Abstract
Leptin has been established as an energy-controlling hormone because of its role in activating the JAK-STAT3 pathway. Temperature has its own prominent role governing appetite regulation and thus, energy expenditure. Previous research has demonstrated consistent decreases in leptin while in a fasted state. Exercising in the heat (1-hour of cycling @60% VO2max in 33°C) has also shown reductions in leptin. However, in order to elucidate the influence of environment, independent of exercise, a fasted resting investigation is needed. PURPOSE: Determine the impact of environmental temperature (33 vs. 20°C) on adipose derived appetite-regulating hormones (leptin and adiponectin) and the impact on energy expenditure. METHODS: 10 college-aged males (27.3 ± 5 y, 86.7 ± 13 kg, and 1.83 ± 4.3 m; 25.8 ± 0.9 kg/m2) completed two randomized, resting experimental trials in the Heat (HT, 33°C) and at Room Temperature (RT, 20°C) at 60% humidity. Blood draws were taken before intervention and after 3 hours for analysis of leptin and adiponectin. Oxygen consumption was measured at 1-, 2-, and 3-hr time-points. RESULTS: HT trial temperatures were greater than RT for both core (mean ± SEM; 37.17 ± 0.08 vs. 36.89 ± 0.08°C, p = 0.002) and skin (37.59 ± 0.10 vs. 32.65 ± 0.48°C; p < 0.001). Oxygen consumption in HT was greater than RT during the 2nd (4.37 ± 0.14 vs. 4.13 ± 0.15 ml/kg/min, p = 0.037) and 3rd hours (4.95 ± 0.26 vs. 4.28 ± 0.19 ml/kg/min, p = 0.002). Fasting leptin concentrations in RT decreased to a greater extent than in HT (mean Δ ± 95% CI; -2.05 ± 1.72 vs. -0.89 ± 1.67 ng/ml; p = 0.036, respectively); however, after adjustment for plasma volume shifts (-7.5%) the interactive effect dissipated (-1.79 ± 1.72 vs. -0.89 ± 1.6 ng/ml; p = 0.068). CONCLUSIONS: The addition of heat stress increased energy expenditure and attenuated the leptin reduction. These data may have implications for appetite control and weight management.
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