Heat shock proteins (HSPs) are expressed when cells are exposed to various types of stress and they may provide protection against cellular insult. Previous data have shown increases in HSP expression following acute exhaustive exercise in rats (Locke et al. 1990, 1995; Salo et al. 1991) and humans (Liu et al. 1999); however, it is not known if chronic exercise will increase resting levels of HSPs. The purpose of this study was to determine if basal protein levels of HSP 72/73 and HSP 60 are increased in cardiac and skeletal muscle of endurance trained Fischer 344 rats. Heart, soleus (SOL) and lateral gastrocnemius (LG) muscles were removed and hearts were sectioned into left ventricle (LV), right ventricle (RV) and atria (AT). Endurance training improved myocardial citrate synthase activity by 88, 90 and 77% and cytochrome c oxidase activity by 58, 51 and 89% in LV, RV and AT, respectively. LV and RV oxidative enzyme activities were greater when compared to AT for both trained and untrained rats (P < 0.05). HSP 72/73 expression was significantly greater (P < 0.05) in LV, RV and SOL from endurance trained versus from control rats (26, 45 and 67%, respectively). HSP 60 was also increased (P < 0.05) in LV, RV and SOL in trained relative to untrained rats. HSP 72/73 and HSP 60 were unchanged in AT and LG after training. These results indicate that endurance training increases the basal expression of stress proteins and this observation is consistent with the hypothesis that endurance training may activate a protective mechanism to stress.

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Cytochrome c oxidase (CCO) is an enzyme complex found on the inner mitochondrial membrane and serves as the final electron acceptor in mitochondrial electron transport. Heat shock proteins (HSPs) are involved in the import of nuclear encoded protein subunits into the mitochondria and induce conformational changes to form active enzyme complexes. As both the nuclear and mitochondrial encoded subunits of CCO have been shown to increase in activity and expression in muscle subsequent to artificial loading, and as exercise has been shown to induce HSPs, we sought to determine whether 16-20 weeks of treadmill exercise would result in enhanced CCO subunit expression, and to determine if there was a relationship between this expression and HSP content in medial gastrocnemius muscle of Fischer 344 rats. Our results indicated that endurance training resulted in a 53%, 87% and 80% increase (P<0.05) in the levels of HSP 60, CCO subunit II and CCO subunit VI, respectively. Enzymatic activity of CCO was 84% greater (P<0.05) after endurance training. Mann Whitney U analyses showed that CCO subunit II and VI increased to the same extent as HSP 60 after endurance training. It appears that 16-20 weeks of endurance training leads to uniform increases in CCO subunits and parts of the transport and assembly mechanisms required for CCO enzyme assembly. The similarity among the increases in CCO subunits II and VI protein levels and the increase in CCO enzyme activity suggest that this increase in activity is due to an increase in the amount of CCO enzyme.