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  • Meeting abstract
  • Open Access

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

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  • 1Email author
Extreme Physiology & Medicine20154 (Suppl 1) :A98

  • Published:


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


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.


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].


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].


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.


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





CVC onset (ΔTb from baseline, °C)

0.31 (0.12)

0.61 (0.21)*


CVC plateau (% of max)

68.4 (27.4)

68.4 (21.6)


CVC sensitivity (Δ%max per °C ΔTb)

82.5 (46.2)

58.9 (23.3)


LSR onset (ΔTb from baseline, °C)

0.35 (0.14)

0.52 (0.19)*


LSR plateau (mg·cm-2·min-1)

0.79 (0.26)

1.00 (0.13)*


LSR sensitivity (Δmg·cm-2·min-1 per °C ΔTb)

0.60 (0.40)

0.63 (0.21)

*Significant difference between groups (p < 0.05).

Authors’ Affiliations

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


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


© Moyen et al.; 2015

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