Causes of Muscle Damage

Ca belongs of Muscle persecuteAn antioxidant has been defined as a substance that reduces oxidative modify such as that caused by free substructures (Halliwell 1984). Oxygen-centred free radicals known as reactive Oxygen Species (ROS) may contribute to compute generate massiveness harm (Mc Ginley 2009). Due to this, it has been widely accepted over the past 20 geezerhood that increasing antioxidants in the body will provide greater protective cover against ROS (Sastre 1992 Hathcock 2005). However, the significance of coif-induce oxidative stress is open for discussion (Cabrera 2008) with unclear conclusions in literature. This has led to the recent investigation on the possibility of increase mathematical product of free radicals during operate and the set up of antioxidant accessory in athletes (Finaud 2006 Gomez-Cabrera 2008Ristow 2009). Free radical proliferation is a widely suggested mechanism in the damage receipt to solve by process of phacocytosis and acti vation of the respiratory burst by neutrophils during the seditious response (Pyne 1994). The most commonly used antioxidants in the sporting cosmos are vitamin C (ascorbic acid) and vitamin E (tocopherol) with an astonishing 84% of athletes using antioxidants during the 2008 capital of Red China Olympics (International Olympic Committee 2008).It has been well documented that in high spirits intensity form results in damage to active bodybuilder fibres resulting in soreness, stiffness and a decline in the energys force producing capabilities (Allen 2001 Armstrong 1990 Clarkson 2002). Peroxidation of muscle fibre lipids causes disturbance in cellular homeostasis which may result in muscle fatigue or injury, possibly implicating free radical organisation as a major cause of delayed-onset muscle soreness (Byrd 1992). Preventing muscle tissue damage during use of goods and services training may help optimize the training effect and ultimate competitive sports performance (S en 2001). In order to minimise tissue cell damage, there must be an equilibrium maintained between oxidants (ROS) and antioxidants (reductants). ROS increases with screaming(prenominal) visible work (Fig 1) which can exceed the contentedness of the bodys natural antioxidant defense reaction (Reid 2001). This was illustrated by Davis (1982) and Ebbeling (1990), whereby strenuous employment led to increased levels of malondialdehyde (MDA), a 3-carbon-chain aldehyde. standard of MDA has become the most commonly used indicator of lipid peroxidation (Mc Bride 1999).Thus, the use of goods and services of exogenous antioxidants has been proposed to attenuate this increase in ROS. Evans (1990) noted that several antioxidants, including vitamin C and especially vitamin E, flummox been shown to decrease the exercise-induced increase in the rate of lipid peroxidation, which could help prevent muscle tissue damage.The effects of Vitamin E have been more extensively investigateed than Vitamin C due to or so promising results in the literature. Vitamin E is the main lipidsoluble, chain-breaking antioxidant (Ji 1996) which accumulates in the phospholipid bilayer of cell membranes and helps attenuate lipid peroxidation (Sjodin 1990) inside the cell membrane acting as an important scavenger of superoxide and lipid radicals (Powers 2000). Vitamin E supplementation has been shown to meaningfully decrease the amount of lipid peroxidation (Kanter 1993) and membrane damage associated with single bouts of economic crisis and high intensity submaximal exercise aswell as opponent exercise (Mc Bride 1998 Ashton 1999). Sumida (1989) stated that 300 mg of vitamin E given for 4 weeks reduced exercise-induced lipid peroxidation . Mc Bride (1998) report the posture of vitamin E supplementation in reducing MDA and creatine kinase (CK) levels. Cannon (1990) reported a decrease in CK and a faster retrieval subsequently supplementation of vitamin E. Furthermore, Kanter (1997) recently reported a 35 % increase in T-lag time (indicative of a diminished LDL oxidation rate) in subjects who consumed metre mg d-a-tocopherol acetate daily for 1 week before exercise. respective(a) studies have also demonstrated beneficial physiological effects of vitamin C supplementation in physically-active people. Jakeman and Maxwell (1993) give that supplementing vitamin C showed slight speciality loss (Fig 2) in the triceps surae post-exercise, and a faster recovery (Fig 3) compared to placebo. The force response to tetanic stimulation was less in the vitamin C group also, indicating a reduction in contractile function. Kaminski and Boal (1992) pre-supplemented subjects for 3 age with 1 g of vitamin C 3 times a day and then induced damage in the posterior calf muscles. Supplementation continued for 7 days post-exercise with vitamin C group reporting reduced soreness ratings ranging from 25-44% less than the control group. Peters (1993) noted fewer cases of upper respi ratory tract transmitting in runners who consumed 600 mg vitamin C/d for 3 weeks before a 42 km road race. Bryer (2006) reported lower DOMS in a high-dose Vitamin C supplementation group 2 weeks prior and 4 days post fleck exercise Studies which have used combinations of antioxidants (consumed 300-800 mg d-cr-tocopherol asset 200 mg vitamin C/d for 4-8 weeks) reported post-exercise declines in blood serum enzymes indicative of muscle tissue damage in subjects (Sumida 1989 Rokitzi 1994). Kanter (1993) reported that a mixture of vitamin E (592 mg), vitamin C (1,000 mg), and 30 mg of beta carotin resulted in a decreased level of a lipid peroxidation chump after exercise. All the previously mentioned studies suggest tangible benefits of antioxidant supplementation in combating detrimental physiological processes that may be initiated by physical activity thus appearing beneficial to sports and exercise participants.Exercise processs numerous overbearing effects on general health (Wartburton 2006), most notably modify glucose metabolism. It is well documented that exercise increases ROS production (Powers 2008), however it is unknown whether this may influence the health promoting effects of exercise. The effects of antioxidant supplementation on the health-promoting effects of exercise have recently been investigated (Gomez-Cabrera 2008 Ristow 2009). Exercise helps initiate mitochondrial metabolism, with a reduction of this metabolism linked with attribute 2 diabetes (Simoneau 1997). Since mitochondria are the main blood of ROS, its been proclaimed that ROS may be a factor in some health promoting effects (Schulz 2007 Birringer 2007). Ristow (2009) investigated this theory and hypothesized that antioxidant supplementation may repeal received health promoting benefits of exercise and oxidative stress. Thus, if increases in oxidative stress exhibit a counteracting effect on insulin-resistance, then the barroom of ROS activation by antioxidants may increa se the risk of disease such as type 2 diabetes.Ristow (2009) proposed an essential role for ROS formation in increasing insulin sensitiveness in exercising humans. The study appoint that vitamin C and vitamin E blockade many of the beneficial effects of exercise such as insulin sensitivity (glucose infusion rates-GIR) and the promotion of muscle antioxidant defence post-exercise. James (1984) found non-supplemented subjects showed significant increase in GIR after 4 weeks training whereas antioxidant group found no significant change (Fig 4). In addition, the non supplemented group also increased adiponectin levels compared to the supplemented group (Fig 5). Adiponectin (secretory protein) has been shown to have a positive correlation with insulin sensitivity and is mutually correlated with risk of type 2 diabetes (Spranger 2003). A recent meta-analysis of 232,550 participants suggests use of antioxidants may increase all-cause mortality (Bjelakovic 2007). Of the 136,023 receivi ng antioxidants, 13.1% died (17,880) whereas of the 96,527 controls, 10.5% died (10,136).Studies in healthy subjects show that low aerophilic skill is a strong predictor of mortality (Myers 2002 Yusuf 2004). impaired regulation of mitochondrial function is an important mechanism for low aerobic capacity (Wisloff 2005). Gomez-Cabrera (2008) found that mitochondrial content is a key de terminationinant of endurance capacity and that vitamin C decreases exercise-induced mitochondrial biogenesis in muscle. Free radicals serve as signals to suit muscle cells to exercise through gene expression (Khassaf 2003). Vitamin C was found to prevent beneficial training effects to decease due to their prevention of activation of two major antioxidants (Mn-SOD and GPx) (Gomez-Cabrera 2008). The aforementioned study also reason out that endurance capacity is directly related to mitochondrial content, which is negatively affected by antioxidants.Antioxidant supplementation is extremely popular a mong athletes, but data indicating beneficial effects on functional capacity of muscle are elusive. There is no strong evidence from literature for the use of antioxidant supplementation in acrobatic populations as there are many poor controlled studies involving unusually high doses, involving low muscle damaging activity and more recent research has alleviated to minimal if any benefits. Antioxidants do not seem beneficial in preventing DOMS, increasing recovery time or protect against muscle damage but in fact long term supplementation (with vitamin E in particular) may increase mortality (Bjelakovic 2007). Most notably for athletes, not only does supplementation appear ineffective in preventing against exercise induced muscle damage, but interferes with the ROS signalling which are needed for adaptation to occur (Gomez-Cabrera 2008).ReferencesAllen DG (2001). Eccentric muscle damage mechanisms of early reduction of force. Acta Physiol Scand 171(3)311-9Aoi W, Naito Y, Takanami Y, Kawai Y, Sakuma K, Ichikawa H (2004). Oxidative stress and delayed-onset muscle damage after exercise. Free Radic Biol Med37480- 7.Armstrong RB (1990). Initial events in exercise-induced muscular injury. Med Sci variations Exerc 22(4) 429-35Ashton T, Young IS, Peters JR, Jones E, Jackson SK, Davies B (1999). Electron spin resonance spectroscopy, exercise, and oxidative stress an ascorbic acid treatment study. J Appl Physiol872032- 6Birringer M, et al. (2007) Improved glucose metabolism in mice absent alphatocopherol transfer protein. Eur J Nutr 46397-405.Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (2007) Mortality in randomize trials of antioxidant supplements for primary and secondary prevention Systematic review and meta-analysis. J Am Med Assoc 297842-857.Bryer SC, Goldfarb AH (2006). Effect of high dose vitamin C supplementation on muscle soreness, damage, function and oxidative stress to eccentric exercise. Int J Sport Nutr Exerc Metab 16(3) 270-80Byrd, S.K.( 1992) Alterations in the sarcoplasmic reticulum A possible link to exercise-induced muscle damage. Med. Sci. Sports Exerc. 24531-536Cannon, J.G, Evans W.J (1990). exquisite phase response in exercise Interaction of age and vitamin E on neutrophils and muscle enzyme release. Am. J. Physiol. 259R1214-R1219. Clarkson PM, Hubal MJ (2002). Exercise-induced muscle damage in humans. Am J Phys Med Rehabil 81(11) S52-59Davies, K.J, BROOKS G.A, and Packer L (1982). Free radicals and tissue damage produced by exercise. Biochem. Biophys. Res. Commun. 1071198-1205.Dillard CJ, Litov RE, Savin RE, Dumelin EE Tappel AL (1978) Effects of exercise, vitamin E, and ozone on pulmonary function and lipid peroxidation. Journal of Applied PhysiologyEbbeling, C.B, and Clarkson P.M(1990). Muscle adaptation prior to recovery chase eccentric exercise. Eur. J. Appl. Physiol. 60 26-31. Finaud J, Lac G, Filaire E (2006). Oxidative Stress kindred with exercise and training. Sports Med36(4)327-58Gomez-Cabrera M C, Domenech E (2008). Moderate exercise is an antioxidant upregulation of antioxidant genes by training. Free Radic Biol Med 44(2) 126-31Gomez-Cabrera MC, et al. (2008) unwritten administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance. Am J Clin Nutr 87142-149.Halliwell, B., Gutteridge J. M (1984). Oxygen toxicity, oxygen radicals, transition metals and disease. J. Biochem. 2191-14.Hartmann A, Nies AM, Grunert-Fuchs M, Poch B Speit G (1995) Vitamin E prevents exercise-induced DNA damage. Mutation Research 346, 195-202.Hathcock JN, Azzi A, Blumberg J (2005). Vitamins E andCare safe across a broad range of intakes. Am J Clin Nutr81736-45Hellsten, Y, Sjodin B (1997) Xanthine oxidase in human careworn muscle following eccentric exercise A role in inflammation. J. Physiol. 498 239-248. James DE, Kraegen EW, Chisholm DJ (1984) Effect of exercise training on whole-body insulin sensitivity and responsiveness. J Appl Physiol 561217-1222.Ji, L.L (1996). Exercise, oxidative stress, and antioxidants. Am. J. Sports Med. 24S20-S24. Ji, L.L. (2000) Free radicals and antioxidants in exercise and sports. G.E. Garrett, and D.T. Kirkendall. Exercise and Sport Science. New York, NY Lippincott Williams and Wilkins. pp. 299- 317.Kaminski, M, Boal M (1992). An effect of ascorbic acid on delayed- onset muscle soreness. Pain 50317-321. Kanter MM, Bartoli WP, Eddy DE Horn MK (1997) Effects of short term vitamin E supplementation on lipid peroxidation, inflammation and tissue damage during and following exercise. Medicine and Science in Sports and Exercise 29, S40.Kanter, M.M., Nolte L ,and Holloszy H (1993). Effects of an antioxidant vitamin mixture on lipid peroxidation at rest and postexercise. J. Appl. Physiol. 74965-969. Kanter, M.M., Nolte L.A and Holloszy J.O (1993). Effects of an antioxidant vitamin mixture on lipid peroxidation at rest and post-exercise. J. Appl. Physiol. 74965-969. Khassaf M, M cArdle A, Esanu C (2003). Effect of vitamin C supplements on antioxidant defence and stress proteins in human lymphocytes and skeletal muscle. J Physiol549645-52.Kosmidou I, Vassilakopoulos T, Xagorari A, Zakynthinos S, Papapetropoulos A, Roussos C (2002). Production of interleukin-6 by skeletal muscle myotubes. Role of reactive oxygen species. Am J Respir cadre Mol Biol26587- 93.Maxwell SRJ, Jakeman P, Thomason H, (1993). Changes in plasma antioxidant status during eccentric exercise and the effect of vitamin supplementation. Free Radic Res Commun19191-202.McBride, J.M., and Kraemer W.J (1998) Effect of resistance exercise on free radical production. Med. Sci. Sports Exerc. 3067-72. McBride, J.M., and Kraemer W.J (1999). Free radicals, exercise, and antioxidants. J. loudness Cond. Res. 13175-183. Myers J, Prakash M, Froelicher V, Do D, Partington S, Atwood JE (2002). Exercise capacity and mortality among men referred for exercise testing. N Engl J Med346793- 801.Powers SK, Jackso n MJ (2008) Exercise-induced oxidative stress Cellular mechanisms and continue on muscle force production. Physiol Rev 881243-1276.Pyne, D.B (1994). Regulation of neutrophil function during exercise. Sports Med. 17245-258. Reid, M.B, Shoji T,Moody M.R, and Entman M.L.(1992) Reactive oxygen in skeletal muscle. II. extracellular release of free radicals.J. Appl. Physiol. 731805-1809. Ristow, M., Zarse, K., Oberbach, A., Kloting, N., Birringer, M., Kiehntopf, M. Stumvoll, M., Kahn, C.R., Bluher, M. (2009). Antioxidants prevent health-promoting effects of physical exercise in humans. Proceedings of the National Academy of Sciences of the United States of America, 106, 8665-8670.Rokitzi L, Logemann E, Sagredos AN, Wetzel-Roth W Keul J (1994) Lipid peroxidation and antioxidative vitamins under extreme endurance stress. Acta Physiologica Scandinavica 154, 149-154.Sastre J, Asensi M, Gasco E (1992). Exhaustive physical exercise causes oxidation of glutathione status in blood prevention b y antioxidant administration. Am J Physiol263R992-5.Schulz TJ, et al. (2007) Glucose restriction extends Caenorhabditis elegans life span by motivator mitochondrial respiration and increasing oxidative stress. Cell Metab 6280-293.Sen, C, K (2001). Antioxidants in Exercise. Nutrition Journal of Sports Medicine- Volume 31 Issue 13 pp 891-908Simoneau JA, Kelley DE (1997) altered glycolytic and oxidative capacities of skeletal muscle contribute to insulin resistance in NIDDM. J Appl Physiol 83166-171.Sjodin, B., Y. And Apple F.S (1990). Biochemical mechanisms for oxygen free radical formation during exercise. Sports Med. 10236-254. Spranger J, et al. (2003) Adiponectin and protection against type 2 diabetes mellitus. Lancet 361226-228.Sumida, S., Tanaka K, Kitao H, Nakadomo F (1989). Exercise- induced lipid peroxidation and leakage of enzymes before and after vitamin E supplementation. Int. J. Biochem. 21835- 838. Warburton DE, Nicol CW, Bredin SS (2006) health benefits of physical activity The evidence. Can Med Ass J 174801-809.Wisloff U, Najjar SM, Ellingsen O (2005). cardiovascular risk factors emerge after artificial selection for low aerobic capacity. Science 307418 -20.Yusuf S, Hawken S, Ounpuu S (2004). Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the Interheart Study) case-control study. Lancet364937-52.