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The purposes of this study were to compare and contrast TSP\u20101 null and wild\u2010type mice by examining the following: (1) capillarity in the skeletal and cardiac muscles; (2) fibre type composition and oxidative enzyme activity in the hindlimb; and (3) the consequences of TSP\u20101 gene deletion for exercise capacity. In TSP\u20101 null mice, maximal running speed was 11% greater and time to exhaustion during submaximal endurance running was 67% greater compared with wild\u2010type mice. Morphometric analyses revealed that TSP\u20101 null mice had higher (<jats:italic>P<\/jats:italic> &lt; 0.05) capillarity in the heart and skeletal muscle than wild\u2010type mice, whereas no differences for fibre type composition or oxidative enzyme activity were present between the two groups. Cardiac function, as measured by transthoracic echocardiography, revealed no difference in myocardial contractility but greater left ventricular end\u2010diastolic and systolic dimensions, corresponding to an elevated heart mass in the TSP\u20101 null mice. The results of this study indicate that TSP\u20101 is an important endogenous negative regulator of angiogenesis that prevents excessive capillarization in the heart and skeletal muscles. The increased capillarity alone was sufficient to increase (<jats:italic>P<\/jats:italic> &lt; 0.05) exercise capacity. These data demonstrate that the capillary\u2010to\u2010muscle interface is a critical factor that limits oxygen transport during exercise.<\/jats:p>","DOI":"10.1113\/expphysiol.2008.045989","type":"journal-article","created":{"date-parts":[[2009,3,19]],"date-time":"2009-03-19T00:44:28Z","timestamp":1237423468000},"page":"749-760","source":"Crossref","is-referenced-by-count":103,"title":["Global deletion of thrombospondin\u20101 increases cardiac and skeletal muscle capillarity and exercise capacity in mice"],"prefix":"10.1113","volume":"94","author":[{"given":"Moh H.","family":"Malek","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I. 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