Global deletion of thrombospondin-1 increases cardiac and skeletal muscle capillarity and exercise capacity in mice.

摘要: Thrombospondin-1 (TSP-1) is a known inhibitor of angiogenesis; however, skeletal muscle phenotype TSP-1 null mice has not been investigated. The purposes this study were to compare and contrast wild-type by examining the following: (1) capillarity in cardiac muscles; (2) fibre type composition oxidative enzyme activity hindlimb; (3) consequences gene deletion for exercise capacity. In mice, maximal running speed was 11% greater time exhaustion during submaximal endurance 67% compared with mice. Morphometric analyses revealed that had higher (P < 0.05) heart than whereas no differences or present between two groups. Cardiac function, as measured transthoracic echocardiography, difference myocardial contractility but left ventricular end-diastolic systolic dimensions, corresponding an elevated mass results indicate important endogenous negative regulator angiogenesis prevents excessive capillarization muscles. increased alone sufficient increase These data demonstrate capillary-to-muscle interface critical factor limits oxygen transport exercise.