Abstract

Many human diseases lead to loss of skeletal muscle function and mass. Local and environmental temperature can alter the exercise-stimulated response of several genes involved in skeletal muscle growth and breakdown. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. PURPOSE: The purpose of this study was to compare the effects of exposure to hot, cold, and room temperature conditions on skeletal muscle gene expression related to myogenesis and proteolysis. METHODS: Recreationally trained male subjects (n=11, age 27 ± 5, height 183 ± 5 cm, weight 84.1 ± 13.0 kg) each completed three trials in hot (33 °C), cold (7 °C), and room temperature (20 °C) conditions. Whole body oxygen consumption was monitored during the 3 h exposure. Muscle biopsies were taken from the vastus lateralis before and after the 3 h temperature exposure. Muscle samples were analyzed for gene expression using qRT-PCR. RESULTS: Temperature had no effect on MSTN (p = 0.987), MYOG (p = 0.444), MYF5 (p = 0.343), MYF6 (p = 0.458), MYOD (p = 0.201), FOXO3 (p = 0.102), atrogin1 (p = 0.543), or MURF1 (p = 0.693). MSTN, MYF5, and FOXO3 decreased over the 3 h trial period (p < 0.001, p = 0.003, p = 0.004 respectively), whereas MYF6 and MYOD increased (p = 0.026, p = 0.004, respectively). Core temperature was significantly higher in hot (37.2 ± 0.1 °C, p = 0.001) and cold (37.1 ± 0.1 °C, p = 0.013) environments compared to room temperature (36.9 ± 0.1 °C). Whole body oxygen consumption was also significantly higher in hot (0.38 ± 0.01 L·min-1, p < 0.001) and cold (0.52 ± 0.03 L·min-1, p < 0.001) compared to room temperature (0.35 ± 0.01 L·min-1). CONCLUSIONS: These data demonstrate that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression related to myogenesis and proteolysis. When considered in conjunction with previous research, exercise appears to be a necessary component to observe gene expression alterations between different environmental temperatures in humans. Supported by the National Institute for General Medical Science (NIGMS; 5P20GM103427 and P20GM109090), a component of the National Institutes of Health (NIH).

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