Is heart muscle or leg muscle the limiting factor?

Both heart muscle and leg muscles play a crucial role in running. The function of both of these types of muscle can be enhanced by training. This raises two major questions:

1) When is the function of the heart the factor that limits our performance and when is skeletal muscle the limiting factor?

2) Are different training regimes required for optimal development of heart and skeletal muscle?

In my next few postings I intend to examine what evidence there is that might help answer these questions, but first is of interest to consider a few similarities and differences between the roles of these two types of muscles.

The heart must beat for life

One of the crucial differences is that the heart must continue to beat throughout life, whereas skeletal muscle is called upon to act for relatively limited periods of time, ranging from a few minutes in middle distance races to a few hours in long distance events such as the marathon. This difference in function necessitates some differences in the options for use of fuel, though during long distance races, both types of muscle rely largely on aerobic metabolism and therefore on an adequate supply of oxygen. From the point of view of the runner, the crucial issue is that a torn skeletal muscle is a frustrating inconvenience whereas serious disruption of the heart is potentially fatal. While the evidence suggests that regular exercise decreases risk of heart attack, unfortunately, there is also clear evidence that very demanding exercise, such as running a marathon, is associated with an increased risk of heart attack within the following 24 hours (Journal of the American College of Cardiology, vol 28, pp 428-431, 1996). In most cases, post mortem examination reveals that such deaths are due to pre-existing abnormality of the heart, especially abnormalities of the coronary vessels that deliver blood to the heart muscle .

The heart is a complex pump

Another crucial difference is in the complexity of the function and therefore on the susceptibility to disruption of that function. In general a skeletal muscle is simply required to either to shorten to achieve the required movement of the bones to which it is attached and thereby flex or extend a joint (i.e concentric contraction), or to resist a forcible extension of the muscle and thereby limit or slow flexion or extension of a joint (eccentric contraction). In fact the amount of tension generated within the muscle must be controlled quite exquisitely if the action of the muscle is to be efficient. Nonetheless the essential requirement is simply to exert the required amount of force along the long axis of the muscle.

In the case of the heart, the required action is much more complex. The heart is a four chambered pump: there are two atria and two ventricles. The right atrium collects the blood that is returned from the tissues of the body (via the two large draining veins known as the inferior and superior vena cava) and transfers it via a valve into the right ventricle. The right ventricle pumps the blood to the lungs to replenish its supply of oxygen and dispose of its burden of carbon dioxide. The freshly oxygenated blood from lungs is collected in the left atrium and transferred into the left ventricle from whence it is pumped into aorta, and thence distributed to the body tissues. This pumping action requires a well coordinated contraction of the four chambers with very precise timing. The timing is controlled by a wave of electrical activity that spreads through the muscular walls of the chambers, from a starting point known as the sinoatrial (SA) node in the wall of the right atrium. The spreading electrical signal is transmitted from the atrial walls to the ventricles via the atrio-ventricular (AV) node.

Left to its own devices, the SA node would fire regularly at a certain base frequency. However various influences including levels of circulating adrenaline and also input from the autonomic nervous system, adjust the rate of firing of the SA node according to the body’s needs.


While the SA node is the usual site from which the spreading electrical impulse that produces contraction is initiated, any heart muscle cell can fire spontaneously, though usually at a rate lower than that of the SA node. If for some reason, such as irritation of the muscle cells by toxins released following damage arising from inadequate blood supply via the coronary arteries, muscle cells other than the SA node fire prematurely and the orderly spread of contraction is disrupted. The wall of the relevant chamber now flaps ineffectually (fibrillation). Provided this fibrillation is confined to the atria, enough blood to fulfill the body’s basic needs is usually drawn into the ventricles as they relax following the previous contraction. Thus the ventricles fill sufficiently to allow ejection of enough blood to meet essential needs provided a ventricular contraction is initiated. In most instances of atrial fibrillation, the AV node takes over the role of initiating an orderly ventricular contraction. Perhaps the person might feel a bit dizzy, but the outcome is not catastrophic. However, if the fibrillation spreads to the ventricles, effective pumping to the tissues of the body cannot occur and the outcome is fatal unless rhythmic contraction is restored very rapidly. Thus ventricular fibrillation is a type of ‘heart attack’ that results in sudden death

Benefits of training

Training might potentially have several benefits to the heart. First of all, there is clear evidence that in heart muscle, as in skeletal muscle, exercise results in increased density of capillaries distributing blood from the coronary arteries to the heart muscle. This would be expected to improve oxygen supply and reduce the risk of heart attack However, as in the case of skeletal muscle, the benefits of training are achieved via compensation for microscopic damage due to the stress of vigorous exercise.

When skeletal muscle is damaged various proteins, including the enzyme creatinine kinase, are released into the blood stream. Following prolonged vigorous exercise, such as running a marathon, blood levels of creatinine kinase rise markedly, indicating appreciable muscle damage. Similarly, when heart muscle is damaged various proteins are released into the blood stream. One characteristic marker of heart muscle damage is a high level of the protein troponin. Elevated troponin levels are observed after prolonged vigorous exercise.

Thus, the mechanism by which the density of capillaries supplying heart muscle is increased, thereby reducing long term risks of a heart attack, appears to involve at least some degree of microscopic damage. Unaccustomed strenuous exercise potentially creates an appreciable short term risk. Hence it is necessary to build up training volume gradually so that the heart gradually accommodates to the demands placed upon it.

As discussed above, in contrast to the risks of damage to skeletal muscle when the athlete might suffer a frustrating but temporary interruption of training, the risks associated with damage to heart muscle are potentially more catastrophic. On the other hand, because the normal demands of an active life style ensure that the heart is continually exercised, it is usually safe for an individual who has been leading an active lifestyle to build up training volume and intensity at a moderate rate. In very rare instances, congenital abnormalities might result in the development of abnormal electrical conducting pathways in the heart, creating the risk of sudden and tragic heart attack in an otherwise fit young person.


Development of capillaries that improve the distribution of blood from the coronary arteries to the heart muscle is not the only beneficial effect of training. It is also possible to increase the size of the heart. There are two principle types of hypertrophy: an increase in the diameter of the ventricles which leads to increased stroke volume; and an increase in the thickness of the walls of the ventricles, which can produce more powerful contraction. Increase in ventricular diameter and stroke volume will result in an increase in aerobic capacity – the ability to deliver oxygen to body tissues, including skeletal muscle, and hence is likely to improve distance running performance.

Various different training strategies have been proposed to maximize the enhancement of stroke volume. I will discuss these training strategies in a future post.

One Response to “Is heart muscle or leg muscle the limiting factor?”

  1. Ewen Says:

    Thanks Canute. I look forward to your next post about training methods to improve stroke volume. The only one I recall reading about is the use of relatively short/fast intervals where the HR is accelerated quickly from a low level to a high level.

    I also wonder about what measurable gain this type of training can produce.

    Re the heart muscle/leg muscle balance, I presume it’s “safer” in events shorter than the marathon if the heart has more “strength” than the legs, so that the legs tire first?

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