Content: Beta₂-agonists evoke potent acute increases in peripheral glucose uptake and energy expenditure at rest. Exercise has been shown to blunt these effects. Whether this attenuation is extended into recovery from exercise is unknown.

Objective: To examine the effect of beta2-agonists on leg glucose uptake and leg metabolic rate in recovery from exercise.

Design: In a randomized, placebo-controlled, cross-over study using arteriovenous balance technique and analysis of thigh muscle biopsies we investigated the effect of 24mg oral salbutamol (a selective beta₂-agonist) on leg glucose, oxygen, and lactate at rest, during exercise, and in recovery, as well as on muscle glycogen resynthesis.

Participants: Healthy, lean, young men (n=12).

Results: Leg glucose uptake tended to be two-fold higher at rest (0.22±0.12mmol/min, P=0.06). Accumulated leg glucose uptake was higher in recovery (21.1±6mmol, P=0.018) with salbutamol, but not during exercise. Leg oxygen uptake was 80% greater at rest (11±2.1mmol/min, P<0.01). Accumulated leg oxygen uptake was higher in recovery (1755±348mL, P<0.01) with salbutamol, but not during exercise. Muscle glycogen was lower with salbutamol 0.5h (109±25mmol/mg dry-weight, P<0.01) and 5h (101±19mmol/mg dry-weight, P<0.01) into recovery, suggestive of augmented glycogen utilization during exercise. There was no difference in glycogen resynthesis or glycogen synthase activity in the 5-hour recovery period with salbutamol.

Conclusions: These findings suggest that while resistance exercise confounds the augmentation of leg glucose uptake and metabolic rate induced by beta₂-agonist at rest, this suppression is not conserved into recovery from exercise.