Archive for April, 2009

The path to fitness or to over-training

April 25, 2009

The path to fitness

Successful training is based on a delicate balance between stressing the body and allowing it to recover. In the short term stress leads to damage and impaired performance but provided there is adequate opportunity for recovery, the body’s response to the challenge is to not only repair the damage but to develop a greater capacity to withstand challenge in future. This is described as super-compensation but in everyday terms, it simply means the body becomes fitter.

The path to over-training

However, if there is inadequate opportunity for recovery, performance continues to deteriorate and the body enters a state of staleness described as overtraining, that can persist for many months. In the over-trained state many aspects of body physiology are prone to be disrupted though there is no single physiological measure that indicates over-training. It is probable that the processes that lead to overtraining involve local trauma to body tissues, excessive production of ‘stress’ hormones such as cortisol, and excessive production of other chemical messengers in the body such as cytokines that re-set the brain mechanisms that regulate the body. It is probable that the derangements of body chemistry in any one case depend on the nature of the initial stress; on the genetic constitution of the individual; and on that individual’s previous history of stress and adaptation.

The first steps on the path to fitness or over-training

For long-distance runners, there are two processes that are the most likely candidates for initiating the processes that lead to either fitness or overtraining. These are damage to muscle fibres produced by the eccentric contraction that occurs on each footfall, and the release of cortisol by the adrenal gland to promote the generation of glucose required to fuel a long run. Understanding these processes is likely to be the key to rationally designing a successful training program.

Catabolic effects of cortisol

When the body faces stress, the initial response is release of cortisol from the adrenal gland. Cortisol plays part in several of the body’s immediate self-protective strategies. Of particular relevance for the long distance runner is the process of gluconeogenesis – the generation of glucose to prevent a fall in blood glucose that would be a catastrophe for the brain, which is heavily reliant on glucose to fuel its operations. Cortisol promotes the release of glucose from glycogen stores in the liver. However cortisol can also promote the breakdown of protein to generate glucose. So unaccustomed long runs are likely to result in the sacrifice of muscle protein for the sake the short term maintenance of blood glucose. This breaking down of body constituents is known as catabolism.

Eccentric damage to muscles

The mechanisms of muscle damage during exercise are not fully understood. It is unlikely that processes such as lactic acid production due to anaerobic metabolism play a significant role. It might be that increased acidity interferes to a limited extent with some beneficial processes such as the generation of mitochondria, (as indicated by the study by David Bishop and colleagues (Medicine & Science in Sports & Exercise:Vol 40(5) Supplement p S33, 2008), discussed in my post on 21st April. However, a substantial amount of evidence indicates that lactate actually protects muscles (Cairns SP, Sports Med. Vol. 36(4):279-91, 2006) Another potential mechanism of damage is the production of free radicals,. These are reactive molecules with an unpaired electron that are formed during oxidative metabolism and can damage tissue, but so far the evidence suggests that free radical damage is on likely to be a serious issue for elderly runners. (I myself am in that group, but in the present discussion I do not want to confine myself to the challenges facing the elderly).

As discussed above, the catabolic effects of cortisol can also promote break-down of muscle. However, the most significant source of damage during running is likely to be simple mechanical trauma. During weight lifting, the eccentric activity involved in controlled lowering of the weight can produce dramatic disruption of the structural integrity of muscles, that far exceeds the damage caused during concentric lifting, even though concentric lifting requires more energy. Forcefully stretching a muscle as it is actively generating an opposing force simply tears many of the muscle fibres apart, producing the pattern known as Z-line streaming (Gibala and colleagues, Journal of Applied Physiology, Vol 78, 702-708, 1995). Unfortunately, eccentric contraction occurs at each footfall during running, as the quads and calf muscles arrest the freefall under the influence of gravity that occurred during the airborne phase. Thus long distance running produces two potentially destructive effects: micro-trauma that tears the muscle fibres apart and the release of the catabolic hormone, cortisol, which acts in the short term to maintain blood glucose levels, but when the supply of glycogen in the lever is inadequate, is likely to breakdown muscle proteins to generate glucose. In the short term, muscle power suffers but in the medium term, these destructive processes can trigger adaptive responses that lead to greater fitness – provided the stress is not excessive. On the other hand, rapid increases in training volume leads to over-training and possible long term impairment of function, as was illustrated ib the study by Lehmann and colleagues discussed in my posting on 14th April (Int J Sports Med. Vol 12(5):pp 444-52, 1991; Br J Sports Med. Vol 26(4):pp 233-42, 1992; Eur J Appl Physiol Occup Physiol. Vol 70(5):pp 457-61, 1995).

The adaptive response to muscle damage

Several adaptive processes can occur. The two most important are closely linked: these are the mobilization of satellite cells and the production of anabolic hormones. Satellite cells are a form of stem cell that occur in muscle adjacent to the muscle fibrils. Following damage to the muscle, the satellite cells fuse with the muscle cells ( GE Adams, Satellite cell proliferation and skeletal muscle hypertrophy, Appl Physiol Nutr Metab. Vol 31, pp782-790, 2006). Muscle cells have multiple nuclei, containing the DNA and other molecular machinery necessary for initiating the synthesis of new proteins. When a satellite cell fuses with a muscle cell, it adds a new nucleus thereby enhancing the regenerative capacity.

Corticosteroid hormones can inhibit the action of satellite cells. This is most clearly established in the case of synthetic steroids such as prenisolone that are used for the treatment of autoimmune disorders (Betters and colleagues, Muscle & Nerve. Vol 37(2):pp 203-9, 2008). However, it would be expected that less potent naturally produced corticosteroids such as cortisol would have a similar, though perhaps less marked effect.

However, the hormonal regulation of metabolism entails not only the production of catabolic hormones such as cortisol that tend to break down body tissues, but also the production of anabolic hormones that promote the building up of body tissues. The most potent of these are the sex steroids, especially testosterone (though oestrogen also has anabolic effects). Vigorous muscular contraction promotes the release of testosterone (Grandys and colleagues, J Physiol Pharmacol. Vol 59 Suppl 7:89-103, 2008). Testosterone promotes the action of satellite cells.

The adrenal cortex also produces anabolic hormones of which DHEA (dihydroepiandrosterone) is the most abundant. DHEA is a multifunctional hormone, and its role in adaptation to training is uncertain. The question of whether DHEA supplements have a beneficial effect on muscle building has been a subject of some controversy. Less controversial are the beneficial anabolic effects of growth hormone. Growth hormone is produced by the pituitary gland and stimulates the building up of body tissues. The production of growth hormone is promoted by vigorous exercise, but the peak release of growth hormone occurs during sleep. Almost certainly, adequate sleep is required to promote the optimum switch from production of the catabolic hormone cortisol (which usually reaches its lowest level 3-5 hours after onset of sleep) to the production of growth hormone.

Failure of adaptation

If the amount of time for recovery is inadequate to allow the repair of muscle fibres and the re-synthesis of glycogen, a vicious cycle sets in. The damaged muscle tissue release cytokines which are small molecules that carry out various signaling functions in the body. Although the details remain speculative, it is likely that the cytokines produced by muscle damage act in the hypothalamus and in other regions of the brain to re-set the regulatory mechanisms that control the various physiological processes in the body (Smith LL,.J Strength Cond Res. Vol. 18(1):pp 185-93, 2004). In particular, the regulatory mechanisms are likely to shut down body functions that might promote further damage. In other words, your brain will not allow you to run far or fast. Cortisol production initially remains high, though eventually it is likely to fail. Anabolic steroid production falls. You will feel stale, de-motivated and possibly even depressed. You are now over-trained and it may be many months before your brain lets you engage in potentially destructive activities such as racing at your best level.

What are the lessons?

This brief (and somewhat speculative) exploration of modern molecular biology confirms what has been discovered by observant athletes and coaches over the years. The simplistic explanations such as the presumed damaging effects of lactate suggested by coaches such as Arthur Lydiard are probably wrong, but many of Lydiard’s observations of what works in practice are probably correct. However a thorough understanding of the molecular biology might allow a somewhat more effective application of the principles.

A few specific points that might be gleaned from the discussion above are:

1) long training runs are potentially beneficial as they provide an enough stress to produce appreciable muscle damage and appreciable cortisol production.

2) Rapid increase in training volume is likely to lead to over-training. On the other hand, if the build up of training volume occurs slowly, the adaptive processes will result in an increased capacity to cope with the stress of heavier training and in turn, to reap greater benefits.

3) Cross training employing a training mode that minimizes eccentric contractions (e.g. elliptical cross training; cycling or swimming) will allow a greater total training load at any given level of fitness, and in particular, might facilitate other valuable adaptations (e.g. increase in blood volume; increased cardiac stroke volume; increased ability to generate glucose from lactate in the liver) without triggering the cytokines that signal to the brain that it further training should be inhibited.

4) Adequate periods of recovery are essential and in particular, adequate sleep is crucial during period of heavy training.

Maximising aerobic development

April 21, 2009

The study by David Bishop and colleagues that Ewen drew my attention to in his comment on my post on base-building on April 12th, demonstrates that interval sessions in the upper part of the aerobic zone produce a marked stimulus to development of mitochondria, and this stimulus to aerobic development is decreased, but not abolished, by acidosis (Medicine & Science in Sports & Exercise:Volume 40(5) Supplement p S33, 2008). Although Bishop and colleagues produced acidosis artificially by administering ammonium chloride, it is likely that marked acidosis arising from highly anaerobic exercise would have a similar effect.

Thus, this study does imply that mixing highly anaerobic work (sufficient to produce marked acidosis) with aerobic work within a session will produce less aerobic development than might be achieved by a purely aerobic session. Although the study does not directly compare lower aerobic with upper aerobic sessions, it certainly demonstrates that upper aerobic work produces a major stimulus to development of mitchondria and hence suggests that the most efficient way to promote development of mitochondria within a limited time is upper aerobic work.

I would expect that fartlek would also be an efficient way to produce aerobic development provided the effort epochs do not become severely anaerobic.  A session that I have been experimenting with recently consists of 6 to 8 uphill stride-outs for about 250 metres on a 1 in 10 gradient grassy path though woodland, separated by easy-paced downhill recoveries. I find this session is not at all stressful (in fact I really enjoy it). By the end of each uphill stride-out, I am near the ventilatory threshold. I do this session in place of the ½ effort sessions in a Lydiard program, because it takes only about 20 minutes (not including warm-up) and hence fits more easily into the time I have available. I hope this will provide good aerobic development while also strengthening my legs.

My current weekly program consists of one longish low aerobic run, a progressive run that gets me near lactate threshold for 5-8 Km (my current equivalent of Lydiard’s ¾ effort session); the uphill strideouts (my replacement of Lydiard’s ½ effort sessions); several easy runs that include a few short ‘alactic’ sprints at the end; and an elliptical session. Overall this program is intended to build an aerobic base while also strengthening my legs and promoting good neuromuscular coordination, with a relatively limited commitment of time. However, it is reasonable to assume that if time was not an issue, I might achieve as much aerobic development by running in the lower aerobic zone for a longer period.  A greater proportion of lower aerobic work would be expected to produce greater development of fat-burning capacity, but less development of type 2a (fast twitch aerobic) muscle fibres than my current program.

I consider that the study by Bishop and colleagues confirms that Lydiard’s recommendation of a moderate amount of upper aerobic work and a large amount of lower aerobic work during base-building is good advice. However, I also think this study indicates that Lydiard’s claim that no further aerobic development can occur once one starts anaerobic development is not correct. Even in a session in which aerobic threshold is exceeded some development of mitochondria will occur. Nonetheless, if you want to achieve aerobic development while also developing speed endurance during a phase of mixed training, it would probably be most efficient to do some entirely aerobic sessions and some separate interval sessions

Risks of increasing volume v increasing intensity

April 14, 2009

In my recent post on base-building, muscle damage and adaptation, I had reported evidence demonstrating that there is are multiple paths to success in training.  Both anecdotal evidence about the training of world record holders and also the evidence from scientific studies suggest that both high volume programs and also high intensity programs can produce an increase in aerobic fitness and enhance performance. 


On the other hand, I also suggested that there are likely to be multiple paths to stunted growth, frustration or outright failure.  My own experience and also the comments of Rick and Ewen in response to that posting, suggest that the risks of ‘stunted growth, frustration and outright failure’ might be greater with high intensity training.  Certainly my own experience confirms that an increase in training intensity increases the risk of overt muscle injuriy.


A study of training and over-training

However, it is salutary to examine the results of the study which I regard as perhaps the most thorough comparison of the risks associated with a major increase in training volume, with the risks associated with a major increase in training intensity.  This was a study conducted almost 20 years ago by Lehmann and colleagues at the University Hospital of Freiberg and reported in a series of papers published in the 1990’s.  (The key papers are:  Int J Sports Med. Vol 12(5):pp 444-52, 1991; Br J Sports Med. Vol 26(4):pp 233-42, 1992; Eur J Appl Physiol Occup Physiol. Vol 70(5):pp 457-61, 1995).


The ITV and ITI programs

It should be noted at the outset that the intention of the investigators was to induce over-training, so the training regimes should not be regarded as typical of sensible training programs.  In the first year, 8 experienced middle or long distance runners took part in a brief Increased Training Volume (ITV) program that entailed a 101% increase is training volume over a three week period, from a baseline of 85.9 Km in week 1, up to 176.6 km in week 4.  Training occurred on 6 days per week.  Virtually all of this training (96-98% of training volume) was performed as long-distance runs at an estimated mean oxygen utilization at 67% of maximum capacity.   This pace corresponds quite closely to Molvar’s interpretation of Lydiard’s 1/4 effort. A year later, 9 experience runners (including 7 of those who took part in the ITV program in the first year) took part in an Increased Training Intensity (ITI) program.  Speed endurance, high-speed and interval runs averaging 9 km at baseline in week 1, increased to 22.7 km in week 4, and the total volume increased from 61.6 to 84.7 km, during ITI.  Thus both programs might be regarded as injudicious, but nonetheless, provide the chance to compare the results of injudicious increase in volume with the results of what appears to be at least an equally injudicious increase in intensity, in almost exactly the same group of athletes a year later.


The consequences of increased volume

During the increased volume program, there was stagnation in endurance performance capacity (running velocity at the aerobic-anaerobic transition range – a key indicator of middle and long distance performance) together with a decrease in maximum working capacity in 6, and a stagnation in 2 of the 8 runners.  Total running distance during an incremental treadmill test decreased from 4719 +/- 912 m to 4361 + /-788 m.  There was an increase in levels of creatine phosphokinase (a marker of muscle damage) and a decrease in neuromuscular excitability (which the investigators regard as a peripheral measure of good muscle function rather than a measure of neural signaling from the brain).  In the subsequent competitive season, these athletes failed to reach their previous personal best levels.


The consequences of increased intensity

In contrast, during the increased intensity program a year later, performance at the aerobic-anaerobic transition (i,e. at lactate level 4 mmol) and also total running distance during the incremental treadmill test improved steadily during the 4 weeks, and there was no significant evidence of muscle damage.



This study does not prove that judicious high volume training is dangerous.  However it does demonstrate that increasing training volume by around 33% per week for three weeks,at moderate aerobic paces (well short of lactate threshold) has a very high probability of producing muscle damage and reduced performance, both during treadmill testing and during the subsequent competitive season. 


The failure to improve performance in competition cannot be attributed to the athletes having already reached their peak, as an increase in high intensity training the following year, which at first sight appeared even more injudicious, resulted in a steady improvement in performance.  This improvement during high intensity training in experienced runners would of course be very unlikely to have occurred in novice runners.  It is almost certain that all of the runners recruited to this study already had a substantial aerobic base before entering the study. 


For runners who already have at least a moderate aerobic base, a ‘crash program’ of high intensity training might be expected to produce greater improvement in performance and less risk of damage, than a ‘crash program’ of increased volume.  The benefits of high volume training are more likely to come from a sustained, long-term program.

Base-building, muscle damage and adaptation

April 12, 2009

One of the challenges of training is getting the right balance between the principle of specificity and the need to build a base.  The principle of specificity dictates that if one wants to run a mile in 4 minutes one should train the body to be able to maintain a pace of 15 miles per hour for 4 minutes.  Hence one might imagine that the best approach is to start by running ¼ mile repeats in 1 minute, and gradually build up the distance at this pace to the stage of running ¾ miles in 3 minutes, before attempting the goal of a 4 minute mile.  Perhaps Zatopek’s famous rhetorical question: Why should I run slowly when I want to learn how to run fast?’ captures the idea of specificity most elegantly.  And perhaps this would be a sensible approach to the final stages of preparation for an assault on the 4 minute mile.


However, to start with a training program based on running at 15 mph is likely to be a prescription for injury and frustration.  To prepare for the rigors of specific training for an event that might test one’s body to its limits, it is necessary to lay a foundation in which many of the tissues of the body are prepared to handle the demands that will be placed upon them.  This is the purpose of base-building.


The goals of base-building

In building a base for middle and long distance running, the two tissues that require the greatest development are skeletal muscles and heart muscle.  However many other tissues require an adequate level of development:

  • lungs to transfer oxygen from air to blood and carbon dioxide from blood to air;
  • ligaments to transmit the force of muscle contraction to joints;
  • bone and joints to withstands the forces generated by muscle, gravity or ground reactions;
  • liver to remove lactate from the blood and regenerate glucose, and replenish glycogen stores;
  • kidneys to assist the lungs in maintaining acid base balance, and to maintain electrolyte levels;
  • the endocrine system to produce the hormones that balance anabolism (building up of tissues) with catabolism (breaking down);
  • and the brain to couple motivation to action and orchestrate all of these actions.  

Base-building prepares all of these tissues, in addtion to skeletal muscle and heart.


Construction v demolition

The essence of base-building is construction, not demolition.  The way in which we build the tissues of the body is by challenging them.  Applying stress stimulates the body to react by strengthening the function that is challenged.  But if we present a challenge that is too great, the net effect is destruction.  The art of base-building is getting the balance right.


From time to time in recent weeks I have mentioned my intention to review the processes that transform muscle during training.  It is in muscle that we can see most clearly the way in which a challenging stress can result in strengthening if applied appropriately, but the process is fraught with risk of both short term damage and possible long term damage.  As with all physiological processes, the topic is complex, and the outcome of the interaction between the processes of destruction and construction is difficult to predict.  I have held back from tackling this topic because the available evidence must be drawn from many sources: historical anecdotes; scientific studies of groups of athletes undergoing specific training routines, and the extensive and rapidly growing body of knowledge about the physiological processes involved.


Reviewing the historical evidence

Much of the information we have to guide training is based on the inspired observations of coaches such as Gerschler in the 1940’s and 50’s and Lydiard in the 1960’s and 70’s who transformed training in their own eras.  Gerschler’s introduction of interval training led, via Franz Stampfl, to Bannister’s four minute mile in 1954, and perhaps also contributed indirectly to Zatopek’s gold medals in the 5000m,10000m and marathon in Helsinki in 1952, though it appears Zatopek developed his training technique independently of Gerschler.  Lydiard’s emphasis on building a base by a large volume of aerobic running followed by a period of intense event-specific training led not only to the middle distance triumphs of Snell but also the longer distance achievements of Halberg, Clarke and others. 


However, world records have continued to improve and in the past decade or so, many African runners, most notably Hicham El Guerrouj in the 1500m and mile, Kenenisa Bekele in the 5000m and 10000m and Haile Gebrselassie in the marathon, have left the records of Bannister, Zatopek, Snell, Halberg and Clarke in tatters.  While there is still some debate about the genetic endowment of African runners, it is more likely that better training provides the main explanation.  However the question of which aspects of training are responsible remains controversial.  Training at altitude is part of the story but more likely a childhood spent building a base, and a large amount of quite high intensity training in the competitive years, are the crucial ingredients.  However, higher intensity training brings with it risks, making it all the more important to understand the mechanisms of both the benefits and of the potential damage.


Historical evidence v. recent scientific evidence

First, we should re-examine the evidence we have touched on in reecent weeks suggesting that Lydiard was wrong to maintain that aerobic capacity could only be developed by aerobic training  There is little doubt that at least in the short and medium term, high intensity training can improve aerobic capacity while providing a more efficient use of time than traditional endurance training.  In the study by Gibala and colleagues comparing 6 sessions of high intensity sprint cycling consisting of 4 to 6 30second sprints with 6 session of endurance training consisting of 90-120 minutes of cycling at 65% of VO2max, over a two week period, similar improvements in performance; muscle oxidative capacity; muscle buffering capacity; and muscle glycogen content were produced even though the total training time commitment was only 2.5 hours for the sprint training compared with 10.5 hours for the endurance training (J Physiol Vol 575, pp 901-911, 2006).


Although the acidity produced by anaerobic training might limit the capacity for aerobic conditioning within a particular training session, I can find no substantial evidence that a reasonable mixture of aerobic and anaerobic sessions damages aerobic development.  In a study mentioned in my recent comparison of Maffetone and Lydiard, Ingjer demonstrated that 24 weeks of training that included one predominantly aerobic session and two interval sessions per week, resulted in an increased proportions of type 2A fibres (fast twitch, aerobic) at the expense of type 2B fibres (fast twitch anaerobic), but without changing the proportion of Type 1 (slow-twitch fibres).  Ingjer also reported that this training program produced substantial improvement in other indices of aerobic function. The mean number of capillaries per muscle fibre increased by 29%   There was a major increase in mitochondrial density in both type 1 and type 2A muscle fibres.  During training the proportion of type 1 fibres that were described as rich in mitochondria increased from  59 to 95%., while the proportion of mitochondria-rich type 2A fibres increased from 21 to 77 % . These increases in proprtion of aerobic fibres, capillary density and mitochondria were associated with an average increase in maximal oxygen uptake capacity of 25% (J. Physiol, vol 294, pp. 419-432, 1979).


Several subsequent studies have confirmed that training can convert fast twitch anaerobic fibres to aerobic fibres.  For example Hather and colleagues demonstrated that a program of eccentric and concentric resistance training increased the proportion of type 2A fibres (fast-twitch aerobic) at the expense of type 2B (anaerobic) fibres, while also increasing the size of type 1 (slow twitch) fibres and increasing capillary density in both type 1 and type 2A fibres ( Acta Physiologica Scandinavica, Vol 143,Pages177–185).  Staron and colleagues demonstrated that heavy resistance training in women produced hypertophy of all three fibre types (European Journal of Applied Physiology, Vol 60, pp1439-6319,  1990).


I am aware of only one study that showed a reduction in type 1 fibres  during training.  That was a study of intense sprint cycling training that resulted in a 7% reduction in proportion of  type 1 fibres and a 6% increase in the proportion of type 2A (aerobic fast twitch fibres) (Jansson and colleagues. Acta Physiologica Scandinavica, Vol 140 pp359-363).  Even in this study, the aerobic slow twitch fibres were replaced by aerobic fast twitch fibres and hence provide no evidence for loss of aerobic capacity.


Thus, recent scientific evidence demonstrates that both aerobic and anaerobic training can lead to enhanced aerobic capacity.  This perhaps explains why coaches and athletes employing quite different strategies have in some instances achieved spectacular success.  There is no single path to success.  However, the large numbers of injured athletes and of athletes who have exhibited great promise early in their careers, but failed to deliver on that promise, demonstrates that despite the multiplicity of paths to success, there are also multiple paths to stunted growth, frustration or outright failure.  Therefore rather than being guided simply by anecdotal evidence of the success of Olympians, or alternatively by scientific studies that reveal group-average benefits in small groups of athletes who have undergone a particular training regime under quite specific circumstances, we might be well advised to understand also what physiological science has revealed about the mechanisms of tissue damage and adaptation.


Use it or lose it

Living tissues are dynamic structures which degenerate unless continuously renewed.  Many of the major functions of living tissues are mediated by proteins. Usually, the process starts when receptor proteins embedded in membranes that enclose the cells in all types of body tissues receive either electrical or chemical messages, arising from the external environment or from within the body, that cause them to adapt their shape in a way that promotes the function of that type of tissue. 


For example, the electrical message from a nerve to a muscle releases a chemical messenger called acetylcholine that binds to receptor proteins on the muscle surface membrane in a region known as the muscle end-plate.  These receptors change their shape when the messenger molecule binds to them, triggering a cascade of signaling processes within the cell.  These signals involve additional chemical messengers which bind to other proteins within the cell, triggering further signaling until ultimately, the proteins that perform the main functions of the cell are activated.  Within muscles, the final signaling messenger is calcium released from a membranous structure surrounding each myofibril known as the sarcoplasmic reticulum.  The calcium acts on the actin and myosin within the myofibril to produce contraction.  Actin and myosin are long chain-like protein molecules that are aligned in parallel and linked by cross-bridges.  In the presence of calcium, the cross-bridges reform creating a ratcheting action that pulls the actin and myosin fibres past each other, producing contraction of the muscle fibre.


However, activation of the receptor proteins on the cell surface not only initiates a cascade of signalling that results in other proteins within the cell executing the function of the cell, the process of activation of the receptor proteins also results in an additional cascade of chemical signals that ultimately act on the DNA in the cell nucleus triggering the genesis of proteins within the cell.  In the case of muscle, binding of acetylcholine triggers the translation of DNA to produce proteins that replace any that have suffered degradation and provide new building material for hypertrophy of the muscle.  Thus muscle, and indeed virtually all body tissues, experience continual repair and remodelling as they are used.  However, if they are not used, they eventually decay due to the inevitable degradation of biological materials.  


It should be noted that the process that leads from the electrical message in the nerve via release of acetylcholine onto receptors on the muscle endplate and subsequent release of calcium from the sarcoplasmic reticulum to the ratcheting of the actin and myosin molecules that results in contraction, occurs on a time scale of milliseconds, whereas the translation of the DNA code and production of new protein takes many hours or even days.  Thus consumption of protein-containing foods which are broken down to produce the amino acids which are the basic building blocks for construction of new protein can occur over a period of hours after exercise; similarly the natural anabolic hormones that promote regeneration and hypertrophy are required to act over a period of many hours.


Mechanisms of muscle damage and adaptation

While processes such as the translation of the DNA code and production of new proteins as a consequence of use, occur in almost types of tissue in the body, the processes of damage and repair are even more dramatic in muscle due to the forceful nature of muscle contraction.  The phenomenon of delayed onset muscle soreness appears to be overt evidence of the damage due to use, and the subsequent increase in strength is an illustration of the hypertrophy due to synthesis of new muscle protein.


The most marked damage to muscle occurs following eccentric contraction – when the muscle attempts to contract while it is actually undergoing stretching due to external forces.  This is a situation that occurs at foot-strike when running.  As the foot contacts the ground, with knee and ankle flexed, the necessity of arresting the free-fall under the influence of gravity in the airborne phase results in stretching of quadriceps and the calf muscles.  This stretching facilitates the storage of gravitational energy as elastic energy which can be recovered at lift off from stance. However, the inevitable eccentric contraction of the quads and calf muscle produces quite marked damage.  Electron microscopic images of muscle fibres after running, especially down-hill running, reveal visible disruption of the points where the actin and myosin chains are attached to the framework of the myofibril.  This manifest evidence of structural damage is known as Z-line streaming.  (For photographs, see for example, Gibala and colleagues, Journal of Applied Physiology, Vol 78, 702-708, 1995).  It is possible that it is due to shorter myofibrils being torn asunder by the powerful contraction of adjacent longer fibrils in the same bundle.


This dramatic damage appears immediately after exercise and is associated with loss of strength that is maximal in the period 24-48 hours after exercise and resolves slowly over a period of up to 96 hours.  Satellite cells appear to play a key role in the recovery from this damage.  Satellite cells are small specialised stem cells found in close association with skeletal muscle fibres. In response to injury they become activated and fuse with the myofibrils promoting repair and regeneration.  They have also been observed to become active during periods of heavy muscle loading and fuse with apparently undamaged myofibres as part of the hypertrophy process  ( GE Adams Satellite cell proliferation and skeletal muscle hypertrophy, Appl Physiol Nutr Metab Vol 31, pp782-790, 2006).  Various factors, including hormonal and nutritional status regulate this process.


In future posts I will review the evidence regarding the likely effect of different training programs on the nature and extent of this damage to muscles, and on the repair and adaptation processes mediated by satellite cells, though there are of course many outstanding questions that remain unanswered.

Where does Hadd fit in the picture with Maffetone and Lydiard?

April 9, 2009

In my recent posting comparing Maffetone and Lydiard, I discussed the fact they both recommend a period of base-building in which the major component is running in the aerobic zone.  The main difference between the two is Maffetone’s recommendation that all of the training during the conditioning phase should be in the lower aerobic zone whereas Lydiard recommended several session per week at paces in the upper part of the aerobic zone.  After reviewing the evidence in support of Maffetone’s recommendations, I had concluded that there was no clear grounds for proposing that a few sessions in the upper aerobic (or even anaerobic) zones would interfere with base-building and hence, came down in support of Lydiard.  In that posting I had implicitly lumped Hadd with Maffetone, but maybe it is only fair to let Hadd speak for himself and in particular, to examine the extent to which he advises against reaching the lactate threshold, and the reasons he advances in support of his advice.


Hadd presents his approach in an article at: .  He argues quite strongly that the anaerobic zone should be avoided during base building.  The core of his argument is that a sound base depends on well conditioned slow twitch fibres and that these fibres can only be recruited and developed at paces in the aerobic zone.  He bases his argument largely on Gary Dudley’s observations of fibre development in rats. 


I will return to a discussion of this evidence later, but first it is useful to review the program that Hadd recommended for a 35 year old marathon runner whom he calls Joe.  He reported that Joe had the potential to run a marathon in 2:25, but at the beginning of the program, he was unfit and 20 lb overweight due to lack of recent training.


Joe’s program

Hadd’s first instruction to Joe was to get his weekly mileage up to 50 miles without concerning himself with pace.  In fact Joe achieved this rapidly.  He then recommend that Joe perform two tests: a test of maximum heart rate, which was to be recorded during a peak effort 400m that followed shortly after a peak effort 800m run  Joe posted a value of 193 bpm.  A few days later, Joe performed the ‘Hadd test’: a set of 5x2400m runs each at a predetermined target heart rate.  The target heart rate increased in steps of 10 BPM in successive runs, ranging from 140 to 180 (and hence extending from lower aerobic zone to the low part of the anaerobic zone.  Joe reported that he found the fastest pace difficult to maintain for the required 2400m, providing confirmation that 180 was above Joe’s current lactate threshold.  With the information from these two tests Hadd defined two key heart rates: a lower heart rate of  140 (approximately HRmax – 50) and an upper heart rate of 160, selected to be about 10-15 BPM below estimated current lactate threshold.  This higher heart rate was in the upper aerobic zone but comfortably below the lactate threshold.  These two heart rate levels (140 and 160)  were used to define the paces for the key workouts. 


Already by this stage, we can see a crucial feature of Hadd’s approach.  He sets training paces according to specific testing of the individual athlete.  Furthermore, although like Maffetone, he argues that it is important to avoid the anaerobic zone, unlike Maffetone, one of Hadd’s key training paces in the comfortable part of the upper aerobic zone.


In early weeks of Joe’s training, majority of sessions were at or near the lower aerobic pace but typically for two sessions per week the target pace was the comfortable upper aerobic pace.  In  week 3 when the weekly mileage was increasing, all runs were near the lower aerobic pace, but once weekly mileage had stabilized at around 100 miles per week, Hadd again introduced 2 runs at the comfortable upper aerobic pace in addition to 60 minutes at the upper pace within a 2 hour run. 


Thus, Hadd’s program bears a strong resemblance to Lydiard’s recommendation that most runs are at ¼ effort, with two or three faster runs at ½ or ¾ effort each week.  Although Lydiard did not define ¼ , ½ and ¾ pace precisely, the overall picture emerging from Lydiard’s writings and lectures suggests that he recommended  sessions that were a little harder than those recommended by Hadd. 


Molvar’s interpretation of Lydiard

John Molvar, who is one of the most thorough students of Lydiard’s writings, defines Lydiard’s paces at  He states:

1/4 effort – easy, but still aerobic pace (not jogging), 65-70% of (Maximum minus resting heart rate). For example, with a resting of 55 and max of 195, 1/4 effort is in the range 145 to 153 beats per minute, though Molvar points out that this might increase later in the base-building phase

1/2 effort – run at a strong aerobic, but sub tempo pace, 70-75% of (Maximum minus resting heart rate). For example 153 to 160 beats per minute.

3/4 effort:  tempo pace/At Threshold (AT) pace, 75-85% of (Maximum minus resting heart rate). For example 160 to 174 beats per minute


Thus. Molvar’s interpretation of Lydiard’s ¼ and ¾ key paces make them a little more demanding than Hadd’s corresponding paces.  There is little doubt that the famous 22 mile Sunday hill run done by Lydiard’s protégés during base building  was more demanding than the 2 hour run with 60 minutes at HR 160 recommended by Hadd.


Speed work

Lydiard also recommended speed work through the conditioning phase.  In somewhat similar manner, in week 8, Hadd introduces 200/200 fartlek sessions to re-establish speed. These session consists of 25 x 200m at 5k pace with 200m recovery at an easy pace.  


Joe’s progress

In a little less than 20 weeks,  Joe reduced his pace at HR 180 (i.e. a little above lactate threshold) from 5:40 min per mile to 5:10 min per mile.  At this stage he entered a marathon with the plan of running with the 2:20 pace group and dropping out half-way.  He covered the half-marathon in 71:xx.  Thus, after 20 weeks his goal of a 2:25 marathon appeared plausible, if not quite within reach at that stage.  Unfortunately , Hadd does not tell us whether or not Joe achieved his marathon target.  Nonetheless, the achievements of the first 20 weeks were impressive. 


In summary, the program recommended by Hadd for Joe is quite different from a typical Maffetone program in which all runs in the conditioning phase are at lower aerobic pace.  In fact Hadd’s paces are only slightly less demanding than the paces recommended by Lydiard.  The major issue in following Hadd’s approach is knowing whether or not it is crucial to avoid reaching the lactate threshold.  Some of his disciples go so far as to slow to a walk when ascending hills to avoid the dreaded threshold


Dudley’s rats

As far as I understand Hadd’s reasoning, it is based largely on the way he interprets the findings of Dudley’s study of rats. (’Influence of Exercise Intensity and Duration on Biochemical Adaptations in Skeletal Muscle,’ Journal of Applied Physiology, vol. 53, pp. 844-850, 1982)   Dudley observed that running at relatively low speed increased mitochondria in the slow twitch fibres while running at faster speeds resulted in an increase in mitochondria in fast twitch fibres.  Hadd interprets this as reason for running at slow speeds if you want to develop the aerobic capacity of the slow twitch fibres essential for distance running  However, in Dudley’s rats, running fast produced a worthwhile increase in mitochondria even in the slow fibres, so overall, fast running is beneficial both fast and slow twitch fibres.  Dudley did not show that faster running obliterates the benefits gained from slow running.  


Perhaps the most striking evidence that a moderate amount of faster running does not destroy the benefits derived from the slower aerobic training is the array of Olympic gold medals won by Lydiard’s protégés, despite the demanding Sunday morning hill run.  However, it is dangerous to draw conclusions from anecdotes alone.  When in doubt, it is can be worthwhile to examine the underlying science – though if you do not feel comfortable trying to keep track of the long names of biological molecules. (or perhaps even worse, trying to keeping track of the abbreviations for the names of molecules), you can skip the next section. 


Some biochemistry

The core reason for advocating development of aerobic metabolism is the fact that aerobic metabolism, in which glucose is converted to carbon dioxide and water, generates 36 molecules of ATP from one molecule of glucose.  In contrast, anaerobic metabolism, in which glucose is converted to lactate (in the absence of oxygen), generates only 2 molecules of ATP.  ATP is the high energy molecule that provides the immediate fuel for muscle contraction.


Hadd and Maffetone imply that training the anaerobic system can damage the aerobic system.  Closer consideration of the aerobic and anaerobic metabolic pathways makes this very unlikely. 


The first important point is that the enzymes involved in anaerobic metabolism are mostly the same enzymes as those involved in the first stage of aerobic metabolism.  In the first stage, glucose is converted to pyruvate.  In the absence of oxygen, pyruvate is converted to lactate by an enzyme known as lactate dehydrogenase (LDH).  LDH is the only enzyme unique to anaerobic metabolism; all others are also part of the aerobic system.  However, as we shall see, LDH has very little ability to control the fate of pyruvate.  It is noteworthy that the production of lactate is also accompanied by the generation of hydrogen ions (i.e. increased acidity) and as discussed in my post on Maffetone on 5th April, this might contribute to a decreased efficiency of fat metabolism and possibly also decreased electro-mechanical coupling within the muscle, during that training session.


When oxygen is available, the pyruvate enters the cycle of chemical processes delineated by Sir Hans Krebs.  Within the Krebs cycle the carbon atoms of pyruvate are converted to carbon dioxide while spare electrons are transferred to a carrier molecule called NADH.  NADH is then processed along a ‘conveyer belt’ known as the respiratory chain in which is it is oxidized by a group of enzymes known collectively as cytochrome oxidase, and in the process, a large amount of ATP is generated.  This process occurs within the organelles known as mitochondria.  One of the main goals of aerobic training is to increase the numbers of mitochondria in muscle cells, and thereby increase the amount of cytochrome oxidase.


Perhaps the crucial question that must be addressed in assessing the plausibility of the claims of Maffetone and Hadd is: might improvement of anaerobic metabolism interfere with aerobic metabolism?  The answer is no.  In fact the opposite is the case: aerobic metabolism switches off anaerobic metabolism.  This is known as the Pasteur effect, in honour of Louis Pasteur, who is famous for developing our understanding of germs and inventing the food sterilizing process known as pasteurization, but among other things, spent a great deal of time investigating energy metabolism in brewers yeast.  


When oxygen is present, and the ATP level is below the maximum required, pyruvate is voraciously sucked into the Krebs cycle and converted to carbon dioxide, meanwhile feeding electrons into the respiratory chain and generating large amounts of ATP.  The crucial question is what enzyme controls the rate of progress of glucose along the path towards pyruvate.  The main regulator is an enzyme called phosphofructokinase (PFK) which is responsible for one of the early steps along the path.  PFK is strongly controlled by the level of ATP.  When the ATP level is below full, PFK works at top speed promoting the conversion of glucose to pyruvate.  If there is any oxygen available, the pyuvate immediately enters the Krebs cycle ultimately generating 36 molecules of ATP per molecule of glucose.  If there is no oxygen available, LDH converts the pyruvate to lactate producing a net output of 2 molecules of ATP per glucose molecule.  When ATP levels are adequate, PFK slows down thereby slowing glucose metabolism.  So, the crucial regulator is an enzyme that in shared by the aerobic and anaerobic pathways.  The unique enzyme of the anaerobic system, LDH, responds passively to the level of pyruvate.  Even if it were possible to produce extra LDH by anaerobic training, this would have minimal influence on the fate of pyruvate.


The bigger picture

So the biochemistry suggests that training the anaerobic system does not damage the aerobic system.  Of course, the bigger picture must take account of other issues.  As Dudley’s rats showed us, if you want to maximize the development of the mitochondria in slow twitch fibres, then this can be achieved with least amount of stress by training at the relatively slow paces where slow twitch fibres are optimally recruited.  Training at higher paces will produce some development of mitochondria in slow twitch fibres, and will also develop the aerobic capacity of the type 2A (aerobic fast twitch fibres)  This is also useful and does not damage the aerobic capacity of the slow twitch fibres. 


The acidity produced by anaerobic metabolism does potentially have an adverse effect on fat burning and perhaps also on electro-mechanical coupling during the current session.    However, there is no evidence to suggest that this damages previously developed aerobic capacity.  Furthermore, Dudley’s rats and also studies of mixed aerobic and anaerobic training in humans (see for example the study by Ingjer, J. Physiol. vol 294, pp. 419-432, 1979) demonstrate that the aerobic capacity of slow twitch fibres is actually enhanced by training that includes moderate amounts of anaerobic running.


However, the even bigger picture includes the role of hormones such as cortisol.  As discussed in my recent comparisons of Lydiard and Maffetone, cortisol is a catabolic hormone that breaks down muscle protein.  Large amounts of stressful training , especially large amount of anaerobic training, will elevate cortisol, and undo the gains of the conditioning phase.


So in conclusion, after considering the arguments of both Maffetone and Hadd, I can see no reason for avoiding moderate amounts of running near or even above the lactate threshold during the conditioning phase, provided excess cortisol production is avoided.  The safest way to train in the conditioning phase is to spend most of the time in the lower part of the aerobic zone, but you do not need to slow to a walk up hills for fear of going anaerobic.  As far as I can see Hadd’s training program is effective, and much nearer to Lydiard than Maffetone, but I cannot find much support for his apparent concern with the need to avoid exceeding the lactate threshold.



Lydiard v. Maffetone

April 5, 2009

Recent advocates of the Lydiard approach, particularly Hadd and Maffetone, have focused on avoiding the anaerobic zone during the conditioning phase.  This focus has led to a greater emphasis on running at the lower end of the aerobic zone than I believe Lydiard himself advocated, though it is not easy to be certain what Lydiard intended.  He stated that running should at a good aerobic pace, and should leave you comfortably tired after the session.  Enigmatically, he recommended longer runs should be at ¼ effort while shorter runs should be at ¾ effort, but did not define these effort levels.


Lydiard ‘mystery coach’

( – pointed out recently by Rick) states that ¼ effort is the effort that would allow you to go straight out and repeat the run, but this does not quite fit with Lydiard’s recommendation of ¼ effort for 22 miles.  I doubt that even Lydiard recommended immediate repetition of a 22 mile run.  In light of his recommendation that runs during the conditioning phase should leave you comfortably tired, I have interpreted ¼ effort to be the maximum pace that you can maintain comfortably for several hours.


Whatever Lydiard meant, Philip Maffetone makes it much clearer that he recommends that most of the training should be in the lower part of the aerobic zone during base-building phase.  His ‘180 formula’ is based on the assumption that the maximum aerobic training pace should be (180-age) with various adjustments for training history.  For me, his formula gives a maximum aerobic training heart rate of 117.  In fact when running, my ventilatory threshold (where breathing depth and frequency increases markedly) occurs at a heart rate around 140-145, so Maffetone’s recommendation is far below my ventilatory threshold.   Even if I adopt Mark Allen’s modified version of Maffetone’s 180 test

  ( and add an extra 5 bpm because I am over 60, my maximum aerobic training heart rate would be 122.


In my easy 2 hour run last Saturday, I covered 21Km in 2 hours (5:43 /km) at heart rate 120.  This would suggest that my maximum aerobic training pace according to Maffetone/Allen should be in the range 5:40-5:45.  This would also match my interpretation of Lydiard’s ¼ effort pace.  So provisionally, I can conclude that my pace for long runs should be in the range 5:40 -5:45 /Km. 


How long is a long run?  Lydiard recommended ¼ effort for runs of 15 miles or more, and he implies that 6 min/mile is a typical aerobic pace for a serious athlete.  Thus when measured in time rather than distance, Lydiard treats runs of 90 minutes or longer as long runs, indicating that for a runner with an aerobic pace of 5:40 /km, 16 Km or more should be regarded as a long run.


According to the above interpretation, Lydiard and Maffetone are in reasonable agreement in their guidance for the pace for long runs,  However when we consider shorter runs, there appears to be a crucial difference between Lydiard and Maffetone.  In his guidelines for marathon conditioning, Lydiard recommends two runs at ½ effort and one run at ¾ effort each week, and in addition, he recommends some speed training throughout the conditioning phase.  The speed training might best be achieved by short sprints fueled by ATP and creatinine (known as alactic metabolism).  As I have described previously, I consider it is crucial for an elderly runner to maintain speed, and therefore I have incorporated short sprints into my program even in the early stage of the conditioning phase.  Lydiard recommends ½ and ¾ effort for medium length runs of duration ranging from 60 to 90 minutes.  He states that these runs should be ‘at a good aerobic pace’. If his ¼ effort is at the lower end of the aerobic zone, it would seem likely that he intended ¾ effort to be near the upper end of the aerobic zone (i.e. near ventilatory threshold which for me is near to a heart rate of 140.  In contrast, in an article on the Road Runners Club of America, Maffetone states that you should train at or below the heart rate determined by the 180 test (117 in my case) throughout the base-building period ( ).


So which of the two offers the best advice? Maffetone offers four reasons for avoiding the anaerobic zone: 1) aerobic training might decrease the number of anaerobic fibres; 2) lactic acid production might inhibit aerobic metabolism; 3) anaerobic metabolism might suppress fat burning; 4) the stress of anaerobic training might raise cortisol which inhibits aerobic activity.  I believe that there is evidence supporting all four of these assertions but I do not consider any of them is reason to justify spending the entire base building period in the lower aerobic zone identified by the 180 test.  Let us consider each of these reasons a little further:


Changes in fibre composition

There is good evidence that fibre composition can change.  For example Ingjer demonstrated that 24 weeks of training that included one predominantly aerobic session and two interval sessions per week, the proportions of type IIA fibres (fast twitch, aerobic) increased while type IIB fibres (fast twitch anaerobic)decreased.  However there was no change in proportion of Type I (slow-twitch fibres) (J. Physiol. vol 294, pp. 419-432, 1979). This evidence suggests that a program including two sessions with some anaerobic work actually increased the proportion of fast twitch fibres capable of functioning aerobically  Thus, in this study, combining aerobic and anaerobic work resulted in a shift towards a distribution of fibres most suited towards running at race paces in the upper aerobic zone.  On the other hand, I have not found any evidence of an appreciable shift towards type IIB (anaerobic) fibres as a result of combining aerobic and anaerobic sessions.


Lactic acid production might suppress aerobic metabolism.

It is true that many biochemical process in muscle slow down in as acidity rises.  Warren and colleagues demonstrated many years ago in a study of isolated soleus muscles dissected from mice that as few as 20 eccentric contractions could result in a reduction in force of contraction to around half the initial value (Journal of Physiology, 1993, 468, pp. 487-499).  Furthermore, even after the debilitating eccentric contractions, the force triggered by applying caffeine (which promotes contraction without the need for an electrical, signal from the nerve) was normal, implying that the contractile machinery (actin and myosin) was still able to function, but the failure was due to impaired coupling of the electrical signal from the nerves to the contractile machinery.  They did not identify what caused the loss of contraction strength, though some metabolic effect, such as altered acidity or possibly changes in some other ions such as potassium ions, essential for efficient electrical conduction, would be likely culprits. 


This rapid loss of strength following powerful eccentric contractions observed by Warren might be responsible for the fact that it is impossible to sprint for more than a few hundred metres, and may even contribute to the inability to sustain a pace in the lower part of the anaerobic zone for more than 10K.  However, the body corrects imbalances in acidity or ion concentration are on a time scale of minutes or at most a few hours.  In the short term increased respiration, which removes carbon dioxide and thereby lowers levels of carbonic acid in the blood, corrects blood acidity within minutes.  Excretion of ions by the kidney will correct any remaining imbalances over a time period of an hour or so.


Thus, adverse effects of acid might effect the ability to deploy aerobic metabolism within a run, and hence suggests that the anaerobic state should be avoided during long runs.  However, acidity developed during one training session will not be sustained to the next day’s session and hence, the acidity itself cannot be a reason for avoiding the anaerobic zone in some sessions, provided the program includes an adequate number of long aerobic runs.


Fat burning

It is probable that the enzymes that metabolise fat function less well as acidity level rises.  Therefore, if one wants to promote the development of these enzymes, it is almost certainly best to do long runs in the lower aerobic zone, but in itself this is no reason to avoid the upper regions of the aerobic zone for all sessions in the conditioning phase.  In fact it might be argued that there is limited value in developing the enzymes that burn fat only in the lower part of the aerobic zone if race pace will be in the upper aerobic zone. It might be helpful to do some sessions in the upper part of the aerobic zone with the explicit goal of increasing the ability to clear hydrogen ions when working in this zone and hence to facilitate fat burning even in the upper aerobic zone. 


Cortisol production

Cortisol is a catabolic hormone produced when the body is stressed. It actually promotes the breakdown of protein and inhibits muscle hypertrophy.  Thus, it is indeed crucial to avoid excessive cortisol production during the base-building phase.  There is little doubt that doing too many hard anaerobic sessions creates a risk of excess cortisol production, as does pushing up total training distance too rapidly.  However, this is not a reason for avoiding upper aerobic sessions provided these do not leave you feeling continually tired and run-down.



So, it does not appear to me that any of the reasons Maffetone proposes are adequate reasons for avoiding the inclusion of some upper aerobic, or even anaerobic, sessions during base-building provided there are an adequate number of low intensity long runs and the total work load is not too stressful.  Thus I consider that Lydiard’s suggestion of one ¾ effort session and two 1/2 effort sessions in the week is fine provided you avoid becoming run-down.  This of course requires judgment, and it is probably best to err on the side of caution when in doubt.


An even more important issue

I think that both Maffetone and Lydiard omit the most important issue of all.  That is the mechanism of muscle damage and adaptation. Recent evidence about the role of satellite cells, which are a form of stem cell that participate in muscle repair, has provide the beginning of an understanding of these mechanisms, but that is a discussion that will have to wait for a future blog.



This week, I have taken two steps to implement the Lydiard conditioning phase.  On Tuesday and again on Thursday, I took the initial step towards including some upper aerobic sessions in my schedule,  On these days, during runs of 6 and 7 Km respectively, I progressively increased pace so that I covered about 4-5 Km in the mid to upper aerobic zone.  Apart from two or three interval sessions during the winter, I have not run in the upper aerobic zone for over six months.  It felt good to be running at a moderate pace, though I found that my muscles felt a little stiff the day afterwards.


Yesterday, as a check on my estimate of the appropriate pace for a long run, I did 16Km at 5:43 /Km.  My mean heart rate was 119, which was very slightly lower than that recorded during a 21 Km run at the same pace the previous Saturday.  Thus, if I wished to follow Maffetone’s recommendation (target heart rate 117), 5:45 /km would be the appropriate pace for long runs, though if I want to follow Mark Allen’s modification, and increase the target heart rate to 122, I should aim for about 5:40 /Km.  I am inclined towards Mark Allen’s recommendation.  This pace is approximately 1 min per Km slower than my target half-marathon time.  This is a fairly modest objective and should allow me to enjoy some relaxed running through the bluebells in the next few weeks.