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Type 2 diabetes causes skeletal muscle atrophy but does not impair resistance training‐mediated myonuclear accretion and muscle mass gain in rats
Author(s) -
Ato Satoru,
Kido Kohei,
Sato Koji,
Fujita Satoshi
Publication year - 2019
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/ep087585
Subject(s) - skeletal muscle , endocrinology , medicine , muscle hypertrophy , insulin resistance , muscle atrophy , atrophy , type 2 diabetes mellitus , basal (medicine) , biology , diabetes mellitus
New FindingsWhat is the central question of this study? Type 2 diabetes mellitus (T2DM) causes skeletal muscle atrophy; does it affect resistance training (RT)‐mediated molecular adaptations and subsequent muscle hypertrophy?What is the main finding and its importance? Although skeletal muscle mass and regulation were not preserved under conditions of T2DM, the response of RT‐induced skeletal muscle hypertrophy was not impaired in T2DM rat skeletal muscle. These findings suggest that the capacity of RT‐mediated muscle mass gain is not diminished in the T2DM condition.Abstract Type 2 diabetes mellitus (T2DM) is known to cause skeletal muscle atrophy. However, it is not known whether T2DM affects resistance training (RT)‐mediated molecular adaptations and subsequent muscle hypertrophy. Therefore, we investigated the effect of T2DM on response of skeletal muscle hypertrophy to chronic RT using a rat resistance exercise mimetic model. T2DM and healthy control rats were subjected to 18 bouts (3 times per week) of chronic RT on unilateral lower legs. RT significantly increased gastrocnemius muscle mass and myonuclei in both T2DM and healthy control rats to the same extent, even though T2DM caused muscle atrophy in the resting condition. Further, T2DM significantly reduced mechanistic target of rapamycin complex 1 (mTORC1) activity (phosphorylation of p70S6K Thr389 and 4E‐BP1 Thr37/46 ) to insulin stimulation and the number of myonuclei in the untrained basal condition, but RT‐mediated adaptations were not affected by T2DM. These findings suggested that although the skeletal muscle mass and regulation were not preserved under basal conditions of T2DM, the response of RT‐induced skeletal muscle hypertrophy was not impaired in T2DM rat skeletal muscle.