Mechanisms of Muscle Growth
Mechanisms of Muscle Growth During Muscle Damage
Physiologically, muscle fiber hypertrophy (growth) is believed to be a result of contractile protein proliferation, and muscle fiber enlargement (Vierck 2000). A positive net protein synthetic response with adequate energy availability is also needed to facilitate further growth (Miyazaki 2009). Simply put, if the adequate nutrients and energy are not present, hypertrophy (muscle growth) cannot occur!
In adults, muscles do not undergo significant cell replacement and growth, making microtrauma essential for muscle growth. The repair is facilitated by satellite cell activation, proliferations, and fusing with existing muscle fibers (Toigo 2006).
Exercise, nutrition, and satellite cells are all complement each other, as they cannot function without each other. Satellite cells mediate hypertrophy, but exercise (or some muscle damage) is needed to signal these satellite cells. Nutrition (energy) is necessary to activate the entire process.
However, individual differences do exist, as some people can perform the same exercise program and eat the same meal, with varying hypertrophic results. This is due to the hormones, gene expression and other factors causing individuality.
Once again, microtrauma is a necessary step for muscle growth. When a microtrauama occurs, calcium ions rush into the cell (Sorichter 1999). This stimulates satellite cells via the hepatocyte growth factor (HGF) and nitric oxide (NO) (Tatsumi 2010). Satellite cells may potentially be activated by calcium ion flux (Hara 2012).
HGF secretion is proportional to the extent muscle damage (Tatsumi 1998). Sateillite cell activation is also specific to the fiber that has become damaged and satellite cells of one fiber do not respond to adjacent fibers (Chargé 2004).
Eccentric exercise increases satellite cell content and activation of Type II muscle fibers (Cermak 2013).
Inflammation may also trigger several cytokines, while white blood cells such as neutrophils and macrophages invade the damaged tissue and release several growth factors, all of which may regulate satellite cell activity (Toigo 2006).
The most notable cytokines which stimulate growth factors and the anabolic response are cytokine interleukin-6 (IL-6), insulin-like growth factor (IGF-1), and HGF.
Also, the use of NSAIDs inhibits the pathway and impairs the hypertrophic response (Schoenfeld 2012). Indeed the use of NSAIDs following eccentric exercise reduces satellite cell activity for up to eight days (Mikkelsen 2009), the likely mechanism decreasing the hypertrophic response.
But, Is Soreness Necessary from Personal Training, Exercise, and/or Boot Camps?
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