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Capsiate supplementation reduces oxidative cost of contraction in exercising mouse skeletal muscle in vivo.

Abstract
Chronic administration of capsiate is known to accelerate whole-body basal energy metabolism, but the consequences in exercising skeletal muscle remain very poorly documented. In order to clarify this issue, the effect of 2-week daily administration of either vehicle (control) or purified capsiate (at 10- or 100-mg/kg body weight) on skeletal muscle function and energetics were investigated throughout a multidisciplinary approach combining in vivo and in vitro measurements in mice. Mechanical performance and energy metabolism were assessed strictly non-invasively in contracting gastrocnemius muscle using magnetic resonance (MR) imaging and 31-phosphorus MR spectroscopy (31P-MRS). Regardless of the dose, capsiate treatments markedly disturbed basal bioenergetics in vivo including intracellular pH alkalosis and decreased phosphocreatine content. Besides, capsiate administration did affect neither mitochondrial uncoupling protein-3 gene expression nor both basal and maximal oxygen consumption in isolated saponin-permeabilized fibers, but decreased by about twofold the Km of mitochondrial respiration for ADP. During a standardized in vivo fatiguing protocol (6-min of repeated maximal isometric contractions electrically induced at a frequency of 1.7 Hz), both capsiate treatments reduced oxidative cost of contraction by 30-40%, whereas force-generating capacity and fatigability were not changed. Moreover, the rate of phosphocreatine resynthesis during the post-electrostimulation recovery period remained unaffected by capsiate. Both capsiate treatments further promoted muscle mass gain, and the higher dose also reduced body weight gain and abdominal fat content. These findings demonstrate that, in addition to its anti-obesity effect, capsiate supplementation improves oxidative metabolism in exercising muscle, which strengthen this compound as a natural compound for improving health.
AuthorsKazuya Yashiro, Anne Tonson, Émilie Pecchi, Christophe Vilmen, Yann Le Fur, Monique Bernard, David Bendahan, Benoît Giannesini
JournalPloS one (PLoS One) Vol. 10 Issue 6 Pg. e0128016 ( 2015) ISSN: 1932-6203 [Electronic] United States
PMID26030806 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Ion Channels
  • Mitochondrial Proteins
  • Ucp3 protein, mouse
  • Uncoupling Protein 3
  • capsiate
  • Capsaicin
Topics
  • Abdominal Fat (drug effects)
  • Animals
  • Biomechanical Phenomena (drug effects)
  • Body Weight (drug effects)
  • Capsaicin (administration & dosage, analogs & derivatives, pharmacology)
  • Cell Respiration (drug effects)
  • Dietary Supplements
  • Dose-Response Relationship, Drug
  • Eating (drug effects)
  • Energy Metabolism (drug effects)
  • Gene Expression Regulation (drug effects)
  • Ion Channels (genetics)
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mitochondria (drug effects, metabolism)
  • Mitochondrial Proteins (genetics)
  • Muscle Contraction (drug effects)
  • Muscle, Skeletal (anatomy & histology, drug effects, metabolism, physiology)
  • Organ Size (drug effects)
  • Oxidation-Reduction (drug effects)
  • Permeability (drug effects)
  • Physical Conditioning, Animal (physiology)
  • Uncoupling Protein 3

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