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This Article Full Text Full Text (PDF) All Versions of this Article: 91/1/73    most recent expphysiol.2005.031179v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by O'Leary, D. S Search for Related Content PubMed PubMed Citation Articles by O'Leary, D. S Related Collections Themed Issue papers Human, Environmental & Exercise

¹ Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201

This brief review summarizes recent studies describing the potential role of the muscle metaboreflex in mediating the altered cardiovascular responses to dynamic exercise in heart failure 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 response. 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 involved in 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 probably 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 probably contributes to the enhanced sympatho-excitation seen during exercise in heart failure.

(Received 1 September 2005; accepted after revision 13 September 2005; first published online 22 September 2005)
Corresponding author D. S. O'Leary: Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA. Email: doleary{at}med.wayne.edu