Salbutamol increases leg glucose uptake and metabolic rate but not muscle glycogen resynthesis in recovery from exercise

Content: Exercise blunts the effect of beta₂-agonist on peripheral glucose uptake and energy expenditure. Whether such attenuation extends into recovery is unknown.

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

Design: Using leg arteriovenous balance technique and analyses of thigh muscle biopsies, we investigated the effect of beta₂-agonist (24 mg oral salbutamol) vs placebo on leg glucose, lactate, and oxygen exchange before, during, and 0.5-5-h in recovery from quadriceps exercise, as well as on muscle glycogen resynthesis and activity in recovery. Twelve healthy, lean young men participated.

Results: Before exercise, leg glucose uptake was 0.42±0.12 and 0.20±0.02 mmol×min^-1 (mean±SD) for salbutamol and placebo (P = .06), respectively, while leg oxygen consumption was around two-fold higher (P < .01) for salbutamol than for placebo (25±3 vs 14±1 mL×min^-1). No treatment differences were observed in leg glucose uptake, lactate release, and oxygen consumption during exercise. But in recovery, cumulated leg glucose uptake, lactate release, and oxygen consumption was 21 mmol (95% CI: 18-24, P = .018), 19 mmol (95%CI: 16-23, P < .01), and 1.8 L (95% CI: 1.6-2.0, P < .01) higher for salbutamol than for placebo, respectively. Muscle glycogen content was around 30% lower (P < .01) for salbutamol than for placebo in recovery, whereas no treatment differences were observed in muscle glycogen resynthesis or glycogen synthase activity.

Conclusions: Exercise blunts the effect of beta₂-agonist on leg glucose uptake, but this attenuation diminishes in recovery. Beta₂-agonist increases leg lactate release in recovery, which may relate to glycolytic trafficking due to excessive myocellular glucose uptake.