Effect of sleep deprivation on exercise-induced growth hormone release

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
Kevin Joseph Ritsche (Creator)
The University of North Carolina at Greensboro (UNCG )
Web Site: http://library.uncg.edu/
Laure Wideman

Abstract: Growth hormone (GH) is released in a pulsatile fashion from the anterior pituitary gland, with the greatest release occurring during sleep and exercise. Under normal conditions, nocturnal GH release is attenuated during sleep deprivation. Acute sleep deprivation can also impair exercise performance and cognitive function. Therefore, the primary purpose of this study was to assess the impact of acute sleep deprivation on exercise-induced GH release. Secondary aims were to investigate alterations in exercise performance and cognitive function during acute sleep deprivation. Ten male subjects (20.6 ± 1.4 years) were screened for normal sleeping patterns before completing two randomized 24-hour laboratory sessions. They completed a brief, high-intensity exercise bout following either a night of adequate sleep (SLEEP) or acute (24-hour) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], time to peak power [TTPP], minimum power [MinP], fatigue index [FI] and total work per sprint [TWPS]) was determined from four maximal 30-sec Wingate sprints on a cycle ergometer followed by four minutes of active recovery between each sprint. Subjects also performed psychomotor vigilance tasks (PVT) and Paced Auditory Serial Addition Tests (PASAT) during each 24-hr session (0800h, 2000h, 0600h and 0730h) with the latter two taken immediately pre- and post-exercise. The average amount of sleep in the 7 days prior to each session was similar between the SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 hr, p = 0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 hours vs. 7.92 ± 0.33 hours, respectively) (p = 0.166). Repeated measures analysis of variance (ANOVA) revealed a significant interaction effect of sprint x session on PP (p < 0.05). Only the peak power output during sprint 1 of the SLEEP vs. SLD session was significantly greater (1207 ± 177 vs. 1150 ± 137 W, respectively, p < 0.01). MP, PP, MinP and TWPS decreased significantly within each session (p < 0.01), but there were no significant main effects of session. Respiratory rate (RR) was significantly elevated at rest during the SLD vs. SLEEP session (14.8 ± 2.2 vs. 13.7 ± 3.2 breaths/min, p < 0.05) while heart rate (HR) was significantly depressed at rest (60 ± 8 vs. 64 ± 8 bpm, p < 0.05) and during exercise (176 ± 9 vs. 182 ± 9 bpm, p < 0.05). Average oxygen consumption (VO2), metablic equivalent (METS), expired carbon dioxide (VCO2), ventilation (VE), respiratory exchange ratio (RER), respiratory rate (RR), tidal volume (VT), peak VO2 and peak METS were all similar between sessions. Resting GH concentration and time to reach exercise-induced peak GH concentration were similar between the SLEEP and SLD sessions (0.57 ± 0.13 vs. 1.35 ± 0.55 µg/L, p = 0.575; 29.5 ± 2.2 vs. 27.0 ± 1.5 min, p = 0.257, respectively). However, GH AUC (exercise + recovery), peak GH concentration and ?GH (peak GH – resting GH) were significantly lower during the SLEEP session (p < 0.01). PVT scores post-exercise were significantly poorer during the SLD session (326.2 ± 36.6 vs. 298.8 ± 21.1 msec, p < 0.05). In conclusion, acute sleep deprivation influenced exercise-induced peak HR and GH but had minimal effects on exercise performance. Furthermore, sleep deprivation had no effect on cognitive measures at rest, but did impair sensory sensitivity following exercise.

Additional Information

Language: English
Date: 2014
Anaerobic, Psychomotor, Sensory, Sleep loss, Sprint exercise
Sleep deprivation $x Health aspects
Somatotropin $x Physiological effect
Exercise $x Physiological aspects
Cognition $x Effect of exercise on

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