Journal of Applied Physiology AJP: Lung Cellular and Molecular Physiology
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J Appl Physiol 105: 1156-1165, 2008. First published August 7, 2008; doi:10.1152/japplphysiol.00194.2008
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Menstrual cycle and oral contraceptive use do not modify postexercise heat loss responses

Glen P. Kenny,1 Emily Leclair,1 Ronald J. Sigal,2 W. Shane Journeay,3 Donald Kilby,4 Lindsay Nettlefold,1 Francis D. Reardon,1 and Ollie Jay1

1Laboratory of Human Bioenergetics and Environmental Physiology, School of Human Kinetics, and 4Health Services, University of Ottawa, Ottawa, Ontario, Canada; 3Dalhousie Medical School, Dalhousie University, Faculty of Medicine, Halifax, Nova Scotia; and 2University of Calgary, Faculties of Medicine and Kinesiology, Departments of Medicine and Cardiac Sciences, Calgary, Alberta, Canada

Submitted 18 February 2008 ; accepted in final form 7 August 2008

It is unknown whether menstrual cycle or oral contraceptive (OC) use influences nonthermal control of postexercise heat loss responses. We evaluated the effect of menstrual cycle and OC use on the activation of heat loss responses during a passive heating protocol performed pre- and postexercise. Women without OC (n = 8) underwent pre- and postexercise passive heating during the early follicular phase (FP) and midluteal phase (LP). Women with OC (n = 8) underwent testing during the active pill consumption (high exogenous hormone phase, HH) and placebo (low exogenous hormone phase, LH) weeks. After a 60-min habituation at 26°C, subjects donned a liquid conditioned suit. Mean skin temperature was clamped at ~32.5°C for ~15 min and then gradually increased, and the absolute esophageal temperature at which the onset of forearm vasodilation (ThVD) and upper back sweating (ThSW) were noted. Subjects then cycled for 30 min at 75% VO2 peak followed by a 15-min seated recovery. A second passive heating was then performed to establish postexercise values for ThVD and ThSW. Between 2 and 15 min postexercise, mean arterial pressure (MAP) remained significantly below baseline (P < 0.05) by 10 ± 1 and 11 ± 1 mmHg for the FP/LH and LP/HH, respectively. MAP was not different between cycle phases. During LP/HH, ThVD was 0.16 ± 0.24°C greater than FP/LH preexercise (P = 0.020) and 0.15 ± 0.23°C greater than FP/LH postexercise (P = 0.017). During LP/HH, ThSW was 0.17 ± 0.23°C greater than FP/LH preexercise (P = 0.016) and 0.18 ± 0.16°C greater than FP/LH postexercise (P = 0.001). Postexercise thresholds were significantly greater (P ≤ 0.001) than preexercise during both FP/LH (ThVD, 0.22 ± 0.03°C; ThSW, 0.13 ± 0.03°C) and LP/HH (ThVD, 0.21 ± 0.03°C; ThSW, 0.14 ± 0.03°C); however, the effect of exercise was similar between LP/HH and FP/LH. No effect of OC use was observed. We conclude that neither menstrual cycle nor OC use modifies the magnitude of the postexercise elevation in ThVD and ThSW.

thermoregulation; body temperature; estrogen; progesterone; postexercise hypotension



Address for reprint requests and other correspondence: G. P. Kenny, Univ. of Ottawa, School of Human Kinetics, 125 Univ., Montpetit Hall, Ottawa, ON, Canada K1N 6N5 (e-mail: gkenny{at}uottawa.ca)







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