The Effect of Exercise in Cool, Control and Hot Environments on Cardioprotective HSP70 Induction

Abstract

A number of environmental and metabolic stimuli rapidly induce the expression of several highly conserved proteins such as heat shock proteins (HSPs) or stress proteins. The purpose of this study was to investigate the effects of a single bout of submaximal exercise in varying ambient temperatures on cardiac and skeletal muscle. Adult male Sprague-Dawley rats were randomly placed in one of three ambient temperature groups; control (23°C), hot (41°C) and cool (11°C). Each exercise bout consisted of treadmill running at 17 m/min and 0% grade. Tissue HSP70 levels for all groups were determined using analysis of variance in two factorial design (2ϫ3). Baseline rectal temperature was similar for all three groups. In the control and hot temperature groups, final rectal temperatures differed from the baseline values (pϽ.05). The rectal temperature from the control/exercise group were 38.5Ϯ0.3°C at rest and 39.8Ϯ0.3°C at exhaustion, the hot/exercise group were 38.4Ϯ0.3°C at rest and 41.2Ϯ0.9°C at exhaustion and the cool/exercise group were 38.2Ϯ0.3°C at rest and 38.5Ϯ0.2°C at exhaustion. The running time was 102.0Ϯ39.5 min at the control/exercise group, 44.1Ϯ18.0 min at the hot/exercise group, and 55.4Ϯ11.9 min at the cool/exercise group. The level of soleus, cardiac and extensor digitorium longus (EDL) HSP70 in cool temperature does not change during a single bout of submaximal exercise. Whereas a single bout of submaximal exercise in hot and control ambient temperatures increases HSP70 accumulation in locomotor muscles, such as the soleus and cardiac, but not in the EDL tissue. This study shows that the changes of HSP70 level induced by a single bout of submaximal exercise at various ambient temperatures (control, hot and cool) depend on the rectal temperature.

Expression of heat shock protein 60 in the tissues of transported piglets

“…2007). Mammalian Hsps has induced by various ambient temperatures or environments in vivo (Fujimori et al 1994;Kim et al 2004). Transportation is thought to be very stressful due to exposure of the animals to unfavorable environments.…”

Exercise-induced cardioprotection — biochemical, morphological and functional evidence in whole tissue and isolated mitochondria

“…Moreover, they revealed that exercise in a cold environment could provide protection against the same insult without increasing cardiac HSPs (HSP10, HSP40, HSP60, HSP70, HSP90). This indicates that the rise in body temperature during exercise is an essential component of the exercise-induced HSP overexpression [90][91][92]. However, Harris and Starnes [91] reported that the limitation of the rise in core temperature during endurance training sessions (room temperature at 4-8°C) with consequent lack of effect on myocardial HSP accumulation, abolished the cardioprotection observed when room temperature during exercise training is maintained neutral (23°C), thus resulting in HSP70 overexpression.…”

Elevated core and muscle temperature to levels comparable to exercise do not increase heat shock protein content of skeletal muscle of physically active men

“…Heat shock was the first known stressor to induce an increase in cellular HSP content (Ritossa 1962, Tissieres et al 1974) and both in vitro (Maglara et al 2003) and in vivo (Oishi et al 2002(Oishi et al , 2003 heating protocols have been shown to induce an increased HSP content in C 2 C 12 skeletal muscle myotubes and rodent muscle, respectively. Furthermore, the exercise-induced production of HSP70 in soleus muscle of rodents is enhanced when exercise is performed under elevated ambient temperatures, an effect attributed to the significantly higher body temperatures in these conditions (Kim et al 2004).…”