Blood flow, lipid oxidation, and muscle glycogen synthesis after glycogen depletion by strenuous exercise

We studied the interrelationship between blood flow, glycogen synthesis, and glucose and lipid utilization in 14 healthy men. A 4-h euglycemic insulin clamp with indirect calorimetry and muscle biopsies were done after a glycogen depletion (exercise) and after a resting day (control). In spite of the exercise induced decrease in leg muscle glycogen content (28% in the basal state, 22% after hyperinsulinemia, P < 0.05 in both as compared with the control study), basal or insulin stimulated glycogen synthase activity remained unchanged. In the basal state, glucose oxidation was 54% lower (P < 0.001) and lipid oxidation 108% higher (P< 0.001) after the glycogen depletion as compared with that in the control study. During the post-depletion insulin clamp, the glucose oxidation rate was 17% lower (P < 0.02) and lipid oxidation 169% higher (P< 0.01), while the whole body total glucose disposal was similar in both studies. Baseline forearm blood flow was similar and increased equally by over 40% during both insulin clamp studies (P < 0.05). Basal glucose extraction after glycogen depletion study was one third of that in the control study (P < 0.05). Both basal and insulin stimulated leg muscle glycogen content correlated inversely with basal forearm blood flow (r =-0.69, P < 0.01 and r = -0.82, P < 0.001, respectively) and basal lipid oxidation (r = -0.54, P < 0.05 and r = -0.64, P < 0.01, respectively) after glycogen depletion. Basal glycogen synthase fractional activity correlated positively with forearm blood flow (r = 0.78, P < 0.001) and forearm glucose uptake (r = 0.71, P < 0.05) during the insulin infusion. In conclusion: 1) the unchanged insulin sensitivity in the face of glycogen depletion is probably a result of increased lipid oxidation, and 2) blood flow is related inversely to muscle glycogen content and directly to glycogen synthase activity.