The purpose of this study was to establish an exercise protocol that demonstrated a relationship between rest-interval duration and the exercise induced human growth hormone (hGH) response. Ten recreationally trained male subjects (23 ± 0.9 yrs) performed three leg extension trials on an Eagle — Cybex leg extension machine that consisted of 4 sets of 10 repetitions. The workload and volume was kept constant, but each trial had different rest-interval durations. Rest-interval durations between sets were at: 30 sec intervals (T-30), 60 sec intervals (T-60), or 120 sec intervals (T-120). Blood samples were obtained pre- and 0 — 30 minutes post-exercise and analyzed for lactate and hGH. All blood lactates rose significantly above baseline after exercise, with no differences in time of occurrence between trials. Blood lactates were significantly greater after the T-30 trials, compared to that of the T-60 and T-120 trials. There was no significant difference in hGH concentrations between trials. However, the data did suggest a relationship between rest-interval duration and the variability of hGH responses. The T-30 trials yielded significantly greater variation in hGH concentrations than the T-120 trials, and the T-120 trials showed significantly less variation than both the T-30 and T-60 trials. Although significant differences were found in these variations between trials, they did not prevent any significant differences in concentrations between trials from being found. In summary, the results of this study demonstrated an exercise related increase in lactic acid that had an inverse relationship to the length of the rest-intervals. hGH data on the other hand, did not show a relationship between rest-interval duration and the hGH concentrations. The connection between rest-interval duration and variability of hGH responses could possibly suggest that hGH values may have been significantly different if an exercise protocol higher in volume were utilized. Additionally, the results indicate that there is no direct relationship between blood lactate and hGH concentrations, as others have suggested. / School of Physical Education, Sport, and Exercise Science

The purpose of this investigation was to determine the effect of passive and active recovery on the resynthesis of muscle glycogen after high intensity cycle ergometer exercise in untrained subjects. In a cross over design, six college-age males performed three, one min exercise bouts, at 130% V02max with a 4 min rest period between each work bout. Subjects refrained from exercise for two days prior to testing, and consumed a 15% carbohydrate solution (300g sugar in 2000ml of water) the day before each trial to help elevate glycogen concentration. The exercise protocol for each trial was identical, while the recovery following exercise was eitheractive (40-50% VO2max) or passive. The initial muscle glycogen values averaged 144.2 mmol•kg-1 w.w. for the active trial and 158.7 mmol•kg-1 w.w. for the passive trial. Corresponding post-exercise glycogen contents were 97.7 and 106.8 mmol•kg-1 w.w., respectively. These differences were not significant (P>0.05). However, the rate of muscle glycogen resynthesis during passive recovery increased 15 mmol•kg-1 w.w. whereas it decreased 6.27 mmol•kg-1 w.w. following active recovery (P<0.01). Also, the decrease in blood lactate concentration during active recovery was much faster than during passive recovery and significantly different at 10 and 30 min of the recovery period (P<0.01). The major finding of this investigation was that the rate of muscle glycogen resynthesis during passive recovery was significantly greater than that during active recovery. These data suggest that lactate can be used as an endogenous glycogenic precusor in muscle, and that glycogenesis was the prevalent pathway of lactate removal during passive recovery following high intensity cycle ergometer exercise. / Human Performance Laboratory