Abstract

While it is well‐established that exercise increases muscle protein synthesis rate, it is still unclear that what role of protein breakdown plays in muscle after exercise. Therefore, the objective of this study was to determine if rates of protein synthesis and breakdown correlate with expression of genes related autophagy and protein degradation in skeletal muscle of healthy adults after a bout of resistance exercise. This is a secondary analysis of a previous published study ( Kim et al., 2016). In total, twenty‐three subjects were divided into two groups, rest (n = 12) and exercised (n = 11). Real‐time PCR was used for analyzing gene expression of baseline muscle samples from both groups, and student t test was used to compare significance (p < 0.05) between two groups. Relationships between variables were assessed using Pearson’s Product‐Moment Correlation, and p value lower than 0.05 was considered as significant. Autophagy‐related genes p62, p53, ATG3, ATG5, LC3B, Beclin1, ATF4, and GADD54A, were significantly upregulated (p < 0.05) in skeletal muscle from exercised subjects versus subjects at rest. Two genes involved in ubiquitin‐proteasome pathway, MuRF1 and Atrogin1, were also upregulated (p < 0.05) after exercise. Neither protein synthesis nor protein breakdown rate was correlated with gene expression in skeletal muscle from subjects at rest. However, protein synthesis rate was positively correlated (p < 0.05) with increased expression of p62, p53, ATG3, ATG5, ATG7, LC3B, Beclin1, ATF4, GADD54A, Atrogin‐1 and MuRF1 in exercised muscle. Protein breakdown rates were positively associated (p < 0.05) with increased expression of ATF4, ATG5, and p62 in exercised skeletal muscle. In conclusion, the results provide preliminary evidence that genes related to autophagy and protein breakdown are upregulated after exercise in skeletal muscle from healthy adults and are positively correlated with muscle protein synthesis rate.Support or Funding InformationThis study is funded by an Arkansas Biosciences Institute grant, we would like to thank thegenerous contribution of muscle samples by Dr. Wolfe.

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