Grant: Travel Awards - Institute Community Support

Hypertension is a cardiovascular disease associated with increased cell death and proteolytic enzyme activity in both skeletal and cardiac muscle. Autophagy is a degradative system that plays an essential role in muscle health and has been shown to influence cell death processes. Although acute exercise can alter markers of autophagy, little is known about the effects of exercise training on autophagy in healthy or diseased states. The purpose of this study was to investigate the effects of exercise training on markers of autophagy, proteolytic activity, and ROS levels in white gastrocnemius (WG) and left ventricle (LV) of Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR. Male WKY and SHR were assigned to a sedentary condition or exercise consisting of treadmill running for 6 wks.In the WG muscle of SHR, significantly greater LC3I protein and a lower LC3II/I ratio was observed compared to WKY rats. Exercise training did not alter the WG LC3II/I protein ratio, a common marker of autophagosome production; however,exercise training significantly upregulated factors contributing to the regulation of autophagy such as Beclin,LC3,and p62 mRNA and reduced ATG7 and Beclin protein levels. Following exercise training, the proteolytic enzyme activity of caspase-3 and cathepsin was lower and a trend towards lower ROS production was observed in the WG. In the LV, SHR had a significantly lower LC3II/I protein ratio and a greater accumulation of p62 protein compared to WKY rats suggesting increased autophagy. Training increased both Beclin and p62 mRNA levels in the LV; however, no change in the LC3II/I protein ratio was observed. Exercise training lowered LV caspase-3 and calpain activity, as well as tended to reduce cathepsin activity and ROS production. Together, these results suggest that autophagy is altered in the SHR muscle and heart, and exercise training can alter upstream regulators of autophagy.