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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 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. Interventions): 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 (F 624 = 186, P .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F 6,24 = 10.1, P .001) and 5 mm Hg (F 624 = 5.4, P .001), respectively. Norepinephrine (F 112 = 12.1, P =.004) and prolactin (F 112 = 30.2, P .001) increased in the plasma (58% and 285%, respectively) (P .05). The HSP72 (F 1,12 = 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名自愿参加的年轻健康成年人(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)。干预):参与者分别在有热(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,血压和热感知。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(F 624 = 186,P <.001),收缩压和舒张压降低分别降低16毫米汞柱(F 6,24 = 10.1,P <.001)和5毫米汞柱(F 624 = 5.4,P <.001)。血浆中去甲肾上腺素(F 112 = 12.1,P = .004)和催乳激素(F 112 = 30.2,P <.001)增加(分别为58%和285%)(P <.05)。 HSP72(F 1,12 = 44.7,P <.001)水平随热应激而增加48.7%±53.9%。对照试验期间(没有坐在热室中安静放置,没有热应力),没有心血管或血液变量显示变化,因此导致热量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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