Maximal Sprint Cycling Research Articles

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

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 (W) during sprint 2, compared with passive recovery [W] 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) mumol .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.

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

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

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 previous dynamic arm exercise on power output during repeated maximal sprint cycling.

This study examined the effects of elevating blood lactate concentration by arm exercise on subsequent performance during repeated 30 s sprints with the legs. Eight male students performed two 30 s cycle ergometer sprints separated by 6 min of recovery, on two occasions. On one occasion the subjects performed only the two 30 s cycle ergometer sprints ('legs'), while on the other occasion 5 min of heavy arm cranking preceded the two sprints ('arms and legs'). Blood lactate concentration was determined from capillary samples at rest, after a standardized warm-up and 3 and 5 min following each exercise bout. In the 'legs' condition, the peak power output (PPO) and mean power output (MPO) in the second sprint were 92% (P < 0.05) and 85% (P < 0.01) of the values attained during the first sprint, respectively. Prior arm exercise, which increased blood lactate to 11.0 +/- 0.6 mM, had no effect on PPO and MPO during the first cycle ergometer sprint (approximately 4% drop, N.S.). However, in the second sprint after prior arm exercise, PPO was 10% lower than the PPO attained during the corresponding sprint in the 'legs' condition (sprint 2 'arms and legs' 963 +/- 42 W, sprint 2 'legs' 1074 +/- 60 W, P < 0.05), while MPO was better maintained (sprint 2 'arms and legs' 517 +/- 17 W, sprint 2 'legs' 549 +/- 24 W, N.S.). The rate of blood lactate accumulation after both cycle ergometer sprints was considerably decreased (by approximately 50%) when blood lactate levels were pre-elevated by arm crank exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Specificity of Test Duration when Assessing the Anaerobic Lactacid Capacity of High-Performance Track Cyclists

The specificity of three maximal cycling sprint tests as a measure of anaerobic lactacid capacity was determined in nine highly trained male cyclists when they performed 10-, 30-, 40-, and 60-s tests on a modified Repco wind-braked cycle ergometer. Peak power (PP), percent power loss (% PO), total work done (TW), and peak blood lactate (PHLa) were determined for each test. The cyclists also performed a 1000-m time trial under competition conditions during which 200-m split times, total time (TT), and peak post-competition blood lactate (TTPHLa) were recorded. While there was no statistically significant difference between the peak blood lactate of the 30-, 40-, and 60-s tests, peak blood lactate achieved after the 1000-m time trial was significantly greater than those after the cycle ergometer tests. Although there were high intercorrelations (0.88-0.99) between the anaerobic power and capacity indices of the laboratory tests, only the PP and TW achieved during the 60-s test correlated significantly (P less than 0.05) with TT. The data suggest that when assessing the anaerobic power and capacity of elite 1000-m time trial cyclists, a cycle ergometer test duration of at least 60 s should be employed.