Physical Training, Vegetative Regulation, and Cardiac Hypertrophy

Dynamic physical training leads to functional and structural adaptations in the cardiovascular system. Functional changes, such as bradycardia, occur after only relatively little training and in advance of structural changes. They are the result of elevated parasympathetic tone at rest and reduced sympathetic activity in the submaximal range. Sympathetic activity cannot be correlated only with the plasma catecholamine level because the affinity and density of the β-receptors and α receptors are influenced by training. In humans, endurance training appears to result in an elevation in β2-receptors and a decrease in α2 receptors: the results of animal experiments are discrepant. Conformant, however, is the increased responsiveness of the myocardium to isoproterenol with respect to the mechanical response. Independent of this, other changes at the membrane level must be discussed since the intrinsic heart frequency is reduced in athletic individuals following autonomic blockade, even before hypertrophy can be observed. The functional changes remain intact or intensify when cardiac hypertrophy is induced by increased training. The maximum values for training-induced hypertrophy left ventricular muscle mass (LVM) = 3.5 g/kg are about 70–80% of the baseline weights (LVM = 2.1 g/kg). The left ventricle is enlarged during end diastole and end systole, the ejection fraction is normal, and the stroke volume is increased. The mass/volume ratio remains constant (LV = 1.2 g/ml), as does the maximum systolic wall stress (196 × 10 dyn/cm). Compared with pathological forms of hypertrophy and to the normal heart, the trained heart is capable of increasing the stroke volume considerably with exercise and maintaining the increase to a high-frequency range. Unlike pathological forms of hypertrophy, training-induced hypertrophy does not produce impairment in compliance or increase in filling pressure, but rather shows more rapid filling. This effect is catecholamine-dependent and thus can be prevented by β-blockade.