How can we built muscle? How do we lose it????
Looking into several degenerative muscular diseases ( Cancer, Diabetes, Heart Disease, Hypertension….) that will progressively deteriorate muscle and organs, whether due to lifestyle choices such as exercise or eating habits, it has been shown that exercise training exerts beneficial effects on skeletal muscle. Furthermore, it has been shown that the expression of myostatin, a key regulator of skeletal muscle mass, is increased in a variety of cachectic states.
Because of its high prevalence and association with several diseases,
muscle wasting is a significante clinical problem. To address it more effectively, a thorough understanding of the underlying molecular pathways is crucial.
WHAT CAN LEAD TO MUSCLE LOSS?
Many mechanisms: Increase the levels of neuroendocrine mediators like (nor)epinephrine, angiotensin II, or proinflammatory cytokines….. Simplifying: Every time that we stimulate our sympathetic nervous system (SNS) we induce a catabolic state in the muscle. The myostatin was identified as an important mediator of muscle wasting. Myostatin acts in an endocrine fashion to communicate to skeletal muscle and induce atrophy. This protein is:
1)Natural regulatory protein
2)Member of TGF-b family
3)Inhibits muscle growth
4)Increases with age
5)An evolutionary circuit breaker to keep muscle growth in check
Probably inhibits recruitment of muscle stem cells
In the picture we can see that Myostatin is recognize by membrane receptors, such as ActRIIB. But it can also be inhibited by other molecules such as Follistatin. Exercise training increases follistatin concentration in the blood and muscle is free to grow without myostatin inhibitor effect. Hard exercise training can increase follistatin in the blood above 50%.
So in disease or in good health, we must think about this molecular pathways to understand «the effort (exercise) is a gain or a lost»