Cross-transfer effects of resistance training with blood flow restriction.
http://www.ncbi.nlm.nih.gov/pubmed/18202577
I came across this very interesting study.
15 people were randomized to two groups, occlusion and normal training. Both groups performed single arm DB curls without occlusion at 3x10 at 50%of 1RM, then the occlusion group continued to perform leg extensions and flexions (30% 1RM) while occluded, while the normal group did the exact same without occlusion.
The elbow flexors of the trained arm in the occlusion group increased its CSA significantly, no other groups did. In other words, the addition of occluded leg exercises somehow increased CSA in the elbow flexors that were trained with only 3x10 at 50%1rm (which was ineffective at causing hypertrophy without the occluded leg exercises)
In another study the hormone response to this training was investigated. GH tended to be higher on occlusion (p=0.12), test was not higher, but noradrenaline was. However, this was done on a different group of subjects with only 5 per group.
The authors suggest this effect can be because of any systemic factor, probably not test or GH, since they were not sig increased. It might be noradrenaline, even though it’s role in hypertrophy is unclear. However, beta agonists (like clenbuterol, for example) are known to stimulate hypertrophy. Also, since the control arm of those who trained with occlusion did not increase in size, the effect of this systemic substance probably only works in muscles that have been trained. Perhaps some sort of basal level of remodeling is required for it to be effective? I know that goes for for example leukemia inhibitory factor in rats. It has been shown in this study “Effects of leukemia inhibitory factor on rat skeletal muscles are modulated by clenbuterol”. LIF injection with or without clenbuterol (which causes remodeling) was tested on soleus and EDL. LIF alone had no effect on soleus without clenbuterol, but had an effect with clenbuterol that was higher than with clenbuterol alone. However, LIF did work on its own in the soleus. LIF is a pretty new and exciting substance in muscular hypertrophy.
So some questions that come to mind now are:
1. It has been assumed that the effect of occlusion training on hypertrophy was because of metabolic disturbances within the muscle. What if the reason for occlusion training’s good effect is because of some systemic factor, not only in other muscles, but in the muscles being trained with occlusion as well?
1. What is this systemic factor, and can we increase it through normal training as well?
1. GH and Test have been viewed as having a systemic muscle building effect after exercise, however, this has been pretty much debunked, but what if other systemic factors actually do have an effect?
EDIT: a 3. question: Would this systemic factor have given greater hypertrophy if the arm was trained with something more realistic like 3x10 to failure? Say this factor improves MPS after exercise in the trained arm, what if you trained the arm so hard that MPS reached a roof? If the systemic factor worked by the same signaling mechanisms then you’d probably see no further increase.. but if it worked through a different pathway to protein synthesis, then perhaps you’d see an increase. (depending on if the “roof” you reach, where no further exercise stimulus gives more MPS is on the level of MPS itself or the signaling that leads to it)
