| Muscle Your Economy | |
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Chronic Disease Adversely Skeletal Muscles Chronic disease also adversely affects the skeletal muscle system. COPD (chronic pulmonary obstruction) and congestive heart failure are disease states that contribute significantly to muscle weakness. In diabetes mellitus, chronic heart failure, chronic obstructive pulmonary disease, renal and liver failure, trauma, sepsis, and senescence, the chemistry of the body shifts so that there is an increase of catabolic hormones (cortisol, epinephrine, nor-epinephrine) and pro-inflammatory chemicals that damage the skeletal muscles. As a consequence, the protein in the skeletal and cardiac muscles breaks down their proteins amino acids. While this helps to meet the body’s indispensable energy requirements, at the same time it decreases the availability of protein for skeletal and cardiac physiological and metabolic functions. Bottom line: All of these conditions have predominant catabolic molecules with significant muscular wasting and metabolic impairment. However, for amino acids to enter the cells for protein synthesis, the hormonal status of an individual is important. Diabetes and the Skeletal Muscles Diabetes profoundly affects the skeletal muscles. By chemical measurement and actual biopsy, the skeletal muscles of diabetic individuals show the following problems: loss of fast muscle fibers, which results in an increased risk of falling, and an increased tendency for muscle fatigue. The efficiency of mitochondria in skeletal muscles also declines in diabetic individuals and this leads to impaired ability of the mitochondria to burn fat. This also holds true for obese individuals without diabetes. Diabetes decreases skeletal muscle contractility, induces atrophy, and reduces the ability of the muscle cells to regenerate. Get a good physical. Have your blood glucose, thyroid hormones, and vitamin D level checked. Don’t forget vitamin D. The active form of vitamin D is both an antioxidant and a powerful anti-inflammatory agent. Studies show that there is a significant association between active vitamin D and leg muscle strength. Japanese researchers studied 76 elderly women who suffered a stroke. In randomized fashion they gave half of the women 1000 I.U. of vitamin D2 (ergocaliciferol) daily. Not only did the vitamin D increase the level of vitamin D hormone in their blood, the women who took the supplement reduced their incidence of falling by 58%. There were also increases in the relative number and size of type 2 muscle fibers (fast-twitched muscle fibers) and improved muscle strength in the vitamin D-treated group. Preserving Your Muscle Economy: Exercise Fortunately, regular, aerobic and resistance-type exercise, especially when combined with a good, corrective diet can increase the number and efficiency of mitochondria including diabetic individuals. Regular moderate exercise induces anti-inflammatory actions and inhibits the production of pro-inflammatory agents that could trigger apoptosis of muscle cells. (Pedersen) The good new is that even short-term, low- and moderate-intensity exercise for sedentary individuals beginning to exercise reduces inflammation within skeletal muscles of obese people, but can increase MGF (mechano growth factor) approximately two fold. MGF is essential for muscle repair. Stretching exercises are important too because they reduce the risk for injury to tendons and joints, increase the range of motion for joints, and reduce muscle tension. Tight muscles reduce blood circulation, increase blood pressure, increase the risk for injury, and decrease coordination. Researchers at the Berck Institute for Aging found that the muscles of older adults were generally 59% weaker than those of the studied younger individuals and showed dramatic age-associative decline of mitochondrial function. After six months of exercise training, the muscle strength in the older individuals improved 21%. These researchers found that regular exercise influences gene activity in older individuals, increases the capacity of the mitochondria, and decreases the markers of oxidative stress and the activity of anti-inflammatory agents in the skeletal muscle. Temperance Temperance is moderate in good things and activities of life and the avoidance of the harmful. Both smoking and continued drinking of alcohol damage the muscle fibers. Smokers also experience greater muscle fatigue than non-smokers. Researchers. found that smokers showed higher levels of myostatin and MAFB-X. These are markers which indicate more inhibited protein growth or synthesis in the muscles of smokers compared with non-smokers. At the same time the biological markers for muscle formation were 40% less in smokers than non-smokers. No wonder smoking ruins endurance and excellence of muscular performance. Alcohol consumption compromises the cellular proteins. The dynamic balance of proteins in striated muscle is dependent upon rates of protein synthesis and protein degradation. Either acute alcohol intoxication or chronic alcohol consumption depresses protein synthesis in skeletal muscles. Conclusion: It is largely up to us whether we engage in activities that build our muscle economy or activities that weaken it. Unless the stock market, we exert a large control over our muscle economy. If you enjoyed this article, you will learned much more about how lifestyle affects muscles in the fall 2010 issue of The Journal of Health & Healing. Learn more about how lifestyle affects the body by enrolling in Lifestyle Physiology from the online College of Health Evangelism at www.healthevangelism.com |
Skeletal muscles, over which we have voluntary control, range from the blinking of an eye to the complex coordination and precision involved in athletic contests. In the average person of normal weight, about 40% of their body weight actually comes from the muscles! Essential to life, skeletal muscles are necessary for movement and posture and contribute to heat production. That is not all: skeletal muscle acts as the major metabolic disposal for glucose and triglyceride disposal and is an important determinant of resting metabolic rate.



