Satellite cell (SC) activation is defined as the time frame during which the stem cell becomes poised to reenter G1 of the cell cycle. The growth factors and events leading to full mitotic activation in equine SCs remain largely unknown. Insulin-like growth factor I (IGF-I), hepatocyte growth factor (HGF), and fibroblast growth factor 2 (FGF2) are sequentially transcribed during the muscle repair and recovery period following strenuous exercise in adult horses.
View Article and Find Full Text PDFOptimal athletic performance requires meeting the energetic demands of the muscle fibers, which are a function of myosin ATPase enzymatic activity. Skeletal muscle with a predominant oxidative metabolism underlies equine athletic success. Sodium butyrate, a short-chain fatty acid, can affect muscle fiber composition in pigs.
View Article and Find Full Text PDFConsumption of β-hydroxy β-methylbutyrate (HMB) alters muscle composition and metabolism leading to strength and agility improvements in human athletes. To determine if HMB affects athletic performance and muscle function in horses, Thoroughbred geldings were fed a control (CON; n = 5) or HMB (n = 6) supplement for 6 wk prior to completing a standardized exercise test (SET). Gluteus medius (GM) muscle biopsies were obtained before the SET for fiber typing.
View Article and Find Full Text PDFSatellite cells are the myogenic stem and progenitor population found in skeletal muscle. These cells typically reside in a quiescent state until called upon to support repair, regeneration, or muscle growth. The activities of satellite cells are orchestrated by systemic hormones, autocrine and paracrine growth factors, and the composition of the basal lamina of the muscle fiber.
View Article and Find Full Text PDFJ Equine Vet Sci
February 2020
A 12-year-old, multiparous, parturient show jumper embryo-recipient mare presented at a veterinary hospital, seven days past her due date and with a dilated cervix, for evaluation of mild colic. Gastrointestinal or metabolic abnormalities and fetal maldispositions were excluded as causes of dystocia, and a diagnosis of uterine inertia was made. There was no uterine response to oxytocin treatment.
View Article and Find Full Text PDF