Two components of the nervous system are intimately involved with metabolic regulation during aerobic exercise.
The somatic nervous system carries the stimuli for contraction of the appropriate muscles, and the arrival of a nervous impulse at the end-plate triggers both contraction and a coordinated activation of glycogen breakdown (Fig. 8.8). This is true just as much during aerobic exercise, and there appears to be 'obligatory' breakdown of muscle glycogen associated with muscle contraction, even if there are plentiful substrates in the blood (e.g. if the athlete has eaten well beforehand).
The sympathetic nervous system, accompanied by adrenaline secretion from the adrenal medulla, brings about the necessary changes in the cardiovascular system and the mobilisation of stored fuels, glycogen and triacylglycerol.
An important part of the physiological response during endurance exercise is an increase in cardiac output (both the rate and force of heart contraction increase), and an increased delivery of blood to skeletal muscle. The increase in cardiac output is mediated mainly by the sympathetic nervous system, acting on P-adrenergic receptors in the heart. An increase in cardiac output in itself might cause an increase in muscle blood flow, but there is an additional specific dilatation of the blood vessels in the muscle. Blood flow to the active muscle increases almost instantaneously at the onset of exercise. The mechanism that brings this about is not entirely clear. It used to be thought that this was mediated by cholinergic impulses from the sympathetic nerves (discussed in Chapter 7, Section 7.3.2 and Fig. 7.5). Skeletal muscle is unusual in that activation of the sympathetic nervous system causes vasodilatation; in other organs (e.g. skin, kidneys and abdominal organs) blood flow is restricted by sympathetic activation. However, the evidence that this occurs in humans is inconclusive and it is now thought to occur more through vasodilatory effects of substances released from the contracting muscle, including lactate ions and the accompanying hydrogen ions. Whatever the mechanism, the effect is that blood is diverted to the muscles, allowing greater delivery of substrates (including O2), and also removal of the products of metabolism (lactic acid and CO2 in particular) (Fig. 8.11).
Increased delivery of O2 to the muscles and removal of CO2 from the body also requires increased depth and rate of breathing. This is brought about mainly by the fall in blood pH (increase in H+ ion concentration) which occurs as lactic acid and CO2 are produced. The change in pH is sensed by receptors in the brainstem (see Section 18.104.22.168) which trigger changes in respiration.
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