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Abstract

Both exercise and passive heating cause acute reductions in blood pressure. It is unknown if exercise-heat stress causes likewise reductions or greater when combined. PURPOSE: This project tested the hypothesis that the resting and exercise-heat stress cause hypotension and improvements in arterial stiffness. METHODS: Seven healthy active (7 day activity: 9887±3564 steps/day; VO2max: 52±10 mL/kg/min ) subjects (5M/2F, 24±9y, 171±6cm, 68±7kg) completed a 30 min baseline rest followed by 60 min at an exercise intensity of their choice that represented their perceived exertion (RPE) of 12 (between light and somewhat hard) on a 20-point rating scale while being blinded to the ergometer (watts) in a hot dry to humid (42.3±0.3℃; initial 10.4±0.4% relative humidity [Rh] that increased to 62.2±5.3%Rh) and control neutral dry (22.9±1.0℃; 11.5±1.9%Rh) condition in random order separated by at least 7 days. Heart rate (HR), peripheral blood pressure (systolic [SYS], diastolic [DIA], mean arterial pressure [MAP]), arterial stiffness (augmentation index [AIX@75]; pulse wave velocity [PWV]) and total vascular resistance (TVR), and central blood pressures (cSYS, cDIA) were measured after the 30 min baseline rest and 60 min of exercise recovery. A 2-way repeated measures analysis of variance was used to examine interaction and main effects for condition x time. RESULTS: Exercise intensity was slightly greater (54±1 vs 48±3%VO2max, P Pre- and post-exercise heat stress resulted in an increase in heart rate (pre-: ∆14±11BPM, post-: ∆26±12BPM) and AIX@75 (pre-: ∆7±7%, post-: ∆14±12%) and a decrease in post-exercise TVR (∆0.1±0.2s*mmHg/ml) (Main effect: Condition; P≤0.03). Only post-exercise heat stress reduced SYS (: ∆12±14mmHg), cSYS (∆9±12mmHg), and PWV(∆0.4±0.4m/s) (Condition x Time; P≤0.03). CONCLUSION: Low intensity exercise heat stress has greater acute cardiovascular benefits for reducing arterial stiffness and peripheral and central systolic pressures compared to exercise in neutral conditions.

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