Review articleNeural mechanisms of cardiovascular regulation during exercise
Introduction
Physical exercise is characterized by increases in arterial blood pressure (AP), heart rate (HR) and cardiac output. The appropriate cardiovascular responses to exercise are largely accomplished by changes in autonomic nervous system activity.
Three mechanisms have been described as playing a role in cardiovascular neural regulation during exercise. In the first mechanism, activation of regions of the brain responsible for the recruitment of skeletal muscle motor units concomitantly activates neuronal circuits within the medulla, establishing changes in parasympathetic and sympathetic efferent activity that determine the cardiovascular responses during skeletal muscle contraction. This mechanism has been termed “Central Command” (Goodwin et al., 1972). In the second mechanism, neural signals arising from stimulation of chemosensitive receptors in the contracting muscles would activate reflexly the cardiovascular control areas in the medulla, and this has been called the “exercise pressor reflex” or the “muscle metaboreflex” Mitchell, 1985, O'Leary, 1993. The third mechanism involves the arterial baroreceptor reflex (Rowell, 1993).
Results from human studies have clearly indicated that both the central command and the reflex neural mechanisms play an important role in determining the cardiovascular responses to exercise and that there is some redundancy of the control systems (Mitchell, 1990).
This brief review addresses current hypotheses concerning the reflex control of circulation during exercise in humans. In particular, the specific objective of this review is to describe how time and frequency domain analysis of blood pressure and heart rate variability signals permitted to gain new insights onto reflex mechanisms of cardiovascular regulation during exercise, without the need of perturbing the cardiovascular system from the outside and utilizing fully noninvasive approaches. For more detailed discussion of cardiovascular control during exercise, the reader is referred to other more complete and extensive reviews Mitchell and Schmidt, 1983, Rowell et al., 1996.
Section snippets
Muscle metaboreflex
Group III and IV myelinated and unmyelinated somatic fibers constitute the afferent arm of this reflex McCloskey and Mitchell, 1972, Kaufman et al., 1988. When blood flow and oxygen delivery to contracting muscles is insufficient for the rate of metabolism, chemical products of muscle metabolism accumulate within the muscle and stimulate group III and IV afferents. Activation of these afferents elicits the reflex increase in sympathetic nerve activity and blood pressure, termed exercise pressor
Arterial baroreflex
Under resting conditions, an increase in AP usually induces a decrease in HR through a baroreceptive reflex mechanism. During muscular exercise, the increase in AP is accompanied by a concomitant increase in HR, which is an important component in blood pressure rise. This phenomenon has raised the question on how arterial baroreflex is altered by exercise to allow this deviation from normal baroreflex physiology to occur. However, whether and how arterial baroreflex is altered is a
Effects of central command and muscle reflexes on the baroreceptor reflex
Another issue of current interest is how the arterial baroreflex is modulated by the central command and the reflex drive from muscles. Rowell (1993) and Rowell et al. (1996) suggested that neural input from central command acts on the central neuron pool, receiving baroreceptor afferents to reset the arterial baroreflex from the onset of exercise. This hypothesis would be supported by the study of Di Carlo and Bishop (1992) who reported a greater increase in HR and renal sympathetic nerve
Conclusions
The objective of this review was to describe how time and frequency domain analysis of arterial pressure and heart rate variability signals could be a valuable tool to investigate the reflex mechanisms of cardiovascular regulation during exercise in a fully noninvasive way.
This experimental approach allowed a distinctive insight into the integrated reflex neural regulation of HR during exercise by having used nonperturbational techniques and by avoiding artificially isolating the influence of
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