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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 (Tgi) 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), Tgi, and mean-weighted skin temperature (Tsk) were taken at baseline and each 0.5 °C Tgi increase. LSR and CVC onsets and sensitivities were calculated with mean body temperature (Tb) = 0.9*Tgi + 0.1*Tsk [4].

Results

No differences existed between SMK and N-SMK for Tgi, Tsk, Tb, heart rate, mean arterial pressure, LSR, CVC, and SGA with each 0.5 °C Tgi 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 Tb 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 Tb) 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

References

  1. 1.

    Alwan A: Global status report on noncommunicable diseases 2010. 2011, World Health Organization

  2. 2.

    Kilaru S, Frangos SG, Chen AH, Gortler D, Dhadwal AK, Araim O, Sumpio BE: Nicotine: a review of its role in atherosclerosis. J Am Coll Surg. 2001, 193 (5): 538-546. 10.1016/S1072-7515(01)01059-6.

  3. 3.

    Ogawa T: Local effect of skin temperature on threshold concentration of sudorific agents. J Appl Physiol. 1970, 28: 18-22.

  4. 4.

    Stolwijk JA: A mathematical model of physiological temperature regulation in man. National Aeronautics and Space Administration. 1971

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Author information

Correspondence to Matthew S Ganio.

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Keywords

  • Nicotine
  • Nicotinic Acetylcholine Receptor
  • Skin Blood Flow
  • Thermoregulatory Response
  • Blood Flow Response