Received September 1, 2005
Revised September 12, 2005
Accepted after revision September 13, 2005

¹ Wayne State University School of Medicine

^* To whom correspondence should be addressed. E-mail: doleary{at}med.wayne.edu.

	Abstract

This brief review summarizes recent studies describing the potential role of the muscle metaboreflex in mediating the altered cardiovascular responses to dynamic exercise and the interaction between the muscle metaboreflex and the arterial baroreflex in these responses. In normal dogs, activation of the muscle metaboreflex (via partial reductions in hindlimb blood flow) during submaximal exercise elicits a powerful pressor responses. This increase in arterial pressure is mediated by an increase in cardiac output with little, if any, peripheral vasoconstriction. The metaboreflex pressor response is buffered by the arterial baroreflex via baroreflex mediated inhibition of metaboreflex induced peripheral vasoconstriction. In contrast, after induction of heart failure, the mechanisms of the muscle metaboreflex are shifted to vasoconstriction with little, if any, increase in cardiac output. The loss of the cardiac output response of the metaboreflex in heart failure likely stems from inability to improve ventricular function. The shift towards vasoconstriction in this setting may be due to depressed ability of the arterial baroreflex to buffer metaboreflex induced peripheral vasoconstriction. The relative underperfusion of active skeletal muscle in heart failure may tonically activate the metaboreflex and this likely contributes to the enhanced sympatho- excitation seen during exercise in heart failure.

Key Words: Autonomic nervous system, Blood pressure, Exercise

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