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J Appl Physiol 95: 1623-1631, 2003. First published July 3, 2003; doi:10.1152/japplphysiol.00415.2003
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Facial cooling-induced bradycardia does not slow pulmonary O2 kinetics at the onset of high-intensity exercise

Masako Endo,1 Shinko Tauchi,1 Naoyuki Hayashi,2 Shunsaku Koga,3 Harry B. Rossiter,4 and Yoshiyuki Fukuba1

1Department of Exercise Science and Physiology, School of Health Sciences, Hiroshima Prefectural Women's University, Hiroshima 734-8558; 2Laboratory of Exercise Physiology, Faculty of Health and Sport Sciences, Osaka University, Toyonaka 560-0043; 3Laboratory for Applied Physiology, Kobe Design University, Kobe 651-2196, Japan; and 4Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, California 92093

Submitted 25 April 2003 ; accepted in final form 2 July 2003

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (O2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the O2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal O2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, O2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 ± 16.0 (SD) vs. CFS1: 69.0 ± 12.8 s and N2: 55.5 ± 11.8 vs. CFS2: 64.0 ± 17.5 s]; however, it did not affect the "primary" O2 kinetics [O2 time constant; N1: 23.7 ± 7.9 (SD) vs. CFS1: 20.9 ± 3.8 s, and N2: 23.3 ± 10.3 vs. CFS2: 17.4 ± 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the O2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of O2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

vagal activation; oxygen uptake adjustment; heavy exercise



Address for reprint requests and other correspondence: Y. Fukuba, Dept. of Exercise Science and Physiology, School of Health Sciences, Hiroshima Prefectural Women's Univ., 1-1-71, Ujina-higashi, Minamiku, Hiroshima 734-8558, Japan (E-mail: fukuba{at}hirojo-u.ac.jp).




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