Remember those stretch position movements I call for during Feast? Well, there’s a method to that madness…
When using ecdy for building new muscle tissue, it is important to focus on maximally stretchinglogs the fascia/muscle in the eccentric or lowering part of the movement.
Recent research is zeroing in on the true mechanism of action for ecdysterones and their ana: The PI3K-AKT pathway. In a recent study, administration of high dose ecdysterones demonstrated much improved protein synthesis in both mouse and human muscle tissue. But when scientists added a known PI3K-AKT inhibitor, administration of ecdysterone failed to improve protein synthesis as seen in the earlier experiment. That begs the question: what else might activate the PI3K-AKT pathway?
Answer: Loaded stretching! In 20 years of running ecdy trials in various forms I have consistently noticed better results when incorporating stretch position movements. Now I know why.
Then there is this abstract I recently stumbled across. Note the last sentence:
Regulation of phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factorkappa B signaling pathways in dystrophin-deficient skeletal muscle in response to mechanical stretch.
Charu Dogra 1, Harish Changotra 1, Jon E.
Wergedal 1 2, Ashok Kumar 1 2 * 1Molecular Genetics Division, Musculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center, Loma Linda, California 2Department of Medicine, Loma Linda University, Loma Linda, California. Funded by: Muscular Dystrophy Association
Phosphatidylinositol 3-kinase (PI3K)/Akt and nuclear factor-kappa B (NF-B) signaling pathways play a critical role in mediating survival signals. In this study we have investigated how loss of dystrophin (the primary cause of Duchenne muscular dystrophy) modulates the activation of PI3K/Akt and NF-B signaling pathways in skeletal muscle in response to mechanical stimulation. Activation of Akt was significantly higher in diaphragm muscle from dystrophin-deficient mdx mice compared to normal mice at both prenecrotic and necrotic states. Higher activation of Akt was also observed in cultured dystrophin-deficient primary myotubes differentiated in vitro. Application of passive mechanical stretch ex vivo synergistically increased the activation of Akt in diaphragm of mdx mice. Stretchinduced activation of PDK-1 and PI3K were also higher in diaphragm of mdx mice compared to normal mice. Pretreatment of diaphragm with PI3K inhibitor LY294002 blocked the activation of Akt in normal and mdx mice. Higher activation of Akt was associated with increased phosphorylation of its downstream targets glycogen synthase kinase 3 (GSK3), FKHR, and mammalian target of rapamycin (mTOR). Treatment of diaphragm muscle with LY294002 inhibited the stretch-induced activation of IkappaB (IB) kinase (IKK) and NF-B transcription factor in normal and mdx mice. Mechanical stretch also reduced the interaction of HDAC1 with RelA subunit of NF-B in diaphragm muscle. Finally, cellular levels of Bcl-2, cIAP1, and integrin 1 and activation of integrin linked kinase were higher in diaphragm muscle of mdx mice compared to normal mice.
Taken together, our data suggest that loss of dystrophin and/or mechanical stretch results in the up-regulation of PI3K/Akt and NF-B signaling pathways in skeletal muscle. J. Cell. Physiol. 208: 575-585, 2006. 2006 Wiley-Liss, Inc.
Using loaded stretches and Synthagen or Progenadrex during your feast phase amps results.
Here’s a list of movements to use in incorporating loaded stretches.
Barbell or dumbell pullovers
Wide grip barbell or dumbell decline press
Weighted chins (focus on bottom position stretch),
Seated cable rows
Quadriceps: Hack squats, sissy squats
Hamstrings: Romanian deadlift, stiff-leg deadlift, leg press (feet higher on platform).
Triceps: Decline close-grip bench, overhead tricep extensions
Biceps: Incline dumbell curls, preacher curl
Your set/rep scheme here (EDT movements) is less stringently regulated than the loading pattern I call for in your big barbell lift. Generally speaking, I’ve found that mirroring the rep pattern of your barbell lift to be very effective. Your loaded stretch movement of choice would follow the same set/rep pattern.
That might not be you, however. Many trainees do well with a flat set/rep scheme such as 6 sets of 6 with the same weight. Still others do well with pyramiding the weights in typical 10, 8, 6, 5, 4, 3 fashion. The point is, it’s flexible.
The advantages of following this protocol are numerous. In addition to the PI3K/Akt and NF-B signaling pathways being amplified, you improve your density overload. That is, you pack more work into the same time period. Think, if you did 6 straight sets of a big barbell lift and then did stretch position movements, it’d take twice as long to complete the workout. Since you’d be lifting the same amount of weight during that longer time period, your overall intensity (pounds per minute you demand your muscles lift) suffers. Not so with this technique, and the higher the stress imposed per unit of time, the more muscle growth! More work done per unit of time encourages tissue (muscle) growth. This is a BIG step in that direction.
One exception: If you’re more focused on gaining strength as opposed to size and you feel this technique is taking away from your barbell lift, you can revert to separating the two. The overall growth stimulation won’t be as great but you may gain the advantage of better neural firing on the big barbell lift. The choice is yours. Neither is right or wrong, it just depends upon your goals.
Don’t leave loaded stretching on the table. It’s an incredibly powerful tool that really juices Blueprint results, especially if you’re using an adaptogen.