RT Journal Article
SR Electronic
T1 Response of growth and myogenic factors in human skeletal muscle to strength training
JF British Journal of Sports Medicine
JO Br J Sports Med
FD BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine
SP 989
OP 993
DO 10.1136/bjsm.2007.045518
VO 42
IS 12
A1 Liu, Y
A1 Heinichen, M
A1 Wirth, K
A1 Schmidtbleicher, D
A1 Steinacker, J M
YR 2008
UL http://bjsm.bmj.com/content/42/12/989.abstract
AB Objective: To investigate the response to different strength training techniques of growth and myogenic factors in human skeletal muscle, with particular emphasis on satellite cell (SC) activation.Methods: 24 volunteers were divided into two groups and performed a 6-week strength training (group A trained with maximum contraction and group B had training combined with maximum contractions, ballistic movement and stretching–shortening cycles). Muscle biopsies were obtained from triceps brachii 3 days before and 7 days after training. For estimating gene expression of insulin-like growth factor (IGF-1), mechano growth factor (MGF), MyoD and myogenin, real-time RT-PCR was performed.Results: In group A, there was an increase in the 1 repeat maximum (1RM), but no change in Vmax (maximum movement velocity) and an increase in MHC (myosin heavy chain) IIa and a decrease in MHC IIx; in group B both 1RM and Vmax increased significantly along with an increase in MHC IIa and a decrease in MHC I. The MGF gene expression increased significantly in both groups (by 1160% and 59%, respectively), and IGF-1 increased only in group A (by 335%). MyoD and myogenin gene expression increased in group A (by 107% and 94%, respectively) but did not change in group B.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.