HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Clanton, T. L. Articles by Klawitter, P. Search for Related Content PubMed PubMed Citation Articles by Clanton, T. L. Articles by Klawitter, P.

---

Original Article

Oxidants and Skeletal Muscle Function: Physiologic and Pathophysiologic Implications

Thomas L. Clanton^*,,1, Li Zuo^*, and Paul Klawitter^,

^* Department of Internal Medicine, Pulmonary and Critical Care Medicine;
Biophysics Program, and
Department of Emergency Medicine, The Ohio State University, Columbus, Ohio 43210

Previous studies have demonstrated that skeletal muscles generate considerable reactive oxygen during intense muscle contraction. However, the significance of this phenomenon and whether it represents normal physiology or pathology are poorly understood. Treatment with exogenous antioxidants suggests that normal redox tone during contraction is influencing ongoing contractile function, both at rest and during intense exercise. This could represent the influence of redox-sensitive proteins responsible for excitation-contraction coupling or redox-sensitive metabolic enzymes. Some conditions associated with intense exercise, such as local tissue hypoxia or elevated tissue temperatures, could also contribute to reactive oxygen production. Evidence that muscle conditioning results in upregulation of antioxidant defenses also suggests a close relationship between reactive oxygen and contractile activity. Therefore, there appears to be a significant role for reactive oxygen in normal muscle physiology. However, a number of conditions may lead to an imbalance of oxidant production and antioxidant defense, and these, presumably, do create conditions of oxidant stress. Ischemia-reperfusion, severe hypoxia, severe heat stress, septic shock, and stretch-induced injury may all lead to oxidant-mediated injury to myocytes, resulting in mechanical dysfunction.

This article has been cited by other articles:

				R. M. Murphy, T. L. Dutka, and G. D. Lamb Hydroxyl radical and glutathione interactions alter calcium sensitivity and maximum force of the contractile apparatus in rat skeletal muscle fibres J. Physiol., April 15, 2008; 586(8): 2203 - 2216. [Abstract] [Full Text] [PDF]

				D. G. Allen, G. D. Lamb, and H. Westerblad Skeletal Muscle Fatigue: Cellular Mechanisms Physiol Rev, January 1, 2008; 88(1): 287 - 332. [Abstract] [Full Text] [PDF]

				A. S. Martins, V. M. Shkryl, M. C. Nowycky, and N. Shirokova Reactive oxygen species contribute to Ca2+ signals produced by osmotic stress in mouse skeletal muscle fibres J. Physiol., January 1, 2008; 586(1): 197 - 210. [Abstract] [Full Text] [PDF]

				M. A. Smith, J. S. Moylan, J. D. Smith, W. Li, and M. B. Reid IFN-{gamma} does not mimic the catabolic effects of TNF-{alpha} Am J Physiol Cell Physiol, December 1, 2007; 293(6): C1947 - C1952. [Abstract] [Full Text] [PDF]

				T. Loizidis, A. Sioga, L. Economou, A. Frosinis, A. Kyparos, A. Zotou, and M. Albani The role of ascorbic acid and exercise in chronic ischemia of skeletal muscle in rats J Appl Physiol, January 1, 2007; 102(1): 321 - 330. [Abstract] [Full Text] [PDF]

				C. L. McGowan, A. S. Levy, P. J. Millar, J. C. Guzman, C. A. Morillo, N. McCartney, and M. J. MacDonald Acute vascular responses to isometric handgrip exercise and effects of training in persons medicated for hypertension Am J Physiol Heart Circ Physiol, October 1, 2006; 291(4): H1797 - H1802. [Abstract] [Full Text] [PDF]

				A. Fredsted, U. R. Mikkelsen, H. Gissel, and T. Clausen Anoxia induces Ca2+ influx and loss of cell membrane integrity in rat extensor digitorum longus muscle Exp Physiol, September 1, 2005; 90(5): 703 - 714. [Abstract] [Full Text] [PDF]

				Y.-P. Li, Y. Chen, J. John, J. Moylan, B. Jin, D. L. Mann, and M. B. Reid TNF-{alpha} acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle FASEB J, March 1, 2005; 19(3): 362 - 370. [Abstract] [Full Text] [PDF]

				C S Bestwick and N Maffulli Reactive oxygen species and tendinopathy: do they matter? Br. J. Sports Med., December 1, 2004; 38(6): 672 - 674. [Full Text] [PDF]

				J. P. Eu, J. M. Hare, D. T. Hess, M. Skaf, J. Sun, I. Cardenas-Navina, Q.-A. Sun, M. Dewhirst, G. Meissner, and J. S. Stamler Concerted regulation of skeletal muscle contractility by oxygen tension and endogenous nitric oxide PNAS, December 9, 2003; 100(25): 15229 - 15234. [Abstract] [Full Text] [PDF]

				M. B. Reid COPD as a Muscle Disease Am. J. Respir. Crit. Care Med., October 1, 2001; 164(7): 1101 - 1102. [Full Text] [PDF]

				M. B. Reid Plasticity in Skeletal, Cardiac, and Smooth Muscle: Invited Review: Redox modulation of skeletal muscle contraction: what we know and what we don't J Appl Physiol, February 1, 2001; 90(2): 724 - 731. [Abstract] [Full Text] [PDF]