A 42.2-km (26.2-mile) marathon race was initiated in the first modern Olympic Game in 1896. Since that time, marathon running has become extremely popular, even in the age group below 18 yr. On the one hand, there has been much discussion regarding potential health risks of marathon running in this age group, and, in fact, young adolescents are forbidden from participating in many marathons by rule, e.g., the Boston Marathon (5). On the other hand, for instance, many thousands of young marathoners participated in the Los Angeles Marathon, and from 1982 to 2005, nearly 300 young runners completed the Twin Cities Marathon with finishing times ranging from 2:53:00 to 6:10:00. The youngest participant in these data sets was 7 yr (27). No one required intravenous fluids or hospitalization, and no severe emergencies occurred (27). On the contrary, several hundred adult runners required urgent medical attention during or after the race for exercise-associated collapse; several runners have died as a result of cerebral and pulmonary edema caused by hyponatremia (3,16,25,31).
The first study investigating hematological and biochemical changes after marathon was done in 1903 (4) and was followed by a large number of studies (6,8,9,18,23,32,37). Significant changes in hematocrit, hemoglobin, red and white blood cell (WBC) counts (9,37), in inflammatory markers (32), and in electrolyte changes (6,8,23) were reported. Sodium concentration, especially, was intensively studied, because large changes, especially hyponatremia, might lead to severe health problems (3,16,25,31). Most of the studies, however, included adults. Only one, focusing on cardiac troponin changes, investigated adolescents who run an entire marathon (36). Others reported respective data after prolonged running in laboratory-based setting and after 21 km of running (11,12,24,35). To our knowledge, no data are available on hematological and plasma electrolyte changes in adolescent marathon runners, but such data would help to judge the risk associated with marathon running of this age group, at least from a biochemical point of view.
Therefore, the goal of this study was to investigate the effects of a whole marathon distance on hematological and electrolyte changes in a larger sample of young male and female runners competing in a standard marathon.
MATERIALS AND METHODS
After approval by the Khon Kaen University Ethics Committee for Human Research, 30 adolescent healthy males and 20 healthy females between ages 13 and 17 yr as well as their parents gave written informed consent for participation in the study. Baseline characteristics are given in Table 1. Participants had no previous marathon experience, but all were regular runners from the Khon Kaen School (Thailand). Each runner had an approximate mean training load of 40 km·wk−1, but active training years varied depending on age. Male participants had an estimated V˙O2max of 66.4 ± 3.8 mL·min−1·kg−1 and female runners 54.8 ± 6.1 mL·min−1·kg−1 derived from submaximal exercise testing and using the Astrand–Ryhming nomogram in conjunction with the Astrand age correction factor (2). They all had to undergo a routine physical examination including red and WBC counts, lung function testing, and ECG records.
All measurements were done before and after the certified Khon Kaen International Marathon. The marathon began at 4:15 a.m. on January 23, 2011. Ambient air temperatures and relative humidities during the race are shown in Table 2. The 42.2-km relatively flat course (altitude displacement, 40 m) consisted of running 10 km on asphalt and the remaining 32.2 km on concrete. Fluids were freely available at drink stations every 5 km along the way. Available fluids consisted of water and sport drinks (electrolyte drink; Sponsor, Bangkok, Thailand). We did not give specific advise how much to drink, but all participants were used to drinking regularly small amounts of water and/or electrolyte drinks during their running activities. Thus, we felt certain that they would have used all drink stations to take one or two cups (200 mL per cup) of the available fluids. All runners were advised to run at an individual pace conforming to their running ability. They were free to stop whenever they perceived overexertion. Along the course, there were 22 first-aid stations, and runners were supervised in total by 45 doctors and nurses.
Blood samples were taken in the early morning 2 d before the marathon race, immediately after the race, and 24 h after the marathon. Ten milliliters of blood was taken from the antecubital vein by a medical technologist from the Faculty of Associated Medical Science, Khon Kaen University. Specimens were immediately centrifuged to separate the plasma, and the plasma was transported on dry ice to the laboratory at Srinakarin Hospital, Faculty of Medical and Faculty of Associated Medical Science, Khon Kaen University.
Whole blood samples were analyzed on the Automate Chemistry cobas® 6000 analyzer (Roche Diagnostics, Indianapolis, IN). The instrument uses ion-selective electrodes to determine sodium, potassium, chloride, calcium, phosphorus, magnesium concentrations, and serum osmolality. Anion gap is calculated by the analyzer.
Complete blood cell counts.
A complete blood cell count was performed with the Xs-800i analyzer (Sysmex Corporation, Kobe, Japan). Red blood cell (RBC) count, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), MCH concentration (MCHC), SD of red cell distribution width, coefficient variation of red cell distribution width, hematocrit, hemoglobin, platelet count, and WBC count were determined. The WBC differential analysis consisted of the percentages of neutrophils, lymphocytes, monocytes, eosinophils, and basophils. Plasma volume changes were calculated according to Dill and Costill (10) and Gillen et al. (13).
Statistical analysis was performed using SPSS statistical software package version 19.0 (SPSS, Inc., Chicago, IL). ANOVA for repeated measures and post hoc Student’s t-tests were used to evaluate hematological and plasma electrolyte changes between baseline and postrace values (immediately and 24 h after the race). Pearson correlation analysis was applied to examine relations between subjects characteristics, measured values, and/or changes in measured values and race time. A P value of <0.05 was considered as significant. All values are expressed as means ± SD.
Fifty adolescent runners started in the 8th Khon Kaen marathon. Three participants dropped out because their shoes got broken. Thus, 47 subjects were considered for further analyses. The mean finishing time was 4 h 57 min 24 s (range: 3 h 17 min 09 s to 6 h 14 min 01 s). None of the participants experienced an adverse medical event requiring medical attention during or after the race.
Electrolyte concentrations before and after the race are shown in Table 3. Plasma concentrations of sodium, potassium, anion gap, calcium, and magnesium had decreased from before to immediately after the race. Twenty-four hours after the race, these values were still lower except for potassium, which had returned to baseline. Phosphorus and serum osmolality significantly increased from before to immediately after the race (P < 0.05). Twenty-four hours after the race, serum osmolality returned to baseline, whereas phosphorus dropped below baseline. None of the participants were hypo- or hypernatremic. Mean sodium levels were 140.1 ± 1.7 mEq·L−1 (range, 136–143 mEq·L−1) immediately after the race and 140.2 ± 1.4 mEq·L−1 (range, 137–143 mEq·L−1) 24 h after the race. Body mass decreased by 1.70 ± 0.70 kg (P < 0.001) from before to after the marathon. Weight loss for the runner with the largest decrease in sodium concentration was 1.58 kg. There were no statistically significant correlations between plasma sodium concentration and race finishing time or plasma sodium concentration and body mass changes (see Figure, Supplemental Digital Content 1, http://links.lww.com/MSS/A251, relation between body mass changes and sodium changes). A significant relation was found between changes in body mass and race finishing times (r = 0.604, P < 0.05, Fig. 1). Changes in plasma calcium and serum osmolality were related to plasma volume changes (r = −0.420, P = 0.003 and r = −0.346, P = 0.036, respectively). There were no different changes between sexes (Table 4).
Complete blood cell counts before and after the race in all participants are shown in Table 5. Twenty-three young runners finished the marathon with leukocytosis (WBC count > 11.0 × 109 L−1). There was a significant (P < 0.05) increase in the WBC count, MCHC, and neutrophils immediately after the race. Twenty-four hours after the race, the values of MCHC and neutrophils were still elevated, whereas WBC count had returned to baseline. The values for hemoglobin, hematocrit, RBC count, MCV, SD of red cell distribution, coefficient variation of red cell distribution width, lymphocytes, monocytes, eosinophils, and basophils were decreased immediately after the marathon and were still lower 24 h after the race, except for MCV, coefficient variation of red cell distribution width, and basophiles. Also, platelet count was reduced 24 h after the race when compared with premarathon. A plasma volume expansion of 11.0% ± 8.0 % and 6.2% ± 8.5% was calculated from changes in Hb and Hct immediately and 24 h after the race, respectively. RBC and platelet count changes were related to plasma volume changes (r = −0.937, P < 0.001 and r = −0.423, P = 0.003, respectively). There were no different changes between sexes (Table 4).
This study aimed at determining plasma electrolyte and hematological changes in adolescent runners completing a standard marathon. To our knowledge, these are the first data on adolescent participants including a relatively large sample size (n = 47). The main findings of the present study were 1) the only slight changes in plasma electrolytes without any cases of hyper- or hyponatremia and 2) a marked increase in WBC count.
In literature, particular attention was paid on changes in sodium concentration due to marathon running as large changes, especially hyponatremia can lead to severe health problems (3,16,25,31). After marathon running increased (6,23,28), unchanged (19,34) or decreased (3,16–18) serum sodium concentrations were reported in adult runners. Inadequate fluid intake (i.e., overdrinking or drinking too little) was suggested to be mainly responsible for the development of abnormal sodium concentrations (29). In the present investigation, slightly but significant reductions in sodium concentrations were found. The values, however, were still within the reference range indicating that the adolescent participants had an adequate fluid intake despite significant lowering of body mass and increases in plasma osmolality, which were considered as markers of dehydration (1). The fact that fluids were provided only every 5 km may likely have prevented from overdrinking. Moreover, loss of body weight during the marathon was inversely related to race finishing time as recently reported in adult runners (38). These findings underline the observation that most successful athletes are often those who lose more body weight.
In addition, slight reductions in magnesium, calcium, and potassium concentration were found. Magnesium has been shown to be released from erythrocytes into the extracellular fluids during sustained exercise and taken up from these fluids by the adipose cells (20). Sodium, calcium, magnesium, and potassium might be lost in sweating during the marathon (28,30). It has to be pointed out that the decreased hematocrit and the lowered hemoglobin values postmarathon suggest an expansion in plasma volume of approximately 11%. This is in agreement with a study of Green et al. (14) who showed that a single exercise session of approximately 5 h led to a plasma volume expansion of 6.7% ± 1.7%. It could be speculated that sodium was mobilized from the osmotically inactive sodium stores hindering larger decreases (26). Therefore, sodium levels were only slightly reduced ( <1%) and remained within the reference range. The disparity between body mass losses and increases in plasma volume might be explained by metabolic water production, substrate utilization, and depletion of the interstitial fluid of the extracellular compartment during long lasting endurance events. Furthermore, plasma volume and tonicity might be independently regulated (15).
The observation of a large increase in WBC count is in agreement to other studies on adults (19,21,33) as was the finding that leukocyte counts reverted to normal 24 h after the race (9,21). The exact mechanisms leading to the leukocytosis are still unclear. It is suggested that leucocytes might congregate along blood vessel walls outside the axial stream of blood flow and increased blood flow and cardiac output during marathon running might wash these cells from blood vessels and cause an increase in WBC count (7,37). It has been suggested that catecholamines produced during exercise increase the ratio of circulating to noncirculating leucocytes, whereas cortisol may act by a mechanism that involves a time lag elevating leucocytes in the vascular compartment (22). In addition, an inflammatory response to local tissue injury may also have contributed to the observed leukocytosis (19,37).
When interpreting present results, it should be emphasized that plasma volume was expanded. Some measurements given as concentration related to blood volume might be influenced by the increased plasma volume. Changes in RBC count, for example, were highly correlated to this changes (r = −0.937, P < 0.001).
One limitation of this study is that the participants were inexperienced with marathon running. Perhaps the findings might be different in more experienced, motivated runners, with different fluid intake volumes, or in different climatic conditions, or on a more challenging course. Another limitation is that we did not give specific advice how and what to drink during the marathon. However, the young runners seem to have done it in the right way without such information.
To our knowledge, this is the first study investigating plasma electrolyte and hematological changes after marathon running in adolescents. Data show that several values were changed immediately and also 24 h after the marathon, but changes were small and not of clinical relevance. Changes did not differ between sexes. Most importantly, there were no cases of hyper- or hyponatremia, and in such a developmentally diverse group, there were no differences in findings compared with those previously described in adult runners. Taken together, well-trained and educated adolescent marathon runners are not at risk to develop clinically significant electrolyte or hematological changes.
We thank the participants from Khon Kaen Sport School and staffs from the Faculty of Associated Medical Science, Khon Kaen University, Khon Kaen, Thailand.
The study was funded by the ASEA-UNINET grant of the Federal Ministry of Science and Research, Austria.
There is no conflict of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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