(-)-Epicatechin Attenuates Degradation of Mouse Oxidative Muscle Following Hindlimb Suspension

J Strength Cond Res. 2016 Jan;30(1):1-10. doi: 10.1519/JSC.0000000000001205.

Abstract

The purpose of this study was to conduct a 14-day hindlimb suspension (HS) with and without (-)-epicatechin supplementation to determine whether (-)-epicatechin treatment can attenuate the loss in muscle degradation, angiogenesis, and mitochondrial signaling in oxidative skeletal muscle. Adult mice were randomized into 3 groups: (a) control (C); (b) HS with vehicle (HS-V); and (c) HS with (-)-epicatechin (HS-(-)-Epi). Animals in the HS-(-)-Epi group received (-)-epicatechin (1.0 mg · kg(-1) of body mass) twice daily through oral gavage. For markers related to muscle degradation, the HS-V group had significantly higher protein expression compared with the control and HS-(-)-Epi groups. Moreover, protein expression for myosin heavy chain type I was significantly reduced by approximately 45% in the HS-V group compared with the control and HS-(-)-Epi groups. In addition, capillarity contact and capillary-to-fiber ratio were significantly higher in the HS-(-)-Epi group compared with the HS-V group. Furthermore, protein expression for thrombospondin-1 was significantly higher in HS-V group compared with the control and HS-(-)-Epi groups. Hindlimb suspension also significantly reduced protein expression for mitochondrial signaling compared with the control and HS-(-)-Epi groups. These findings suggest that (-)-epicatechin supplementation attenuates degradation in oxidative muscles after HS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / drug effects
  • Animals
  • Capillaries / drug effects
  • Capillaries / pathology
  • Capillaries / physiopathology
  • Capillary Action / drug effects
  • Catechin / pharmacology*
  • Hindlimb Suspension / adverse effects
  • Hindlimb Suspension / physiology
  • Male
  • Mice
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Muscle, Skeletal / drug effects*
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Myosin Heavy Chains / metabolism*
  • Myosin Type I / metabolism*
  • Neovascularization, Physiologic / drug effects
  • Signal Transduction / drug effects
  • Thrombospondin 1 / metabolism

Substances

  • Thrombospondin 1
  • Thbs1 protein, mouse
  • Catechin
  • Myosin Type I
  • Myosin Heavy Chains