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We investigated the effects of an ultra-marathon on cell-free plasma DNA as well as on mRNA expression of pro-apoptotic (Bax, Bad), anti-apoptotic (Bcl-2) and cell-protective (Hsp70, Hsp27 and Hsp32) genes in mononuclear blood cells (MNCs). Blood samples were drawn from 14 athletes before and immediately after 6-h run. In addition, blood samples were also collected and analyzed 2 and 24 h after the end of the run. Levels of plasma DNA were significantly increased immediately after the marathon (P < 0.001) and were still higher 2 h later (P < 0.005), but significantly lower than those immediately after the race (P < 0.05). Cell-free plasma DNA returned to pre-race levels 24 h after the run. mRNA expressions of Hsp70, Hsp32 and Bax significantly increased in MNCs after the race, whereas Hsp27 and Bad mRNA expression levels showed no significant changes. Bcl-2 expressions decreased immediately after the race (P < 0.001), but increased in the 24 h later (P < 0.05). We conclude that apoptotic ladders of cell-free DNA following exhaustive exercise originate from apoptotic cells and that not only skeletal muscle cells but also leukocytes contribute to this phenomenon.

The present study aimed to investigate the acute effects of a single bout of high-intensive strength training on the production of cell-free plasma DNA (cf-DNA), as well as on the degradation of purine nucleotides as assessed by the concentration of xanthine (XA) and hypoxanthine (HX) in urine and serum. Twelve trained weightlifters performed six sets of six lifting exercises with 90-95% of the one repetition maximum. Blood samples and urine were obtained 1 h before training, immediately after finishing the exercise session and following 2 h of recovery. Cf-DNA, HX, and XA (in serum) significantly increased (P < 0.05-P < 0.001) immediately after heavy lifting exercise when compared with baseline levels, and significantly decreased (P < 0.05-P < 0.001) after 2 h of recovery. These results indicate that, cf-DNA and oxypurines might be relevant biomarkers for cellular damage, mechanical, energetic, and/or ischemic stress in context with exercise.

The present study was designed to investigate whether the stress of a half-marathon race can induce myocardial cell injury or left ventricular dysfunction in moderately trained runners of both gender, as assessed by post-race plasma concentrations of biochemical cardiac-specific markers and by quantitative echocardiographic measurements. We examined 12 male (mean+/-SD); age: 42.8+/-7.3 yr; height: 177.6+/-7.4 cm; body mass: 75.6+/-9.4 kg; BMI: 24.1+/-1.8 and 13 female (mean+/-SD); age: 39.0+/-6.5 yr; height: 164.6+/-6.2 cm; body mass: 58.4+/-9.8 kg; BMI: 21.5+/-3.4 recreational runners, who completed a half-marathon race. Blood samples were collected from each subject before the half-marathon race as well as 20 min and 2 h post-race and cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured. Quantitative echocardiographic analyses of wall dimensions and ejection fraction were also obtained from 14 of 25 subjects within 1 wk after the race. Both blood markers showed significant changes (p<0.05-0.001) over the time course of the three blood draws. A significant percentage of laboratory analytes analyzed in this study were outside the reference ranges and fulfilled conventional criteria for cardiac muscle damage. However, echocardiography within one week following the competition did not show any evidence that running a half-marathon competition damages the myocardium. Strenuous endurance exercise in middle-aged recreational runners induces a significant elevation of biochemical cardiac-specific markers, which may reflect transient subclinical myocardial damage, but can also reflect a physiological reparative or adaptive process.

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