Interstitial glucose concentration in insulin-resistant human skeletal muscle: influence of one bout of exercise and of local perfusion with insulin or vanadate.
The present study investigated the changes occurring in interstitial metabolite concentrations and blood flow in insulin-resistant human skeletal muscle during the post-exercise recovery period following a single 2-h bout of one-legged exercise. In addition, the effect of microdialysis perfusion with insulin or the insulin-mimetic trace element vanadate was explored. Eight microdialysis catheters, four in each leg, were inserted in the quadriceps femoris muscle of nine insulin-resistant obese male subjects 2 h following exercise. Two catheters in each leg were perfused at 0.2 microl/min for metabolite determinations and two at 1.33 microl/min for the determination of blood flow. Samples were collected until 9 h after the end of exercise had passed. The interstitial glucose concentration (mean +/- SD) was significantly lower in the exercised (2.8 +/- 1.3 mM) than in the rested leg (3.7 +/- 0.9 mM), P = 0.001, a difference that lasted at least 8 h after the exercise bout. On the other hand, blood flow was not different in the two legs. Microdialysis perfusion with insulin (14 mU/ml) or sodium metavanadate (100 mM) decreased the interstitial glucose concentration (P = 0.001) in both the exercised and rested leg. With vanadate, this decrease was similar in the exercised (-69%) and the rested leg (-71%), whereas insulin had a larger effect in the exercised leg (-29 vs. -6.9%), P = 0.05. This study shows that the interstitial glucose concentration in insulin-resistant skeletal muscle is markedly decreased for several hours following a single exercise session. This is in accordance with recent findings in healthy subjects. This change is accompanied by an increased insulin effect on the interstitial glucose concentration. The effect of vanadate was not decreased in insulin-resistant human skeletal muscle and was not augmented by exercise.
Hamrin
K
K
Department of Physiology and Pharmacology, Karolinska Institutet, 171 77, Stockholm, Sweden. Kerstin.Hamrin@ki.se
Henriksson
J
J
D001642:Bicycling / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D045604:Extracellular Fluid / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007004:Hypoglycemic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage / Q000494:pharmacology*; D007333:Insulin Resistance / Q000502:physiology*; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism; D007866:Leg / Q000502:physiology; D008297:Male; D017551:Microdialysis; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism*; D019289:Pyruvic Acid / Q000097:blood / Q000378:metabolism; D012146:Rest / Q000502:physiology; D014508:Urea / Q000097:blood / Q000378:metabolism; D014638:Vanadates / Q000494:pharmacology*
D007004:Hypoglycemic Agents; D007328:Insulin; D019344:Lactic Acid; D014638:Vanadates; D019289:Pyruvic Acid; D014508:Urea; D005947:Glucose