Effect of high-intensity intermittent swimming on postexercise insulin sensitivity in rat epitrochlearis muscle.
A bout of prolonged aerobic exercise can enhance the sensitivity of muscle glucose uptake to insulin, and this may be mediated by activation of 5'-adenosine monophosphate-activated protein kinase (AMPK). The aim of this study was to examine whether high-intensity short-term exercise resulting in a significantly greater increase in the activation of AMPK is more effective in enhancing muscle insulin sensitivity compared with low-intensity prolonged aerobic exercise. We measured insulin sensitivity after high-intensity intermittent swimming (HIS) or low-intensity continuous swimming (LIS) exercise in rat epitrochlearis muscle. During HIS, the rats underwent eight 20-second bouts of swimming with a weight equal to 18% of body weight. The LIS rats swam with no load for 3 hours. High-intensity intermittent swimming increased (P < .05) 2-deoxyglucose uptake approximately 8-fold, whereas LIS increased it (P < .05) approximately 2-fold immediately after exercise compared with rested muscle. This response was associated with an increase (P < .05) in phosphorylation of AMPK Thr(172) and its downstream target acetyl-coenzyme A carboxylase (ACC) Ser(79) in HIS (13- and 6-fold, respectively) and LIS (2.8- and 2-fold, respectively) immediately after exercise. In contrast, submaximal (30 microU/mL) insulin-stimulated 2-deoxyglucose uptake measured 4 hours after exercise was 73% and 46% higher (P < .05) in LIS and HIS, respectively, compared with rest. The HIS exercise resulted in a greater activation of AMPK compared with LIS, but insulin sensitivity was higher after LIS compared with HIS. The results suggest that HIS is not more effective in enhancing insulin sensitivity than LIS. Thus, AMPK activation immediately after exercise may not be the only factor that determines the magnitude of the exercise-induced increase in insulin sensitivity in rat epitrochlearis muscle.
Koshinaka
Keiichi
K
Department of Health and Nutrition, Niigata University of Health and Welfare, 1398 Shimami-cho, Kita-ku, Niigata City, Niigata 950-3198, Japan.
Sano
Akiko
A
Howlett
Kirsten F
KF
Yamazaki
Takako
T
Sasaki
Maiko
M
Sakamoto
Kei
K
Kawanaka
Kentaro
K
D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000263:Adenylate Kinase / Q000378:metabolism; D000818:Animals; D005947:Glucose / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000032:analysis; D006003:Glycogen / Q000032:analysis; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D018482:Muscle, Skeletal / Q000737:chemistry / Q000378:metabolism*; D010766:Phosphorylation; D010805:Physical Conditioning, Animal; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013550:Swimming; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D051275:Glucose Transporter Type 4; D007328:Insulin; D006003:Glycogen; D051057:Proto-Oncogene Proteins c-akt; D048051:p38 Mitogen-Activated Protein Kinases; D000263:Adenylate Kinase; D000103:Acetyl-CoA Carboxylase; D005947:Glucose