α-Stimulation protects exercise increment in skeletal muscle oxygen consumption

Oxygen consumption (VO₂) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P₀) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO₂ were evaluated at rest [Q(c) and VO(2c)], after 5 min of exercise [Q(e) and VO(2e)] and after 5 more min of exercise with either NE or MO [Q(t) and VO(2t)]. Data were normalized and plotted as the [VO(2e) - VO(2t)]/[VO(2c) - VO(2e)] vs. [Q(e) - Q(t)]/[Q(c) - Q(e)] and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P < 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced increment in VO₂ was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO₂ was secondary to a β-adrenergic-receptor-mediated stimulation of skeletal muscle metabolic processes, the experiments were repeated in the presence of β-blockade with propranolol. In the presence of β-blockade, the effects of NE on skeletal muscle VO₂ were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.