Cardiac fitness

Recently I said that I would post some thoughts on running and the heart. The topic is vast. Today I want to address the question of whether athletic performance is limited by fitness of the heart or fitness of the skeletal muscles. This has been a topic of debate since the 1920’s when Nobel prize winner, AV Hill, first put forward the concept that a governor protects the heart by ‘slowing the circulation’ (Quart J Med 1923;16:135–71). In the past decade, two of the main protagonists in the debate have been Tim Noakes in Capetown and Bjorn Ekblom at the Karolinska Institute in Stockholm. As might be expected, the answer appears to depend on circumstances.

Can cardiac work increase at power output above VO2max?

Ekblom and colleagues (J Appl Physiol 2007; 102:781-786) measured oxygen utilization (VO2), cardiac output, heart rate and blood pressure in 8 well trained young men during two brief bouts of exercise (lasting about 4 minutes each) at a power output above that achievable at VO2 max. During these bouts of ‘supramaximal’ exercise (i.e. above power output at VO2 max), blood pressure rose with increasing power output despite constant VO2 and heart rate, demonstrating that the work done by the heart continued to increase. This suggests that the cardiac work under the circumstance of that study was not the limiting factor.

What happened to cardiac output when the oxygen supply is low?

In contrast, in a review of studies of cardiac output when running at high altitude (or other circumstances where a decreased amount of oxygen is delivered via the lungs) by Noakes’ team, suggests that under these circumstances, cardiac output falls as availability of oxygen falls (Journal of Experimental Biology 2001; 204, 3225–3234). If the heart was not the limiting factor, it might be expected that cardiac output would rise to maintain the rate of delivery of oxygen to skeletal muscles. However, this might be a risky strategy. Increasing cardiac output and therefore increasing the oxygen requirements of the heart, when the availability of oxygen is less would create the risk of starving the heart muscle of oxygen, thereby creating the risk of disturbance of the exquisitely synchronized rhythm of heart muscle contraction and potentially fatal fibrillation. Perhaps not surprisingly under conditions where oxygen delivery via the lungs is less (eg at high altitude), it appears that Noakes ‘central governor’ takes action to prevent the heart being damaged with catastrophic consequences.

My central governor

My asthma frequently restricts the supply of oxygen to my lungs. I do not regularly measure my peak expiratory flow before and after training, but when I do, it typically falls from around 500 litres per minutes to around 250 litres/minute during a training session. The most extreme I have observed was a fall from 610 litres per minute to 130 litres per minute. My subjective experience is that over shorter distances, I am limited mainly by my ability to get enough oxygen into my lungs. Interestingly, I find it very hard to get my heart rate much above 150 (though on some occasions I do manage to get it to 160). I suspect that my non-conscious brain is very reluctant to allow me to push myself to the limit. So the effect of diminished oxygen supply is not a compensatory increase in heart rate, but rather my brain appears to curtail how fast I can run, possibly to protect my heart.

In fact I have little desire to push myself to VO2 max and beyond at present. I would quite like to run a fairly fast mile again one day (ie, anything faster than 6 minutes – the pace that I once regarded as the slowest worthwhile training pace even for long distance runs, but at present I am unable to sustain that pace for even one mile), though I am prepared to put that day off until my asthma settles. I use a steroid inhaler which keeps my asthma under moderately good control. So far I have resisted taking oral steroids; I would only accept the risks of oral steroids if asthma was seriously interfering with my everyday life. For the time being I would prefer to work on gradually building my aerobic capacity and increasing the endurance of my leg muscles, since those are the characteristics that limit me when running long distances in the aerobic zone. Nonetheless, I am also eager to increase my cardiac fitness as much as possible to give myself a good buffer zone so that I can safely push myself a little beyond lactate threshold at the end of a race.

Creating a safety buffer zone

Cardiac deaths among athletes are not restricted to those competing in short anaerobic events. The risk of cardiac death in the 24 hours after a marathon is estimated to be around 1 in 50,000 (Journal of the American College of Cardiology, 1996; 28, 428-431). This is a small risk but nonetheless, even among those who do not suffer asthma or any known cardiac disease, it would seem to be worthwhile to increase cardiac fitness as much a possible before strenuous endurance events. But this raises the question of how can we best make the heart fitter?

First we must ask what aspects of heart structure or function can be strengthened by training. There is good evidence that training can produce improvements in three main domains:

1) Hypertrophy of cardiac muscle. Both ventricular diameter (and hence stroke volume) and also cardiac wall thickness can be increased by training. When I was young, there was much discussion as to whether or not the hypertrophy of an athlete’s heart was healthy. In non-athletes, a large heart can be a sign of serious disease. In the past few decades it has become clear that the hypertrophy seen in athletes is generally healthy. Unlike pathological hypertrophy, which is usually associated with decreased coronary reserve ( decreased ability to increase blood flow in the coronary arteries when required), in athletes cardiac hypertrophy is usually associated with increased coronary reserve (Hildick Smith and colleagues, Heart 2000;84:383–389).

2) Increased capacity of small blood vessels supplying the heart muscle.  The evidence for this was controversial for some years because some measurements suggested that capillary density was not increased in athletes compared with sedentary people. However, this debate was resolved by a study of Yucatan mini-pigs carried out by White, Bloor and colleagues (J Appl Physiol 85:1160-1168, 1998.) Pig heart resembles human heart in many ways. White and colleagues trained their pigs on a treadmill for 16 weeks, following a program that entailed a gradual increase from running for 30 minutes, five days per week at 70-80% maximum heart rate, up to running for 70 minutes, 5 days per week, after 8 weeks. The pigs maintained that training load for a further 8 weeks. After the initial 3 weeks capillary density had increased, but at 16 weeks capillary density was not greater than at baseline – however the number of arterioles (blood vessels intermediate in diameter between capillaries and arteries) was increased, indicating that number of capillaries had initially increased, but subsequently the diameter of these capillaries increased and they became arterioles.

The most important aspect of coronary blood supply for the athlete is how much it can increase above resting level when required. This is known as coronary reserve. It is probable that coronary reserve depends not only on the number and diameter of blood vessels, but also on the hormonal or other biochemical mechanisms that produce dilation the blood vessels when demand increases. Another similar measure that is more appropriate for measurement in animals, is capillary transport reserve. In White’s study of Yucatan mini-pigs, capillary transport reserve increased even more dramatically than coronary blood flow. Whereas blood flow increased by 22%, capillary transport reserve increased by almost 60%

3) Increased capacity for metabolizing fuel to produce energy. One of the metabolic adaptations that occurs with training is an increase in the ability to transport lactate from the blood stream into the heart. In general heart muscle works in the aerobic zone, but it can nonetheless use lactate (produced for example by skeletal muscle) as fuel. The transport system that moves lactate across the sarcolemma (cell membrane) of heart muscle responds well to training (Bonen, Eur J Appl Physiol, 2001, 86, 6-11) It seems to me that this might be a very valuable adaptation for the long distance runner. If blood glucose reserves begin to fall in the later stages of a long run in the upper aerobic zone, the capacity to utilize the lactate that has accumulated in the blood following extrusion from skeletal muscle, should at least ensure that the heart has an adequate supply of fuel.

White and Bloor’ study of Yucatan mini-pigs demonstrated that a training program similar to that which might be recommended for base building prior to a half marathon or marathon program (though perhaps a little monotonous for my own taste) resulted not only in increased small blood vessels number and diameter, but also increased capillary transport reserve and cardiac muscle hypertrophy. However, not all types of training produce the same profile of benefits for the heart. In a future post, I will examine what little evidence there is regarding the optimum training program for achieving improvements in each of the different aspects of cardiac fitness.

8 Responses to “Cardiac fitness”

  1. Ewen Says:

    Another interesting post Canute, thanks.

    At the moment when racing, I feel a little like I’m at altitude in regards to heart function. I’m running ‘hard’, but the heart patiently sits on about 90% of maximum, no matter how hard I try. I’d expect to be able to sit on a HR of 92-95% of maximum for these short races.

    So, in my case (at the moment) I think it’s the “muscles” that are the limiting factor. I wonder if this is due to not being “fresh”. Interestingly, when I was doing regular interval/speed type training over summer, I could sit on a higher HR, so perhaps the constant base training has temporarily reduced that ability, and it’s not just lack of “freshness” that’s the problem?

    Something related, is that when I’ve been coming back from an injury (for example the 3 weeks or so after my calf problem in 2006, I was easily able to run at 95% of maximum (even though the pace was very slow – 5:26/km). I’d like to be able to run at 95% in my current condition!

  2. Thomas Says:

    I start wheezing very badly when running above a certain threshold. As I’m also suffering from hay fever twice a year I think I do have a very mild form of asthma. If I weren’t a runner I would most likely never even notice anything, but at high effort my breathing becomes increasingly difficult and I’m wheezing like a steam engine.

    In a 5k 2 months ago, I started wheezing within the first k. The runners around me must have thought I was going to keel over at any moment. At then end I even apologized to one of them for all the noise I had been making. As it does not affect me in my everyday life, I don’t take any medicine for it. Do you think it would be worthwhile talking to a doctor about it? I’m generally very cautious when it comes to using pills and avoid them whenever possible, and since I’m not really concentrating on my 5k results, it doesn’t have that much impact on my running either.

  3. canute1 Says:

    Thomas, I am very cautious about offering advice, but quite happy to tell you about my own experience and the judgments I have made. Like yourself, I try to avoid medication wherever possible.
    My earliest memories of upper airway obstruction date from age 4 when I nearly died from a severe episode that was described at the time as croup. Since then I have found that house dust, cold air and vigorous exercise, alone or in combination, trigger asthma. I suspect that the episode at age 4 was due to a combination of acute infection causing inflammation and swelling in my upper airways, and a hyper-active allergic type response of the smooth muscles of my airways causing constriction – the core feature of asthma. In those days effective bronchodilators did not exist so I spent the night in a steam tent. I still remember the horror of the visual hallucinations generated by my oxygen-starved brain. However I seemed to grow out of it. Occasionally, in my teens I became wheezy when I inhaled cold air, and I always suffered mild airways constriction during middle distance races. However I did not seek treatment, and the problem settled down entirely for about thirty years.
    However when I started running again in my mid fifties I was again aware of mild constriction when trying to run fast, but it was still not a significant problem. Then I developed a persistent irritation of my upper airways (I think due to house dust as much as running) so stopped running for 18 months. In fact the problem got worse. When I started running again in my sixties, things came to a head the following winter. I was very wheezy when I exerted myself, but I was also waking breathless in the night. That was the point when I decide to discuss it with my GP. Initially he recommended a bronchodilator (salbutamol inhaler) which dealt with the acute episodes but the underlying problem persisted so I started on a steroid inhaler.

    I use a Wright peak flow meter (relatively cheap, and available from Pharmacies under prescription in the UK) to monitor the situation. As long as my peak flow rarely falls below 300 litres per minute, I consider the problem is reasonably well under control – though this is my own arbitrary decision. My best value in the past year or so is around 600 but my usual upper level values are in the range 500-540, which is good for a person of my age and height. Tables of normal values are readily available via internet. At present I use the steroid inhaler daily, and am content with my present situation. The only limitation it places upon me is that I cannot train at levels near to VO2max – but I do not want to do this anyway.
    If you have a GP who is willing to talk about the advantages and disadvantages of medication with you, I think it would be worth talking to your GP. There is some evidence that continued use of bronchodilators results in loss of sensitivity to the beneficial effects, so you should not use any medication without good monitoring. The GP will probably measure your peak flow during the consultation. It might even be worth getting a peak flow meter for home use and measuring values before and after vigorous training. If there is a marked decrease after training, discuss these values with your doctor.
    The IOC has produced a useful document:

  4. canute1 Says:

    Ewen, I agree that it is probable that your leg muscles are the limiting factor for you at present. My very speculative hypothesis is that your current daily high volume training has created a situation where the muscle damage you suffer each day is only approximately balanced by the amount of compensation (through mechanisms such as satellite cell activation) each day. As a result you might have a chronic level of mild impairment of muscle function relative what you might expect if you had a rest day in which repair exceeds damage. Due to the hypothetical sustained mild level of damage, there is some inflammation and some inefficiency of recruitment of muscle fibres. The ability of your leg muscles to extract oxygen from blood is not quite as good as it would be after a rest day. At a specific heart rate in the upper aerobic zone, there will be a greater accumulation of lactate, so running in the upper aerobic zone will be somewhat less pleasant.
    Provide you have adjusted your training level so that compensation slightly outweighs damage most days, you will slowly improve in fitness, but racing will not be much fun. If you want to enjoy racing, I would suggest a mild taper for two days preceding the race. But this is of course wild speculation.
    The observation of being able to achieve a higher HR on return from injury is an interesting observation, that I suspect might be partly explained by lower blood volume and hence smaller stroke volume at that time. Therefore, heart rate will be higher for a given level of cardiac work, but I suspect other factors also play a role in this phenomenon.

  5. speedygeoff Says:

    Hmmm. My rheumatic fever (3 bouts taking many months out of my early life) left me with heart arrhythmia and valve damage. But this was the main motivation for me to take up and continue running. Despite the risks I kept running to extreme, after ten years build-up racing many marathons and running 150km per week + for at least 15 years. And yet … i think my heart was never my limiting factor. I remember racing a half marathon with Farrington, Zeuner and others in the leading pack and being how amazed at how laboured they sounded whereas I was hardly drawing breath in comparison. But my leg soreness as usual slowed me in that race. Five days out of seven at the time my training was long/slow, plus a race day and a km interval day, never shorter. Also I had a very light body-weight. My heart rate could be quite fast but was very low at rest. My conclusion is that despite starting with a very weak heart, hard training brought about benefits to the point that the heart was no longer the limiting factor.

  6. canute1 Says:

    Geoff, On the whole your training program over a period of years was near ideal for developing good blood supply to the heart muscle, good heart rate variability, large stoke volume and also good capacity of your heart to metabolize lactate. There is a little bit of evidence that aerobic training plus resistance work can be beneficial for developing heart rate variability in older runners, but you had probably already established a very sound level of cardiac fitness before you got into the veteran’s age range. In any case, I would not be rush to recommend heavy resistance work for a person with a history valvular heart disease.
    I strongly endorse the idea that if one trains appropriately, one can overcome many potentially serious limitations.

  7. Ewen Says:

    Canute, I’ve been thinking about this again, in view of how easy my HR went to a very high % in my race on Sunday afternoon 28 June. It averaged 93% (quite high for a 2.5k race, starting from ‘rest’) – I was sitting on 95%, yet didn’t feel like I was pushing that hard.

    I’m wondering if the heart just does “the minimum required” to pump enough blood up to lactate threshold. In other words, there’s nothing we can do during a race (short of sprinting) to raise the heart-rate. I recall a blog post by Steve L: where Eric Wainaina said he runs the first half of a marathon at a heart-rate of 61%. So in this case, heart-rate is not limiting speed. If it was, surely he’d push his HR higher and thus run faster?

    Relating this to my case – before my recent injury and loss of fitness a short race would produce a HR of 90%, and there didn’t seem to be anything I could do to raise the HR higher during the race. This leads me to think that a low racing HR is just a by-product of training and doesn’t really help us to race faster – it just means there’s less stress on the heart. The limiting factors to speed are other things – muscular, ‘spring’, stride, economy, etc.

  8. canute1 Says:

    Ewen, You are right that heart rate below the maximum will not limit speed, though maximum cardiac output does depend on the product of maximum heart rate and stoke volume , so if heart rate is relatively low, you are far from peak cardiac output. It is of course good to be far from peak cardiac output, provided you are going as fast as you want to. However, if there is a problem, such as over-training that is limiting your work rate as a protective mechanism (either acting directly on heart or on muscles), then both the pace and the heart rate will be lower than you might have expected, relative to the effort. I would not want to jump to any conclusions about over-training in your case, though I think the fact that you had recently increased training load substantially is reason to weigh up the evidence carefully. On the other hand, you have a well established fitness base, built over many years, so I do not think you should be too alarmed – just vigilant

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