Effects of training and immobilization on VO2 and DO2 in dog gastrocnemius muscle in situ

Abstract

To investigate the effects of exercise training and immobilization on peak O2 uptake (VO2) and effective O2 diffusive conductance (DO2) in skeletal muscle, three groups of purpose-bred hounds [control (C), exercise trained (E), and immobilized (I)] were studied. Group E exercised on a treadmill 1 h/day, 5 days/wk for 8 wk, while groups C and I were cage confined for 8 wk, with group I undergoing left hindlimb immobilization for the last 3 wk. Thereafter, each dog's left gastrocnemius was surgically isolated, pump perfused, and electrically stimulated to elicit peak VO2 in situ at three levels of arterial oxygenation. O2 delivery [(arterial O2 concentration x muscle blood flow)/100 g muscle] was kept constant among the three groups at each level of arterial oxygenation. Compared with group C, peak VO2/100 g muscle was 38, 33, and 19% greater and DO2/100 g muscle was 71, 75, and 68% greater during normoxia, moderate hypoxia, and severe hypoxia, respectively, in group E (P < 0.02), whereas no differences from control were found in group I. We conclude that O2 delivery is not the unique determinant of peak VO2 and that exercise training improves the functional blood-tissue gas exchange properties of the muscle itself. Immobilization sufficient to reduce muscle weight by 31% and citrate synthase activity by 68% has no effect on peak VO2/100 g muscle or DO2/100 g muscle.

Exercise training in chronic heart failure: improving skeletal muscle O2transport and utilization

“…205) during submaximal exercise. Central to these adaptations is the substantial improvement in both D mO 2 and Q m after exercise training (27,42,204,260,279). Importantly, skeletal muscle plasticity is preserved in CHF and thus similar improvements in D mO 2 and Q mO 2 have been reported in HFrEF patients (74).…”

Vascular-Specific Growth Factor mRNA Levels in the Human Diaphragm

“…Such changes in the capillary bed of skeletal muscles in athletes have been detected in the mid-70s [1] and were attributed to reduced muscle oxygen tension [2] . Since then, angiogenesis was extensively studied and found to be an extremely complex process involving, among others, the dissolution of the extra-cellular matrix underlying endothelium, cell migration and endothelial cell proliferation [3] .…”

Myocyte vascular endothelial growth factor is required for exercise-induced skeletal muscle angiogenesis

“…Last, because there is evidence that the muscle-capillary interface is a critical determinant for O 2 transport (12, 17, 18, 29) and that muscle O 2 conductance (and consequently muscle V O 2 ) is dependent on skeletal muscle capillarity (5,25,26,30,31), it could be hypothesized that a lack of capillary adaptation to training contributed to the impaired exercise performance. Corroborating evidence comes from untrained thrombospondin-1 knockout mice, which have elevated skeletal muscle capillarity (and normal cardiac function) compared with WT mice and display a significant increase in exercise capacity (40).…”