THE RELATION OF HEART RATE TO EXERCISE FITNESS: AN ATTEMPT AT PHYSIOLOGICAL INTERPRETATION OF THE BRADYCARDIA OF TRAINING
Authors: Hall Victor E. 
Published: December 2021

It is painfully obvious that, at this time, no clearly demonstrated mechanism for the bradycardia of training is at hand. Accordingly the present attempt at its explanation has necessarily been speculative. It has, however, proposed a number of possible factors:

(a) A decrease in the intensity of the central cardiovascular discharge made possible by the increased strength of skeletal muscles;

(b) An increase in blood volume, acting through nervous mechanisms regulating central venous pressure; and

(c) A diminished cardioaccelerator effect of the Alam-Smirk chemoreceptor reflex permitted by reduced concentration of metabolites in the interstitial fluid of active muscles made possible by greater capillarization of their fibers.

(d) A diminished cardioaccelerator effect resulting reflexly from the increase in respiratory efficiency induced by training.

As a result of these factors the heart rate at any given level of work is slowed, so reducing the oxygen consumption of the heart and achieving greater myocardial efficiency.

One cannot but feel dissatisfied with such a picture: in it the bradycardia appears merely as a chance result of the action of various heterogeneous factors, rather than the consequence of operation of an integrated system for organismic adaptation to a high level of physical activity. True it would be possible to restate this picture formally as a system with multiple sensors, located in the skeletal muscles, the lungs and the venous system, playing on the central structures controlling the heart rate. What is disturbing is, for instance, the absence of a means whereby there could be transmitted to the centers the effect of such an outstanding consequence of training as strengthening of the left ventricular myocardium. Surely some fairly direct and reliable channel of communication from the ventricle to its pacemaker must exist! Further, it is disturbing that nothing has been said involving cardiac output in the causation of the bradycardia, even though training apparently achieves greater work capacity at lowered total blood flow. Our knowledge of the changes in circulatory adjustment to prolonged heavy exercise is too meager to warrant setting up a formal hypothesis to account for the bradycardia involved therein.

A philosophical question suggests itself at this point: if the circulatory changes resulting from training are adaptive to a high level of physical activity, then is it not possible that the circulatory state of a sedentary individual is equally adaptative to his level of activity? This question suggests studies which would explore the efficiency of circulatory adjustment at levels above, at and below that of common daily life. Indeed, it may be that the relative tachycardia, characteristic of the bedridden, the chronically ill and the denizen of the easy chair may be of value to them. Is it possible that the "unfit" in reality possess a better circulatory adaptation to their restful way of life than those rated "fit" by a test of "exercise fitness"?