Abstract

Autophagy is a proteolytic pathway that functions within cells to degrade damaged or dysfunctional organelles, and to remove harmful protein aggregates. Recently, this intracellular signaling pathway was shown to be involved in the regulation of muscle mass, and it is known that muscle fiber types appear to atrophy at different rates. To examine whether this is related to oxidative capacity, we investigated the levels of autophagic proteins in various fiber types (soleus, plantaris, and heart), in response to a 9 week voluntary wheel training protocol, or to unilateral chronic muscle stimulation (CCA, 10Hz, 3h/day, 7 days). Beclin-1 and LC3II protein expression was highest in muscles possessing a high oxidative capacity (heart) and lowest in the least oxidative plantaris muscle. In response to training and CCA, mitochondrial content increased by 35–40%. The autophagic proteins ATG7, ULK1, LC3II and Beclin1 were elevated 2- to 3-fold following CCA, but were not significantly elevated following 9 weeks of training. Therefore, these data demonstrate a relationship between muscle oxidative capacity and autophagic protein expression under steady state conditions, but also indicate that autophagy may be an early event in the muscle remodeling that occurs with exercise.

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