UE was closed for the Holiday, so I took the opportunity to get a workout in. I slept late after working New Years Eve, so I was well-rested. Today was legs/abs day.
Calf Exercise on MedX Leg Press
TSC Hip Abduction
MedX Leg Press
Since my last posting I also did my shoulder and arm rotation. It has been hectic, so I don’t recall the exact dates, but I have compressed my rotation down from every 5th day, to every 3rd or 4th day. So far, recovery has been fine.
Shoulders: MedX overhead press, rear delt fly, lateral raise, shrug
Arms: Nautilus Plate Load Biceps with SS cam, close grip pulldown, Nautilus Plate Load Triceps, MedX Chest Press (narrow grip on vertical handles), Compound Row, Formulator flex/ext
Things have been relatively quiet on the Myostatin front since the Myostatin blocking drug MYO-029 fell off the map in Phase II trials. However, Novartis has recently been given approval to proceed with clinical trials on their new drug “Bimagrumab” or BYM338. This drug reportedly blocks binding of the Activin II receptor where Myostatin and Activan A attach. Myostatin and Activin A are proteins that inhibit muscle growth and act as major governors of muscle growth and differentiation. These proteins are over-expressed in certain disease states such as cancer, AIDS, COPD, glucocorticoid and corisol-induced atrophy, sarcopenia of aging, as well as atrophy related to inactivity or low-gravity environments. The fact that this drug blocks a receptor rather than abolishing the production of the regulatory protein is promising because it can avoid the unintended side-effects of completely eliminating a regulatory protein, and it allows for a potential dose-dependent effect. This drug holds great promise for those with muscle wasting diseases that are refractory to the exercise stimulus. From my own standpoint, I am fascinated to learn what this drug may teach us about the regulation of muscular potential. While there is certainly a potential for abuse in athletics, there is also the potential for leveling the playing field such that athletes in a given endeavor could have their engines “governed” in an equal way much like the rules in NASCAR racing. Hopefully, fear of the drug’s potential use (or abuse) in the athletic realm will not prevent it from being available to those with legitimate disease states.
An Antibody Blocking Activin type II Receptors Induces Strong Skeletal Muscle Hypertrophy and Protects from Atrophy.
The myostatin/Activin type II receptor (ActRII) pathway has been identified as critical in regulating skeletal muscle size. Several other ligands, including GDF11 and the Activins, signal through this pathway, suggesting that the ActRII receptors are major regulatory nodes in the regulation of muscle mass. We have developed a novel, human anti-ActRII antibody (“Bimagrumab”, aka BYM338) to prevent binding of ligands to the receptors, and thus inhibit downstream signaling. BYM338 enhances differentiation of primary human skeletal myoblasts, and counteracts the inhibition of differentiation induced by myostatin or Activin A. BYM338 prevents myostatin or Activin A induced atrophy through inhibition of Smad2/3 phosphorylation, thus sparing myosin heavy chain from degradation. BYM338 dramatically increases skeletal muscle mass in mice, beyond sole inhibition of myostatin as detected by comparing the antibody with a myostatin inhibitor. A mouse version of the antibody induces enhanced muscle hypertrophy in myostatin-mutant mice, further confirming a beneficial effect on muscle growth through blockade of ActRII ligands beyond myostatin inhibition alone. BYM338 protects muscles from glucocorticoid-induced atrophy and weakness, via prevention of muscle and tetanic force losses.These data highlight the compelling therapeutic potential of BYM338 for the treatment of multiple settings of skeletal muscle atrophy and weakness.
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