Charles Glass is een amateur, kijk wat hij Gunter heeft aangedaan. WORSE SHAPE EVER!!!
Ja maar lage reps verhoogt het myostatine gehalte wat de spieropbouw tegengaat dus waar zit de logica dan? Ik train gewoon: eens 12 reps, 8 reps, 15 reps, 6 reps, door elkaar.
PURPOSE: Myostatin is a negative regulator of muscle mass and its effects seem to be exacerbated by glucocorticoids; however, its response to resistance training is not well known. This study examined 12 wk of resistance training on the mRNA and protein expression of myostatin, follistatin-like related gene (FLRG), activin IIb receptor, cortisol, glucocorticoid receptor, myofibrillar protein, as well as the effects on muscle strength and mass and body composition. METHODS: Twenty-two untrained males were randomly assigned to either a resistance-training [RTR (N = 12)] or control group [CON (N = 10)]. Muscle biopsies and blood samples were obtained before and after 6 and 12 wk of resistance training. RTR trained 3 x wk(-1) using three sets of six to eight repetitions at 85-90% 1-RM on lower-body exercises, whereas CON performed no resistance training. Data were analyzed with two- and three-way ANOVA. RESULTS: After 12 wk of training, RTR increased total body mass, fat-free mass, strength, and thigh volume and mass; however, they increased myostatin mRNA, myostatin, FLRG, cortisol, glucocorticoid receptor, and myofibrillar protein after 6 and 12 wk of training (P < 0.05). CONCLUSIONS: Resistance training and/or increased glucocorticoid receptor expression appears to up-regulate myostatin mRNA expression. Furthermore, it is possible that any plausible decreases in skeletal muscle function from the observed increase in serum myostatin were attenuated by increased serum FLRG levels and the concomitant down-regulation of the activin IIb receptor. It is therefore concluded that the increased myostatin in response to cortisol and/or resistance training appears to have no effects on training-induced increases in muscle strength and mass.
-> In deze studie deed men 8-12 herhalingen en hier daalde het myostatin gehalte in het bloed.Myostatin inhibits myoblast proliferation and differentiation in developing muscle. Mounting evidence suggests that myostatin also plays a limiting role in growth/repair/regeneration of differentiated adult muscle by inhibiting satellite cell activation. We tested the hypothesis that myostatin mRNA expression would decrease after resistance loading (RL) with a blunted response in older (O) females (F) who have shown minimal hypertrophy [vs. males (M)] after long-term RL. As myostatin is thought to modulate cell cycle activity, we also studied the response of gene transcripts key to stimulation (cyclin B1 and D1) and inhibition (p21cip and p27kip) of the cell cycle, along with the muscle-specific load-sensitive mitogen mechano-growth factor (MGF). Twenty young (Y; 20-35 yr, 10 YF, 10 YM) and 18 O (60-75 yr, 9 OF, 9 OM) consented to vastus lateralis biopsy before and 24 h after a bout of RL (3 sets x 8-12 repetitions to volitional fatigue of squat, leg press, knee extension). Gene expression levels were determined by relative RT-PCR with 18S as an internal standard and analyzed by age x gender x load repeated-measures ANOVA. A load effect was found for four transcripts (P < 0.005) including myostatin, cyclin D1, p27kip, and MGF as mRNA levels decreased for myostatin (-44%) and p27kip (-16%) and increased for cyclin D1 (34%) and MGF (49%). For myostatin, age x load and gender x load interactions (P < 0.05) were driven by a lack of change in OF, while marked declines were noted in YM (-56%), YF (-48%), and OM (-40%). Higher cyclin D1 levels in OF led to a main age effect (36%, O > Y) and an age x gender interaction (66%, OF > YF vs. 10%, OM > YM; P < 0.05). An age x gender x load interaction (P < 0.05) for cyclin D1 resulted from a 48% increase in OF. Post hoc testing within groups revealed a significant increase in MGF after RL in YM only (91%, P < 0.05). Higher levels of cyclin B1 in O (27%, O > Y) led to a main age effect (P < 0.05). An age x load interaction for cyclin B1 (P < 0.05) was driven by a 26% increase in Y with no change in O after RL. No age or gender differences, or load-mediated changes, were detected in levels of p21cip mRNA expression. These data clearly demonstrate that RL downregulates myostatin expression and alters genes key to cell cycle progression. However, failure to reduce myostatin expression may play a role in limiting RL-induced hypertrophy in OF.