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To meet the metabolic demands of skeletal muscle, the vasculature supplying these vascular beds has to be connected to respond in a coordinated uniform manner, thus providing the necessary oxygen and nutrients during increased activity. The skeletal muscle microcirculation is the major resistance network controlling vascular blood supply and it is the integrity of the endothelium lining the blood vessels that is paramount in facilitating this action. Aging is a major risk factor for cardiovascular disease and is associated with significant increases in inflammatory agents that negatively impact the vasculature. Several inflammatory agents such as cytokines (tumor necrosis factor-a), advanced glycation products (AGEs), and matrix metalloproteinases (MMPs) along with storage cells for inflammatory mediators (mast cells) are associated with a chronic "low-grade inflammation" state that has been observed over the course of the aging process. Current research suggests that these age-related increases in inflammatory agents can disrupt the microvascular endothelium and thus impair blood flow. This impairment could exacerbate the common age-related disease states such as hypertension, diabetes, congestive heart failure, and sarcopenia, leading to increased mortality and morbidity.

Microvascular structure and function are key aspects of tissue and organ health. At approximately 40% of total body mass, skeletal muscle contains more microvessels than any other organ system in the body. Moreover, skeletal muscle is the most dynamic tissue in the body with the capacity to increase blood flow and metabolic rate 30- to 50- fold. Aging is associated with decrements in microvascular function and exercise tolerance that are poorly understood. Here, experts in their respective fields of microvascular structure and function are brought together to review the current state of knowledge regarding microvascular adaptations to aging. Reviews are drawn from human and animal studies and focus on age-related changes in sympathetic nervous system control of microvessels, capillary hemodynamics and oxygen pressure, microvascular network structure and functional integration, microvascular reactivity, whole muscle perfusion, and cellular contacts and inflammation.

Physical diminishes with ageing, but little is known of how the microvascular supply to skeletal muscle fibres is affected. To test the hypothesis that ageing alters blood flow control, we investigated network architecture and vasomotor responses of arterioles in the gluteus maximus muscle of young (2-3 months), adult (12-14 months) and old (18-20 months) C57BL6 male mice (n = 83) (Young, Adult and Old, respectively). Microvascular casts revealed that the total number, length and surface area of arteriolar segments (diameter, 10-50 microm) were not significantly different across age-groups. However, for arterioles with diameter of 30 microm, tortuosity and branch angles increased with age (P < 0.05). In anaesthetized mice, second-order (2A) distributing arterioles had similar resting (17 +/- 1 microm) and maximal (37 +/- 1 microm) diameters and similar responsiveness to cumulative (10(-10)-10(-4) M) superfusion of acetylcholine or phenylephrine. With superfusate oxygen level raised from 0 to 21%, 2A arteriolar constriction in Young (11 +/- 1 microm) was greater (P < 0.05) than Adult and Old (5 +/- 1 microm). Observed 1 mm upstream from microiontophoresis of ACh (1 microA, 1 s), conducted vasodilatation was 10 +/- 1 microm in Young, 17 +/- 1 microm in Adult and 6 +/- 1 microm in Old (P < 0.05). With muscle contractions (2, 4 and 8 Hz; 30 s) arteriolar diameter increased similarly across age-groups (6 +/- 1, 11 +/- 1 and 18 +/- 1 microm, respectively). Muscle mass and active tension were similar across age-groups yet postcontraction vasodilatation recovered more rapidly in Old versus Adult and Young (P < 0.05). With arteriolar network architecture maintained during ageing, the impairment in conducted vasodilatation and attenuation of postcontraction vasodilatation may compromise exercise tolerance.