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Jeremy P Loenneke
Smoke to Sarcopenia
Smoking is the number one cause of preventable death. Smoking is highly correlated with many known diseases. The American Heart Association (AHA) reports that, “Cigarette smoking increases the risk of coronary heart disease by itself. When it acts with other factors, it greatly increases risk. Smoking increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot. Smoking also increases the risk of recurrent coronary heart disease after bypass surgery. Cigarette smoking is the most important risk factor for young men and women. It produces a greater relative risk in persons under age 50 than in those over 50. Women who smoke and use oral contraceptives greatly increase their risk of coronary heart disease and stroke compared with nonsmoking women who use oral contraceptives. Smoking decreases HDL cholesterol. Cigarette smoking combined with a family history of heart disease also seems to greatly increase the risk. Studies show that cigarette smoking is an important risk factor for stroke. Inhaling cigarette smoke produces several effects that damage the cerebrovascular system. Women who take oral contraceptives and smoke increase their risk of stroke many times. Smoking also creates a higher risk for peripheral arterial disease and aortic aneurysm (Cigarette smoking and cardiovascular diseases).”
The AHA detailed many negative affects of smoking but what affect does smoking have on muscle? Peterson and colleagues have recently shown that smoking decreases muscle protein fractional synthesis rate and increases the expression of myostatin and MAFBx. Myostatin and MAFBx are genes which are involved in the regulation of muscle mass (Peterson, et al., 2007). Myostatin belongs to the TGF- super
family and it has been proposed that myostatin inhibit muscle growth by up-regulating the expression of p21, which inhibits cyclin-E·Cdk2 activity, thus causing the hypophosphorylation of retinoblastoma (Rb) protein and G1 arrest (Thomas, et al., 2000). Basically, smoking increases this signaling which in turns leads to decreased myoblast proliferation. Myogenic differentiation is also inhibited by myostatin due to the inability of MyoD to become fully functional, resulting in the inactivation of certain myogenic genes (Langley, Thomas, Bishop, Sharma, Gilmour, & Kambadur, 2002).
In conclusion smokers may be adversely affecting their health even more so then previously thought. Smoking has been shown to decrease muscle mass by way of an increased expression of myostatin and a decreased protein synthesis rate (Peterson, et al., 2007). It has been shown that increasing levels of myostatin decreases myoblast proliferation and myogenic differentiation (Thomas, et al., 2000 and Langley, Thomas, Bishop, Sharma, Gilmour, & Kambadur, 2002). Table 1(A) shows how myostatin decreases the ability to develop myotubues, by up-regulating genes to inactivate Rb and G1 arrest. Myotubes develop into muscle fibers, so a decreased ability of myotubes to differentiate from myoblasts can be very detrimental (MacIntosh, Gardiner, & McComas, 2006). In summation, smoking not only increases the risk of CHD and stroke, it also increases the risk of developing sarcopenia.
References
Cigarette smoking and cardiovascular diseases. (n.d.). Retrieved from American Heart Association: http://www.americanheart.org/present...dentifier=4545
Langley, B., Thomas, M., Bishop, A., Sharma, M., Gilmour, S., & Kambadur, R. (2002). Myostatin inhibits myoblast differentiation by down-regulating MyoD Expression. J. Biol. Chem. , 277 (51), 49831-49840.
MacIntosh, B. R., Gardiner, P. F., & McComas, A. J. (2006). Muscle Formation. In Skeletal Muscle Form and Function (2nd Edition ed., pp. 52-70). Human Kinetics.
Peterson, A. M., Magkos, F., Atherton, P., Selby, A., Smith, K., Rennie, M. J., et al. (2007). Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFbx in muscle. AM J Physiol Endocrinol Metab. , 293 (3), 843-848.
Thomas, M., Langley, B., Berry, C., Sharma, M., Kirk, S., Bass, J., et al. (2000). Myostatin, a negative regulator of muscle growth, functions by inhibiting myoblast proliferation. J. Biol. Chem. , 275 (51), 40235-40243.
Table 1 (Thomas, et al., 2000)
Jeremy P Loenneke
Smoke to Sarcopenia
Smoking is the number one cause of preventable death. Smoking is highly correlated with many known diseases. The American Heart Association (AHA) reports that, “Cigarette smoking increases the risk of coronary heart disease by itself. When it acts with other factors, it greatly increases risk. Smoking increases blood pressure, decreases exercise tolerance and increases the tendency for blood to clot. Smoking also increases the risk of recurrent coronary heart disease after bypass surgery. Cigarette smoking is the most important risk factor for young men and women. It produces a greater relative risk in persons under age 50 than in those over 50. Women who smoke and use oral contraceptives greatly increase their risk of coronary heart disease and stroke compared with nonsmoking women who use oral contraceptives. Smoking decreases HDL cholesterol. Cigarette smoking combined with a family history of heart disease also seems to greatly increase the risk. Studies show that cigarette smoking is an important risk factor for stroke. Inhaling cigarette smoke produces several effects that damage the cerebrovascular system. Women who take oral contraceptives and smoke increase their risk of stroke many times. Smoking also creates a higher risk for peripheral arterial disease and aortic aneurysm (Cigarette smoking and cardiovascular diseases).”
The AHA detailed many negative affects of smoking but what affect does smoking have on muscle? Peterson and colleagues have recently shown that smoking decreases muscle protein fractional synthesis rate and increases the expression of myostatin and MAFBx. Myostatin and MAFBx are genes which are involved in the regulation of muscle mass (Peterson, et al., 2007). Myostatin belongs to the TGF- super
family and it has been proposed that myostatin inhibit muscle growth by up-regulating the expression of p21, which inhibits cyclin-E·Cdk2 activity, thus causing the hypophosphorylation of retinoblastoma (Rb) protein and G1 arrest (Thomas, et al., 2000). Basically, smoking increases this signaling which in turns leads to decreased myoblast proliferation. Myogenic differentiation is also inhibited by myostatin due to the inability of MyoD to become fully functional, resulting in the inactivation of certain myogenic genes (Langley, Thomas, Bishop, Sharma, Gilmour, & Kambadur, 2002).
In conclusion smokers may be adversely affecting their health even more so then previously thought. Smoking has been shown to decrease muscle mass by way of an increased expression of myostatin and a decreased protein synthesis rate (Peterson, et al., 2007). It has been shown that increasing levels of myostatin decreases myoblast proliferation and myogenic differentiation (Thomas, et al., 2000 and Langley, Thomas, Bishop, Sharma, Gilmour, & Kambadur, 2002). Table 1(A) shows how myostatin decreases the ability to develop myotubues, by up-regulating genes to inactivate Rb and G1 arrest. Myotubes develop into muscle fibers, so a decreased ability of myotubes to differentiate from myoblasts can be very detrimental (MacIntosh, Gardiner, & McComas, 2006). In summation, smoking not only increases the risk of CHD and stroke, it also increases the risk of developing sarcopenia.
References
Cigarette smoking and cardiovascular diseases. (n.d.). Retrieved from American Heart Association: http://www.americanheart.org/present...dentifier=4545
Langley, B., Thomas, M., Bishop, A., Sharma, M., Gilmour, S., & Kambadur, R. (2002). Myostatin inhibits myoblast differentiation by down-regulating MyoD Expression. J. Biol. Chem. , 277 (51), 49831-49840.
MacIntosh, B. R., Gardiner, P. F., & McComas, A. J. (2006). Muscle Formation. In Skeletal Muscle Form and Function (2nd Edition ed., pp. 52-70). Human Kinetics.
Peterson, A. M., Magkos, F., Atherton, P., Selby, A., Smith, K., Rennie, M. J., et al. (2007). Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFbx in muscle. AM J Physiol Endocrinol Metab. , 293 (3), 843-848.
Thomas, M., Langley, B., Berry, C., Sharma, M., Kirk, S., Bass, J., et al. (2000). Myostatin, a negative regulator of muscle growth, functions by inhibiting myoblast proliferation. J. Biol. Chem. , 275 (51), 40235-40243.
Table 1 (Thomas, et al., 2000)
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