Whole body heat stress attenuates the pressure response to muscle metaboreceptor stimulation in humans

Jian Cui, Cheryl Blaha, Lawrence I Sinoway, Jian Cui, Cheryl Blaha, Lawrence I Sinoway

Abstract

The effects of whole body heat stress on sympathetic and cardiovascular responses to stimulation of muscle metaboreceptors and mechanoreceptors remains unclear. We examined the muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate in 14 young healthy subjects during fatiguing isometric handgrip exercise, postexercise circulatory occlusion (PECO), and passive muscle stretch during PECO. The protocol was performed under normothermic and whole body heat stress (increase internal temperature ~0.6°C via a heating suit) conditions. Heat stress increased the resting MSNA and heart rate. Heat stress did not alter the mean blood pressure (MAP), heart rate, and MSNA responses (i.e., changes) to fatiguing exercise. During PECO, whole body heat stress accentuated the heart rate response [change (Δ) of 5.8 ± 1.5 to Δ10.0 ± 2.1 beats/min, P = 0.03], did not alter the MSNA response (Δ16.4 ± 2.8 to Δ17.3 ± 3.8 bursts/min, P = 0.74), and lowered the MAP response (Δ20 ± 2 to Δ12 ± 1 mmHg, P < 0.001). Under normothermic conditions, passive stretch during PECO evoked significant increases in MAP and MSNA (both P < 0.001). Of note, heat stress prevented the MAP and MSNA responses to stretch during PECO (both P > 0.05). These data suggest that whole body heat stress attenuates the pressor response due to metaboreceptor stimulation, and the sympathetic nerve response due to mechanoreceptor stimulation.

Keywords: autonomic; hyperthermia; mechanoreceptor; metaboreceptor; sympathetic.

Copyright © 2016 the American Physiological Society.

Figures

Fig. 1.
Fig. 1.
Representative tracings of handgrip force, passive stretch force (EOW), heart rate (HR), muscle sympathetic nerve activity (MSNA), and arterial blood pressure (BP) in normothermic (top) and heat stress (bottom) conditions in one subject. bpm, Beats/min. In some subjects, the EOW started at 1 min from the onset of cuff inflation, as shown here, and the PECO data in these subjects were obtained in the 1.5-min window following the EOW. In other subjects, the EOW was performed during the last 1.5 min of the 4-min occlusion, and the PECO data in those subjects were obtained in the 1.5-min window before the EOW.
Fig. 2.
Fig. 2.
Absolute mean arterial pressure (MAP), HR, and MSNA burst rate and total activity, before exercise resting baseline (Rest) and during the last minute of the handgrip exercise (HG), PECO, and passive stretch during the occlusion (PECO + EOW) in normothermic (open bars) and heat stress (solid bars) conditions. MAP was calculated from the blood pressure waveform obtained from the Finometer. Values are means ± SE. *Significantly different from the respective normothermic period (P < 0.05). †Significantly different from the respective resting baseline before exercise (P < 0.05).
Fig. 3.
Fig. 3.
Increases in MAP, HR, and MSNA relative to resting baseline [i.e., change (Δ)] during postexercise circulatory occlusion (PECO) only and the passive stretch during the occlusion (PECO + EOW), while subjects were in normothermic and heat stress conditions. Open bars: PECO only under normothermia; shaded bars: PECO + EOW under normothermia; hatched bars: PECO only under heat stress; shaded hatched bars: PECO + EOW under heat stress. Values are means ± SE. *Significantly different from normothermia (P < 0.05). The passive stretch in normothermic condition evoked significant increases in MSNA and MAP (shaded vs. open bars), while these responses in heat stress were not significant (shaded hatched vs. hatched bars).

Source: PubMed

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