Subcellular movement and expression of HSP27, αB-crystallin, and HSP70 after two bouts of eccentric exercise in humans

Abstract

The aims of this study were to investigate the sarcomeric accumulation and expression of heat shock proteins (HSPs) after two bouts of maximal eccentric exercise. Twenty-four subjects performed two bouts of 70 maximal voluntary eccentric actions using the elbow flexors in one arm. The bouts were separated by 3 wk. The changes in concentric (60 degrees/s) and isometric (90 degrees) force-generating capacity were monitored for 9 days after each bout, and biopsies were taken 1 and 48 h and 4 and 7 days after bout 1 and 1 and 48 h after bout 2. The content of HSP27, alphaB-crystallin, HSP70, and desmin in the cytosolic and cytoskeleton/myofibrillar fractions of homogenized muscle samples was determined by immunoassays, and the cellular and subcellular localization of the HSPs in the myofibrillar structure was analyzed by conventional and confocal immunofluorescence microscopy and quantitative electron microscopy. The force-generating capacity was reduced by approximately 50% and did not recover completely during the 3 wk following bout 1. After bout 2, the subjects recovered within 4 days. The HSP levels increased in the cytosolic fraction after bout 1, especially HSP70 (approximately 300% 2-7 days after exercise). Increased levels of HSP27, alphaB-crystallin, and HSP70 were found in the cytoskeletal/myofibrillar fraction after both bouts, despite reduced damage after bout 2. At the ultrastructural level, HSP27 and alphaB-crystallin accumulated in Z-disks, in intermediate desmin-like structures (alphaB-crystallin), and in areas of myofibrillar disruption. In conclusion, HSP27 and alphaB-crystallin accumulated in myofibrillar structures, especially in the Z-disks and the intermediate structures (desmin). The function of the small HSPs is possibly to stabilize and protect the myofibrillar structures during and after unaccustomed eccentric exercise. The large amount of HSP27, alphaB-crystallin, and HSP70 in the cytoskeletal/myofibrillar fraction after a repeated bout of exercise suggests a protective role as part of the repeated-bout effect.

Repeated muscle damage blunts the increase in heat strain during subsequent exercise heat stress

“…This process is thought to be mediated, in part, by intra-cellular heat shock proteins (Hsp's), and it has been suggested that acquired thermotolerance (the accumulation of protective Hsp's within cells following heat exposure), and systemic adaptations to heat acclimation share a common pathway (Kuennen et al 2011). This may be pertinent since EIMD has been shown to increase Hsp72 and Hsp27 expression within muscle cells following EIMD (Paulsen et al 2009;Thompson et al 2001), and that the changes we observed during HS on EIMD trial 2, reflect similar adaptations to that observed during heat acclimation (reduced exercising Tre, earlier sweating onset, reduced thermal sensation).…”

Heat shock response and autophagy—cooperation and control

“…156,157 However, a significant effect of exercise on HSP70 protein expression in human skeletal muscle has been observed as early as 8 h post exercise 158 and expression remains elevated up to 7 d after exercise termination. [158][159][160][161][162][163][164][165][166] When examining exercise training effects on HSP70 protein expression in humans, it has been shown that a 7-d heat acclimation protocol consisting of 2 50-min exercise bouts in a warm environmental chamber elevates subjects' core temperature to 39 C and results in a significant increase in HSP70 protein expression in peripheral leukocytes at 4-h post-exercise. 144 Similarly, a 10-d acclimation program involving treadmill walking or running in a hot environment augments HSP70 content in peripheral blood mononuclear cells.…”

A change of heart: oxidative stress in governing muscle function?

“…In the heart, α-B-crystallin and HSP27 are induced during ischemic injury, heat stress, or end-stage failure (Martin et al 1997;Benjamin and McMillan 1998;Knowlton et al 1998;Yoshida et al 1999;Dohke et al 2006). Small HSPs are induced in both myopathic skeletal (Kley et al 2012) and normal muscles after intense exercise (Paulsen et al 2009) and during aging (Doran et al 2007). HSP27 has been shown to preserve cytoskeletal architecture (Mounier and Arrigo 2002) and to play roles in the resistance to oxidative (Huot et al 1996;Dalle-Donne et al 2001), thermal and ischemic stress (Vander Heide 2002;Hollander et al 2004), and to participate in the regulation of cellular redox states (Arrigo 2001) which in turn prevent apoptosis (Mehlen et al 1996) and correlate with hypoxia (Martin et al 1997).…”