Muscle Metaboreflex Modulates Dynamic Cardiovascular Responses to Acute Hypotension in Humans

Abstract

During heavy exercise, the arterial baroreflexes and the muscle metaboreflex are hypothesized to be activated, and moreover to interact in ways that lead to modulation of the primary cardiovascular reflex responses. However, this interaction and its consequences are not fully understood. PURPOSE: We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflex [as reflected by alterations in the dynamic responses of mean arterial blood pressure (MAP), heart rate (HR), cardiac output (CO: by the ultrasound Doppler method) and total vascular conductance (TVC) to acute hypotension] in humans. METHODS: Acute hypotension was induced nonpharmacologically in twelve healthy subjects by releasing bilateral thigh cuffs after nine minutes of suprasystolic resting ischemia with and without muscle metaboreflex activation [via post exercise muscle ischemia after one minute static handgrip exercise at 50% MVC]. RESULTS: The thigh cuff release evoked rapid reduction in MAP and rises in HR, CO and TVC in both control and during muscle metaboreflex activation. The decrease in MAP from baseline was greater (control vs. muscle metaboreflex activation: -28 ± 2.4 vs. -33 ± 2.4 mmHg, p < 0.05), while increase in TVC was smaller (111 ± 8.4 vs. 86 ± 6.8 ml/min/mmHg, p < 0.05) during muscle metaboreflex activation compared to the control condition. Meanwhile, the HR and CO responses were not different between two conditions (ΔHR, 25 ± 1.7 vs. 25 ± 1.2 beats/min; ΔCO, 4.73 ± 0.28 vs. 4.62 ± 0.31 L/min). In addition, the muscle metaboreflex activation enhanced the arterial baroreflex mediated peripheral vasoconstriction as evidenced by a faster return of MAP and TVC to the baseline (The recovery responses were assessed by comparisons of area under the hemodynamic responses-time curve (AUC) during first minute after the thigh cuff release: AUC for MAP, -1165 ± 147 vs. -877 ± 97 mmHg · sec, p < 0.05; AUC for TVC, 4667 ± 489 vs. 2469 ± 369 ml/min/mmHg · sec, p < 0.05.). CONCLUSIONS: These results show that during muscle metaboreflex activation in humans, the arterial baroreflex mediated peripheral vasoconstriction to acute hypotension is augmented. We suggest that this interaction is one of the mechanisms that helps to maintain the elevated arterial blood pressure during activation of the muscle metaboreflex.