Date of Graduation

12-2012

Document Type

Thesis

Degree Name

Master of Science in Kinesiology (MS)

Degree Level

Graduate

Department

Health, Human Performance and Recreation

Advisor/Mentor

Ganio, Matthew S.

Committee Member

Washington, Tyrone A.

Second Committee Member

Fort, Inza L.

Keywords

Social sciences; Biological sciences; Exercise; Females; Obesity; Thermoregulation

Abstract

Previous research has shown that obese individuals are at greater risk for heat illnesses because of impaired thermoregulation. However, laboratory studies investigating cardiovascular and thermoregulatory function in obese individuals are difficult to interpret because of low sample sizes and methodological concerns. The purpose of this study was to determine if there are differences in thermoregulatory and cardiovascular function between obese and non-obese females. Twenty-four females, 13 obese (43.3 ± 4 .3 % fat, 77.2 ± 13.7 kg) and 11 non-obese (27.8 ± 6.0 % fat, 55.7±6.7 kg), cycled for 60 min in a warm environment (~40°C, 30% humidity) at a work load that elicited either 300 W of metabolic heat production (fixed heat production; FHP) or 175 W/m2 of skin surface area (body surface area; BSA). In the FHP trial, when heat production was similar between obese (290 ± 16 W) and non-obese (299±18 W) individuals (P > 0.05), no differences in rectal temperature (Tre), mean skin temperature (Tsk), VO2 (l/min), or sweat rate (l/hr) occurred (all P > 0.05). As expected because of greater skin surface area, the obese individuals in the BSA trial had a greater heat production (316±33 W) compared to the non-obese individuals (284 ± 23W) which was a result of higher VO2 during exercise (1.14 ± 0.10 vs. 1.01 ± 0.09 l/min; P > 0.05). The rise in Tre and Tsk, over time in the BSA trial was not dependent on subject grouping (i.e., non-significant interaction P > 0.05). In conclusion, when obese and non-obese individuals exercise at a fixed metabolic heat production or a heat production relative to body surface area there are no thermoregulatory differences between groups. The overall relatively minor increases in Tre (0.55 ± 0.28 and 0.61 ± 0.34°C for FHP and BSA trials, respectively), may partially explain why differences were not observed in this setting.

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