Muscle metaboreflex activation speeds the recovery of arterial blood pressure following acute hypotension in humans

Abstract

It has been suggested that the arterial baroreflex and muscle metaboreflex are both activated during heavy exercise and that they interact to modulate primary cardiovascular reflex responses. This proposed interaction and its consequences are not fully understood, however. The purpose of present study was to test our hypothesis that dynamic arterial baroreflex-mediated cardiovascular responses to acute systemic hypotension in humans are augmented when the muscle metaboreflex is active and that this results in a faster recovery of arterial blood pressure. Acute hypotension was induced nonpharmacologically in 12 healthy subjects by releasing bilateral thigh cuffs after 9 min of suprasystolic resting ischemia, with and without muscle metaboreflex activation via postexercise muscle ischemia (PEMI) after 1 min of isometric handgrip exercise at 50% maximum voluntary contraction. The thigh-cuff release evoked rapid reductions in mean arterial pressure (MAP) and increases in heart rate, cardiac output (Doppler), and total vascular conductance (TVC) under control conditions and during PEMI. The reductions in MAP from baseline were greater and the increases in TVC were smaller during PEMI than control. In addition, arterial baroreflex-mediated peripheral vasoconstriction was augmented during PEMI, as evidenced by a near doubling of the rate of recovery of MAP and TVC. These results show that when the muscle metaboreflex is activated in humans, arterial baroreflex-mediated peripheral vasoconstriction elicited in response to acute hypotension is augmented, which halves the time needed for MAP recovery. Such modulation of baroreflex function would be advantageous for maintaining an elevated arterial blood pressure during activation of the muscle metaboreflex.