By Joao H. Bastos
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Extra resources for Athlete Performance and Injuries
2008). Although none of these mutations have been studied in the context of physical fitness or performance-related phenotypes, both contributions could affect them, by increasing oxidative stress and decreasing the energy supply during exercise. , 2008), besides exerting an impact on femoral mechanical characteristics, impairing femoral bending strength and stiffness in growing knockout female mice. , 2003). Mitochondria are the major source of reactive oxygen species in a resting cell. If antioxidant protection is inadequate this will result in oxidative stress and cause mitochondrial dysfunction.
2. , 2011). , 2009). In general, IL-1 acts synergistically with TNF-, activating proinflammatory responses in a wide range of cells and promoting the acute phase response. , 2010). , 2011). Additionally, it may modify the regulation of energy balance, by actings as an energy sensor, being dependent on the glycogen content in the muscle. , 2004). , 2004). , 2004; Petersen and Pedersen, 2005). , 2004; Petersen and Pedersen, 2005; Petersen and Pedersen, 2006). Polymorphisms in the promoter region of the IL-6 gene (locus 7p21) that affect the IL-6 expression level may consequently influence performance, immunodepression and risk of upper respiratory symptoms (URS), besides contributing to insulin resistance and CVD risk.
3. , 1997). , 1998). During early stages of embryogenesis, GDF8 expression is restricted to the myotome compartment of developing somites. , 1998). , 2004). , 2007). , 2011). , 1998). Mice with null mutations of the myostatin gene have increased muscle mass. , 2007). In humans, a loss-of-function mutation in the myostatin gene in a child increased muscle bulk and strength. , 2004). , 2011). , 2004). , 2010). Also other genes within the myostatin pathway as well as regulatory elements in myostatin expression should be studied as candidate genes.
Athlete Performance and Injuries by Joao H. Bastos