Our laboratory recently reported that chronic resistance training (RT) improved insulin-stimulated glucose transport in normal rodent skeletal muscle, owing, in part, to increased GLUT-4 protein concentration (Yaspelkis BB III, Singh MK, Trevino B, Krisan AD, and Collins DE. Acta Physiol Scand 175: 315-323, 2002). However, it remained to be determined whether these improvements resulted from alterations in the insulin signaling cascade as well. In addition, the possibility existed that RT might improve skeletal muscle insulin resistance. Thirty-two male Sprague-Dawley rats were assigned to four groups: control diet (Con)-sedentary (Sed); Con-RT; high-fat diet (HF)-Sed; and HF-RT. Animals consumed their respective diets for 9 wk; then RT animals performed 12 wk of training (3 sets, 10 repetitions at 75% one-repetition maximum, 3x/wk). Animals remained on their dietary treatments over the 12-wk period. After the training period, animals were subjected to hindlimb perfusions. Insulin-stimulated insulin receptor substrate-1-associated phosphatidylinositol-3 kinase activity was enhanced in the red gastrocnemius and quadriceps of Con-RT and HF-RT animals. Atypical PKC-zeta/lambda and Akt activities were reduced in HF-Sed and normalized in HF-RT animals. Resistance training increased GLUT-4 protein concentration in red gastrocnemius and quadriceps of Con-RT and HF-RT animals. No differences were observed in total protein concentrations of insulin receptor substrate-1, Akt, atypical PKC-zeta/lambda, or phosphorylation of Akt. Collectively, these findings suggest that resistance training increases insulin-stimulated carbohydrate metabolism in normal skeletal muscle and reverses high-fat diet-induced skeletal muscle insulin resistance by altering components of both the insulin signaling cascade and glucose transporter effector system.

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The aim of this investigation was to determine if resistance training exercise improved glucose uptake and transport in rodent skeletal muscle. Sprague-Dawley rats were assigned to one of the three groups: control (CON), resistance trained (RT) and aerobic exercise trained (AT). Resistance trained rats were placed in a rodent squat apparatus and performed three sets of 10 repetitions at 75% of their one repetition maximum 3 days week-1 for 12 weeks. Aerobic exercise training consisted of running the rats 3 days week-1 for 45 min over a 12-week period on a motor-driven treadmill (32 m min-1, 15% grade). Following the training period, all animals were subjected to hind limb perfusion in the presence of 500 microU mL-1 insulin. Hind limb glucose uptake was similar in the RT (9.91 +/- 0.7 micromol g-1 h-1) and AT (10.23 +/- 1.0 micromol g-1 h-1) animals and significantly greater than control (CON) (6.40 +/- 0.6 micromol g-1 h-1). Rates of 3-O-methyl-d-glucose transport in the RT animals were elevated in the muscles utilized for RT while in the AT animals rates of 3-O-methyl-d-glucose transport were increased in those muscles recruited for running. The increased rates of 3-O-methyl-d-glucose transport in the skeletal muscles of the resistance trained and aerobic exercise trained animals appeared to be, in part, because of an increased GLUT4 protein concentration. These findings suggest that both resistance or aerobic training exercise can improve insulin-stimulated skeletal muscle glucose uptake and transport, but the training adaptations are restricted to the muscles recruited for the exercise performance.

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The goal of the study was to assess whether endothelin-1 levels are increased in tissue and plasma in free flaps. To assess this hypothesis, blood samples were taken from the general circulation before and after reperfusion and from the flap after reperfusion in 20 patients undergoing breast reconstruction with free transverse rectus abdominis musculocutaneous or deep inferior epigastric perforator flaps. Tissue samples were also taken from the flap before and after the period of ischemia. Peripheral blood samples of 10 ml each were taken before the vessels were clamped and at 10 minutes and 1 hour after the flap was recharged. The flap vein was catheterized with a smooth catheter to avoid endothelial trauma, and ischemic blood from the flap was obtained immediately after the artery was unclamped and 10 minutes later. Two skin samples of 2 cm each were taken: one after dissection of the flap before division of the vessels and one after reanastomosis of the veins (one or two veins). Statistical analyses were performed with the (nonparametric) Wilcoxon signed rank test. Flap ischemia time, from vessel division to the completion of the arterial anastomosis, ranged from 35 to 120 minutes (mean, 48 minutes). The plasma endothelin-1 level extracted from the flap was 4.34 +/- 0.85 pg/ml, significantly higher than baseline, 3.87 +/- 0.81 pg/ml (p < 0.0001). There was a small increase, 4.5 +/- 1.03 pg/ml (p = NS), 10 minutes after reperfusion. The peripheral level after venous anastomosis was 3.78 +/- 0.79 pg/ml, not significantly different from the peripheral plasma level, before the flap was raised. The peripheral plasma level 1 hour after reperfusion was 3.83 +/- 0.8 pg/ml, with no difference from baseline. The tissue level of endothelin-1 before clamping was 3.8 +/- 0.8 pg/mg and in postischemic tissue, 5.2 +/- 0.6 pg/mg, a statistically significant increase. The authors concluded that endothelin-1 levels are elevated in free flaps. This could be an explanation for vasospasm and may lead to therapy directed against the no-reflow phenomenon.