Mitochondrial Bioenergetics of Skeletal Muscles

  • Janka Lipková

Myofibril is the main contractile structure of a muscle; sarcomere is a functional unit comprising thin actin and thick myosin filaments. The process of muscular fiber shortening takes place through insertion of thin actinic filaments in between the thick myosin ones. The whole process is regulated by regulatory proteins troponin and tropomyosin. Energy necessary for muscle contraction is obtained from adenosinetriphosphate (ATP) produced in mitochondria. Energy necessary for ATP resynthesis is obtained by cleavage of phosphocreatine (PCr), carbohydrates, fats and proteins. During the aerobic ATP production, the majority of received oxygen is reduced by hydrogen to water. However a part of oxygen which is not reduced completely produces the so-called free oxygen radicals – univalent oxygen forms escaping from the transport chain. Production of oxygen radicals and their highly reactive derivatives, the so-called reactive oxygen species, increases during endurance exercise and may negatively affect the function of muscles and accelerate the process of fatigue.

Exercise can cause imbalance between the levels of oxidants and antioxidants. This state, so-called oxidative stress, causes damage to enzymes, protein receptors, lipid membranes and DNA. On the other hand, exercise positively affects oxidative stress reduction and improves the function of mitochondria. Results of human studies are however frequently inconclusive.

The antioxidative defense systemdepends on the intake of antioxidative vitamins and minerals with the diet (vitamins C, E, β-carotene and selenium), as well as on endogenous production of other substances with antioxidative effects (such as glutathione, coenzyme Q10) and of enzymes (such as superoxide dismutase), whose task it is to suppress free radicals. In most cases, antioxidant supplementation is unnecessary. The question whether supplementation with vitamins and other antioxidants increases sports performance and facilitates regeneration has not yet been explicitly answered.


Energy muscle contraction oxidative damage physical activity reactive oxygen species supplementation 


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  1. 1.
    Dawn BM (1994) Biochemistry. Williams & Wilkins, Baltimore, MD, pp 337Google Scholar
  2. 2.
    Gvozdjáková A (1998) unpublished resultsGoogle Scholar
  3. 3.
    Hartmann A et al. (1995) Vitamin E prevents exercise-induced DNA damage. Mutat Res 346:195–202PubMedCrossRefGoogle Scholar
  4. 4.
    Irrcher I et al. (2003) Regulation of mitochondrial biogenesis in muscle by endurance exercise. Sports Med 33(11):783–793PubMedCrossRefGoogle Scholar
  5. 5.
    Koves TR et al. (2005) Subsarcolemmal and intermyofibrillar mitochondria pay distinct roles in regulating skeletal muscle fatty acid metabolism. Am J Physiol: Cell Physiol 57(5):1074–1083CrossRefGoogle Scholar
  6. 6.
    Maughan RJ, Burke LM (2004) Sports Nutrition. Handbook of Sports Medicine and Science. Blackwell, MA, Oxford, Victoria, pp 187Google Scholar
  7. 7.
    Maughan R, Gleeson, M (2004) The Biochemical Basis of Sport Performance. Oxford University Press, Oxford, pp 257Google Scholar
  8. 8.
    Menshikova EV et al. (2005) Effect of weight loss and physical activity on skeletal muscle mitochondrial function in obesity. Am J Physiol: Endocrinol Metab 51(4):818–826Google Scholar
  9. 9.
    Menshikova EV (2006) Effect of exercise on mitochondrial content and function in aging human skeletal muscle. J Gerontol Series A: Biol Sci Med Sci 61(6):534–540Google Scholar
  10. 10.
    Mooren FC, Völker K (2005) Molecular and Cellular Exercise Physiology. Human Kinetics. Champaign, Windsor, Leeds, Lower Mitcham, Auckland, pp 453Google Scholar
  11. 11.
    Navarro A et al. (2004) Beneficial effects of moderate exercise on mice aging: survival, behavior, oxidative stress and mitochondrial electron transfer. Am J Physiol: Regul Integr Comp Physiol 55(3):505–512Google Scholar
  12. 12.
    Servais S et al. (2003) Effect of voluntary exercise on H2O2 release by subsarcolemmal and intermyofibrillar mitochondria. Free Radic Biol Med 35(1):24–28PubMedCrossRefGoogle Scholar
  13. 13.
    Short KR et al. (2003) Impact of aerobic exercise training on age-related changes in insulin sensitivity and muscle oxidative capacity. Diabetes 52(8):1888–1897PubMedCrossRefGoogle Scholar
  14. 14.
    Sibernagel S, Despopoulos A (1993) Atlas fyziologie člověka. Grada Avicenum, Praha, 352 (Atlas of Human Physiology; In Czech)Google Scholar
  15. 15.
    Tsakiris S, Parthimos T (2006) Alpha tocopherol supplementation reduces the elevated 8-hydroxy-2 deoxyguanosine blood levels induced by training in basketball players. Clin Chem Lab Med 44(8):1004–1008PubMedCrossRefGoogle Scholar
  16. 16.
    Vasilaki I et al. (2006) Free radical generation by skeletal muscle of adult and old mice: effect of contractile activity. Aging Cell 5(2):109–117PubMedCrossRefGoogle Scholar
  17. 17.
    Vollaard NB et al. (2005) Exercise induced oxidative stress: myths, realities and physiological relevance. Sports Med 35(12):1045–1062PubMedCrossRefGoogle Scholar
  18. 18.
    Wilmore JH, Costil DL (1999) Physiology of Sport and Exercise. Human Kinetics, Champaign, Windsor, Leeds, Lower Mitcham, Auckland, pp 710Google Scholar
  19. 19.
    Yeo S, Davidge ST (2001) Possible beneficial effect of exercise, by reducing oxidative stress, on the incidence of preeclampsia. J Wom Health 10:983–989Google Scholar

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© Springer Science + Business Media B.V 2008

Authors and Affiliations

  • Janka Lipková
    • 1
  1. 1.Sport's FacultyComenius UniversitySlovakia

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