UC Irvine

Extended periods of skeletal muscle disuse can cause a significant loss of contractile proteins, which compromises the ability to generate force, mechanical work or power, thus compromising locomotor performance. Several hibernating organisms can resist muscle atrophy despite months of inactivity. This resistance has been attributed to a reduction in body temperature and metabolic rate and activation of physiological pathways that counteract pathways of protein degradation. However, in these systems, such strategies are not mutually exclusive and the effects of these mechanisms can be difficult to separate. In this study, we used the western fence lizard, Sceloporus occidentalis, as an ectothermic model to determine whether a reduction in metabolic rate is sufficient to resist muscle atrophy. We induced atrophy through sciatic denervation of the gastrocnemius muscle and housed lizards at either 15 or 30°C for 6-7 weeks. Following treatment, we used muscle ergometry to measure maximum isometric force, the force-velocity relationship and contractile dynamics in the gastrocnemius. This approach allowed us to relate changes in the size and morphology to functional metrics of contractile performance. A subset of samples was used to histologically determine muscle fiber types. At 30°C, denervated muscles had a larger reduction in muscle mass, physiological cross-sectional area and maximum isometric force than at 15°C. Maximum shortening velocity of the muscle decreased slightly in animals housed at 30°C but did not change in those housed at 15°C. Our results suggest that metabolic rate alone can influence the rate of muscle atrophy and that ectothermic vertebrates may have an intrinsic mechanism to resist muscle atrophy during seasonal periods of inactivity.