Heat stress and cardiovascular, hormonal, and heat shock proteins in humans.

Heat stress and cardiovascular, hormonal, and heat shock proteins in humans.
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DOI:
10.4085/1062-6050-47.2.184
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发表时间:
2012-12
影响因子:
3.3
通讯作者:
Masaki Iguchi;A. Littmann;S. Chang;Lydia A Wester;Jane S. Knipper;R. Shields
Masaki Iguchi;A. Littmann;S. Chang;Lydia A Wester;Jane S. Knipper;R. Shields
中科院分区:
医学2区
文献类型:
--
作者:
Masaki Iguchi;A. Littmann;S. Chang;Lydia A Wester;Jane S. Knipper;R. Shields

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骨关节炎、肥胖和脊髓损伤等疾病限制了患者的运动能力,使他们无法经历许多有据可查的生理应激源。最近的证据表明,这些压力源中的一些可能来自运动引起的体温升高。目的:确定无运动全身热应激是否触发运动引起的心血管、激素和细胞外蛋白反应。设计随机对照试验。设置大学研究实验室。患者或其他参与者25名年轻健康成人(13名男性,12名女性;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)自愿参加。干预(S)参与者在不同的日子坐在有热(73°C)和没有热(26°C)应激的热应激室中30分钟。我们从13名参与者(7名男性,6名女性)的子集中获得了暴露于热应激之前和之后的血液样本。主要观察指标(S)细胞外热休克蛋白(HSP 72)和儿茶酚胺血浆浓度、心率、血压和热感觉。结果热应激30 min后,直肠温度传感器测得的体温升高0.8°C。心率线性增加至131.4 ± 22.4次/分钟(F = 186,P <0.001),收缩压和舒张压分别降低16 mm Hg(F = 10.1,P <0.001)和5 mm Hg(F = 5.4,P <0.001)。血浆中的去甲肾上腺素(F_(12),P = 12.1,P = 0.004)和催乳素(F_(12),P = 30.2,P <0.001)增加(分别为58%和285%)(P <0.05)。HSP 72(F = 44.7,P <0.001)水平随热应激的增加而升高48.7% ± 53.9%。在对照试验期间(安静地坐在热室中,没有热应激),没有心血管或血液变量显示出变化,导致热试验和对照试验之间的差异。结论:我们发现全身热应激触发了运动中观察到的一些生理反应。未来的研究是必要的,以调查是否精心规定的热应激构成一种方法,以增加或补充运动。
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 extracellular 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.