Effect of High-Frequency Resistance Exercise on Adaptive Responses in Skeletal Muscle

COFFEY, VERNON G.1; REEDER, DONALD W.2; LANCASTER, GRAEME I.3; YEO, WEE KIAN1; FEBBRAIO, MARK A.3; YASPELKIS, BEN B. III2; HAWLEY, JOHN A.1

Medicine & Science in Sports & Exercise: December 2007 - Volume 39 - Issue 12 - pp 2135-2144
doi: 10.1249/mss.0b013e31815729b6
BASIC SCIENCES: Original Investigations

Purpose: Regulation of skeletal muscle mass is highly dependent on contractile loading. The purpose of this study was to examine changes in growth factor and inflammatory pathways following high-frequency resistance training.

Methods: Using a novel design in which male Sprague-Dawley rats undertook a "stacked" resistance training protocol designed to generate a summation of transient exercise-induced signaling responses (four bouts of three sets × 10 repetitions of squat exercise, separated by 3 h of recovery), we determined the effects of high training frequency on signaling pathways and transcriptional activity regulating muscle mass.

Results: The stacked training regimen resulted in acute suppression of insulin-like growth factor 1 mRNA abundance (P < 0.05) and Aktser473 phosphorylation (P < 0.05), an effect that persisted 48 h after the final training bout. Conversely, stacked training elicited a coordinated increase in the expression of tumor necrosis factor alpha, inhibitor kappa B kinase alpha/beta activity (P < 0.05), and p38 mitogen-activated protein kinase phosphorylation (P < 0.05) at 3 h after each training bout. In addition, the stacked series of resistance exercise bouts induced an increase in p70 S6 kinasethr389 phosphorylation 3 h after bouts ×3 and ×4, independent of the phosphorylation state of Akt.

Conclusions: Our results indicate that high resistance training frequency extends the transient activation of inflammatory signaling cascades, concomitant with persistent suppression of key mediators of anabolic responses. We provide novel insights into the effects of the timing of exercise-induced overload and recovery on signal transduction pathways and transcriptional activity regulating skeletal muscle mass in vivo.

1Exercise Metabolism Group, RMIT University, Bundoora, AUSTRALIA; 2Exercise Physiology and Biochemistry Laboratories, California State University, Northridge, CA; and 3Cellular and Molecular Metabolism Laboratory, RMIT University, Bundoora, AUSTRALIA

Address for correspondence: Vernon G. Coffey, Ph.D., School of Medical Sciences, RMIT University, Bundoora, Victoria 3083, Australia; E-mail: vernon.coffey@rmit.edu.au.

Submitted for publication February 2007.

Accepted for publication July 2007.

©2007The American College of Sports Medicine