Abstract
We examined the effect of repeated heat stress on muscle atrophy, and apoptotic and proteolytic regulation in unloaded rat slow- and fast-type skeletal muscles. Forty male Wistar rats (11 week-old) were divided into control (CT), hindlimb unweighting (HU), intermittent weight-bearing during HU (HU + IWB), and intermittent weight-bearing with heat stress during HU (41–41.5°C for 30 min; HU + IWB + HS) groups. The HU + IWB + HS and HU + IWB groups were released from unloading for 1 h every second day, during which the HU + IWB + HS group underwent the heating. Our results revealed that repeated bouts of heat stress resulted in protection against disuse muscle atrophy in both soleus and plantaris muscles. This heat stress–induced protection against disuse-induced muscular atrophy may be partially due to reduced apoptotic activation in both muscles, and decreased ubiquitination in only the soleus muscle. We concluded that repeated heat stress attenuated skeletal muscle atrophy via suppressing apoptosis but the response to proteolytic systems depend on the muscle phenotype.
Highlights
Skeletal muscle mass is balanced between protein synthesis and degradation
Body weights in the HU + IWB and HU + IWB + HS groups were significantly lower than that in the CT group, but no differences were observed among the three hindlimb unweighting groups (Table 1)
The HU+IWB+HS and HU+IWB groups were released from unloading for 1 h every second day because of a limitation in the experimental method; no significant changes in muscle weight or myofiber Cross-sectional area (CSA), the number of transferase dUTP nick end labeling (TUNEL)-positive nuclei, calpain autolysis, or ubiquitinated protein expression were observed between the HU and HU + IWB groups
Summary
Protein synthesis and breakdown are regulated through multiple signaling pathways; decreased protein synthesis and/or increased protein degradation contribute to loss of muscle protein (Thomason and Booth 1990; Booth and Criswell 1997). Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society Heat Stress and Signaling During Disuse Muscle Atrophy tein synthetic rate declines rapidly following hindlimb unloading, disuse-induced muscle atrophy is mainly due to an increase in the protein degradation rate in rat skeletal muscle (Booth and Criswell 1997; Powers et al 2005, 2007). Recent evidence has revealed that the apoptotic system may contribute to select forms of disuse muscle atrophy (Du et al 2004; McClung et al 2007; Powers et al 2007)
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