Reid Stephen A, Speedy Dale B, Thompson John M D, Noakes Timothy D, Mulligan Guy, Page Tony, Campbell Robert G D, Milne Chris
SportsMed, Christchurch, New Zealand.
Clin J Sport Med. 2004 Nov;14(6):344-53. doi: 10.1097/00042752-200411000-00004.
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 parameters.
Observational cohort study.
City of Christchurch (New Zealand) Marathon, June 2002.
One hundred fifty-five of the 296 athletes entered in the 2002 City of Christchurch Marathon were enrolled in the study.
Athletes were weighed at race registration and immediately after the race. Blood was drawn postrace for measurement of serum sodium, potassium, creatinine, and urea concentrations and for hematological analysis (hemoglobin concentration, hematocrit, leukocyte distribution).
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 potassium (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).
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 hydration practices were not promoted. Consumption of NSAIDs in the 24 hours prior to distance running was associated with altered renal function.
前瞻性研究完成标准42.2公里马拉松赛跑的跑步者的血液学和生化参数。确定跑步者低钠血症的发生率，以及非甾体抗炎药（NSAIDs）的使用是否与血清生化参数的改变有关。
观察性队列研究。
2002年6月，克赖斯特彻奇市（新西兰）马拉松赛。
2002年克赖斯特彻奇市马拉松赛报名的296名运动员中有155名参加了本研究。
在比赛报名时和比赛结束后立即对运动员进行称重。赛后采集血液，测量血清钠、钾、肌酐和尿素浓度，并进行血液学分析（血红蛋白浓度、血细胞比容、白细胞分布）。
收集了134名马拉松完赛者包括赛前和赛后体重以及赛后血液学和生化分析的完整数据集。赛后血清钠浓度与体重变化直接相关（P<0.0001）。没有生化性或症状性低钠血症病例。13%的跑步者在比赛前24小时服用了NSAIDs。服用NSAIDs的跑步者血清肌酐（P=0.03）和血清钾（P=0.007）浓度的平均值显著更高。服用NSAIDs的运动员赛后血清肌酐浓度均不低于0.09 mmol/L。98%的跑步者赛后出现白细胞增多（平均白细胞计数，18.97×10⁹/L），其中主要成分是中性粒细胞计数升高（平均中性粒细胞计数，15.69×10⁹/L）。
本研究发现完成标准距离马拉松的跑步者中没有低钠血症病例。这一发现与在理想条件下（最小气候压力）进行的马拉松赛跑有关，且该马拉松赛的补给站间隔（每5公里）比北美马拉松赛（每1.6公里）更稀疏。此外，未提倡激进的补液做法。长跑前24小时服用NSAIDs与肾功能改变有关。
