Increase In Capillary Recruitment Research Articles

Non-invasive evaluation of the capillary recruitment in the human muscle during exercise in hypoxia

This study proposes a non-invasive evaluation of capillary recruitment in human muscle from resting state to maximal exercise while under hypoxic conditions. Our work is based on the analysis of oxygen transport variables measured during incremental exercise in endurance-trained men (n=8) and in their sedentary counterparts (n=8). Maximal exercise tests were performed on a cycloergometer in normoxia and at three simulated normobaric levels of hypoxia (altitude equivalent to 1000, 2500 and 4500 m). We made the assumption that the relationship between the oxygen diffusion coefficient (Kt) and cardiac output (Qc) was: Kt=kQcNc where Nc is the capillary recruitment coefficient during exercise. Our results demonstrate that Nc increases with altitude and that the increase is greater in trained compared with untrained subjects at high altitude (4500 m). Moreover, the venous PO2 threshold beyond which capillary recruitment increases is lower in trained men. Despite their greater increase in capillary recruitment, trained men are not able to compensate for their drastic drop in arterial oxygen content during exercise in acute hypoxia, which results in a greater drop in maximal oxygen consumption than in sedentary men.

Microvascular recruitment is an early insulin effect that regulates skeletal muscle glucose uptake in vivo.

Insulin increases glucose disposal into muscle. In addition, in vivo insulin elicits distinct nitric oxide synthase-dependent vascular responses to increase total skeletal muscle blood flow and to recruit muscle capillaries (by relaxing resistance and terminal arterioles, respectively). In the current study, we compared the temporal sequence of vascular and metabolic responses to a 30-min physiological infusion of insulin (3 mU. min(-1). kg(-1), euglycemic clamp) or saline in rat skeletal muscle in vivo. We used contrast-enhanced ultrasound to continuously quantify microvascular volume. Insulin recruited microvasculature within 5-10 min (P < 0.05), and this preceded both activation of insulin-signaling pathways and increases in glucose disposal in muscle, as well as changes in total leg blood flow. Moreover, l-NAME (N(omega)-nitro-l-arginine-methyl ester), a specific inhibitor of nitric oxide synthase, blocked this early microvascular recruitment (P < 0.05) and at least partially inhibited early increases in muscle glucose uptake (P < 0.05). We conclude that insulin rapidly recruits skeletal muscle capillaries in vivo by a nitric oxide-dependent action, and the increase in capillary recruitment may contribute to the subsequent glucose uptake.

Exercise training improves insulin-mediated capillary recruitment in association with glucose uptake in rat hindlimb.

Exercise training is considered to be beneficial in the treatment and prevention of insulin insensitivity, and much of the effect occurs in muscle. We have recently shown that capillary recruitment by insulin in vivo is associated with and may facilitate insulin action to increase muscle glucose uptake. In the present study, we examined the effect of 14 days of voluntary exercise training on euglycemic-hyperinsulinemic clamped (10 mU. min(-1). kg(-1) for 2 h), anesthetized rats. Whole-body glucose infusion rate (GIR), hindleg glucose uptake, femoral blood flow (FBF), vascular resistance, and capillary recruitment, as measured by metabolism of infused 1-methylxanthine (1-MX), were assessed. In sedentary animals, insulin caused a significant (P < 0.05) increase in FBF (1.6-fold) and capillary recruitment (1.7-fold) but a significant decrease in vascular resistance. In addition, hindleg glucose uptake was increased (4.3-fold). Exercise training increased insulin-mediated GIR (24%), hindleg glucose uptake (93%), and capillary recruitment (62%) relative to sedentary animals. Neither capillary density nor total xanthine-oxidase activity in skeletal muscle were increased as a result of the training regimen used. We concluded that exercise training improves insulin-mediated increases in capillary recruitment in combination with augmented muscle glucose uptake. Increased insulin-mediated glucose uptake may in part result from the improved hemodynamic control attributable to exercise training.