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Hoshino D, Tamura Y, Masuda H, et al. Effects of decreased lactate accumulation after dichloroacetate administration on exercise training-induced mitochondrial adaptations in mouse skeletal muscle. Physiol Rep. 2015;3(9)doi: 10.14814/phy2.12555.
Hoshino, D., Tamura, Y., Masuda, H., Matsunaga, Y., & Hatta, H. (2015). Effects of decreased lactate accumulation after dichloroacetate administration on exercise training-induced mitochondrial adaptations in mouse skeletal muscle. Physiological reports, 3(9), . https://doi.org/10.14814/phy2.12555
Hoshino, Daisuke, et al. "Effects of decreased lactate accumulation after dichloroacetate administration on exercise training-induced mitochondrial adaptations in mouse skeletal muscle." Physiological reports vol. 3,9 (2015). doi: https://doi.org/10.14814/phy2.12555
Hoshino D, Tamura Y, Masuda H, Matsunaga Y, Hatta H. Effects of decreased lactate accumulation after dichloroacetate administration on exercise training-induced mitochondrial adaptations in mouse skeletal muscle. Physiol Rep. 2015 Sep;3(9). doi: 10.14814/phy2.12555. PMID: 26416973; PMCID: PMC4600395.
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Physiol Rep. 2015 Sep;3(9). doi: 10.14814/phy2.12555.

Effects of decreased lactate accumulation after dichloroacetate administration on exercise training-induced mitochondrial adaptations in mouse skeletal muscle.

Physiological reports

Daisuke Hoshino, Yuki Tamura, Hiroyuki Masuda, Yutaka Matsunaga, Hideo Hatta

Affiliations

  1. Department of Sports Sciences, The University of Tokyo, Tokyo, Japan [email protected].
  2. Department of Sports Sciences, The University of Tokyo, Tokyo, Japan.

PMID: 26416973 PMCID: PMC4600395 DOI: 10.14814/phy2.12555

Abstract

Recent studies suggested that lactate accumulation can be a signal for mitochondrial biogenesis in skeletal muscle. We investigated whether reductions in lactate concentrations in response to dichloroacetate (DCA), an activator of pyruvate dehydrogenase, attenuate mitochondrial adaptations after exercise training in mice. We first confirmed that DCA administration (200 mg/kg BW by i.p. injection) 10 min before exercise decreased muscle and blood lactate concentrations after high-intensity interval exercise (10 bouts of 1 min treadmill running at 40 m/min with a 1 min rest). At the same time, exercise-induced signal cascades did not change by pre-exercise DCA administration. These results suggested that DCA administration affected only lactate concentrations after exercise. We next examined the effects of acute DCA administration on mRNA expressions involved with mitochondrial biogenesis after same high-intensity interval exercise and the effects of chronic DCA administration on mitochondrial adaptations after high-intensity interval training (increasing intensity from 38 to 43 m/min by the end of training period). Acute DCA administration did not change most of the exercise-induced mRNA upregulation. These data suggest that lactate reductions by DCA administration did not affect transcriptional activation after high-intensity interval exercise. However, chronic DCA administration attenuated, in part, mitochondrial adaptations such as training-induced increasing rates of citrate synthase (P = 0.06), β-hydroxyacyl CoA dehydrogenase activity (P < 0.05), cytochrome c oxidase IV (P < 0.05) and a fatty acid transporter, fatty acid translocase/CD36 (P < 0.05), proteins after exercise training. These results suggest that lactate accumulation during high-intensity interval exercise may be associated with mitochondrial adaptations after chronic exercise training.

© 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

Keywords: Dichloroacetate; exercise training; lactate; mitochondria; skeletal muscle

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