TY - JOUR
T1 - Exercise heat acclimation causes post-exercise hypotension and favorable improvements in lipid and immune profiles
T2 - A crossover randomized controlled trial
AU - Rivas, Eric
AU - Crandall, Craig G.
AU - Suman, Oscar E.
AU - Moustaid-Moussa, Naima
AU - Ben-Ezra, Vic
N1 - Funding Information:
The authors acknowledge the financial support from The American Heart Association Predoctoral Fellowship , SouthWest Affiliate, United States and the National Swimming Pool Foundation, United States, Grants to E.R.
Publisher Copyright:
© 2019 Elsevier Ltd
PY - 2019/8
Y1 - 2019/8
N2 - Background: Passive hyperthermic exposure causes an acute hypotensive response following the cessation of heat stress. Chronic heat stress is well documented in animal studies to instigate metabolic and lipid alterations. However, it is unknown if exercise-heat acclimation also causes favorable chronic blood pressure, lipid, and immune responses in humans. Purpose: This project tested the hypothesis that 10-day exercise-heat acclimation (HA) would cause greater post-exercise reductions in arterial blood pressure and favorable metabolic, lipid, and immune responses compared to 10-day exercise under neutral conditions (CON). Methods: Thirteen healthy sedentary participants (8M/5F, 28 ± 6y, 78 ± 17 kg), completed a 10-day (90 min/day exercise bout) clamped hyperthermia HA (increase internal temperature 1.5 °C, in 42 °C, 28% Rh) and control (CON: 23 °C, 42% Rh) protocols in a counterbalanced design with a 2 month washout. Pre- and post-exercise HA/CON blood pressures were taken 1-h post-exercise on exercise days 1 and 10. Metabolic, lipid and immune panels were taken pre-post HA/CON. Results: Exercise under heat stress had greater post-exercise hypotension (systolic; -6 mmHg, diastolic; -8 mmHg; and mean arterial pressure; -7 mmHg) on both days 1 and 10 compared to exercise under neutral conditions (main effect for condition, P ≤ 0.004). Only from pre-to-post HA, total cholesterol (168 ± 19 to 157 ± 15; P < 0.03) and triglycerides (137 ± 45 to 111 ± 30; P < 0.03) were reduced, while absolute lymphocytes (−26%), monocytes (−22%), and basophils (−49%) significantly decreased (each P ≤ 0.04). Relative values of neutrophils increased (18%) and lymphocytes decreased (−20%) only after HA (P ≤ 0.04). Conclusion: These data indicate that exercise in the heat (regardless of acclimation status) causes a profound post-exercise hypotensive response, while HA causes favorable lipid, and immune profile changes. Further examination of exercise-heat acclimation on vascular, metabolic, and immune responses will offer insight for benefits in other clinical populations with vascular, metabolic and immune dysfunction.
AB - Background: Passive hyperthermic exposure causes an acute hypotensive response following the cessation of heat stress. Chronic heat stress is well documented in animal studies to instigate metabolic and lipid alterations. However, it is unknown if exercise-heat acclimation also causes favorable chronic blood pressure, lipid, and immune responses in humans. Purpose: This project tested the hypothesis that 10-day exercise-heat acclimation (HA) would cause greater post-exercise reductions in arterial blood pressure and favorable metabolic, lipid, and immune responses compared to 10-day exercise under neutral conditions (CON). Methods: Thirteen healthy sedentary participants (8M/5F, 28 ± 6y, 78 ± 17 kg), completed a 10-day (90 min/day exercise bout) clamped hyperthermia HA (increase internal temperature 1.5 °C, in 42 °C, 28% Rh) and control (CON: 23 °C, 42% Rh) protocols in a counterbalanced design with a 2 month washout. Pre- and post-exercise HA/CON blood pressures were taken 1-h post-exercise on exercise days 1 and 10. Metabolic, lipid and immune panels were taken pre-post HA/CON. Results: Exercise under heat stress had greater post-exercise hypotension (systolic; -6 mmHg, diastolic; -8 mmHg; and mean arterial pressure; -7 mmHg) on both days 1 and 10 compared to exercise under neutral conditions (main effect for condition, P ≤ 0.004). Only from pre-to-post HA, total cholesterol (168 ± 19 to 157 ± 15; P < 0.03) and triglycerides (137 ± 45 to 111 ± 30; P < 0.03) were reduced, while absolute lymphocytes (−26%), monocytes (−22%), and basophils (−49%) significantly decreased (each P ≤ 0.04). Relative values of neutrophils increased (18%) and lymphocytes decreased (−20%) only after HA (P ≤ 0.04). Conclusion: These data indicate that exercise in the heat (regardless of acclimation status) causes a profound post-exercise hypotensive response, while HA causes favorable lipid, and immune profile changes. Further examination of exercise-heat acclimation on vascular, metabolic, and immune responses will offer insight for benefits in other clinical populations with vascular, metabolic and immune dysfunction.
KW - Blood pressure
KW - Exercise heat therapy
KW - Hyperthermia
KW - Thermal stress
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U2 - 10.1016/j.jtherbio.2019.07.017
DO - 10.1016/j.jtherbio.2019.07.017
M3 - Article
C2 - 31466764
AN - SCOPUS:85068968682
SN - 0306-4565
VL - 84
SP - 266
EP - 273
JO - Journal of Thermal Biology
JF - Journal of Thermal Biology
ER -