Journal of the American College of Nutrition, Vol. 17, No. 2, 124-127 (1998)
Published by the American College of Nutrition
The Effect of a Marathon Run on Plasma and Urine Mineral and Metal Concentrations
Alan L. Buchman, MD, MSPH, FACN1,
Carl Keen, PhD2,
Joel Commisso, BS2,
Donna Killip, RN3,5,
Ching-Nan Ou, PhD4,
Cheryl L. Rognerud, MS, MT4,
Kenneth Dennis, MD5,6 and
J. Kay Dunn, PhD,,,,,
Division of Gastroenterology, Hepatology and Nutrition (A.L.B.), University of Texas Houston Health Science Center, Houston
Department of Nutrition (C.K., J.C.), University of California, Davis
Division of Gastroenterology, Hepatology and Nutrition (D.K.), Baylor College of Medicine, Houston, Texas
Department of Pathology (C-N.O., C.L.R.), Baylor College of Medicine, Houston, Texas
Baylor College of Medicine; Houston, Texas (K.D., D.K.)
Section of Design and Analysis (K.D.), Baylor College of Medicine, Houston, Texas
Address reprint requests to: Alan L. Buchman, MD, MSPH, FACN, Division of Gastroenterology, Hepatology and Nutrition, 6431 Fannin, MSB 4.234, Houston, TX 77030
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ABSTRACT
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Background: Little data exist on the requirements of trace metals and minerals for endurance athletes. Changes in body status of these elements must be examined before specific nutritional recommendations can be made. This study was designed to determine whether a marathon run was associated with changes in serum and urine metal and mineral concentrations.
Methods: Forty subjects who planned to complete the 1996 Houston-Tennaco marathon were recruited. Subjects had blood and urine samples collected 2 weeks prior to the race and immediately following the race. Blood and urine specimens were analyzed for copper, iron, magnesium and zinc concentrations. Blood was also analyzed for calcium concentration and ceruloplasmin activity.
Results: Twenty-six subjects (24 male, 2 female) completed the marathon. Finish times varied between 2 hours 43 minutes and 5 hours 28 minutes. There was no significant change in serum calcium, copper or zinc concentrations or ceruloplasmin activity. Serum and urine magnesium concentration decreased significantly (19.55±1.73 to 16.55±1.53 ppm, p=0.00001; 34.02±8.64 to 21.80±12.24 ppm, p=0.003, respectively). Serum iron concentration increased significantly (1.06±0.48 to 1.35±0.42 ppm, p=0.006), while urine copper and iron concentrations were below the limits of detection, zinc concentration did not change.
Conclusions: Serum and urinary magnesium concentrations decrease during endurance running, consistant with the possibility of magnesium deficiency. This may be related to increased demand in skeletal muscle. Serum iron concentration increases, possibly related to tissue injury. The exact etiology for these observations, as well as their clinical significance, requires further investigation.
Key words: calcium, ceruloplasmin, copper, exercise, iron, magnesium, zinc
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INTRODUCTION
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Little data exist on the effect of endurance exercise, especially long-distance running, on body metal status. Previous investigation has suggested marathon running may be associated with a decline in serum magnesium [1] and zinc [2] concentrations, although it is unclear if this decline was related to ion shifts or body depletion. We sought to determine whether changes in the serum concentration of various metals occurred during a marathon run, and whether such changes would be related to increased urinary excretion of that metal.
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METHODS
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Subjects
Forty male and female volunteers who planned to run in, and complete the 1996 Houston-Tennaco Marathon were recruited via flyers distributed at various local running clubs, pre-marathon training races and direct mail. Requirements for participation in the study included aged 18 to 55 years, successful completion of at least one marathon in the previous 12 months, and agreement to refrain from nonsteroidal antiinflammatory drugs (NSAID) for 24 days prior to, and during the race,and vitamin C, E (other than prescribed for the study) or selenium supplements beginning 30 days prior to, and during the race. Potential participants were excluded if they had a history of peptic ulcer disease, abdominal pain, nausea or vomiting, hematochezia or melena, Crohn’s disease or celiac sprue, hypertension, or use of warfarin anticoagulant. All subjects signed an informed consent approved by the Baylor Affiliates Institutional Review Board.
Procedures
Subjects were part of a vitamin E/placebo study to determine the effects of vitamin E on intestinal permeability and occult bleeding. Subjects received either 1000 IU of a water-soluble form of d-alpha tocopherol (Pharmavite, Mission Hills, CA), or a similar appearing and tasting placebo (soya lecithin, 19 grains, Pharmavite) provided in a gel capsule, once daily in the morning beginning 14 days prior to the marathon. Vitamin E supplementation has no known or theoretical effects on mineral and metal homeostasis; results are reported for all subjects together because vitamin E supplementation had no effect on either serum or urine concentration on any of the metals evaluated (data not shown). Therefore, data from both vitamin E and placebo groups were pooled for analysis in this study.
Blood was obtained for analysis of calcium, copper, ceruloplasmin, iron, magnesium and zinc concentrations 2 weeks prior to the race, and immediately following the race. These were measured using techniques described by Clegg et al [3,4]. Urine was collected for 6 hours 2 weeks prior to the race, prior to morning training runs, and 10 to 15 minutes following the race with aliquots taken for creatinine, magnesium and zinc measurements. Post-race blood specimens were obtained within 10 minutes of race completion in the medical area, immediately after the finish line. Specimens were placed on ice immediately. Blood samples were centrifuged, and plasma and urine samples were frozen at -70°C until assayed. Urine creatinine was analyzed using a Vitro 950 automated chemistry analyzer (Johnson & Johnson Clinical Diagnostics, Rochester, NY).
The paired t test was used to compare biochemical data pre and post-race. All results are expressed as the mean±standard deviation (SD) except where noted. A p value of <0.05 constituted statistical significance.
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RESULTS
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Twenty-six subjects (24 males, 2 females) completed the marathon. Fourteen subjects were dropped from the study before the race because of admitted NSAID use, vitamin C or E intake (other than prescribed in the study), injuries or insufficient training mileage that would prohibit successful marathon completion. Finish times varied between 2 hours 43 minutes and 5 hours 28 minutes. There was no significant change in serum calcium, copper or zinc concentrations or ceruloplasmin activity (table). Serum magnesium concentration decreased significantly at the end of the race compared with baseline (19.55±1.73 to 16.65±1.53 ppm, p=0.00001). This observation was accompanied by a significant decrease in urinary magnesium excretion (34.02±8.64 to 21.80±12.24 ppm, p=0.003). Serum iron concentration increased significantly (1.06±0.48 to 1.35±0.42 ppm, p=0.006). Urinary zinc excretion did not change. Urinary copper and iron concentrations were below the level of detection.
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DISCUSSION
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We observed that serum magnesium concentration decreased significantly in marathon runners following their race to levels consistant with mild deficiency. Other investigators have described similar percent decreases in serum magnesium, not only during endurance running, but during other endurance activities as well including bicycle ergometry, swimming and treadmill exercise [1,5].
We expressed urinary magnesium (and zinc) concentrations as a ratio to urinary creatinine in order to correct for volume changes that might have been associated with dehydration since there was no possibility of accurately measuring oral liquid intake during the race. Because urinary magnesium losses decreased, we speculate the body attempts to conserve magnesium most likely because of increased skeletal muscle requirements. There may also be a shift of magnesium from serum into erythrocytes during a marathon, which could contribute to a decrease in serum concentration, but not magnesium depletion [6,7]. It is unlikely magnesium depletion resulted from losses in sweat. Although marathon runners may lose up to 2.8 l/hour of sweat [8], there is little magnesium in sweat as most magnesium is contained in the intracellular space. Despite a 5.8% body weight reduction from sweat, only 13 mmol of magnesium was lost in sweat [9]. Terblanche et al found skeletal muscle magnesium concentration 48 hours following a marathon was similar to pre-race concentration, although by this time post-race the decline observed in serum magnesium had been reversed and was also similar to baseline [10]. In addition, none of the runners in that study developed sub-normal serum magnesium concentration, unlike the participants in our study.
Magnesium deficiency has been associated with decreased endurance during treadmill testing in rats [11]. Maximum oxygen consumption during maximal treadmill testing in humans was also correlated with plasma magnesium concentration in trained, but not untrained individuals [6]. This suggests the possibility that magnesium deficiency could result in impaired endurance and performance. However, at least in one study, magnesium supplementation failed to enhance performance. Terblanche et al supplemented marathon runners with 1.33g Mg-L-Asp-HCL (equivalent to 122.6mg of elemental Mg) three times daily [10]. Neither the treatment group or the placebo group developed sub-normal serum magnesium concentration. This modest supplement may have been inadequate since neither serum or muscle magnesium concentration were affected. Alternatively, runners may not benefit from magnesium supplementation in the absence of depletion, or that oral magnesium supplements are largely lost in the stool, unabsorbed.
Serum calcium concentration did not change, similar to data reported following a 6 mile run by Anderson et al or after the Boston Marathon [2,5]. However, Olha et al reported a significant increase in plasma calcium concentration following another form of endurance exercise, bicycle ergometry [1]. These authors were unable to account for the variance.
We observed significantly increased serum iron concentration in marathon runners following their race. This observation has not been described previously, to our knowledge. Previous study has indicated hemoconcentration following marathon-like activity exerts only a minimal effect on measured iron concentrations [12]. Our results are contrary to those observed during weight training and in triathletes following a competition. In fact, serum iron concentration tended to decrease with a longer period of weight training [13]. A similar, but more substantial decrease was observed in triathletes following a competition [12,14]. It had been postulated that the decrease in serum iron may have occurred because of redistribution to the reticuloendothelial system (RES) as part of an acute phase response, and iron losses in sweat [12]. However, iron may be released from cells when tissues are crushed or torn [6]. We suspect that was the etiology for the increased serum iron concentration observed in our study. Subclinical hemolysis also may be a factor; this was not investigated. Why increased serum iron was not observed in weight lifters or triathletes is unclear. Increased free extracellular iron could lead to free radical-mediated tissue damage via the conversion of O2 and H2O2 into OH [15], although the magnitude of the increase in extracellular iron required is unknown.
We found no significant change in plasma copper concentration or ceruloplasmin activity, consistent with that reported by Anderson et al in subjects following a 6 mile run [2]. On the contrary, both Ohla et al and Ohno et al found serum copper concentration increased significantly following bicycle ergometry [1,16]. Ohno also observed a significant increase in serum ceruloplasmin concentration [16]. The reasons for discrepencies in the data between endurance running and bicycle ergometry are not readily apparent.
Serum zinc concentration did not change post-race in our runners, although significant decreases following a 10 mile run and 2 to 4 hours post-stair climbing have been described [2,17]. We observed no change in urinary zinc losses. It is possible increased urinary zinc losses accounted for the decreased serum zinc concentration observed in the other studies. However, the reported zinc losses appear insufficient to have caused any decline in total body zinc status, which could affect skeletal muscle performance.
We conclude that serum and urinary magnesium concentrations decrease significantly, consistant with the possibility of at least transient magnesium deficiency. Further investigation with magnesium supplements in runners is warranted. Whether or not adequate magnesium supplementation will enhance performance should be the subject of future investigation. Although we found no evidence for a decline in body zinc status, previous data cannot be discounted, and a study of zinc supplementation during endurance exercise may be warrented. Serum iron concentration increases during endurance running. The etiology for this observation, as well as its potential role in antioxidant metabolism and its clinical significance, requires further study.
Received May 1, 1997.
Accepted October 1, 1997.
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ABSTRACT
INTRODUCTION
