Effects of Low and High-Intensity Swimming on Post-Exercise Insulin Sensitivity in Rat Skeletal Muscle
Abstract Number: 1000-P
Authors: KEIICHI KOSHINAKA, AKIKO SANO, KENTARO KAWANAKA.
Institutions: Niigata, Japan.
Results: Rats swim models, low-intensity prolonged swim (LIS; 180∼360min swim without weight) and high-intensity intermittent swim (HIS; eight 20-s swim with a weight equal to 18% of body mass), have been often used for studying the effect of exercise on muscle glucose transport. Although it was reported that both LIS and HIS training induced about 2 fold increases in GLUT4 protein and insulin-stimulated maximal glucose transport in rat epitrochlearis (EPI) muscles, no studies characterized the effects of acute bout of LIS and HIS on post-exercise insulin sensitivity. Since previous study provides evidence that the increase in insulin sensitivity follows exercise is mediated by activation of AMPK, we examined the effects of LIS and HIS on AMPK activation and post-exercise insulin sensitivity.
Fasted rats underwent LIS or HIS. Immediately after LIS, AMPK phosphorylation was not significantly increased in EPI muscles as compared with sedentary control, whereas 800% increase was observed immediately after HIS. Furthermore, muscle AMP level was higher after HIS than after LIS. These changes in AMPK phosphorylation and AMP level lead to HIS induced greater activation of AMPK. Therefore, we hypothesized that HIS increases post exercise insulin sensitivity in EPI muscle to higher level than LIS.
However, submax (30μU/ml) insulin stimulated glucose transport was 1.7 fold higher 4 h after LIS as compared with sedentary control, whereas it was 1.4 fold higher 4 h after HIS than control (3.01±0.30, 5.22±0.30, and 4.39±0.12 μmol/g tissue/20min in the control, LIS, and HIS, respectively). Neither LIS nor HIS increased max (10mU/ml) insulin stimulated glucose transport as compared with control (7.48±0.47, 7.54±0.17, and 7.18±0.20μmol/g tissue/20min in the control, LIS, and HIS, respectively). Thus, in spite of HIS induced greater activation of AMPK, HIS did not increase post-exercise insulin sensitivity to higher level than LIS.
These results suggest that AMPK independent mechanisms may regulate the extent of increase in post-exercise insulin sensitivity.