Key result
Endurance exercise training in aged rats significantly increased precontraction baseline microvascular PO2 (37.5 vs 24.7 Torr) and improved maximal vasodilation in nonrecruited skeletal muscle.
Why the study?
Does exercise training improve microvascular PO2 dynamics and vasomotor control in nonrecruited skeletal muscle of aged rats?
RCT (n=69)
Randomly assigned
No
Does exercise training improve microvascular PO2 dynamics and vasomotor control in nonrecruited skeletal muscle of aged rats?
Endurance training in aged rats improves microvascular oxygenation and vascular smooth muscle function even in nonrecruited skeletal muscles.
Answers are grounded in this paper and cite their sources.
Suggests exercise benefits for aged muscle microvasculature; leaves open human translation and clinical outcomes.
With advancing age, there is a reduction in exercise tolerance, resulting, in part, from a perturbed ability to match O(2) delivery to uptake within skeletal muscle. In the spinotrapezius muscle (which is not recruited during incline treadmill running) of aged rats, we tested the hypotheses that exercise training will 1) improve the matching of O(2) delivery to O(2) uptake, evidenced through improved microvascular Po(2) (Pm(O(2))), at rest and throughout the contractions transient; and 2) enhance endothelium-dependent vasodilation in first-order arterioles. Young (Y, ∼6 mo) and aged (O, >24 mo) Fischer 344 rats were assigned to control sedentary (YSED; n = 16, and OSED; n = 15) or exercise-trained (YET; n = 14, and OET; n = 13) groups. Spinotrapezius blood flow (via radiolabeled microspheres) was measured at rest and during exercise. Phosphorescence quenching was used to quantify Pm(O(2)) in vivo at rest and across the rest-to-twitch contraction (1 Hz, 5 min) transition in the spinotrapezius muscle. In a follow-up study, vasomotor responses to endothelium-dependent (acetylcholine) and -independent (sodium nitroprusside) stimuli were investigated in vitro. Blood flow to the spinotrapezius did not increase above resting values during exercise in either young or aged groups. Exercise training increased the precontraction baseline Pm(O(2)) (OET 37.5 ± 3.9 vs. OSED 24.7 ± 3.6 Torr, P < 0.05); the end-contracting Pm(O(2)) and the time-delay before Pm(O(2)) fell in the aged group but did not affect these values in the young. Exercise training improved maximal vasodilation in aged rats to acetylcholine (OET 62 ± 16 vs. OSED 27 ± 16%) and to sodium nitroprusside in both young and aged rats. Endurance training of aged rats enhances the Pm(O(2)) in a nonrecruited skeletal muscle and is associated with improved vascular smooth muscle function. These data support the notion that improvements in vascular function with exercise training are not isolated to the recruited muscle.
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McCullough et al. (2011) conducted an RCT in Aging-related microvascular dysfunction (n=69). Exercise training vs. Sedentary control was evaluated on Precontraction baseline microvascular PO2 (PmO2) in aged rats (p=<0.05). Endurance exercise training in aged rats significantly increased precontraction baseline microvascular PO2 (37.5 vs 24.7 Torr) and improved maximal vasodilation in nonrecruited skeletal muscle.
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