Exercise heat acclimation causes post-exercise hypotension and favorable improvements in lipid and immune profiles: A crossover randomized controlled trial.


Journal

Journal of thermal biology
ISSN: 0306-4565
Titre abrégé: J Therm Biol
Pays: England
ID NLM: 7600115

Informations de publication

Date de publication:
Aug 2019
Historique:
received: 24 05 2019
revised: 17 06 2019
accepted: 11 07 2019
entrez: 31 8 2019
pubmed: 31 8 2019
medline: 28 1 2020
Statut: ppublish

Résumé

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. 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). 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. 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). 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.

Sections du résumé

BACKGROUND 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 OBJECTIVE
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 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 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 CONCLUSIONS
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.

Identifiants

pubmed: 31466764
pii: S0306-4565(19)30288-8
doi: 10.1016/j.jtherbio.2019.07.017
pii:
doi:

Substances chimiques

Triglycerides 0
Cholesterol 97C5T2UQ7J

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

266-273

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Eric Rivas (E)

Exercise & Thermal Integrative Physiology Laboratory, Department of Kinesiology & Sport Management, Texas Tech University, Lubbock, TX, USA; Obesity Research Institute, Texas Tech University, Lubbock, TX, USA. Electronic address: eric.rivas@ttu.edu.

Craig G Crandall (CG)

Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Oscar E Suman (OE)

Department of Surgery, University of Texas Medical Branch Galveston, TX, USA.

Naima Moustaid-Moussa (N)

Obesity Research Institute, Texas Tech University, Lubbock, TX, USA; Department of Nutritional Sciences, Texas Tech University, Lubbock, TX, USA.

Vic Ben-Ezra (V)

Department of Kinesiology, Texas Woman's University, Denton, TX, USA.

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