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Am J Physiol Regul Integr Comp Physiol (March 2, 2006). doi:10.1152/ajpregu.00918.2005
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Submitted on December 29, 2005
Accepted on February 25, 2006

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

G. P Kenny1*, O. Jay1, W. Zaleski2, M. L Reardon3, Ronald J Sigal3, W. S Journeay4, and F. D Reardon1

1 Faculty of Health Sciences, University of Ottawa, Ottawa, Ontario, Canada
2 Radiology, London Health Sciences Centre, London, Ontario, Canada
3 Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada
4 Veterinary Biomedical Sciences, University of Saskatchewan, Saskatoon, Saskatchewan, Canada

* To whom correspondence should be addressed. E-mail: gkenny{at}uottawa.ca.

We examined the effect of two levels of exercise induced hypotension on esophageal (Tes) and active and non-active 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 pre-exercise 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 pre-exercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP in comparison to 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 pre-exercise 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.




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