During high-intensity dynamic exercise, O2 delivery to active skeletal muscles is enhanced through marked increases in both cardiac output and skeletal muscle blood flow. When the musculature is vigorously engaged in exercise, the human heart lacks the pumping capacity to meet the blood flow demands of both the skeletal muscles and other organs such as the brain. Vasoconstriction must therefore be induced through activation of sympathetic nervous activity to maintain blood flow to the brain and to produce the added driving pressure needed to increase flow to the skeletal muscles. In this review, we first briefly summarize the local vascular and neural control mechanisms operating during high-intensity exercise. This is followed by a review of the major neural mechanisms regulating blood pressure during high-intensity exercise, focusing mainly on the integrated activities of the arterial baroreflex and muscle metaboreflex. In high cardiac output situations, such as during high-intensity dynamic exercise, small changes in total peripheral resistance can induce large changes in blood pressure, which means that rapid and fine regulation is necessary to avoid unacceptable drops in blood pressure. To accomplish this rapid regulation, arterial baroreflex function may be modulated in various ways through activation of the muscle metaboreflex and/or other neural mechanisms. Moreover, this modulation of the arterial baroreflex may change over the time course of an exercise bout, or to accommodate changes in exercise intensity. Within this model, integration of arterial baroreflex modulation with other neural mechanisms plays an important role in cardiovascular control during high-intensity exercise.
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