Effects of Different Intensities of Resistance Exercise on Regulators of Myogenesis

Abstract

A single bout of high-intensity resistance exercise is capable of activating the expression of various genes in skeletal muscle involved in hypertrophy such as myosin heavy chain (MHC) isoforms, myogenic regulatory factors (MRFs), and growth factors. However, the specific role exercise intensity plays on the expression of these genes is not well defined. The purpose of this study was to investigate the effects of exercise intensity on MHC (type I, IIA, IIX), MRF (Myo-D, myogenin, MRF-4, myf5), and growth factor (insulin-like growth factor [IGF]-1, IGF-1 receptor [IGF-R1], mechano-growth factor [MGF]) mRNA expression. Thirteen male participants (21.5 +/- 2.9 years, 86.1 +/- 19.5 kg, 69.7 +/- 2.7 in.) completed bouts of resistance exercise involving 4 sets of 18-20 repetitions with 60-65% 1 repetition maximum (1RM) and 4 sets of 8-10 repetitions with 80-85% 1RM. Vastus lateralis biopsies were obtained immediately before exercise, and at 30 minutes, 2 hours, and 6 hours after each bout. The levels of mRNA expression were determined using real-time polymerase chain reaction. Data were analyzed using 2 x 4 multivariate analysis of variance (p <or= 0.05). For both intensities, MHC type IIX, IGF-1, IGF-R1, MGF, Myo-D, myogenin, MRF-4, and myf5 mRNA were all significantly increased in response to resistance exercise by 2 hours after exercise, whereas myostatin and the cyclin-dependent kinase inhibitor p27(kip) were decreased at 2 hours after exercise (p < 0.05). Resistance exercise between 60-85% 1RM upregulates the mRNA expression of MHC and factors involved in myogenic activation of satellite cells while concomitantly decreasing expression of myogenic inhibitors.

Co-ingestion of carbohydrate with branched-chain amino acids or l-leucine does not preferentially increase serum IGF-1 and expression of myogenic-related genes in response to a single bout of resistance exercise

“…Following our previously established procedures (Wilborn et al 2009;Willougbhy et al 2007), approximately 20 mg of muscle tissue was homogenized in a of monophasic solution of phenol and guanidine isothiocyanate contained within the TRI-reagent (Sigma Chemical Co., St. Louis, MO). Total RNA concentrations were determined spectrophotometerically (Helio γ, Thermo Electron, Milford, MA) by optical density (OD) at 260 nm using an OD260 equivalent to 40 μg/μl (Ausubel et al 2002), and the final concentration expressed relative to muscle wet weight.…”

“…The cDNA concentration was determined by using an OD260 equivalent to 50 μg/μl (Ausubel et al 2002), and the starting cDNA template concentration was standardized by adjusting all samples to 200 ng prior to PCR amplification (Wilborn et al 2009;Willoughby et al 2007). …”

“…Primer pairs were synthesized commercially (Integrated DNA Technologies, Coralville, IA). β-actin was used as an external control standard for each reaction due to its consideration as a constitutively expressed "housekeeping gene," and the fact that it has been shown to be an appropriate external reference standard in real-time PCR in human skeletal muscle following acute exercise (Mahoney et al 2004;Wilborn et al 2009;Willoughby et al 2007). …”

“…Following our previous procedures (Wilborn et al, 2009;Willoughby et al 2007), each reaction was amplified using real-time quantitative PCR system (iCycler IQ Real-Time PCR Detection System, Bio-Rad, Hercules, CA, USA). To help control for differences in amplification efficiency during thermocycling, all PCR reactions were prepared from the same stock solution.…”

Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspective

“…COPD patients display elevated levels of oxidative stress, which may lead to increased DNA damage and requires increased removal of damaged nuclei. Although exercise induces oxidative stress, which is even accentuated in COPD patients,105 exercise also triggers myogenesis 106. In COPD, this myogenic response to exercise seems intact, although it is specifically impaired in cachectic COPD 40, 98.…”