Response of growth and myogenic factors in human skeletal muscle to strength training

Yuefei Liu ^1*, Markus Heinrichen ¹, Klaus Wirth ², Dietmar Schmidtbleicher ² and Jürgen Michael Steinacker ¹

¹ Sports Medicine, University of Ulm, Germany
² Sports Sciences, Johann-Wolfgang-Goethe University, Germany

^* To whom correspondence should be addressed. E-mail: yuefei.liu{at}uniklinik-ulm.de.

Accepted 9 February 2008

Abstract

Objective: To investigate the response of growth and myogenic factors in human skeletal muscle to different strength trainings with special respect to satellite cell (SC) activation.<br> Methods: 24 volunteers divided into two groups performed a six-week strength training (Max-group for training with maximal contraction while Combi-group for training combined with maximal contractions, ballistic movement and stretching-shortening circles). Muscle biopsies were obtained from triceps brachii three days before and seven days after the training. For estimating gene expression of IGF-1, MGF, MyoD and myogenin real-time RT-PCR was performed.<br> Results: In Max-group, there was an increase in 1 repeat maximum (1RM), but no change in Vmax (maximal movement velocity) along with an increase in MHC (myosin heavy chain) IIa and a decrease in MHC IIx; in Combi-group both 1RM and Vmax increased significantly along with an increase in MHC IIa and a decrease in MHC I. MGF gene expression increased significantly in both Max- and Combi-group (by 1160% and 59%, respectively), and IGF-1 increased only in Max-group (by 335%). MyoD and myogenin gene expression increased in Max-group (by 107% and 94%, respectively) but did not change in Combi-group.<br> Conclusions: Response of growth and myogenic factors occurs during muscular adaptation to a prolonged training, and strength training with different strategies caused different responses with respect to gene expression of these factors. These results suggest that SC activation is involved in the muscular adaptation process to training and might be attributed to MHC isoform transition.