NE Moyen, MS Ganio, HA Anderson, JB Burchfield, MA Tucker, MA Gonzalez, & FB Robinson

Human Performance Laboratory, Department of Health, Human Performance, and Recreation, University of Arkansas, Fayetteville, Arkansas

Convection (cutaneous blood flow) and evaporation (sweating) are the main avenues for heat loss during heat-stress. Although some drugs such as cocaine impair heat loss, it is unknown if nicotine use with smokers leads to thermoregulatory impairments. Specifically, it is not known if smokers have impairments in the onset, sensitivity, and capacity for cutaneous blood flow and sweating during heat stress. PURPOSE: To compare cutaneous vascular and sudomotor (i.e., sweating) responses to passive heat stress between smokers and non-smokers. METHODS: 12 regularly smoking (S; 8.8 ± 5.5 cigarettes/day for >4 years) and 14 non-smoking (NonS) males matched for age, body mass, and exercise habits participated (S: 26 ± 8 y, 80.6 ± 21.1 kg; NonS: 28 ± 9 y, 77.2 ± 8.2 kg). Subjects were passively heated until achieving a 1.5°C core temperature (TC) increase. Forearm local sweat rate (LSR; via ventilated capsule) and skin blood flow (CVC; via Laser Doppler) were continuously recorded. Blood pressure, heart rate, sweat gland activation (SGA), sweat gland output (SGO), TC, and skin temperature (Tsk) were taken at baseline and each 0.5°C TC increase. LSR and CVC onsets and sensitivities were calculated using mean body temperature (Tb). RESULTS: No differences existed between S and NonS for TC, Tsk, Tb, LSR, CVC, SGA, and SGO with each 0.5°C TC increase (all p > 0.05). However, medium effect sizes (ES) suggested S had a lower Tb at the onset of sweating (­S = 37.37 ± 0.21°C vs. NonS = 37.58 ± 0.32°C; ES = 0.66) and vasodilation (S = 37.45 ± 0.32°C vs. NonS = 37.63 ± 0.30°C; ES = 0.69). LSR plateau (maximal LSR during heating) was significantly lower in S than NonS (0.63 ± 0.31 vs. 0.94 ± 0.21 mg·cm-2·min-1, respectively; p = 0.01). Maximal CVC was lower in S than NonS (90.6 ± 39.1 vs. 115.7 ± 42.6 arbitrary units/mmHg, respectively; ES = 0.61; p = 0.13). The degree of increase in LSR and CVC per °C increase in Tb (i.e., sensitivities) were not different between groups (p > 0.05). CONCLUSION: During passive heating, smokers’ had an earlier onset for sweating and cutaneous vasodilation but a lower maximal CVC and LSR. Therefore, some aspects of thermoregulation in smokers appear enhanced and some impaired. Future studies should utilize exercise heat-stress to fully understand the physiological differences in smokers and whether or not they are at increased risk for heat illness.

Funding: This project was funded by the University of Arkansas and the Arkansas Biosciences Institute, the major research component of the Arkansas Tobacco Settlement Proceeds Act of 2000.

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