Circulating Ang Ii Modulates The Effects Of Exercise Training On Skeletal Myopathy In Heart Failure

Previous studies show that angiotensin II (AngII) mediates muscle wasting. In chronic heart failure (CHF), exercise training reduces AngII and improves skeletal myopathy. Unknown is whether the improvement in skeletal myopathy in CHF provoked by exercise training depends on AngII reduction. Thus, we studied the effects of exercise training on muscle ubiquitin‐proteasome pathway in CHF rats submitted to an AngII clamp (osmotic minipump). Male Wistar rats underwent coronary artery ligation for CHF induction. At fourth week of surgery, the CHF rats were divided into three groups: 1) Untrained; 2) exercise‐trained and 3) exercise‐trained with AngII. Exercise training was conducted on a treadmill 60min/day, 5 days/wk at 60% VO 2 max during 8wk. Exercise training reduced E3a, Atrogin and MuRF mRNA expression (RT‐PCR), carbonylated and ubiquitinated proteins (Western Blot), and 26S proteasomal activity (Fluorimetry) in plantaris muscle of CHF rats. AngII infusion, set at the same levels of untrained rats, restrained the exercise‐mediated changes in the ubiquitin‐proteasome pathway. We concluded that circulating AngII modulates the effects of exercise training on skeletal myopathy in CHF. Grant Funding Source : Supported by FAPESP (2010/50048‐1), CAPES, CNPq, and Fundação Zerbini