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LETTER TO THE EDITOR
This study examined the growth hormone (GH) response to repeated bouts of sprint cycling. Eight healthy men completed three trials consisting of two 30-s sprints on a cycle ergometer separated by either 60 min (Trial A) or 240 min (Trial B) of recovery and a single 30-s sprint carried out the day after Trial B (Trial C). Trials A and B were separated by at least 7 days. Blood samples were obtained at rest and during recovery from each sprint. In Trial A, GH was elevated immediately before sprint 2, and there was no further increase in GH following the second sprint [area under the curve: 460 (SD 348) vs. 226 min·µg–1·l–1 (SD 182), P = 0.05]. Free insulin-like growth factor I tended to be lower immediately before sprint 2 than sprint 1 (P = 0.06). Serum free fatty acids were not different immediately before each of the sprints. In Trial B, there was a trend for a smaller GH response to the second sprint [GH area under the curve: 512 (SD 396) vs. 242 min·µg–1·l–1 (SD 190), P = 0.09]. Free insulin-like growth factor I tended to be lower (P = 0.06), and serum free fatty acids were higher (P = 0.01) immediately before sprint 2 than sprint 1. There was no difference in the GH response to sprinting on consecutive days (Trials B and C). In conclusion, repeated bouts of sprint cycling on the same day result in an attenuation or even ablation of the exercise-induced increase in GH, depending on the recovery interval between sprints.
Growth hormone responses to repeated bouts of aerobic exercise with different recovery intervals
To the Editor: We read with interest the paper by Stokes et al. (5), concerning growth hormone (GH) responses to two repeated 30-s bouts of sprint exercise with different recovery periods (60 min and 240 min) between bouts.
We recently studied (3) GH responses to two consecutive 30-min cycling sessions at 80% of individual maximal oxygen consumption (
O2 max) in amateur competitive cyclists (mean age ± SE: 28.7 ± 2.3 yr; mean weight: 65.2 ± 2.4 kg). Subjects were tested on three occasions with different time intervals between the two bouts: 120 min (experiment A), 240 min (experiment B), and 360 min (experiment C). As reported in Figs. 1 and 2, peak GH concentration and GH incremental area under the curve (GH AUC, ng·ml–1·90 min–1) in response to the second bout was significantly lower (P < 0.01) than that observed after the first bout in experiments A and B, whereas no difference was detected between the two bouts in experiments C.
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O2 max. In our hands, the attenuation of the GH response was eliminated when greater recovery time (i.e., 360 min) was provided between exercise bouts, thus indicating that pituitary refractoriness was fully reversible. The trend of decreasing GH responsiveness to repeated bouts of exercise resembles the pattern of responsiveness found with repeated administration of 1 µg/kg body wt GH-releasing hormone at the same intervals in normal adults (2, 4), thus suggesting that both pharmacological and exercise repeated stimuli may exert a comparable negative feedback on GH secretion and/or elicit a transient depletion of the promptly releasable pituitary GH pool.
The blunting of GH responsiveness to short-term repeated exercise bouts does not seem related to the intensity and duration of the exercise, being present in different experimental conditions, and to the amount of GH released after the first exercise bout (range of GH peaks: 6–23 ng/ml), as reported in Refs. 1, 3, and 5.
The knowledge of this pattern of exercise-induced GH secretion could be useful to athletes when planning their training sessions for producing physiological greater amounts of GH-IGF-I. Although all these data may have some implications for exercise prescription in athletes (in terms of the optimal combination of intensity and recovery in between training sessions), further additional studies are necessary to extend these observations to different sport activities, both aerobic and anaerobic.
REFERENCES
Claudio L. Lafortuna
Institute of Bioimaging and Molecular Physiology
CNR, Milan, Italy
Nicola A. Maffiuletti
Schulthess Klinik
Zurich, Switzerland
To the Editor: It is interesting to compare the findings of our recent study (7) and the paper by Sartorio et al. (6) relating to the GH responses to repeated bouts of exercise. The similar pattern of GH responses to repeated bouts of exercise in these two papers is striking, and it is of particular interest that the attenuation of the GH response to a second bout of exercise occurred despite the fact that the exercise stimulus was very different in each investigation. However, it must also be pointed out that other investigators have reported an augmented GH response with repeated exercise (4, 5). Kanaley et al. (4) determined integrated GH in response to three 30-min bouts of exercise, separated by either 60 min or 210 min. Integrated GH increased with each subsequent exercise bout and tended to be greater when recovery between bouts was longer. Similarly, Ronsen et al. (5) reported a greater GH response to the second of two 65-min bouts of exercise that were separated by 180 min of recovery. The reason for the disparity between these findings is not clear, demonstrating that our understanding of the mechanisms regulating exercise-induced GH release is far from complete.
Furthermore, the mechanism behind the refractory period for GH release proposed when the GH response to a second bout is attenuated (6, 7) is not fully understood. We feel that it is unlikely to be due to a depletion of the releasable pituitary pool of GH, due largely to the very fact that some investigations have demonstrated an augmented response to a second bout of exercise (4, 5). Furthermore, it has been suggested that pituitary GH content far exceeds the amount of GH released after GHRH administration, yet repeated GHRH administration results in an attenuated GH response (3). As proposed in our paper (7), it appears that there may be at least a two-phase refractory period in response to sprint exercise, with an initial period of GH autoinhibition, followed by later inhibition of GH release by the action of circulating free fatty acids.
Finally, we recognize the need to better understand the role of GH release in response to exercise. It is possible that GH has a role in the regulation of protein synthesis after exercise, but pituitary GH is not essential for exercise-induced muscle hypertrophy (1). It is also possible that GH contributes to the regulation of substrate metabolism during or after exercise, yet administering GH during exercise had no effect on substrate oxidation (2). Until the role for exercise-induced GH release is better defined, the relationship between serum GH and signaling pathways in target tissues is better understood, and the influence that these have on long-term changes in body composition and exercise performance has been identified, we must be cautious about value of prescribing exercise in a manner designed to maximize GH release.
REFERENCES
Mary Nevill
Henryk Lakomy
School of Sport and Exercise Sciences
Loughborough University
Loughborough, United Kingdom
Jan Frystyk
Medical Research Laboratories
Aarhus University Hospital
Aarhus, Denmark
George Hall
Department of Anaesthesia and Intensive Care Medicine
St. George's Hospital Medical School
University of London
London, United Kindgom
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) and heart rate (HR, continuous trace) determined as a function of time during 2 consecutive exercise bouts with different time intervals (A: experiment A, 120 min; B: experiment B, 240 min; C: experiment C, 360 min).