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The Role of Androgens in the Exercise Induced Decrease in Protein Breakdown
Author(s) -
Rossetti Michael L,
Gordon Bradley S
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb733
Subject(s) - medicine , castration , endocrinology , androgen , oxidative stress , oxidative phosphorylation , autophagy , chemistry , hormone , apoptosis , biochemistry
Androgens play an important role in the regulation of muscle protein balance. The decrease in androgen production and/or bioavailability observed in various atrophic conditions is associated with increased rates of muscle protein breakdown in the fasted metabolic state. While the increase in muscle protein breakdown is accompanied by a decrease in oxidative capacity, the contribution of muscle oxidative capacity to muscle protein breakdown in the absence of androgens is unclear. To shed light on this, male mice that were 10 weeks of age were subjected to a sham or castration surgery. Ten days post‐surgery, mice from both groups were further randomized to remain sedentary or perform aerobic treadmill exercise (6 days a week for 8 weeks) to increase oxidative capacity. At the conclusion of the 8‐week training, mice underwent a run to fatigue to assess training effectiveness. Mice were fasted overnight prior to sacrifice to induce a fasted metabolic state. All mice subjected to the training ran significantly longer compared to the sedentary groups with no effect of castration observed. Plantaris muscle mass was significantly higher in sham exercised mice compared to the castration exercised group. While exercise training increased expression of the mitochondrial protein, cytochrome c oxidase subunit IV (COX IV), in both sham and castration conditions, this measure was significantly lower in castrated mice relative to sham values. Interestingly, exercise training decreased the LC3 II/I ratio, a marker of autophagy activation, only in sham mice which could not be explained by corresponding changes in putative autophagy regulatory factors. However, a strong inverse relationship between COX IV and the LC3 II/I ratio was observed, suggesting that muscle oxidative capacity contributed to the change in autophagy activation. In all, these data support a role of muscle oxidative capacity in the androgen‐mediated regulation of autophagy activation during the fasted metabolic state. Support or Funding Information UCF Office of Research and Commercialization Grant to Bradley Gordon