Journal of Applied Physiology
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J Appl Physiol (January 5, 2004). doi:10.1152/japplphysiol.01054.2003
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Submitted on September 29, 2003
Accepted on December 29, 2003

RESISTANCE TRAINING ENHANCES COMPONENTS OF THE INSULIN SIGNALING CASCADE IN NORMAL AND HIGH FAT-FED RODENT SKELETAL MUSCLE

Adam D Krisan1, Dale E Collins1, Andrew M Crain1, Connie C Kwong1, Mohenish K Singh1, Jeffrey R Bernard1, and Ben B Yaspelkis, III1*

1 Kinesiology, California State University Northridge, Northridge, CA, USA

* To whom correspondence should be addressed. E-mail: ben.yaspelkis{at}csun.edu.

We recently reported that chronic resistance training (RT) improved insulin-stimulated glucose transport in normal rodent skeletal muscle, in part, to an increased GLUT4 protein concentration (Acta Physiol. Scand. 175: 315-23, 2002). However, it remained to be determined if these improvements resulted from alterations in the insulin-signaling cascade as well. In addition, the possibility existed that RT might also improve skeletal muscle insulin resistance. Thirty two male Sprague Dawley rats were assigned to one of four groups: control diet, sedentary (CON-Sed); control diet, resistance trained (CON-RT); high-fat diet, sedentary (HF-Sed); or high-fat diet, resistance trained (HF-RT). Animals consumed their respective diets for 9 wk and then RT animals performed 12 wk of training (3 sets, 10 repetitions at 75% 1-RM, 3X/wk). All animals remained on their dietary treatments over the 12 wk period. Following the training period, animals were subjected to hind limb perfusions. Insulin-stimulated IRS-1 associated PI-3 kinase activity was enhanced in the red gastrocnemius (RG) and quadriceps (RQ) of the CON-RT and HF-RT animals. aPKC-{zeta}/{lambda} and Akt activities were reduced in the HF-Sed and normalized in the HF-RT animals. RT increased GLUT4 protein concentration in the RG and RQ of the CON-RT and HF-RT animals. No differences were observed in the total protein concentrations of IRS-1, Akt, aPKC-{zeta}/{lambda} or phosphorylation of Akt. Collectively, these findings suggest that RT 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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