Delayed onset muscle soreness does not alter O2 uptake kinetics during heavy-intensity cycling in humans.

The purpose of this study was to determine if exercise-induced delayed onset muscle soreness (DOMS) would alter O2 uptake kinetics during heavy cycling in 9 untrained females. O2 uptake kinetics were characterised during 8-min of constant-load cycling performed with and without DOMS. DOMS was caused by completing 30 min of bench-stepping at a rate of 15 steps.min(-1). Two days after bench stepping, all subjects reported significant leg muscle soreness. Both phase II kinetics (without DOMS tau1: 26.6 +/- 2.4 s; with DOMS tau1: 27.2 +/- 3.7 s) and the slow component amplitude (without DOMS: 277 +/- 15 mL.min(-1); with DOMS: 291 +/- 21 mL.min(-1)) were unaffected by DOMS. The change in blood lactate concentration from rest to end-exercise was significantly greater during exercise performed with DOMS. Eccentric exercise causing a moderate degree of DOMS does not appear to impact upon the mechanisms mediating phase II or the slow component of O2 uptake kinetics.

VE and VCO2 remain tightly coupled during incremental cycling performed after a bout of high-intensity exercise.

The purpose of the present study was to determine whether the linear relationship between CO2 output (VCO2) and pulmonary ventilation (VE) is altered during incremental cycling performed after exercise-induced metabolic acidosis. Ten untrained, female subjects performed two incremental cycling tests (15 W x min(-1) up to 165 W) on separate days. One incremental exercise test was conducted without prior exercise, whereas the other test was preceded by a 1-min bout of maximal cycling. The ventilatory equivalent for O2 (VE/VO2) was only elevated above control values at 15-60 W during incremental cycling performed after high-intensity exercise. In contrast, the ventilatory equivalent for CO2 (VE/VCO2) was significantly increased above control levels at nearly every work stage of incremental work (all except 165 W). Hyperventilation relative to VCO2 was confirmed by the significantly lower end-tidal CO2 tension (P(ET)CO2) obtained throughout the incremental cycling that was performed after high-intensity exercise (except at 165 W). VE and VCO2 were significantly correlated under both treatment conditions (r > 0.99; P < 0.001). Moreover, both the slope and y-intercept of the linear regression were found to be significantly elevated during the incremental cycling performed after high-intensity cycling compared to control conditions (P < 0.01). The increase in the slope of the VE-VCO2 relationship during incremental exercise performed under these conditions does not represent an uncoupling of VE from VCO2, but could be accounted for by the significantly lower P(ET)CO2 observed during exercise.

Creatine supplementation and the total work performed during 15-s and 1-min bouts of maximal cycling.

Nine untrained male subjects participated in a placebo (Pl)/creatine (Cr), single-blind study conducted over a 5-wk period. Placebo and Cr treatments were presented in a sequential manner because muscle Cr washout time after supplementation is unknown. The mean ( +/- SE) age, height, and initial body mass for the subjects was 25.7+/- 1.2 yr, 177 +/- 2 cm, and 78.5 +/- 3.8 kg, respectively. Each subject performed five 15-s bouts of maximal cycling (1-min rest periods) after 7 d of Pl (6 g glucose X 5 doses daily) and again after ingesting Cr for 7 d (5 g creatine plus 1 g glucose X 5 doses) with a 2-wk intervention period. Only 6 of 9 subjects were able to complete five 1-min bouts of maximal cycling (5-min rest periods) after an additional 2 d of Pl and Cr treatment. Cr ingestion resulted in a significant increase in the work performed during each 15-s bout of maximal cycling compared to Pl trials. Moreover, the total work completed during five 15-s bouts of cycling increased significantly from 47.5 +/- 2.3 kJ with Pl treatment to 50.6 +/- 2.3 kJ after Cr supplementation (P < 0.05). Peak blood lactate concentrations determined 4 min after the fifth 15-s work bout were 14.4 +/- 0.5 mmol.L-1 and 14.3 +/- mmol.L-1 for Pl and Cr trials, respectively (P < 0.05). Total work completed during five 1-min bouts of maximal cycling was not significantly increased after Cr supplementation (P > 0.05). Additionally, Cr supplementation did not slow the rate of decline in the work accomplished during repeated bouts of maximal cycling. These findings suggest that Cr ingestion may augment the rate of ATP resynthesis from phosphocreatine during exercise in untrained subjects.