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This Article Full Text Full Text (PDF) All Versions of this Article: 564/3/765    most recent jphysiol.2005.083840v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sahlin, K. Articles by Pedersen, P. K. Search for Related Content PubMed PubMed Citation Articles by Sahlin, K. Articles by Pedersen, P. K.

¹ Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Denmark
² Department of Health and Human Performance, Memorial Coliseum, Auburn University, Auburn, AL, USA
³ Department of Medicine, Division of Physiology, University of California, San Diego, CA, USA

We investigated the hypothesis that the pulmonary oxygen uptake slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak for 10 min before (CON) and after (AC) PHE. 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 kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in 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 and reduced gross exercise efficiency during AC. It is concluded that the 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 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 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.

(Received 26 January 2005; accepted after revision 28 February 2005; first published online 3 March 2005)
Corresponding author K. Sahlin: Institute of Sports Science and Clinical Biomechanics, University of Southern Denmark, Campusvej 55, DK-5230 Odense M, Denmark. Email: ksahlin{at}health.sdu.dk

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