Mary E. Nevill

Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man.

1. The recovery of power output and muscle metabolites was examined following maximal sprint cycling exercise. Fourteen male subjects performed two 30 s cycle ergometer sprints separated by 1.5, 3 and 6 min of recovery, on three separate occasions. On a fourth occasion eight of the subjects performed only one 30 s sprint and muscle biopsies were obtained during recovery. 2. At the end of the 30 s sprint phosphocreatine (PCr) and ATP contents were 19.7 +/‐ 1.2 and 70.5 +/‐ 6.5% of the resting values (rest), respectively, while muscle lactate was 119.0 +/‐ 4.6 mmol (kg dry wt)‐1 and muscle pH was 6.72 +/‐ 0.06. During recovery, PCr increased rapidly to 65.0 +/‐ 2.8% of rest after 1.5 min, but reached only 85.5 +/‐ 3.5% of rest after 6 min of recovery. At the same time ATP and muscle pH remained low (19.5 +/‐ 0.9 mmol (kg dry wt)‐1 and 6.79 +/‐ 0.02, respectively). Modelling of the individual PCr resynthesis using a power function curve gave an average half‐time for PCr resynthesis of 56.6 +/‐ 7.3 s. 3. Recovery of peak power output (PPO), peak pedal speed (maxSp) and mean power during the initial 6 s (MPO6) of sprint 2 did not reach the control values after 6 min of rest, and occurred in parallel with the resynthesis of PCr, despite the low muscle pH. High correlations (r = 0.71‐0.86; P < 0.05) were found between the percentage resynthesis of PCr and the percentage restoration of PPO, maxSp and MPO6 after 1.5 and 3 min of recovery. No relationship was observed between muscle pH recovery and power output restoration during sprint 2 (P > 0.05). 4. These data suggest that PCr resynthesis after 30 s of maximal sprint exercise is slower than previously observed after dynamic exercise of longer duration, and PCr resynthesis is important for the recovery of power during repeated bouts of sprint exercise.

Effects of active recovery on power output during repeated maximal sprint cycling

AbstractThe 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 (

Modelling the relationship between isokinetic muscle strength and sprint running performance

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Effect of a school-based intervention to promote healthy lifestyles in 7–11 year old children

) during sprint 2, compared with passive recovery [

Repeated bouts of sprint running after induced alkalosis

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Growth hormone responses to treadmill sprinting in sprint- and endurance-trained athletes.

] 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 · 1−1;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) 1 · 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.