Advertisement

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
  • 260 Downloads

Keywords

Nicotine Nicotinic Acetylcholine Receptor Skin Blood Flow Thermoregulatory Response Blood Flow Response 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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

Personalised recommendations