11-28-2008, 05:24 PM
I read this....
15. Don't train too heavy for too long
>> Yes, training with a heavy weight that prevents you from getting more than 4-5 reps is good for strength and overall mass when done in conjunction with lighter training that allows you to get 8-12 reps. Yet too much heavy training may work against muscle growth. Baylor University (Waco, Texas) scientists found that when athletes trained using their 6RMs, they had higher levels of active myostatin (a protein that limits muscle growth) than when they did the same workout using their 18RMs. Keep to your heavy rep ranges for no longer than 6-8 weeks, then switch to a lighter-weight, higher-rep scheme to keep your myostatin levels in check.
at this site...
and I couldn't find the original study. Maybe I am not good at scholarly searching. Anybody have any insight into whether or not the claims are valid and taken in context? Or can any find the original study?
11-28-2008, 05:32 PM
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.
11-28-2008, 05:38 PM
its just another reason not to take science out of context as the author from muscle and fiction did...
Discussion:The results from the present study demonstrate that after 12 wk of heavy resistance training there were significant increases in skeletal muscle myostatin mRNA (32%), skeletal muscle myostatin (53%), serum myostatin (56%), and FLRG (127%), whereas activin IIb receptor decreased (18%). In addition, muscle strength and myofibrillar protein content increased 41% and 67%, respectively, whereas indicators of muscle mass underwent respective increases of 19% and 28% for thigh volume and thigh mass. Our present results suggest that heavy resistance training is associated with increases in myostatin mRNA expression, along with subsequent increases in both skeletal muscle and serum myostatin. Even though research has shown that increases in serum myostatin appear to attenuate muscle growth and mass, the presence of increased serum myostatin levels in the present study did not appear to affect the ability of the resistance-trained group to undergo significant increases in muscle strength and mass. The resistance-training program appeared effective at producing muscle hypertrophy based on the significant increases in thigh volume and mass, along with increases in fat-free mass and myofibrillar protein, but no increases in fat mass and total body water.
It is likely that the increased FLRG may have inhibited myostatin from binding to the activin IIb receptor. This is conceivable because serum myostatin is bound, inhibited, and negatively regulated by FLRG (11). Moreover, in a negative feedback loop that regulates activin function, FLRG regulates activin-induced expression and displays an antagonistic effect on activin signaling through the activin IIb receptor (3). Therefore, the observed increases in serum myostatin that occurred in response to heavy resistance training were likely inhibited by the concomitant increase in serum FRLG along with the concomitant down-regulation of the activin IIb receptor.
Intriguing, however, is that our observed increase in myostatin mRNA is in agreement with Peters and colleagues (18), who showed increased myostatin mRNA expression 30 min after a single bout of 30 eccentric contractions of rat dorsiflexors. Although, our present results are in disagreement with Roth and colleagues (20), who showed that 9 wk of unilateral resistance training of the knee extensors, 3× wk-1, with a total of 50 moderate intensity repetitions each exercise session, and employing one training exercise involving only the concentric contraction from a variable resistance, hydraulic modality resulted in decreases in myostatin mRNA expression. In our study, however, we employed three high-intensity training exercises 3× wk-1, each being performed for a total of 36-48 repetitions at 85-90% 1-RM each exercise session. Two of the three exercises (leg press and leg extension) targeted the knee extensors, one of the three exercises (leg curl) targeted the knee flexors, and one of the three exercises (leg press) targeted the hip extensors. In addition, all three exercises involved both the concentric and eccentric phases of the dynamic, isotonic contraction. In view of these aforementioned studies, it appears that expression of the myostatin gene may be more responsive to eccentric contractions. This may be due to the premise that eccentric contractions produce more muscle stress and damage than concentric contractions due to the fact that fewer motor units are recruited during the eccentric phase of contraction. There are data showing eccentric contractions to have 40% less EMG activity compared with concentric contractions (10). This indicates that during an eccentric contraction a smaller cross-sectional area takes on an equivalent load as that handled in the concentric contraction (9). This issue of concentric and eccentric contractions could be important in attempting to clarify the possible differences between our present results and those of Roth and colleagues (20) because it is likely that the subjects in our present study underwent greater amounts of muscle stress and damage, which could have conceivably played a role in the observed increases in myostatin mRNA expression. In light of this, it is conceivable that eccentric contractions, along with a higher intensity of dynamic resistance training, may have a more profound influence on up-regulating myostatin gene expression than resistance exercise with only moderate intensity concentric contractions.
Another possible explanation for our results is due to the observed increases of 40% and 104%, respectively, in the resistance-trained group for postexercise serum cortisol and the content of skeletal muscle glucocorticoid receptor. Acute increases in serum cortisol are associated with high-intensity exercise training (5) and are also known to up-regulate the glucocorticoid receptor (7). Furthermore, increases in serum glucocorticoids are also known to induce a glucocorticoid receptor-mediated up-regulation in the transcription of myostatin due to the presence of putative glucocorticoid response elements present in the promoter of the myostatin gene (15). There are data showing that exposure of rodents to a glucocorticoid agonist increased myostatin gene expression whereas exposure to a glucocorticoid antagonist inhibited expression (13,15,16). In addition, when compared with pretreatment with a glucocorticoid agonist before burn injury, a glucocorticoid antagonist inhibited myostatin expression and attenuated the significant loss in muscle protein content observed with burn injury and glucocorticoid exposure (13).
Because we observed significant increases in serum cortisol immediately postexercise after both 6 and 12 wk of training, it is not unreasonable to assume that serum cortisol was consistently elevated after each exercise session due to the fact that all subjects continued to train with the same exercises and relative intensity. This consistent elevation in postexercise serum cortisol could have conceivably instigated the observed up-regulation in the glucocorticoid receptor. Therefore, herein we demonstrate a possible glucocorticoid receptor-mediated mechanism for the observed increase in myostatin mRNA expression occurring in response to heavy resistance training. Furthermore, in light of the increased serum myostatin expression in conjunction with heavy resistance training, our data also appear to illustrate a potential mechanism that seems to attenuate any negative regulatory effects on muscle mass and function through the possible inhibitory effects of serum FRLG and activin IIb receptor down-regulation. As a result, we conclude that 12 wk of heavy resistance training employing dynamic concentric and eccentric contractions increases myostatin mRNA expression, thereby leading to a subsequent increase in serum myostatin, which is possibly inhibited by increases in FRLG and concomitant decreases in the activin IIb receptor
11-28-2008, 05:44 PM
perhaps myostatin increased because muscle growth was at a higher than normal rate...
These studies tend to be discussion pieces and not anything actually weight lifters should worry about. Strength, muscle, and fitness do not occur in a vacuum, and for every aspect of the human body they track in these studies, there's 1000 they didn't consider.
11-28-2008, 06:45 PM
Thank you andro for finding the study and taking the time to point out what the author of the M&F article clearly missed (at best) or avoided (at worst). It seemed odd to me, which is why I posted it with skepticism.
Thank you maverick for making an excellent point.
11-29-2008, 05:21 PM
Not to mention guys have been getting big and strong for years using that rep range.
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