title: (-)-Epicatechin maintains endurance training adaptation in mice after 14 days of detraining.
abstract: The purpose of this study was to determine whether (-)-epicatechin (mainly found in cocoa) could attenuate detraining effects in the hindlimb muscles of mice. Thirty-two male mice were randomized into 4 groups: control, trained, trained with 14 d of detraining and vehicle (DT-14-W), and trained with 14 d of detraining and (-)-epicatechin [DT-14-(-)-Epi]. DT-14-(-)-Epi received (-)-epicatechin (1.0 mg/kg 2 ×/d), whereas water was given to the DT-14-W group. The latter 3 groups performed 5 wk of endurance training 5 ×/wk. Hindlimb muscles were harvested, and Western blots, as well as enzyme analyses, were performed. Training significantly increased capillary-to-fiber ratio (≈ 78.8%), cytochrome-c oxidase (≈ 35%), and activity (≈ 144%) compared to controls. These adaptations returned to control levels for the DT-14-W group, whereas the DT-14-(-)-Epi group was able to maintain capillary-to-fiber ratio (≈ 44%), CcO protein expression (≈ 45%), and activity (≈ 108%) above control levels. In addition, the increase in capillarity was related to decreased protein expression of thrombospondin-1, an antiangiogenic regulator. Furthermore, there were no significant differences in endurance capacity between the trained and DT-14-(-)-Epi groups. Our data suggest that (-)-epicatechin may be a suitable compound to maintain exercise-induced improved capillarity and mitochondrial capacity, even when exercise regimens are discontinued.
authors.affiliation: Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, MI 48201, USA.
authors.forename: Maik
authors.initials: M
authors.lastname: Hüttemann
authors.forename: Icksoo
authors.initials: I
authors.lastname: Lee
authors.forename: Moh H
authors.initials: MH
authors.lastname: Malek
mesh_terms: D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D002392:Catechin / Q000737:chemistry / Q000494:pharmacology*; D042967:Electron Transport Complex I / Q000502:physiology; D014450:Electron Transport Complex III / Q000502:physiology; D003576:Electron Transport Complex IV / Q000378:metabolism / Q000502:physiology; D006614:Hindlimb / Q000033:anatomy & histology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008928:Mitochondria / Q000378:metabolism; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D010807:Physical Endurance / Q000187:drug effects* / Q000502:physiology; D011897:Random Allocation; D019700:Thrombospondin 1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D019700:Thrombospondin 1; D042461:Vascular Endothelial Growth Factor A; D002392:Catechin; D003576:Electron Transport Complex IV; D042967:Electron Transport Complex I; D014450:Electron Transport Complex III