J Physiol Pharmacol. 2008 Dec;59 Suppl 7:71-88.
Mechanisms for exercise training-induced increases in skeletal muscle blood flow capacity: differences with interval sprint training versus aerobic endurance training.
Department of Biomedical Sciences, University of Missouri, Columbia, MO 65211, USA.
Skeletal muscle blood flow capacity (BFC) is increased by exercise training due to structural vascular remodeling (in the form of angiogenesis of capillaries and remodeling of the arterial tree within skeletal muscle) and/or altered control of vascular resistance. Changes in control can be central or the result of changes in reactivity of arteries and arterioles (due to changes in vascular smooth muscle and/or endothelium). The purpose of this review is to evaluate the relative importance of these mechanisms for increased BFC following interval sprint training (IST) and endurance exercise training (ET). Based on the results discussed herein we conclude that the importance of each of these mechanisms varies throughout muscle tissue due to interactions of muscle fiber-type composition and muscle fiber recruitment patterns during exercise. The distribution of vascular adaptive changes varies with mode of training. For example, IST has been shown to produce the greatest relative increase in contractile activity in fast-twitch, white, skeletal muscle (i.e. white gastrocnemius muscle (Gw) and Gw muscle exhibits the largest increase in oxidative capacity, capillary density, BFC, and changes in vascular cells with IST. In contrast, ET has been shown to produce the greatest relative increase in contractile activity in red gastrocnemius muscle (Gr), and Gr muscle exhibits the largest increase in oxidative capacity, capillary density, and BFC after ET training. Results demonstrate that the increases in BFC are not mediated solely by structural adaptation. Rather, changes in vascular control predominate in Gr and soleus muscle, while increases in arteriolar and capillary density predominate following IST in Gw. Finally, evidence indicates that ET and IST induce non-uniform changes in smooth muscle and endothelium throughout skeletal muscle arteriolar networks.