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.
Institute for Exercise and Environmental Medicine, Texas Health Presbyterian Hospital of Dallas, University of Texas Southwestern Medical Center, Dallas, TX, USA.
J Therm Biol. 2019 Aug;84:266-273. doi: 10.1016/j.jtherbio.2019.07.017. Epub 2019 Jul 13.
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.
被动性体温过高暴露会在停止热应激后引起急性低血压反应。动物研究充分证明了慢性热应激会引发代谢和脂质改变。然而，目前尚不清楚运动热适应是否也会导致人类的慢性血压、脂质和免疫反应更有利。
本研究旨在测试以下假设，即 10 天的运动热适应（HA）会导致运动后动脉血压降低更大，代谢、脂质和免疫反应更有利，而中性条件下（CON）的 10 天运动则不会。
13 名健康的久坐参与者（8M/5F，28±6 岁，78±17kg），以平衡设计完成 10 天（90 分钟/天的运动回合）的热适应（内部温度升高 1.5°C，在 42°C，28%Rh）和对照（CON：23°C，42%Rh）方案，间隔 2 个月洗脱期。在运动日 1 和 10 的运动后 1 小时，分别在 HA/CON 之前和之后测量血压。在 HA/CON 之前和之后测量代谢、脂质和免疫参数。
与中性条件下的运动相比（条件主效应，P≤0.004），在 HA/CON 下进行热应激运动时，运动后的低血压（收缩压；-6mmHg，舒张压；-8mmHg，和平均动脉压；-7mmHg）在第 1 天和第 10 天都更大。仅从 HA 前到 HA 后，总胆固醇（168±19 到 157±15；P<0.03）和甘油三酯（137±45 到 111±30；P<0.03）降低，而绝对淋巴细胞（-26%）、单核细胞（-22%）和嗜碱性粒细胞（-49%）显著减少（每个 P≤0.04）。只有在 HA 后，中性粒细胞的相对值（增加 18%）和淋巴细胞的相对值（减少 20%）才会发生变化（每个 P≤0.04）。
这些数据表明，无论热适应状态如何，在热环境中运动都会引起剧烈的运动后低血压反应，而 HA 则会导致有利的脂质和免疫特征变化。进一步研究运动热适应对血管、代谢和免疫反应的影响，将为血管、代谢和免疫功能障碍的其他临床人群提供益处。
