Cutaneous vascular & sudomotor responses to heat-stress in smokers & non-smokers

Introduction

As approximately one billion people worldwide are chronic smokers [1] it is important to determine smokers' thermoregulatory responses to heat-stress. Although local maximal vasodilation may be attenuated in smokers [2], skin blood flow responses during whole-body heat stress are unknown. Moreover, it is unknown if sweat rate is altered in smokers; theoretically the binding of nicotine to nicotinic acetylcholine receptors [2] may initiate an earlier onset of sweating during whole-body heat stress compared to non-smokers [3]. The purpose of this study was to compare cutaneous vascular and sudomotor responses to whole-body passive heat-stress between smokers and non-smokers.

Methods

Nine male chronic smokers [SMK; 10 (6) cigarettes/day for 11.8 (9.5) y; 26 (8) y; 177.7 (6.6) cm; 80.6 ± 21.1 kg] and 13 male non-smokers [N-SMK; 28 (9) y; 177.6 (6.8) cm; 77.2 (8.2) kg] were matched for age, height, body mass, and exercise habits (all p > 0.05). Subjects were passively heated via water-perfused suits until gastrointestinal temperature (T_gi) increased 1.5 °C. Local sweat rate (LSR) via ventilated capsule and cutaneous vasomotor activity (CVC) via Laser Doppler on the forearm were continuously recorded; blood pressure, heart rate, sweat gland activation (SGA), sweat gland output (SGO), T_gi, and mean-weighted skin temperature (T_sk) were taken at baseline and each 0.5 °C T_gi increase. LSR and CVC onsets and sensitivities were calculated with mean body temperature (T_b) = 0.9*T_gi + 0.1*T_sk [4]_.

Results

No differences existed between SMK and N-SMK for T_gi, T_sk, T_b, heart rate, mean arterial pressure, LSR, CVC, and SGA with each 0.5 °C T_gi increase (all p > 0.05). Overall, SGO tended to be lower in SMK than N-SMK [SMK = 5.94 (3.49) vs. N-SMK = 8.94 (3.99) µg·gland^-1·min^-1; p = 0.08].

Discussion

Smokers' CVC and LSR onsets occurred at an earlier T_b than non-smokers, possibly because heat stress enhances nicotine kinetics (i.e. binding of nicotine to nicotinic acetylcholine receptors; [2, 3]). The lower LSR at plateau during whole-body heating might indicate a thermoregulatory impairment in young smokers, and is likely a result of decreased sweat gland output and not activation.

Conclusion

Compared to non-smokers, smokers had an earlier onset but similar sensitivity (i.e. increase in response per increase in T_b) for sweating/cutaneous vasodilation. These data suggest that overall, most young chronic smokers' thermoregulatory responses to whole-body passive heat stress are not impaired.

Table 1 Mean (SD) CVC and LSR parameters on the forearm for SMK and N-SMK during passive heat stress