ArticlePflugers Archiv : European journal of physiology2006
Tricarboxylic acid cycle intermediates accumulate at the onset of intense exercise in man but are not essential for the increase in muscle oxygen uptake.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Single sodium pyruvate ingestion modifies blood acid-base status and post-exercise lactate concentration in humans.Nutrients · 2014Trial
- Signals from the Circle: Tricarboxylic Acid Cycle Intermediates as Myometabokines.Metabolites · 2021Review
- Comparative NMR and NIRS analysis of oxygen-dependent metabolism in exercising finger flexor muscles.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Hyperpolarized 13C NMR observation of lactate kinetics in skeletal muscle.The Journal of experimental biology · 2015Article
- Long-chain fatty acid combustion rate is associated with unique metabolite profiles in skeletal muscle mitochondria.PloS one · 2010Article
- Tricarboxylic acid cycle intermediate pool size: functional importance for oxidative metabolism in exercising human skeletal muscle.Sports medicine (Auckland, N.Z.) · 2007Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It was proposed that a contraction-induced increase in tricarboxylic acid cycle intermediates (TCAI) is obligatory for the increase in muscle oxygen uptake at the start of exercise. To test this hypothesis, we measured changes in muscle TCAI during the initial seconds of intense exercise and used dichloroacetate (DCA) in an attempt to alter the level of TCAI. Five men performed strenuous leg kicking exercise (64+/-8 W) under noninfused control (CON) and DCA-supplemented conditions; biopsies (vastus lateralis) were obtained at rest and after 5, 15, and 180 s of exercise. In CON, the total concentration of three measured TCAI (SigmaTCAI: citrate, malate, and fumarate) increased (p<0.05) by 71% during the first 15 s of exercise. The SigmaTCAI was lower (p<0.05) in DCA than in CON at rest [0.18+/-0.02 vs 0.64+/-0.09 mmol kg(-1) dry weight (d.w.)], after 5 s (0.30+/-0.07 vs 0.85+/-0.14 mmol kg(-1) d.w.), and 15 s of exercise (0.60+/-0.07 vs 1.09+/-0.16 mmol kg(-1) d.w.), but not different after 3 min (3.12+/-0.53 vs 3.23+/-0.55 mmol kg(-1) d.w.). Despite differences in the level of muscle TCAI, muscle phosphocreatine degradation was similar in DCA and CON during the first 15 s of exercise (17.5+/-3.3 vs 25.6+/-4.1 mmol kg(-1) d.w.). Taken together with our previous observation that DCA does not alter muscle oxygen uptake during the initial phase of intense leg kicking exercise (Bangsbo et al. Am J Physiol 282:R273-R280, 2002), the present data suggest that muscle TCAI accumulate during the initial seconds of exercise; however, this increase is not essential for the contraction-induced increase in mitochondrial respiration.
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