hoertnagl H. (2005) Effect of competitive marathon cycling on plasma N-terminal pro-brain natriuretic peptide and cardiac troponin T in healthy recreational cyclists. Am J Cardiol.;96(5):732-5.

[9]  Binici Z, Intzilakis T, Nielsen OW, Køber L, Sajadieh A. (2010) Excessive supraventricular ectopic activity and increased risk of atrial fibrillation and stroke. Circulation. 121(17):1904-11.

[10] Molina L, Mont L, Marrugat J, Berruezo A, Brugada J, Bruguera J, Rebato C, Elosua R. (2008)  Long-term endurance sport practice increases the incidence of lone atrial fibrillation in men: a follow-up study. Europace. 10(5):618-23.

[11] Lie H, Erikssen J. (1984)  Five-year follow-up of ECG aberrations, latent coronary heart disease and cardiopulmonary fitness in various age groups of Norwegian cross-country skiers. Acta Med Scand. 216(4):377-83.

[12] Schwartz JG, Merkel-Kraus S, Duval S, Harri K, Peichel G, Lesser JR, Knickelbine T, Flygenring B, Longe TR, Pastorius C, Roberts WR, Oesterle SC, Schwartz RS (2010) Does long term endurance running enhance or inhibit coronary artery plaque formation? A prospective multidetector CFA study of men completing marathons for least 25 consecutive years.  J. Am. Coll. Cardiol. 55;A173.E1624

Integrating the runner’s mind and body: the role of HRV

September 12, 2010

In his response to the post in which I presented my daily Heart Rate Variability (HRV) recording for August, Rick provided a link to the blog by Carl Valle in which he raises the provocative question that HRV is the ‘new lactate’ [1].   On the whole Carl’s posting was typical of a coach who brashly denies the value of scientific data yet takes for granted that he/she knows how to advise his/her clients.  This implies that there is some mystical source of wisdom that transcends science.  I believe a good coach observes, draws conclusions, makes predictions and offers advice, though sometimes he or she cannot put the underlying series of logical deductions into words.   The thinking style of such a coach is indeed almost pure science but it is a science that sometimes defies words.  This might be called intuition but it is not magic.   There is indeed a rich stream of activity in the human mind/brain that defies words yet is crucial for excellent performance in almost any sphere of activity, physical or mental.  My own interest in HRV and the question of how it might be best understood and used, is closely related to my speculations about how best to achieve the coordination between mind and body necessary for optimal performance, taking account of the fact that most of the communication between mind and body is non-verbal.

One piece in the kaleidoscope of memories and ideas that fuel my speculation is the most memorable race of my life.  It was a very low-key event; a 10,000m in a meeting in my home town, Adelaide, one summer evening almost 45 years ago ago.   I had not made any advance plan to run.  I had finished work rather late but on the spur of the moment decided that I would see if I could get to the track on time for the start, because in those days there were few opportunities to run 10,000m on the track. It was my first, and so far, only 10,000m race.  I arrived in time to line up for the start, but without any opportunity for a proper warm up.   However from the moment the starter’s gun fired, I was into my stride.  I did not consciously plan my pace as I had never run a 10,000 race before, though I frequently ran distances around 8-10K for recreation, so I suppose my body had a good non-conscious estimate of the magnitude of the task.  As the race unfolded, I ran with an amazing feeling of grace and power.  I was calmly aware that I was headed for victory, but winning was of little importance.    Perhaps endorphins contributed to my transcendental state but any circulating endorphins were not a reaction to pain; I was simply running well and enjoying it.  I have kept no record of the finishing time, nor indeed of my PB for any other event run in my youth, but that matters little.  The memory I treasure is the feeling of grace and power.  I doubt that my family or friends would use words like graceful to describe me, but in fact from time to time since then, I have had flashes of that same sense of grace and power – though sadly, not often in recent times.

Another sparkling fragment in the kaleidoscope comes from a different time and place, Beijing 2008, and a different level of performance entirely: Usain Bolt’s victory in the 100m final, in the world record time of 9.69 seconds.  With 15 metres to go he was about 8 metres clear of the rest of the field; his arms spread in celebration; not a triumphant thrust of the arms, but an open gesture accompanied by turning his head to the crowd as if inviting everyone to celebrate with him.  It is tempting to think that he might have recorded an even faster time if only he had been concentrating on the race – but I doubt if that is true.  In fact his legs still drove powerfully forward to the finishing line.  It is more likely that he is such an amazing runner because he does not concentrate on his running in the conventional manner.  In the press conference afterwards he grinned: ‘“I was havin’ fun. That’s just me. Just stayin’ relaxed. I like dancin’.”


Although perhaps the differences are more prominent than the similarities, what both of these illustrations have in common is a mental state, a ‘zone’, in which there is time and space to savour the moment; the body does not need to be driven by conscious determination.  It is state of unhurried awareness; but not detachment.  Perhaps this mental state is a variant of what is known in contemporary psychology as mindfulness: a calm awareness of ones breathing and heart beat, one’s muscle tone and posture, one’s thoughts and feelings, and of consciousness itself.

Although mindfulness-based therapy has recently become a popular form of therapy for the stresses of modern life [2,3], the concept of mindfulness is deeply rooted in all human cultures.  The Oxford English Dictionary unhelpfully defines it as “The state or quality of being mindful; attention; regard”, and notes that it was first recorded in the English language as ‘myndfulness’ in 1530.  The concept is even more strongly associated with the teaching Buddha who lived around 500 years before the beginning of the Christian era.  In the celebrated but perhaps apocryphal ‘flower sermon’, Buddha’s disciples were puzzled as he silently contemplated a lotus flower.  After it dawned on one of the disciples that the message was that enlightenment comes through contemplation, Buddha is reported to have claimed that this wisdom was transmitted by some mystical form of communication that transcends time and space and does not depend on letters or words.

But one does not need to invoke mystical power to account for non-verbal communication.  Modern neuroscience provides abundant evidence for non-verbal modes of processing and transmitting information.  Since the French neurologist Paul Broca established in the middle of the nineteenth century that the left frontal lobe of the brain plays a crucial a role in the generation of speech, a great deal of evidence has been assembled to demonstrate that logical, verbally mediated goal orientated mental processing is largely the work of the left hemisphere.  The right hemisphere has a gross structure similar to that of the left hemisphere but the subtle details of its internal and external connections facilitate non-verbal processes.   However, it would be simplistic to regard the brain as an organ with two competing halves, one verbal and one non-verbal.  The functions of the brain and body are integrated via a complex web of connections, neural and hormonal.  Neuroscience is beginning to unravel the principles underlying this communication web to an extent that was inaccessible to Buddha, but the details are complex and for practical purposes we are only a little further than Buddha in understanding how to tap into the power of non-verbal mind-body interactions.

Integration of mind and body

The understanding of the natural world provided by modern science frees us from many of the superstitions of our forebears, but there is a danger that we will lose that intuitive grasp of the wisdom that defies words.  There appears to be a contradiction between science that reduces the natural world to laws expressed in the language of mathematics and the intuitions that coach Carl Valle appears to extol in his blog. I do not accept that there is a real contradiction. Science is does not have to be purely reductive and it can certainly encompass non-verbal communication without resorting to mysticism. I believe that monitoring of HRV in combination with the practice of mindfulness, provides one way of using technology to foster constructive non-verbal mind body interaction

One of the communication systems within the complex web that mediates non-verbal mind-body interaction is the autonomic nervous system.  The parasympathetic division of the autonomic system mediates recovery from stress and can be engaged by meditation that encourages mindfulness. In light of the role that acute inflammation plays in the damage to muscles, tendons ligaments and joints that is an inevitable, indeed crucial part of the response to athletic training, it is of particular interest that mindfulness can modify the levels of the messenger molecules, such as interleukins and other cytokines that communicate to the brain information about tissue damage and help to regulate the inflammatory process.  The parasympathetic nervous system is intimately involved in the anti-inflammatory process, and HRV, both high frequency variability but also low frequency  variability, is associated with levels of cytokines circulating in the blood stream [4, 5].

Reliable measurement of HRV

As I have discussed on several occasions previously (eg 13 July 2010), two studies by Antii Kiviniemi and colleagues from Oulu in Finland demonstrate that adjusting one’s training regime according to a daily measurement of high frequency HRV (such that training intensity is decreased on days when HRV is reduced) can lead to greater improvement in fitness than training according to a fixed schedule [6.7].  However, my own experience is that high frequency HRV fluctuates erratically from day to day unless you adopt a standardized procedure for the measurement.

I have found that the most consistent measurements are obtained by recording HRV during two minutes shortly after getting out of bed each morning.  To standardise my physical state, I stand in a relaxed posture while breathing slowly and regularly.   To standardise the state of my mind I practice mindfulness.  I focus on the flow of air into and out of my lungs, the pulsation of my heart in my chest and the tension of my postural muscles.  Although I merely observe my thoughts and feeling in a manner that is not goal orientated, the awareness of oxygen flowing into and out of my body often prompts thoughts along the paths related to James Lovelock’s Gaia hypothesis – the proposal that all living organisms can be considered as components of a single self-regulating organism capable of keeping the earth’s environment healthy [8].  Sometimes I am reminded of the lesson that Hilary Stellingwerff learned during high altitude training in Ethiopia; ‘Finally, on all my recovery runs, the Ethiopian athletes stressed the importance of running on soft ground in the forest to make sure you go slow enough to really recover. They don’t worry too much about their pace, but instead about “getting good oxygen” from the trees and “soft ground” for the body.’

I believe that my daily ritual serves two purposes.  First, it leads to relatively consistent day-to-day HRV measurements.  Significant departures from the usual range of values indicate either excessive stress from training or from some other aspect of my life, as described in my post on 29th August, and help me adjust training intensity appropriately.  Second, in light of my hectic lifestyle, I think that starting the day with two minutes of relaxed contemplation makes a small but valuable contribution to maintaining a degree of calm throughout the day.  But the value of this is speculative, and I agree with Carl Valle that measurement of HRV is of limited proven value so far.  My own motivation is as much driven by a curiosity about what might work as by what is proven.

There is a third and even more speculative purpose in my ritual.  To what extent can training in mindfulness create the ability to invoke that mental state in which the body produces its best without the need for potentially obstructive gritty determination; a state in which there is time and space to savour the moment, to feel grace and power while running? Maybe this is an unrealistic romantic goal.  It flies in the face of our inclination to believe that it is only by disciplining our bodies in training and while racing, that we can achieve our peak.  But perhaps in the attempt to get the most from our minds and bodies we exult the power of discipline and struggle, and we lose the magic that allowed Usain Bolt to celebrate his victory in Beijing 15 metres before the tape.

My own experience provides some limited evidence that mindfulness can improve running performance.  When running intervals, my breathing rate increases to around 85 breaths per minute when I become anaerobic.  If at this point I focus on the distance still to be run, my breathing feels laboured and painful.  If instead I focus on the sensation of powerful expulsion of air from my lungs and then the subsequent surge of air back into my lungs, the feeling is usually an exhilarating sense of power.  When I employ a similar exercise in mental focus during intervals on the elliptical cross trainer (which has a power meter) my power output increases by an extra few percent without a corresponding increase in conscious effort.

Why not simply listen to the body?

One might argue that there is no need to invest in a heart rate monitor with the capacity to record R-R intervals in order to learn how to listen to the body.  I accept that the findings of the studies of HRV guided training by Kiviniemi and colleagues [6.7] are encouraging but not compelling.  Nonetheless, the evidence demonstrates that HRV can be a good index of autonomic nervous system function if interpreted appropriately, and that autonomic nervous system function is a useful index of the interactions between mind and body that mediate inflammation and recovery.  Perhaps the autonomic system also plays a key role in producing the optimal interaction between mind and body while running.

My own experience suggests that achieving optimum consistency in measuring HRV requires development of the skill of mindfulness – the objective awareness of one’s own bodily and mental function.  I suspect that this mindfulness has some similarity to the state of detached contemplation advocated by Buddha, though I suspect Buddha might have concluded that any concern with quantitative measurement was alien to his concept detached contemplation.  However, Buddha did not have the benefit of our current knowledge of physiology and neuroscience.  I believe that both the traditional oriental understanding of the interaction between mind and body, and the understanding provided by modern neuroscience, are useful models of reality.  Like all scientific theories, both are only models. As outlined by Isaac Asimov in his famous essay entitled ‘The Relatively of Wrong’ charting the development from mankind’s belief in a flat earth to our current understanding of a slightly pear shaped earth, all scientific models are wrong [10]; most have some utility within a certain domain in which they fit the observed evidence.  Better models provide a more accurate description over a wide range of circumstances.  I believe that it is likely that a traditional oriental understanding of the interaction between mind and body can be very helpful in creating as situation in which mind and body harmonise to produce maximal performance, but if this is the case, the traditional understanding must also harmonise with the evidence from modern science.

If we adopt the simplistic view that the goal of training is merely to improve physiological quantities such as aerobic capacity or strength, we might miss out on some of the wisdom embedded in traditional oriental understanding of mind-body interactions.  Some approaches to running, such as that advocated by Danny Dreyer in his method of Chi running [11], appeal to traditional oriental wisdom.  Insofar as such approaches encourage harmony between mind and body they might be helpful, though I think that ultimately it is likely to be more effective to integrate traditional wisdom with a realistic application of knowledge of physiology, mechanics and neuroscience.  Chi running, like Pose, assigns a mystical role to gravity that is contrary to the laws of Newtonian mechanics.  Hence, while Chi and Pose might be useful for many recreational runners whose major goal is avoiding injury, especially for individuals prone to knee injury, these methods are unlikely to be of much use for elite runners who need not only to harmonise mind and body but also need to maximise the efficiency of movement.

I think that the skill of mindfulness might play a useful role in helping integrate traditional oriental wisdom into an approach to training that also takes account of modern science.  Hence, I believe that curiosity in this concept is well justified, even though I cannot at this stage claim compelling evidence that it is worthwhile. I am not trying to sell snake oil.  There is no point expecting that simple mental exercise will abolish the need for training.  Without well developed aerobic capacity and adequate strength, running is unlikely to be either graceful or powerful, but neither will it be so without good coordination between mind and body.



[2] Kabat-Zinn J (1990)  Full Catastrophe Living: Using the wisdom of your body to face stress, pain and illness. Delcorte press, New York

[3] Williams M, Teasdale J, Segal Z and Kabat-Zinn J (2007) The Mindful Way Through Depression: Freeing Yourself from Chronic Unhappiness.  Guilford press, New York & London

[4]  Haensel A, Mills PJ, Nelesen RA, Ziegler MG, Dimsdale JE (2008) The relationship between heart rate variability and inflammatory markers in cardiovascular diseases. Psychoneuroendocrinology 33, 1305—1312.

[5] Taylor AG, Goehler LE, Galper DI, Innes KE, Bourguignon C. (2010) Top-down and bottom-up mechanisms in mind-body medicine: development of an integrative framework for psychophysiological research.  Explore (NY). 6(1):29-41.

[6] Antti Kiviniemi, Arto Hautala, Hannu Kinnunen & Mikko Tulppo (2007) Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol. 101(6):743-751.

[7] Kiviniemi AM, Hautala AJ, Kinnunen H, Nissilä J, Virtanen P, Karjalainen J, Tulppo MP . (2010) Daily exercise prescription based on Heart Rate Variability among men and women. Med Sci Sports Exerc. 42(7):1355-63

[8] Lovelock JE and Margulis L. (1974). “Atmospheric homeostasis by and for the biosphere- The Gaia hypothesis”. Tellus 26 (1): 2–10.


[10] Asimov I. (1989) The Relativity of Wrong. The Skeptical Inquirer, 14 (1), 35-44


Heart Rate Variability (HRV) during exercise

July 18, 2010

The evidence discussed in my recent posts indicates that for moderately fit individuals there is only a narrow gap between the training load required to produce useful improvement in performance and that which results in the over-reaching that leads to reduced  benefits of training.  Hence to obtain optimum benefit from training, it is necessary to  have a reliable way of estimating recovery from previous training sessions.  Furthermore, the evidence, especially the evidence for the recent studies by Kiviniemi and colleagues [1, 2] indicates that adjusting training according to heart rate variability HRV) measured in the resting state each morning might lead to more efficient training.  As discussed in my post on 13th July, I think this evidence is promising but not compelling.

Heart rate during exercise

Many athletes use heart rate during exercise itself as a guide to progress with their training.  Assessment of fitness such as that proposed by Hadd, which employs the relationship between pace and heart rate, assessed over a range of different heart rates, are based on the assumption that a lower heart rate at a given pace is an indication of increased fitness.  On the other hand, when fatigue begins to build up during moderately heavy training, heart rate at a given pace tend to rise indicating the first phase of over-reaching.  In contrast, during very heavy training, a decreased heart rate at a given pace can actually indicate parasympathetic over-reaching.   Provided the measurements are interpreted in context, gradual changes in heart rate at a given pace over a period of many weeks can be a useful guide to changing level of fitness, while short term changes can provide an indication of over-training.

HRV during exercise

These observations raise the possibility that HRV during exercise might be a useful guide to the degree of exhaustion during a training session.  However, there is surprisingly little published information regarding the interpretation of HRV during exercise.  Why should this be so?  The main problem is that whereas HRV at rest is very strongly influenced by the autonomic nervous system, it is not clear what are the main factors influencing HRV during vigorous exercise.

Figure 1 shows a trace which I recorded last year using my Polar RS800cx in R-R mode, during a graded exercise session on the elliptical cross trainer in July.  (Note the figure shows beat-by-beat values of heart rate, which is the reciprocal of R-R interval).  After two minutes of standing still, I exercised at a cadence of 80 cycles per minute and adjusted the resistance such that the power output increased from 30 watts in 7 approximately equal steps, each lasting 4 minutes, up to 230 watts.  After completing 4 minutes at  230 watts, I maintained an output of 30 watts for a further 4 minutes and then stood still for another 4 minutes.

Fig 1. R-R record during progressive increase in Elliptical power output. (18July 2009)

There are a number of idiosyncratic features of the trace which I will ignore for the present discussion.  These include sharp spikes which might be premature atrial beats (or artifact due to disrupted electrode contact).  The dip in heart rate to a value below 80 bpm lasting for around 20 seconds at 5 minutes is a typical feature which I observe in many of my recordings while in the lower part of the aerobic zone, and at present remains a mystery to me.  I have seen this feature in the recordings of other athletes but have not found any descriptions of these dips in published research reports.  However, for present purposes, let us ignore both the spikes and the dips.

The main features of note are:

1)  a large amount of high frequency fluctuation (indicated by the thickness of the fuzzy line) when standing still, in the first two minutes;

2) the amount of high frequency fluctuation reduces subsantially (the line becomes less fuzzy) as HR increases into the range from 80 to 120 bpm, if we ignore the aberrant spikes and dips.  By HR 120 bpm, at around 12 minutes, there is relativley little high frequency variability, though of course HR is continuig to rise slowy under the influence  of the sympathetic nervous system.

3) the high frequency variability then builds up again as HR approaches 140 (my ventilatory threshold, where breathing rate rapidly increases from 40 breaths per minute to 80 breaths per minute), as indicated by the increased fuzziness at around 24 minutes;

4) and finally the variability diminishes slightly as HR approaches its maximum, at around 28 minutes.  (My true maximum HR is probably around160 bpm though I have not actually pushed myself to the maximum in recent years) .

Figure 2a shows the Poincare plot of each interval between consecutive beats against the interval between the preceding pair of consecutive beats, over a 60 second interval around 24 minutes (power output, 200watts).  If a series of beats were equally spaced, the point representing each pair of consecutive beats in the Poincare plot would lie on a straight line inclined at 45 degrees.  The degree of scatter away from the 45 degree line indicates beat by beat fluctuations in HR.  The amount of scatter can be quantified by calculating the quantity, SD1, the standard deviation of the scatter away from the 45 degree line.  In this plot, sd1 is 4.4 ms which is typical of values I observe at the upper end of the aerobic zone.  Figure 2b shows the natural log of SD1 calculated for 60 second epochs at the end of each of the 4 minute steps, when HR is relatively stable.

2a. Poincare plot at 200watts. 2b. Plot of log (SD1) against heart rate (18 Jul 2009). Red arrow denotes HR at 200watts

It should be noted that estimating HRV during a period when HR is varying due to increasing work load presents problems.  Various  measures other than SD1, such as a scaling factor designated alpha computed on the basis of the theory of nonlinear systems (i.e. chaos theory), have been proposed, but the interpretation of such measurements is fraught with difficulty.  This is illustrated by poor consistency between measurement of alpha in the same person in  sessions a week apart [3].  Hence I think it is best to employ SD1 despite the limitations of this measurement.   The reason that it is conventional to plot the log of SD1 is that during the early phase of increasing exercise intensity, parasympathetic influence falls away exponentially.  An exponential decay would be expected to produce a straight line when plotted on a logarithmic scale.

Figure 2b confirms that high frequency HRV (as quantified by the log of SD1) falls rapidly from standing to low intensity exercise; continues to diminish gradually in the lower aerobic zone and then increases around the anaerobic threshold before decreasing again as HR approaches maximum.  This is fairly typical of what is seen in other athletes, though I exhibit a more abrupt initial withdrawal than I observe in others.

What determines HRV during exercise?

It is widely accepted that the initial fall off in high frequency HRV (as HR increases from its resting value) is due to withdrawal of parasympathetic influence.  Once in the aerobic zone, parasympathetic input is minimal and further increase in heart rate is driven by increased sympathetic activity [4].   However, high frequency variation at around respiratory frequency is not entirely abolished even in the mid-aerobic zone, suggesting that some other factor is contributing.  It is quite likely that intrinsic variability in the function of the sinoatrial node (the collection of  specialized muscle cells in the right atrial wall which fire spontaneously and normally act as pace-maker) plays a substantial role.  In a transplanted heart, which does not receive any input for the parasympathetic or sympathetic nervous system, heart rate variability during exercise is similar to that in a heart with intact input from the nervous system.  Casadei and colleagues from Oxford carried out a study in which they used the pharmaceutical agent, atropine, to block parasympathetic nervous activity, and observed that about a third of the variability of heart rate in the lower aerobic zone, can be accounted for by non-neural mechanisms [5].   Perini and colleagues [6] have argued that the most plausible alternative mechanism is mechanical.  For example, respiration would be expected to produce rhythmic stretching of tissues that might change the excitability of the pace-maker leading to variability at the respiratory frequency.  Furthermore, mechanical effects are a plausible explanation for the prominent increase in the magnitude of high frequency fluctuation around the anaerobic threshold, at which point respiratory effort increases markedly.

However, I remain a little skeptical that mechanical effects account fully for the high frequency variation in the upper aerobic and anaerobic zones.  In particular, excessive high frequency fluctuation during vigorous exercise appears to be a significant predictor of poor long term health.  For example, in a large study of 1335 subjects, mainly males, Dewey and colleagues from Stanford University [7] demonstrated that increasing magnitude of high frequency fluctuation during vigorous exercise (and also during the recovery phase) was a significant predictor of mortality  in general, and especially of cardiac mortality, in the following five years.   This suggests that HRV during vigorous exercise might reflect some physiological process that is indicative of impaired cardiac well being, probably something more subtle than the simple mechanical effects of respiration.  Might that putative physiological marker of impaired cardiac well-being be sensitive to the state of recovery during training?

HRV during exercise when fatigued

Observations of my own HRV during exercise confirm this hypothesis.  Last summer, my preparation for the Robin Hood half marathon had been seriously disrupted by quite severe bout of illness in June.  I had missed about 4 weeks of training, and attempted to build up training volume in July, in preparation for the  race in early September.  As described in my blog posting on 31st August 2009, I developed quite marked fatigue during August.  In an attempt to determine if the fatigue was affecting my heart, I had repeated the graded increase in exercise on the elliptical cross trainer at the end of August, following an identical schedule with 4 minutes at a series of seven steps spanning a range of power output from 30 to 230 watts, to that employed on 18th July. The R-R trace for 31st August is shown in figure 3, while fig 3a is an expanded view comparing the variability in the period 23-25 minutes  on 31st Aug with that on 18th July.  Figure 4a depicts the Poincare plot based on R-R intervals at 23-24 minutes on 31st August and Figure 4b shows the natural log of SD1 calculated for 60 second epochs at the end of each of the 4 minute steps.

R-R trace during progressive increase in Elliptical power output (31 August 2009; fatigued)

fig 3a: Expanded view of HR variability in the period 23 to 25 minutes, before (18 July) and during fatigue (31 August)

4a. Poincare plot at 200watts. 4b Plot of log (SD1) against heart rate (31 August 2009, red arrow denotes HR at 200watts)

The most prominent feature is that on 31st August, there was a much more dramatic increase in high frequency HRV as I approached the anaerobic threshold (shown by the marked fuzziness of the line around 24 minutes).  Furthermore, despite a subsequent increase in power output from 200 to 230 watts,  heart rate scarcely rose in the following 4 minutes.  In contrast to the similar test on 18th July, when HR rose to 157 bpm at a power output of 230 watts, on 31st August the peak heart rate was 145 bpm.  Subjectively, I experienced tremendous fatigue and found it very difficult to complete the 4 minutes at 230 watts.  Thus, on this occasion overwhelming feelings of fatigue limited my power output and were associated with excessive high frequency HRV.

The greater amount of high frequency variability is also clear from the wide scatter of points away from the 45 degree line in the Poincare plot and the relatively large peak in the value of log (SD1) at a heart rate of 145 bpm, visible in the plot of log (SD1) against HR.   (Compare fig 4a and 4b with fig 2a and 2b).

Although I have not subsequently experienced such overwhelming fatigue, there have been a number of occasions in which I have observed excessive high frequency HRV in association with moderate fatigue, sometimes when exercising in the lower aerobic zone and sometimes near anaerobic threshold.  For example, a few weeks ago I became increasingly tired during a hectic week at work.  On the Friday evening (18th June) I set out to do an easy 7.2Km run in the lower aerobic zone.  I felt tired and lethargic throughout.  The R-R trace (figure 5)  for a 15 minute segment in the middle of the run, when my pace was stable at 5:56 min/Km, shows marked high frequency fluctuation in heart rate.  Average heart rate was 124 bpm and SD1 was 9.0 ms.  For comparison figure 6 shows a similar 15 minute segment in the mid-stage of a 7.2Km low aerobic run on the same path in January.   Pace was somewhat faster at 5:39 min/Km, average heart rate was a little lower at 122 bpm, and high frequency variability was much less (SD1= 3.8ms).

Fig 5. R-R record in the mid-section of a 7.2Km low aerobic run when exhausted (18 Jun 2010)

Fig 6. R-R record during the mid-section of a low aerobic run (3 Jan 2010)

The following week I developed signs of an upper respiratory tract infection.  The R-R trace during an interval session on the elliptical machine is shown in Figure  7.  High amplitude fluctuation in heart rate can be seen in the second, third and fourth effort epochs.  During the crest of the second effort epoch, SD1 = 12.8ms

For comparison the R-R trace during a virtually identical elliptical interval session performed a week later when the respiratory tract infection had resolved, is shown in figure 8.  The magnitude of HRV is much less, and SD1 at  a comparable period in the 2nd effort epoch is 2.5 ms.

Fig 7. R-R record during an interval session while suffering a mild viral infection (24 Jun 2010)

Fig 8. R-R record duirng an interval session after recovery from the viral infection (9 Jul 2010). (Vertical arrows denote dips in HR possibly due to sympathetic withdrawal)

Although not all of the data provides quite such clear-cut information as the illustrations I have presented here, on many occasions on which I have felt fatigued or sluggish, there as been excessive high frequency HRV.  This feature is observed in various different types of session including steady running in the lower aerobic zone, tempo sessions, interval sessions and progressive increases in exercise intensity from the low aerobic to the anaerobic zone.  In contrast to resting HRV, where increased high frequency HRV is generally an indication of good recovery (except during advanced stages of over-reaching)  increased high frequency HRV during vigorous exercise generally appears to be an indicator of greater stress.

I do not know what physiological process is responsible for this. Perhaps some central governor generates ‘protective’ parasympathetic activity even at exercise intensities at which parasympathetic influence would normally be minimal.  Alternatively, in view of the fact that I suffer from asthma, it is possible that these episodes of fatigue are associated with subliminal constriction of my airways that results in more labored breathing and hence greater mechanical forces on my heart.  However, I have observed this phenomenon on many occasions when I am not aware of any breathing difficulty.  I would be very interested to hear if anyone else has observed similar increases in high frequency variability during exercise when under stress.

The dips: could they be due to transient sympathetic withdrawal?

[Note added 29 Nov 2010: the dips are almost certainly due to a transient surge of parasympathetic actviity associated with relaxation of smooth muslce at the the oesophageal-gastric junction – as  discussed with Steve in the comment section below]

Although I have not hitherto focused on the dips in HR that I frequently observe when exercising in the lower aerobic zone, or as my heart rate drops during the recovery from intense exercise, I have marked these by black arrows in figure 8.  Similar dips are also visible in figs 1,5,6 & 7 .   I have no reason to connect these to the increases in HRV associated with fatigue.  In fact the duration of these dips is typically 10-20 seconds.  If they are due to influence of the autonomic nervous system, they might possibly reflect sympathetic withdrawal, which would be expected to act on this time scale   They do not appear to be a marker for fatigue, but nonetheless I wonder whether they too might reflect a protective effect generated by a putative central governor.  I  have observed these dips in the traces of other athletes, but would also be very pleased to hear from others who have observed similar dips.  Because of the relatively long time scale, such dips would in fact be seen more readily in a record of HR averaged over 5 second intervals.

Is ‘real time’ assessment of HRV during exercise practical?

If indeed the excess HRV during exercise is a reliable marker for undue stress, would this be of any practical use?   The R-R trace is not generally available for inspection until after the completion of the session. However, in principle it should be possible to produce a continuous read-out of HRV averaged over a preceding period of about 20 seconds.  In fact the Polar RS800cx produces a measure called RLX.  Although it is difficult to obtain a precise account of the computation on which RLX is based, it appears to be very closely related to a continuous estimate of SD1.  Furthermore, according to the Polar manual, it should be possible to present the continuously updated value of RLX in the display of the wrist unit.  I have been unable to do this, and think that it is yet another manifestation of the fact that my particular RS800cx is infested with gremlins.  However as far as I can tell from retrospective examination of RLX values, the Polar computation of RLX is based on computation over too short an interval to provide reliable values.  I suspect that if I can convince myself that it would be worthwhile having access to a continuous read-out of high frequency HRV while exercising, it would probably be necessary to develop some more sophisticated way of performing the computation.


[1] Antti Kiviniemi, Arto Hautala, Hannu Kinnunen & Mikko Tulppo (2007) Endurance training guided individually by daily heart rate variability measurements. Eur J Appl Physiol. 101(6):743-751.

[2] Kiviniemi AM, Hautala AJ, Kinnunen H, Nissilä J, Virtanen P, Karjalainen J, Tulppo MP . (2010) Daily exercise prescription based on Heart Rate Variability among men and women. Med Sci Sports Exerc. 42(7):1355-63

[3] Tan CO, Cohen MA, Eckberg DL, Taylor JA (2009) Fractal properties of human heart period variability:physiological and methodological implications J Physiol 587.15 pp 3929–3941

[4] Rowell LB, O’Leary DS (1990) Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes J. Appl. Physiol. 69(2): 407-418

[5} Casadei B, Moon, J, Johnston J, Caizza S, Sleight P (1996)  Is respiratory sinus arrhythmia a good index of cardiac vagal tone in exercise? J.Appl. Physiol. 81(2): 556-564,

[6] Perini R, Veicsteinas A (2003) Heart rate variability and autonomic activity at rest and during exercise in various physiological conditions. Eur J Appl Physiol  90: 317–325

[7] Dewey FE  Freeman JV, Engel G, Oviedo R, Abrol N, Ahmed N, Myers J, Floelicher VF (2007) Novel predictor of prognosis from exercise stress testing: heart rate variability response to the exercise treadmill test. Am Heart J, 153(2) 281-8.