ORIGINAL RESEARCH Study of Hematological and Biochemical Parameters in Runners Completing a Standard Marathon Stephen A. Reid,* Dale B. Speedy,† John M. D. Thompson,‡ Timothy D. Noakes,§ Guy Mulligan,  Tony Page,* Robert G. D. Campbell,* and Chris Milne¶ Objective: To study hematological and biochemical parameters prospectively in runners completing a standard 42.2-km marathon run. To determine the incidence of hyponatremia in runners, and whether consumption of nonsteroidal anti-inflammatory medications (NSAIDs) was associated with alterations in serum biochemical pa- rameters. Design: Observational cohort study. Setting: City of Christchurch (New Zealand) Marathon, June 2002. Participants: One hundred fifty-five of the 296 athletes entered in the 2002 City of Christchurch Marathon were enrolled in the study. Main Outcome Measures: Athletes were weighed at race regis- tration and immediately after the race. Blood was drawn postrace for measurement of serum sodium, potassium, creatinine, and urea con- centrations and for hematological analysis (hemoglobin concentra- tion, hematocrit, leukocyte distribution). Results: Complete data sets including prerace and postrace weights, and postrace hematological and biochemical analyses were collected on 134 marathon finishers. Postrace serum sodium concentrations were directly related to changes in body weight (P < 0.0001). There were no cases of biochemical or symptomatic hyponatremia. Thirteen percent of runners had taken an NSAID in the 24 hours prior to the race. Mean values for serum creatinine (P = 0.03) and serum potas- sium (P = 0.007) concentrations were significantly higher in runners who had taken an NSAID. No athlete who had taken an NSAID had a postrace serum creatinine concentration less than 0.09 mmol/L. Ninety-eight percent of runners had a postrace leukocytosis (mean white cell count, 18.97 b/L), of which the major component was a raised neutrophil count (mean neutrophil count, 15.69 b/L). Conclusions: This study found no cases of hyponatremia in runners completing a standard distance marathon. This finding relates to a marathon run under ideal conditions (minimal climatic stress) and in which there were fewer aid stations (every 5 km) than is common in North American marathons (every 1.6 km). Also, aggressive hydra- tion practices were not promoted. Consumption of NSAIDs in the 24 hours prior to distance running was associated with altered renal func- tion. Key Words: marathon runners, hyponatremia, creatinine, nonsteroi- dal anti-inflammatory medication, renal function, potassium (Clin J Sport Med 2004;14:344–353) A considerable body of literature has been published during the last 40 years to document hematological and bio- chemical changes that occur in endurance athletes. There is evidence that some athletes finish endurance events with a raised serum creatinine 1,2 or a raised serum sodium concentra- tion 3–5 or both. The cause of this is thought to be multifactorial, with both dehydration (with consequent hemoconcentration) and reduced renal blood flow (with consequent reduced glo- merular filtration) likely to be contributing factors. 2,6 Renal function may be so severely compromised in some athletes that they develop renal failure. 7–9 There is, however, a subgroup of endurance athletes who develop hyponatremia rather than hypernatremia. 10–12 In tri- athlons of Ironman distance (3.8-km swim, 180-km cycle, 42.2-km run), this subgroup has been shown to be as large as 17% of race finishers. 13 The etiology for this has been contro- versial for some years. One hypothesis that has been put for- ward is that salt losses in sweat are the basis of athletic hypo- natremia. 14 The second hypothesis is that overhydration with hypotonic fluids is the cause of this condition. A number of studies have now been published that support the fluid over- load theory. 11,15–24 In recent years, there have been a number of reports of hyponatremia developing in runners completing a standard distance marathon. 21–29 Several runners have died as a result of cerebral and pulmonary edema caused by hyponatre- mia. 24,25,28 Recently, studies of runners in marathons in the United States have reported incidences of hyponatremia rang- ing from 5.6% to 13%. 21,23,27 Received for publication August 2003; accepted January 2004. From *SportsMed, Christchurch, New Zealand; †SportsCare, Auckland, New Zealand; ‡University of Auckland, Auckland, New Zealand; §MRC/UCT Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town and Sports Science Institute of South Africa, Cape Town, South Africa;  MedLab South, Christchurch, New Zealand; and ¶Clarence Street Medical, Hamilton, New Zealand. Reprints: Stephen A. Reid Sports Medicine Practice, St. Helen’s Hospital, 186 Macquarie Street, Hobart, Tas 7000, Australia (e-mail: stevenlyn@ ozemail.com.au). Copyright © 2004 by Lippincott Williams & Wilkins 344 Clin J Sport Med • Volume 14, Number 6, November 2004