Prior heavy exercise eliminates VO2 slow component and reduces efficiency during submaximal exercise in humans.

We investigated the hypothesis that the pulmonary oxygen uptake (VO2) slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters VO2 kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak VO2 (VO2peak) for 10 min before (CON) and after (AC) PHE. VO2 was measured continuously (breath-by-breath) and muscle biopsies were obtained prior to and after 3 and 10 min of exercise. Muscle lactate concentration was stable between 3 and 10 min of exercise but was 2- to 3-fold higher during AC (P < 0.05 versus CON). Acetylcarnitine (ACn) concentration was 6-fold higher prior to AC and remained higher during exercise. Phosphocreatine (PCr) concentration was similar prior to exercise but the decrease was 2-fold greater during AC than during CON. The time constant for the initial VO2 kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in VO2 between 3 and 10 min of exercise during CON (+7.9 +/- 0.2%) was not correlated with muscle or blood lactate levels. PHE eliminated the slow increase in VO2 and reduced gross exercise efficiency during AC. It is concluded that the VO2 slow component cannot be explained by a progressive acidosis because both muscle and blood lactate levels remained stable during CON. We suggest that both the VO2 slow component during CON and the reduced gross efficiency during AC are related to impaired contractility of the working fibres and the necessity to recruit additional motor units. Despite a pronounced stockpiling of ACn during AC, initial VO2 kinetics were not affected by PHE and PCr concentration decreased to a lower plateau. The discrepancy with previous studies, where initial oxidative ATP generation appears to be limited by acetyl group availability, might relate to remaining fatiguing effects of PHE.