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首页> 外文期刊>Journal of athletic training >Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans
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Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

机译：人类的热应激以及心血管，激素和热休克蛋白

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Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.
机译：背景：骨关节炎，肥胖和脊髓损伤等疾病限制了患者的运动能力，使他们无法承受许多有据可查的生理应激源。最近的证据表明，其中一些压力源可能是运动引起的体温升高。目的：确定不进行运动的全身热应激是否会触发运动的心血管，激素和细胞外蛋白反应。设计：随机对照试验。地点：大学研究实验室。患者或其他参与者：25位自愿参加的年轻健康成年人（13位男性，12位女性;年龄= 22.1±2.4岁，身高= 175.2±11.6 cm，体重= 69.4±14.8 kg，体重指数= 22.6±4.0）。干预措施：参与者在分开的日子中，在有热（73°C）和无热（26°C）压力的热应激室内坐了30分钟。在接触热应激前后，我们从13名参与者（7名男性，6名女性）的子集中获得了血液样本。主要观察指标：细胞外热休克蛋白（HSP72）和儿茶酚胺血浆浓度，心率，血压和热知觉。结果：热应激30分钟后，通过直肠传感器测得的体温升高了0.8°C。心率线性增加至每分钟131.4±22.4次搏动（F6,24 = 186，P <.001），收缩压和舒张压降低16 mm Hg（F6,24 = 10.1，P <.001）和5 mm Hg （F6,24 = 5.4，P <.001）。血浆中去甲肾上腺素（F1,12 = 12.1，P = .004）和催乳素（F1,12 = 30.2，P <.001）增加（分别为58％和285％）（P <.05）。 HSP72（F1,12 = 44.7，P <.001）水平随热应力增加48.7 ％±53.9 ％。在对照试验期间（无热量压力的安静坐在加热室中），没有心血管或血液变量显示变化，从而导致热试验和对照试验之间存在差异。结论：我们发现，全身热应激会触发运动中观察到的某些生理反应。有必要进行进一步的研究，以调查精心规定的热应激是否构成增加或补充运动的方法。

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