A single 30 s treadmill sprint would appear to produce a near-maximal growth hormone (GH) response based on results from pharmacological intervention studies, with GH levels remaining elevated for at least 60 min post-exercise (Nevill et al. 1996). However, repeated bouts of exercise have been shown to both augment and attenuate the GH response to exercise. Sprint cycling at different pedal speeds has been found to elicit similar metabolic changes in muscle and blood despite differences in the fatigue profile. There is, however, no information regarding the hormonal response to sprint exercise at different pedal speeds. Therefore the aim of this study was (1) to examine the GH response to repeated bouts of maximal sprint cycling whilst (2) studying the effect of different pedal speeds on GH response. After ethical approval was obtained, ten male subjects completed two all-out 30 s efforts separated by 1 h of passive recovery on two occasions. During one trial the subjects completed both sprints against 75 g kg body mass-1 resistive mass (Fast) and during the other trial both sprints were completed against 100 g kg body mass-1 (Slow) resistive mass. Blood samples were taken in a seated position via a venous cannula at rest, post-warm-up and 10 s, and 2, 4, 10, 30 and 60 min after each sprint. Data were analysed using a two- or three-way ANOVA with repeated measures over time. Fig. 1. Mean serum growth hormone concentrations at rest and during 1 h of recovery after two 30 s maximal sprints (A, sprint 1; B, sprint 2) for the Fast and Slow trials. Peak (PPR) and mean (MPR) pedal revolutions were greater in Fast than Slow (mean ± S.E.M. = 156 ± 4 vs. 128 ± 5 rev min-1, P < 0·01 and 118 ± 3 vs. 95 ± 4 rev min-1, P < 0·01). Blood lactate and blood pH did not differ between trials or between sprints in each trial, although plasma ammonia concentration was higher in sprint 1 than sprint 2 (P < 0·05) and higher in Fast than Slow (P < 0·05). The first sprint in each trial resulted in a distinct GH pulse (Fast, 46 ± 10 vs. Slow, 23 ± 7 mU l-1, P < 0·05) and serum GH was still elevated 60 min post-exercise, but there was no apparent GH pulse in response to the second sprint (Fig. 1). A weak correlation was found between MPR and peak GH response (sprint 1, r = 0·61, P < 0·01; sprint 2, r = 0·56, P < 0·01) and PPR and peak GH response (sprint 1, r = 0·54, P < 0·05; sprint 2, r = 0·57, P < 0·01), but no significant correlation was found between GH and any metabolic response. This study has shown that the GH response is attenuated in repeated sprint cycling and that cycling at fast pedal speeds results in a greater GH response than at slower speeds, despite a similar metabolic response to the two sprints and the two speeds. Thus it would appear that GH release is not controlled by the metabolic response to exercise .
© Copyright 1992 Journal of Applied Physiology. American Physiological Society. Alle Rechte vorbehalten.