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Increased Concentrations of Cell-Free Plasma DNA after Exhaustive Exercise

¹ Institute of Laboratory Diagnostics, Kaiser Franz Josef Hospital, Vienna, Austria;² Institute of Sports Science, Department of Sports and Exercise Physiology, University of Vienna, Vienna, Austria;³ Ludwig Boltzmann Institute for Rheumatology, Vienna, Austria;

^aaddress correspondence to this author at: Institute of Laboratory Diagnostics, Kaiser Franz Josef Hospital, Kundratstrasse 3, A-1100 Vienna, Austria; fax 43-60191-3309, e-mail johanna.atamaniuk@wienkav.at

The first 300 words of the full text of this article appear below.

Physical exercise leads to temporary ischemia in muscles, followed by increased oxygen supply during recovery as a result of reperfusion. It is thought that the sudden influx of oxygen causes a calcium overload in cells, leading to an influx of inflammatory cells into reperfused tissue. This leads to the generation of reactive oxygen radicals and subsequent oxidative damage to DNA, proteins, and lipids. For example, increased oxidant production in the mitochondria of muscles during acute exercise, followed by reoxygenation, was shown to cause cellular damage (1). In addition, exercise may cause transient muscle damage, characterized by muscle soreness, muscle fiber disarrangement, muscle protein release into plasma, an acute immune response, and decreased muscle performance (2).

Regional ATP depletion during reperfusion, disruptions in calcium homeostasis, and the presence of oxygen free radicals have all been implicated in the etiology of muscle fiber damage and necrosis. Furthermore, postexercise lymphocytopenia (2) is well documented and attributed to the exit of lymphocytes from the vascular compartment (3). Other studies have reported exercise-induced DNA damage in leukocytes and raised the question of a possible link to apoptosis (3). This effect is thought to be caused by reactive oxygen species, which are released from peripheral monocytes.

The aim of this study was to investigate the effects of physical activity, in particular muscle damage and oxidative stress, during and after a half-marathon race and the subsequent recovery period; we also wanted to measure whether oxidative stress attributable to reoxygenation may be a relevant factor in cellular damage. Cell-free plasma DNA concentrations were used as a sensitive tool for quantification of cellular damage and compared with the conventional measurements of myoglobin and uric acid in blood samples.

In this study, blood samples from half-marathon runners were taken before . . . [Full Text of this Article]

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				M. P. Langford, T. B. Redens, N. R. Harris, S. Lee, S. K. Jain, S. Reddy, and R. McVie Plasma Levels of Cell-Free Apoptotic DNA Ladders and Gamma-Glutamyltranspeptidase (GGT) in Diabetic Children Experimental Biology and Medicine, October 1, 2007; 232(9): 1160 - 1169. [Abstract] [Full Text] [PDF]

				I. G. Fatouros, A. Destouni, K. Margonis, A. Z. Jamurtas, C. Vrettou, D. Kouretas, G. Mastorakos, A. Mitrakou, K. Taxildaris, E. Kanavakis, et al. Cell-Free Plasma DNA as a Novel Marker of Aseptic Inflammation Severity Related to Exercise Overtraining Clin. Chem., September 1, 2006; 52(9): 1820 - 1824. [Abstract] [Full Text] [PDF]

				J. Atamaniuk, K. Ruzicka, K. M. Stuhlmeier, A. Karimi, M. Eigner, and M. M. Mueller Cell-Free Plasma DNA: A Marker for Apoptosis during Hemodialysis. Clin. Chem., March 1, 2006; 52(3): 523 - 526. [Abstract] [Full Text] [PDF]