Oxygen exchange in muscle of young and old rats: muscle-vascular-pulmonary coupling

Sustained performance of muscular exercise is contingent upon increasing muscle O(2) delivery (Qo2; the product of blood flow and arterial O(2) content, i.e. Q X Cao2) and utilization (Vo2m ) rapidly at exercise onset and sustaining necessary conductive and diffusive O(2) fluxes throughout exercise. A tight co-ordination of pulmonary, cardiovascular and muscle system responses is therefore required to prevent muscle microvascular O(2) pressures (P(mvO(2))) from falling to levels that impair blood-muscle O(2) exchange and/or impact metabolic control and reduce exercise tolerance. Microvascular O(2) pressures are determined by the balance between and Qo2 and Vo2m, and emerging evidence indicates that this balance is regulated differently across muscle fibre types and also in aged muscle. Moreover, disease states such as diabetes (type I and II) and chronic heart failure (CHF) also impact P(mvO(2)). This brief review primarily examines evidence obtained in animals that ageing: (1) redistributes exercising away from highly oxidative muscles and muscle fibres; (2) alters muscle capillary haemodynamics; and (3) reduces the O(2) pressure head within the microcirculation (P(mvO(2))) that serves to facilitate blood-muscle O(2) transfer. In many respects, these alterations found in healthy ageing animals bear a striking resemblance to those present in some chronic diseases (e.g. diabetes, CHF) and may help explain the compromised exercise tolerance present in aged individuals. Putative mechanistic insights are explored within the context of current knowledge and future investigative approaches.