Enhancement of parasympathetic cardiac activity during activation of muscle metaboreflex in humans

Abstract

We measured the changes in heart rate (HR) variability estimated from the standard deviation of the R-R intervals to evaluate cardiac parasympathetic tone noninvasively before and during activation of muscle metaboreflex induced by postexercise muscle ischemia. Eight healthy male subjects performed sustained handgrip at 50% maximal voluntary contraction followed by forearm occlusion. Mean arterial pressure, cardiac stroke volume, and ratio of cardiac preejection period to left ventricular ejection time (PEP/LVET) were also measured. During the 2-min occlusion after 60 s of handgrip with voluntary respiration, HR variability and mean arterial pressure were significantly increased from baseline (54.4 +/- 6.1 to 80.1 +/- 12.8 ms and 81 +/- 1 to 99 +/- 3 mmHg, respectively) and PEP/LVET was decreased from resting level of 0.404 +/- 0.022 to 0.363 +/- 0.036. During occlusion and recovery, HR did not change from baseline level in any experiment. There was no influence of occlusion itself or of cessation of exercise per se on any parameters. Although overall enhanced HR variability was seen, probably due to lower breathing frequency and larger tidal volume, similar results were also obtained from an experiment with controlled respiration, showing that the increase in HR variability was not due to the changes in tidal volume or breathing frequency during occlusion. In conclusion, the HR variability is increased during activation of the muscle metaboreflex induced by postexercise muscle ischemia in humans. This finding shows that the parasympathetic cardiac tone is enhanced during activation of the muscle metaboreflex in humans and balances enhanced cardiac sympathetic activity to result in an unchanged HR.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle metaboreflex modulates the arterial baroreflex dynamic effects on peripheral vascular conductance in humans

“…3D). Changes in cardiac stroke volume could also alter the cardiac output; however, previous studies have shown that little change in stroke volume is elicited either by neck chamber stimuli (18) or during PEMI (15). Moreover, according to recent findings by Ogoh et al (18), the peak MAP response (normally observed at 6 -8 s after the start of a 5-s neck chamber stimulus) is mainly due to reflex changes in total vascular conductance, with little contribution being made by any change in cardiac output.…”

“…It was demonstrated 10 or more years ago that the arterial baroreflexes oppose the pressor response evoked by the muscle metaboreflex (15,19,29,31). Later, evidence was provided of modulations of the arterial-baroreflex control of both blood pressure and MSNA during muscle metaboreflex activation (6 -9, 20).…”

“…Because the HR responses to neck chamber stimuli are predominantly mediated by the CBR control of cardiac parasympathetic activity (5), our results suggest that the interaction between the muscle metaboreflex and the arterial baroreflex does not affect the CBR-mediated regulation of cardiac parasympathetic tone. Nishiyasu et al (15) suggested that cardiac parasympathetic tone would increase during activation of the muscle metaboreflex (i.e., during PEMI) in humans. They suggested that such an increase might form part of the counteraction by the arterial baroreflex of the raised blood pressure induced by the muscle metaboreflex in humans.…”

“…Two types of interaction between these reflexes have been demonstrated to lead to such modulation. In the first type, the arterial baroreflexes act to oppose the pressor response elicited via the muscle metaboreflex (15,19,29,31). Evidence for this effect has been obtained during dynamic exercise in dogs (31) as well as during static handgrip exercise (29) and postexercise muscle ischemia (PEMI) in humans (15).…”

“…In the first type, the arterial baroreflexes act to oppose the pressor response elicited via the muscle metaboreflex (15,19,29,31). Evidence for this effect has been obtained during dynamic exercise in dogs (31) as well as during static handgrip exercise (29) and postexercise muscle ischemia (PEMI) in humans (15). The second type of interaction involves a modulation of arterial baroreflex function during muscle metaboreflex activation (6 -9, 20).…”