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Am J Physiol Regul Integr Comp Physiol 291: R580-R588, 2006. First published March 2, 2006; doi:10.1152/ajpregu.00918.2005
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Physiology and Pharmacology of Temperature Regulation

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery

Glen P. Kenny,1 Ollie Jay,1 Wytek M. Zaleski,3 Mark L. Reardon,2 Ronald J. Sigal,2 W. Shane Journeay,4 and Francis D. Reardon1

1Faculty of Health Sciences, School of Human Kinetics, and 2Department of Medicine, University of Ottawa, Ottawa, Ontario, Canada; 3London Health Sciences Centre, London, Ontario, Canada; and 4Department of Veterinary Biomedical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, Canada

Submitted 29 December 2005 ; accepted in final form 25 February 2006

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located ~10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P ≤ 0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (all P ≤ 0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P ≤ 0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.

heat load; thermoregulation; hyperthermia; heat content; and heat balance



Address for reprint requests and other correspondence: G. P. Kenny, Univ. of Ottawa, School of Human Kinetics, 125 Univ. Priv., Montpetit Hall (367), PO Box Stn. A, Ottawa, ON, Canada




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