Postexercise Skeletal Muscle Glucose Transport Is Normal in Kininogen-Deficient Rats

SCHWEITZER, GEORGE G.1; CARTEE, GREGORY D.1,2

Medicine & Science in Sports & Exercise: July 2011 - Volume 43 - Issue 7 - pp 1148-1153
doi: 10.1249/MSS.0b013e31820a7f65
Basic Sciences

A single exercise bout stimulates skeletal muscle glucose transport (GT) in the absence or presence of insulin. It has been suggested that the kallikrein-kinin system may contribute to exercise effects on both insulin-independent and insulin-dependent GT. Plasma kininogen, a key kallikrein-kinin system component, is a protein substrate for the enzyme kallikrein and the source of the peptide bradykinin.

Purpose: This study aimed to determine whether the postexercise (PEX) increase in insulin-dependent or insulin-independent GT is reduced in rats deficient in plasma kininogen versus normal rats.

Methods: Male Brown Norway (BN) and Brown Norway Katholiek (BNK; plasma kininogen-deficient) rats were studied. BN and BNK rats were assigned to exercise (4 × 30-min swim) or sedentary (SED) groups. Rats were anesthetized immediately (0hPEX) or 3 h (3hPEX) after exercise. For 0hPEX and 0hSED rats, one epitrochlearis muscle per rat was used for AMPK phosphorylation and muscle glycogen analyses. The contralateral muscle was incubated with [3H]-3-O-methylglucose (3-MG) for GT assay. For 3hPEX and 3hSED rats, one muscle from each rat was incubated without insulin, and the contralateral muscle was incubated with 60 μU·mL−1 insulin, and both muscles were incubated with 3-MG for GT measurement.

Results: For 0hPEX versus 0hSED, both BN and BNK rats had greater insulin-independent GT and AMPK phosphorylation with reduced glycogen after exercise. No genotype effects were found 0hPEX. There was a significant main effect of exercise (3hPEX > 3hSED) and no interaction between exercise and genotype for basal or insulin-stimulated GT.

Conclusions: Plasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation, or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX, suggesting that normal plasma kininogen is not essential for these important exercise effects.

1Muscle Biology Laboratory, School of Kinesiology, University of Michigan, Ann Arbor, MI; and 2Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI

Address for correspondence: Gregory D. Cartee, Ph.D., School of Kinesiology, Muscle Biology Laboratory, 401 Washtenaw, Ann Arbor, MI 48109; E-mail: gcartee@umich.edu.

Submitted for publication October 2010.

Accepted for publication December 2010.

© 2011 American College of Sports Medicine