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

  • Nicole E Moyen
  • Hannah A Anderson
  • Jenna M Burchfield
  • Matthew A Tucker
  • Melina A Gonzalez
  • Forrest B Robinson
  • Matthew S Ganio
Open Access
Meeting abstract
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Keywords

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

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

Measurement

Smokers

Non-smokers

CVC

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

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).

References

  1. 1.
    Alwan A: Global status report on noncommunicable diseases 2010. 2011, World Health OrganizationGoogle Scholar
  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.CrossRefPubMedGoogle Scholar
  3. 3.
    Ogawa T: Local effect of skin temperature on threshold concentration of sudorific agents. J Appl Physiol. 1970, 28: 18-22.PubMedGoogle Scholar
  4. 4.
    Stolwijk JA: A mathematical model of physiological temperature regulation in man. National Aeronautics and Space Administration. 1971Google Scholar

Copyright information

© Moyen et al.; 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors and Affiliations

  • Nicole E Moyen
    • 1
  • Hannah A Anderson
    • 1
  • Jenna M Burchfield
    • 1
  • Matthew A Tucker
    • 1
  • Melina A Gonzalez
    • 1
  • Forrest B Robinson
    • 1
  • Matthew S Ganio
    • 1
  1. 1.Human Performance Laboratory, Department of Health, Human Performance, and RecreationUniversity of ArkansasFayettevilleUSA

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