Hormonal and metabolic responses to repeated cycling sprints under different hypoxic conditions
Introduction
Exercise is a potent stimulus for growth hormone (GH) secretion. The GH response to acute exercise is related to exercise intensity with greater GH secretion observed at higher exercise intensities [1]. Although the precise physiological role of high intensity exercise-stimulated GH secretion has not been fully elucidated, it has been associated with a post-exercise rise in lipolysis [2]. Octreotide infusion blocks exercise-induced GH secretion and inhibits post-exercise adipose tissue lipolysis [3]. These results suggest that high intensity exercise-induced GH release enhances adipose tissue lipolysis during the post-exercise recovery period.
Exercise performed in acute severe systemic hypoxia also increases GH release [4], [5], [6]. We have recently reported that moderate- [4] and low- [5] intensity resistance exercise performed during acute severe hypoxia (13% oxygen) causes a larger increase in GH concentrations than when exercise is performed in normoxia. Additionally, submaximal endurance (cycle ergometer) exercise (750 kpm/min) performed under severe hypoxic conditions (4550 m above sea level; approx. 12% oxygen) increases levels of circulating GH and free fatty acids (FFA) to a greater extent than when exercise is performed under normoxic conditions [6]. In contrast, low-intensity (30% 1RM) resistance exercise performed under moderate hypoxia (15% oxygen) or normoxia caused similar levels of GH secretion [7]. Similarly, 30 min of submaximal endurance exercise (50% of peak oxygen uptake) performed under moderate hypoxia (2000 m above sea level; approx. 16.5% oxygen) or normoxia elicited similar GH and FFA responses [8]. These results suggest that the severity of hypoxia affects the exercise-induced GH secretion and adipose tissue lipolysis, and subsequent FFA mobilization.
All-out sprint cycling exercise is a powerful stimulus for GH release. Previous studies report a marked increase in circulating GH levels following sprint exercise [9], [10], [11], [12]. However, as far as we know, there are no data concerning the effect of different hypoxic levels on circulating GH and FFA responses during and post-sprint exercise. Improved repeated sprint ability performance in athletes occurs following sprint exercise training under hypoxia [13]. Indeed athletes, in particular international-level athletes, utilize hypoxic training rooms to gain a greater improvement in their physical performance. A reduction in body fat can further enhance athlete physical performance. Therefore, a better understanding of the relationship between hypoxia and circulating GH and FFA responses during and post-sprint exercise may assist in improving athlete performance. Here, we examined the effects of sprint exercise performed under both moderate and severe hypoxic conditions on hormonal and metabolic responses. We hypothesized that following sprint exercise performed in severe hypoxic conditions GH and circulating FFA levels would be elevated to a greater extent when compared to the sprint exercise performed in normoxic and moderate hypoxic conditions.
Section snippets
Subjects
Seven healthy male subjects (age = 20.4 ± 0.7 yr, height = 170.4 ± 1.5 cm, body mass = 68.3 ± 1.9 kg, BMI = 23.5 ± 0.9 kg/m2) participated in this study. The subjects were non-smokers and not taking regular medications. They belonged to a University Cycling Club and trained 6 days per week. The subjects were not exposure to an altitude of > 3000 m within 1 month before each trial and had no history of severe acute mountain sickness. All subjects were informed about the purpose of the present study as well as the
Power outputs
Table 1 shows the results for the peak and mean power outputs. There was a significant main effect of time on peak (F = 47.65, P < 0.01) and mean (F = 79.47, P < 0.01) power outputs. In all trials, peak power significantly decreased in bouts 3 and 4 compared with bout 1 (P < 0.01), but no significant differences between the three trials were observed. Mean power in all the trials progressively decreased over the intermittent exercise session compared with bout 1 (P < 0.01). However, there were no
Discussion
In the present study, we demonstrated that the HSE 13.6 trial caused larger elevations in GH than the NSE and HSE 16.4 trials. In addition, we performed correlation analysis and found a significant correlation between the peak value of GH and the peak value of FFA. The SpO2 in the HSE 13.6 trial (mean value after exposure: 84.5% ± 0.8%) was significantly lower than that in the NSE (mean value after exposure: 97.0% ± 0.2%) and HSE 16.4 (mean value after exposure: 93.0% ± 0.5%) trials. These results
Conflict of interest
There were no conflicts of interests.
Acknowledgments
We thank members of the hypoxic research project in Japan Institute of Sports Sciences for their excellent technical support. We also thank clinical laboratory technicians in Japan Institute of Sports Sciences and University of Tsukuba for help with conduct of the clinical portion of this study. We also thank Yusuke Ikeda and Wataru Takashima for their excellent experimental assistances. This work was supported by a grant-in-aid for Young Scientists (B) from the Ministry of Education, Culture,
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