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The purpose of this study was to determine the effects of exercise in hot, cold, and temperate environments on plasma interleukin-6 (IL-6). Eleven recreationally trained males (age = 25 ± 4 years, height = 178 ± 5 cm, weight = 79.4 ± 13.5 kg, body fat = 14.7 ± 3.6%, VO2 peak = 54.6 ± 11.5 ml kg-1 min-1) performed a 1 hr cycling bout in hot (33 °C), cold (7 °C), and temperate (20 °C) environments at 60% of Wmax followed by 3 hr of supine recovery in temperate conditions. Expired gases were measured every 15 min during exercise and once every hour during recovery. Heart rate was continuously measured throughout the trials. Blood samples were obtained from the antecubital vein pre-exercise, immediately post-exercise, and 3 hr post-exercise. Blood samples were analyzed for plasma concentrations of IL-6 using a commercial ELISA kit. Plasma IL-6 concentrations were significantly higher immediately post-exercise (14.8 ± 1.6 pg ml-1, p = 0.008) and 3 hr post-exercise (14.8 ± 0.9 pg ml-1, p = 0.018) compared to pre-exercise (11.4 ± 2.4 pg ml-1), across all trials. There were no differences in plasma IL-6 concentrations (p = 0.207) between temperature conditions.Oxygen consumption and heart rate were higher and respiratory exchange ratio was lower in the hot compared to other conditions (p < 0.05). These data indicate that the temperature in which exercise occurs does not affect acute plasma IL-6 response despite differences in metabolic state.

Many human diseases lead to a loss of skeletal muscle metabolic function and mass. Local and environmental temperature can modulate the exercise-stimulated response of several genes involved in mitochondrial biogenesis and skeletal muscle function in a human model. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. Thus, 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 mitochondrial biogenesis and muscle mass. Recreationally trained male subjects (n = 12) had muscle biopsies taken from the vastus lateralis before and after 3 h of exposure to hot (33 °C), cold (7 °C), or room temperature (20 °C) conditions. Temperature had no effect on most of the genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Core temperature was significantly higher in hot and cold environments compared with room temperature (37.2 ± 0.1 °C, p = 0.001; 37.1 ± 0.1 °C, p = 0.013; 36.9 ± 0.1 °C, respectively). Whole-body oxygen consumption was also significantly higher in hot and cold compared with room temperature (0.38 ± 0.01 L·min−1, p < 0.001; 0.52 ± 0.03 L·min−1, p < 0.001; 0.35 ± 0.01 L·min−1, respectively). In conclusion, these data show that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression. 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.

Effects on Oxygen Consumption and Metabolic Gene Expression when Determining Experimental Exercise Intensity Based on Exercise Capacity Tests Conducted in Hypoxic and Normoxic Environments Exercise intensities utilized in experimental designs are usually determined relative to maximal aerobic capacity (i.e. 65% VO2 max). This becomes a challenge when studying the effects of hypoxia and altitude versus normoxic control conditions since acute hypoxia decreases VO2 max when compared to normoxic conditions. Endurance trained individuals with an average sea level VO2 max of 65.5 ml x kg-1 min-1 would be projected to have an average VO2 max at 2500 m of 57.7 ml x kg-1 min-1, or a 7.8% decrease.