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J Appl Physiol (July 3, 2003). doi:10.1152/japplphysiol.00415.2003
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Submitted on April 25, 2003
Accepted on July 2, 2003

Facial cooling-induced bradycardia does not slow pulmonary VO2 kinetics at the onset of high-intensity exercise

Masako Endo1, Shinko Tauchi1, Naoyuki Hayashi2, Shunsaku Koga3, Harry B Rossiter4, and Yoshiyuki Fukuba1*

1 Department of Exercise Science & Physiology, School of Health Sciences, Hiroshima Prefectural Women's University, Hiroshima, Japan
2 Laboratory of Exercise Physiology, Faculty of Health & Sport Sciences, Osaka University, Toyonaka, Japan
3 Laboratory for Applied Physiology, Kobe Design University, Kobe, Japan
4 Division of Physiology, Department of Medicine, University of California San Diego, La Jolla, CA, USA

* To whom correspondence should be addressed. E-mail: fukuba{at}hirojo-u.ac.jp.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (VO2) 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 delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the VO2-kinetics during repeated bouts of heavy intensity cycling exercise. Five healthy subjects (aged 21-43 years) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: {Delta}50 % between LT and VO2max) 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 1st bout (CFS1) or 2nd bout (CFS2) of repeated heavy intensity exercise. In the control protocol, VO2 responses in N2 showed a facilitated adaptation compared to 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 ({tau}HR; N1: 55.6 (±16.0, SD) vs. CFS1: 69.0 (12.8) and N2: 55.5 (11.8) vs. CFS2: 64.0 (17.5)), however it did not affect the 'primary' VO2 kinetics ({tau}VO2; N1: 23.7 (±7.9, SD) vs. CFS1: 20.9 (3.8) and N2: 23.3 (10.3) vs. CFS2: 17.4 (6.3)). In conclusion, increased vagal withdrawal delayed and slowed the circulatory response, but did not alter the VO2-kinetics at the onset of supra-LT cycling exercise. As the facilitation of VO2 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.




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