Does Acute Exercise Increase Insulin‐Stimulated Skeletal Muscle Glucose Uptake, Blood Flow And Insulin Signalling In Response To A Meal?

A single bout of exercise increases skeletal muscle insulin sensitivity measured by euglycemic, hyperinsulinemic clamp (EHC) through coordinated increases in skeletal muscle insulin‐stimulated microvascular perfusion and molecular signalling at the level of TBC1D4 (2 , 3) . Surpringly, however, skeletal muscle interstitial glucose concentration decreases substantially during a EHC, especially after one‐legged exercise, reaching 2–3 mM (1) . This result may, however, be a artifact of the EHC because, unlike after a meal, blood glucose does not rise during a EHC but is “clamped” at around 5 mM while plasma insulin is elevated. Therefore, the aim of this project was to determine the effect on leg blood flow and skeletal muscle glucose metabolism of meals begun 4 hours after one‐legged exercise. We hypothesized that hyperglycemia after the meal would prevent a drop in muscle interstitial glucose concentrations and result in large increases in leg glucose uptake. Four healthy young males performed 60 min of 1‐legged knee extensor exercise involving at 80% of 1‐legged peak work load (PWL) with three 5 min intervals at 100% 1‐legged PWL. Participants then rested for 4 hours and catheters were inserted into the femoral artery of one leg and the femoral vein of both legs and two microdialysis catheters for measurement of interstitial glucose concentration were inserted into the vastus lateral muscle of both legs. A solid meal was ingested (40 kJ.kg BW−1) 4 hrs after the 1‐legged exercise with smaller liquid meals (20 kJ.kg BW−1) ingested 4.5 and 5 hrs after the exercise. Four hours after exercise there was no significant difference between the exercised and rested leg for leg blood flow, leg arteriovenous glucose difference, leg glucose uptake, vastus lateralis interstitial glucose concentration or apparent muscle membrane glucose permeability. Meal ingestion increased arterial blood glucose concentration and increased leg blood flow, leg arteriovenous glucose difference and leg glucose uptake more in the exercised leg than the rested leg. Meals increased vastus lateralis interstitial glucose concentration, especially in the rested leg. Vastus lateralis apparent muscle membrane glucose permeability increased with the meals in both legs and moreso in the previously exercised leg. Ingestion of meals several hours after 1‐legged exercise results in hyperglycemia, increased skeletal muscle interstitial glucose concentration and increased muscle membrane permeability to glucose. This results in larger increases in muscle glucose uptake in the previously exercised than the rested leg. Real life feeding after exercise confirms and extends findings from clamp studies.