Question

3. Describe the control of cardiovascular function during exercise including local control, the metaboreflex, central control and baroreceptor resetting.

Please give a detailed answer. Add supportive equations if possible.

Answer 1

Physical activities with large muscle mass, such as running, cycling, and rowing, can produce a reduction in systemic vascular resistance (SVR) because of the intense metabolic vasodilatation in the muscle vasculature via functional sympatholysis. This fact constitutes a challenge for the cardiovascular apparatus and it would cause a drop in blood pressure if control mechanisms did not contemporarily augment cardiac output (CO). Thus, the active muscle competes with blood pressure regulation for blood flow. Despite the vasodilation-induced SVR decrease, dynamic exercise in normal subjects is characterized only by a small to moderate increase in mean arterial pressure (MAP). Convincing evidence demonstrates that this fine hemodynamic tuning is determined by the activity of neural mechanisms which control the cardiovascular system and regulate circulation to guarantee adequate oxygen supply and washout of metabolic end-products to exercising muscles. These mechanisms also regulate arterial blood pressure, so that perfusion of the vital organs is reached and blood pressure does not vary excessively.

There are at least three neural mechanisms participating in this cardiovascular regulation: (1) the exercise pressor reflex, (2) the central command, and (3) the arterial baroreflex.

The medulla contains the major nuclei that control blood pressure and the cardiovascular system. These nervous circuits are extensively reviewed in other excellent papers . It is believed that the “central command” sets a basal level of sympathetic activity and vagal withdrawal closely related to the intensity of the strain and to motor drive from the motor cortex. In this neural mechanism, the cardiovascular control areas located in the medulla are activated by regions of the brain responsible for motor unit recruitment. This basic level of autonomic activation is then modulated by the exercise pressor reflex, which originates from peripheral signals arising from mechano- and metaboreceptors (types III and IV nerve endings within the muscle) that reflexively modulate sympathetic activity taking into account the mechanical and metabolic conditions in the working muscle. In detail, it is known that groups III and IV nerve endings excite neurons in the nucleus of the solitary tract (NST) in the medulla. A subset of the NTS neurons activated by these afferents is thought to directly excite neurons of the ventrolateral medulla, which are the primary output for sympathetic activity. This autonomic modulation originating from the central command and the exercise pressor reflex increases HR and enhances myocardial contractility, which together concur in raising CO. Sympathetic stimulation is in turn modulated by baroreflexes, which oppose any mismatch between vascular resistance and CO by controlling muscle vasodilatation and cardiac chronotropism in order to avoid excessive variation in blood pressure.

Thus, dynamic exercise elicits marked cardiovascular and autonomic adjustments which include increases in CO, MAP, and SVR reduction. This hemodynamic status is regulated by the nervous system by the integration of information coming from the motor cortex (central command), from muscle receptors (exercise pressor reflex), and from receptors in the aortic, carotid, heart, and pulmonary arteries (arterial and cardiopulmonary baroreflexes).

One key point of the functioning of these reflexes is how they interact during dynamic exercise. There is some redundancy between them and neural occlusion can be operative. Moreover, from several observations it appears that both the central command and the exercise pressor reflex can modulate the activity of the baroreflex. In this review, we will briefly summarize the activities of these neural reflexes with particular emphasis on their integration during dynamic exercise.