Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

Abstract

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 (F 6,24 = 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 6,24 = 5.4, P < .001), respectively. Norepinephrine (F 1,12 = 12.1, P = .004) and prolactin (F 1,12 = 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.

Irisin and Fibronectin Type III Domain-Containing 5 Responses to Exercise in Different Environmental Conditions

“…Elevated levels of epinephrine and norepinephrine are observed after exercise in all exercise conditions with greater increases in hot environments (17). This study corroborates that epinephrine and norepinephrine increase during exercise, more so in the heat than at RT and cold environment.…”

Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure

“…Whitham et al (2006) demonstrated increased eHsp72 was associated with higher plasma levels of catecholamines and heart rate, whilst it has also been observed that following passive heating, neither epinephrine nor norepinephrine was solely responsible for eHsp72 release (Whitham et al 2007). Johnson and Fleshner (2006) identified α-adrenergic stimulation, notably through norepinephrine elevation (Nielsen et al 1997;Ortega et al 2006;Whitham et al 2006;Giraldo et al 2010;Iguchi et al 2012) as responsible for Hsp72 release into the circulation, this alongside the work of Whitham et al (2006Whitham et al ( , 2007 suggest a requirement for individuals to be presented with sustained physiological challenge during exercise-heat stress (Johnson and Fleshner 2006). Exercise intensity, or α-adrenergic stimulation via norepinephrine is likely required to be above an intensity threshold to elicit significant eHsp72 response with the greater exercise intensity data from Périard et al (2012) leading to data contrasting that of Marshall et al (2006).…”

“…Exercise in hot and humid environments increases physiological strain on the body in comparison with temperate conditions (Galloway and Maughan 1997). Combined with exercise (exercise-heat stress), environmental manipulation to induce hyperthermia (Fehrenbach et al 2001;Oishi et al 2002;Moran et al 2006;Whitham et al 2007;Sandström et al 2008;Iguchi et al 2012) have been reported as stimuli for further increasing eHsp72 compared to exercise alone. Indeed a strong relationship exists between plasma eHsp72 and core temperature (Ruell et al 2006;Sandström et al 2009).…”

Heat therapy promotes the expression of angiogenic regulators in human skeletal muscle

“…For example, as discussed above, whole body heat stress has been shown to trigger the release and recruitment of bone marrow-derived proangiogenic cells (49,66). Further, whole body heat stress evokes a marked increase in sympathoadrenal activity and an associated elevation in circulating levels of catecholamines (27). Catecholamines have been previously shown to contribute to skeletal muscle angiogenesis in a model of peripheral vascular insufficiency (7).…”