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This article discusses the potential benefits of taking aspirin before participating in a marathon to reduce the risk of cardiac arrest. The author references a study that found a link between endurance exercise and coronary atherosclerosis, as well as evidence that male gender and marathons are significant risk factors for cardiac arrest. The article suggests that aspirin use may attenuate the elevated risk of acute cardiac events during races, particularly for runners with elevated coronary artery calcium scores. The author concludes that aspirin is a safe and effective intervention to mitigate cardiac morbidity and mortality during marathons. [Extracted from the article]

Cerebral edema due to exercise-associated hyponatremia and cardiac arrest due to atherosclerotic heart disease cause rare marathon-related fatalities in young female and middle-aged male runners, respectively. Studies in asymptomatic middle-aged male physician-runners during races identified inflammation due to skeletal muscle injury after glycogen depletion as the shared underlying cause. Nonosmotic secretion of arginine vasopressin as a neuroendocrine stress response to rhabdomyolysis mediates hyponatremia as a variant of the syndrome of inappropriate antidiuretic hormone secretion. Fatal hyponatremic encephalopathy in young female runners was curtailed using emergent infusion of intravenous hypertonic (3%) saline to reverse cerebral edema on the basis of this paradigm. This treatment was arrived at through a consensus process within the medical community. An increasing frequency of cardiac arrest and sudden death has been identified in middle-aged male runners in 2 studies since the year 2000. Same-aged asymptomatic male physician-runners showed post-race elevations in interleukin-6 and C-reactive protein, biomarkers that predict acute cardiac events in healthy persons. Hypercoagulability with in vivo platelet activation and release of cardiac troponin and N-terminal pro-brain natriuretic peptide were also observed post-race in these same subjects. High short-term risk for atherothrombosis during races as shown by stratification of biomarkers in asymptomatic men may render nonobstructive coronary atherosclerotic plaques vulnerable to rupture. Pre-race aspirin use in this high-risk subgroup is prudent according to conclusive evidence for preventing first acute myocardial infarctions in same-aged healthy male physicians. On the basis of validated clinical paradigms, taking a low-dose aspirin before a marathon and drinking to thirst during the race may avert preventable deaths in susceptible runners. [ABSTRACT FROM AUTHOR]

Abstract: Prolonged strenuous exercise such as marathon running transiently increases the absolute and relative risk for sudden cardiac death. A 17-fold increase in the latter over resting baseline in previously sedentary middle-aged men is reduced due to cardioprotection from training in experienced marathon runners. Exertional rhabdomyolysis as a common occurrence during the race is accompanied by neutrophilia and elevated biomarkers of inflammation, including interleukin-6 and C-reactive protein. A hemostatic imbalance with prothrombotic effects includes in vivo platelet activation during the race. Suggesting a pathogenic role for these findings, plaque rupture due to atherothrombosis triggers acute exertional cardiac events, including sudden death, in low-risk runners as in high-risk patients such as those with diabetes mellitus. Strategies including prophylactic aspirin are considered to decrease the risk for acute cardiac events. [Copyright &y& Elsevier]

Exercise-associated hyponatraemia (EAH) is an acute-onset imbalance in the tonicity of extracellular fluids during or after endurance exercise which results in a blood sodium concentration <135 mmol/L. Both excessive fluid intake and a concurrent decrease in urine formation contribute to this rapid-onset, predominantly dilutional, decrease in serum sodium, which can result in life-threatening pulmonary and cerebral oedema. Marathon runners with hypotonic encephalopathy related to EAH. including two cases with fatal cerebral oedema, demonstrated non-osmotic secretion of arginine vasopressin and fulfilled the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The pathophysiology of SIADH as the proximate cause of EAH accounts for otherwise puzzling clinical observations such as cases occurring after only moderate fluid intake or presenting hours after races. This formulation provides a framework for enhancing prevention by monitoring weight changes during races to detect positive fluid balance before the onset of mental status changes. Most importantly, SIADH supports a strategy for use of oral and intravenous hypertonic solutions, including 3% sodium chloride, for the emergent treatment of moderate and life-threatening symptoms of hypotonic encephalopathy, respectively. [ABSTRACT FROM AUTHOR]

Discusses the effect of marathon running on inflammatory and homeostatic markers. Mean age of participants in the 100th to 105th Boston Athletic Association Marathons from 1996 to 2001; Effects of strenuous physical exercise.

Reports on the effect of marathon running on inflammatory and hemostatic markers. Increase in the relative risk for acute myocardial infarction and sudden cardiac death; Increase in prothrombotic factors and fibrinolytic activity; Postrace increase in novel inflmmatory markers of cardiac risk in middle-aged runners.

Context.--Prostate-specific antigen (PSA) is an important tumor marker for the most frequently diagnosed cancer in the United States. A major limitation of this marker is falsely elevated results in patients who are found not to have prostate cancer. The effects of vigorous physical exertion on PSA concentrations are controversial. Objective.--To determine the effects of marathon running on PSA levels. Design.--Measurement of total and free PSA levels in the sera of participants in a marathon before and within 4 and 24 hours after the race. Results.--None of the participants had elevated total PSA levels before the race. Although we found no statistically significant changes in average total or free PSA concentrations at either time point, after the marathon, 2 (11%) of 18 runners had total PSA concentrations outside the standard reference range. Changes in total PSA levels did not correlate with age or prerace PSA concentrations. Free PSA levels were not statistically significantly changed after the race and did not allow a reliable determination of exercise-induced PSA elevations. Conclusions.--Although it may not be necessary for men to abstain from exercise involving running before blood draws for PSA analysis, elevated PSA concentrations may be observed in some individuals after participation in a major sporting event. In these cases, repeat measurements should be considered at a time significantly removed from such exercise. [ABSTRACT FROM AUTHOR]