This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10-and 30-s sprints. At the end of sprint 1, PCr was 16.9 ± 1.4% of the resting value, and muscle pH dropped to 6.69 ± 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 ± 0.03), but PCr was resynthesized to 78.7 ± 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 ± 9 mmol/kg dry muscle during the first sprint but was decreased to 139 ± 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a  45% decrease in glycolysis. Despite this  41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only  18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 ± 0.10 vs. 3.17 ± 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part ( 49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.

The effects of active recovery on metabolic and cardiorespiratory responses and power output were examined during repeated sprints. Male subjects (n = 13) performed two maximal 30-s cycle ergometer sprints, 4 min apart, on two separate occasions with either an active [cycling at 40 (1)% of maximal oxygen uptake; mean (SEM)] or passive recovery. Active recovery resulted in a significantly higher mean power output (W̄) during sprint 2, compared with passive recovery [W̄] 603 (17) W and 589 (15) W, P < 0.05]. This improvement was totally attributed to a 3.1 (1.0)% higher power generation during the initial 10 s of sprint 2 following the active recovery (P < 0.05), since power output during the last 20 s sprint 2 was the same after both recoveries. Despite the higher power output during sprint 2 after active recovery, no differences were observed between conditions in venous blood lactate and pH, but peak plasma ammonia was significantly higher in the active recovery condition [205 (23) vs 170 (20) μmol·l-1; P < 0.05]. No differences were found between active and passive recovery in terms of changes in plasma volume or arterial blood pressure throughout the test. However, heart rate between the two 30-s sprints and oxygen uptake during the second sprint were higher for the active compared with passive recovery [148 (3) vs 130 (4) beats min-1; P < 0.01) and 3.3 (0.1) vs 2.8 (0.1) l·min-1; P < 0.01]. These data suggest that recovery of power output during repeated sprint exercise is enhanced when low-intensity exercise is performed between sprints. The beneficial effects of an active recovery are possibly mediated by an increased blood flow to the previously exercised muscle.

This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10-and 30-s sprints. At the end of sprint 1, PCr was 16.9 ± 1.4% of the resting value, and muscle pH dropped to 6.69 ± 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 ± 0.03), but PCr was resynthesized to 78.7 ± 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 ± 9 mmol/kg dry muscle during the first sprint but was decreased to 139 ± 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a  45% decrease in glycolysis. Despite this  41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only  18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 ± 0.10 vs. 3.17 ± 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part ( 49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.

The effects of active recovery on metabolic and cardiorespiratory responses and power output were examined during repeated sprints. Male subjects (n = 13) performed two maximal 30-s cycle ergometer sprints, 4 min apart, on two separate occasions with either an active [cycling at 40 (1)% of maximal oxygen uptake; mean (SEM)] or passive recovery. Active recovery resulted in a significantly higher mean power output (W̄) during sprint 2, compared with passive recovery [W̄] 603 (17) W and 589 (15) W, P < 0.05]. This improvement was totally attributed to a 3.1 (1.0)% higher power generation during the initial 10 s of sprint 2 following the active recovery (P < 0.05), since power output during the last 20 s sprint 2 was the same after both recoveries. Despite the higher power output during sprint 2 after active recovery, no differences were observed between conditions in venous blood lactate and pH, but peak plasma ammonia was significantly higher in the active recovery condition [205 (23) vs 170 (20) μmol·l-1; P < 0.05]. No differences were found between active and passive recovery in terms of changes in plasma volume or arterial blood pressure throughout the test. However, heart rate between the two 30-s sprints and oxygen uptake during the second sprint were higher for the active compared with passive recovery [148 (3) vs 130 (4) beats min-1; P < 0.01) and 3.3 (0.1) vs 2.8 (0.1) l·min-1; P < 0.01]. These data suggest that recovery of power output during repeated sprint exercise is enhanced when low-intensity exercise is performed between sprints. The beneficial effects of an active recovery are possibly mediated by an increased blood flow to the previously exercised muscle.

This study examined the contribution of phosphocreatine (PCr) and aerobic metabolism during repeated bouts of sprint exercise. Eight male subjects performed two cycle ergometer sprints separated by 4 min of recovery during two separate main trials. Sprint 1 lasted 30 s during both main trials, whereas sprint 2 lasted either 10 or 30 s. Muscle biopsies were obtained at rest, immediately after the first 30-s sprint, after 3.8 min of recovery, and after the second 10-and 30-s sprints. At the end of sprint 1, PCr was 16.9 ± 1.4% of the resting value, and muscle pH dropped to 6.69 ± 0.02. After 3.8 min of recovery, muscle pH remained unchanged (6.80 ± 0.03), but PCr was resynthesized to 78.7 ± 3.3% of the resting value. PCr during sprint 2 was almost completely utilized in the first 10 s and remained unchanged thereafter. High correlations were found between the percentage of PCr resynthesis and the percentage recovery of power output and pedaling speed during the initial 10 s of sprint 2 (r = 0.84, P < 0.05 and r = 0.91, P < 0.01). The anaerobic ATP turnover, as calculated from changes in ATP, PCr, and lactate, was 235 ± 9 mmol/kg dry muscle during the first sprint but was decreased to 139 ± 7 mmol/kg dry muscle during the second 30-s sprint, mainly as a result of a ~45% decrease in glycolysis. Despite this ~41% reduction in anaerobic energy, the total work done during the second 30-s sprint was reduced by only ~18%. This mismatch between anaerobic energy release and power output during sprint 2 was partly compensated for by an increased contribution of aerobic metabolism, as calculated from the increase in oxygen uptake during sprint 2 (2.68 ± 0.10 vs. 3.17 ± 0.13 l/min; sprint 1 vs. sprint 2; P < 0.01). These data suggest that aerobic metabolism provides a significant part (~49%) of the energy during the second sprint, whereas PCr availability is important for high power output during the initial 10 s.