Whole body heat stress attenuates baroreflex control of muscle sympathetic nerve activity during postexercise muscle ischemia.
Both whole body heat stress and stimulation of muscle metabolic receptors activate muscle sympathetic nerve activity (MSNA) through nonbaroreflex pathways. In addition to stimulating muscle metaboreceptors, exercise has the potential to increase internal temperature. Although we and others report that passive whole body heating does not alter the gain of the arterial baroreflex, it is unknown whether increased body temperature, often accompanying exercise, affects baroreflex function when muscle metaboreceptors are stimulated. This project tested the hypothesis that whole body heating alters the gain of baroreflex control of muscle sympathetic nerve activity (MSNA) and heart rate during muscle metaboreceptor stimulation engaged via postexercise muscle ischemia (PEMI). MSNA, blood pressure (BP, Finometer), and heart rate were recorded from 11 healthy volunteers. The volunteers performed isometric handgrip exercise until fatigue, followed by 2.5 min of PEMI. During PEMI, BP was acutely reduced and then raised pharmacologically using the modified Oxford technique. This protocol was repeated two to three times when volunteers were normothermic, and again during heat stress (increase core temperature approximately 0.7 degrees C) conditions. The slope of the relationship between MSNA and BP during PEMI was less negative (i.e., decreased baroreflex gain) during whole body heating when compared with the normothermic condition (-4.34 +/- 0.40 to -3.57 +/- 0.31 units x beat(-1) x mmHg(-1), respectively; P = 0.015). The gain of baroreflex control of heart rate during PEMI was also decreased during whole body heating (P < 0.001). These findings indicate that whole body heat stress reduces baroreflex control of MSNA and heart rate during muscle metaboreceptor stimulation.
Cui
Jian
J
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, TX 75231, USA.
Shibasaki
Manabu
M
Davis
Scott L
SL
Low
David A
DA
Keller
David M
DM
Crandall
Craig G
CG
D000328:Adult; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects; D001831:Body Temperature / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D018737:Hand Strength; D006339:Heart Rate / Q000502:physiology; D018882:Heat Stress Disorders / Q000503:physiopathology*; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D012039:Regional Blood Flow; D012867:Skin / Q000098:blood supply; D013546:Sweating / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine