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Plasma Free, Phospholipid-Bound and Urinary Free Choline All Decrease During a Marathon Run and May Be Associated with Impaired Performance

Division of Gastroenterology, Hepatology and Nutrition, University of Texas Houston Health Science Center, Houston, Texas (A.L.B.)
Department of Pharmacology, UCLA Medical School, Los Angeles, California (D.J., M.R.)

Address reprint requests to: Dr. Alan L. Buchman, Division of Gastroenterology, Hepatology and Nutrition, University of Texas Houston Health Science Center, 6431 Fannin MSB 4.234, Houston, Texas

	ABSTRACT

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Background: Previous investigations have shown that plasma free choline decreases during long distance running.

Objective: This study was undertaken to determine if body choline status changes during a marathon run and whether performance is thereby adversely affected.

Design: Twenty-three accomplished marathon runners 25 to 49 years of age were studied before and after the 1997 Houston-Methodist Marathon. Fasting blood and five-hour urine samples were obtained in the morning, 14 days prior to the race, immediately after the race and approximately 48 hours after completion of the race. Runners were asked to predict their finish times two weeks prior to the race. Performance was indicated by the ratio of predicted to actual time.

Results: Both plasma free and phospholipid-bound choline concentrations as well as urinary free choline concentration decreased immediately following the race (19.2±4.5 to 14.6±4.2 nmol/mL, p=0.005, and 2565.2±516.4 to 2403.4±643.0 nmol/mL, p=0.068, respectively) and, except for the phospholipid-bound choline, rebounded towards baseline after 48 hours (15.6±3.2 and 2299.9±426.7 nmol/mL), although plasma concentrations remained significantly below baseline. Plasma free and phospholipid-bound choline concentrations were significantly correlated (r=0.46, p=0.0001), although urinary free choline concentration was not correlated with either. There was no correlation between plasma free, phospholipid-bound or urinary free choline concentration and actual finish time or the ratio of predicted to actual finish time. However, the percent decrease in urinary free choline concentration was significantly correlated with the ratio of predicted to actual time (r=0.47, p=0.036). No relationship was seen between this ratio and the percent decrease in either plasma free or phospholipid-bound choline concentrations immediately after the race.

Conclusion: Our finding of both decreased free and phospholipid-bound choline suggests the decrease in choline status is related to accelerated choline metabolism or enhanced choline uptake by tissues rather than decreased hepatic choline release. The role of choline supplementation during endurance running requires further investigation.

Key words: choline, marathon

	INTRODUCTION

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Choline is a quaternary amine that is the precursor of acetylcholine, which is involved in neural transmission and skeletal muscle innervation [1]. Previous investigations have shown that plasma free choline decreases during long distance running [2,3]. This study was undertaken to determine if body choline status changes during a marathon run and whether performance is thereby adversely affected.

	MATERIALS AND METHODS

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Twenty-three male and female runners, 25 to 49 years of age, who had successfully completed at least one marathon within the 12 months preceding the 1997 Houston-Methodist Marathon were recruited from local running clubs, through newsletters and newspaper announcements. Fasting blood and five-hour urine samples were obtained in the morning, 14 days prior to the race, immediately after the race and approximately 48 hours after completion of the race. Blood samples were immediately placed on ice and centrifuged at 2000g for 10 minutes. Plasma was decanted and frozen at -70°C until analysis. Urine containers were kept refrigerated during collection and were frozen at -70°C within one hour of completion of collection. Plasma and urinary free choline were measured by gas chromatography and mass spectrophotometry [4,5]. Plasma phospholipid-bound choline was determined following extraction as described by Folch et al. [6] and hydrolysis as described by Jope and Jenden [7]. Runners were asked to predict their finish times two weeks prior to the race. Performance was indicated by the ratio of predicted to actual time. All subjects signed an informed consent approved by the Baylor Affiliates Institutional Review Board.

Continuous variables are reported as mean±standard deviation (SD). Concentrations at the study time points were compared using the Wilcoxan Signed Rank Test. Pearson correlation coefficients were obtained. A p value of 0.05 constituted statistical significance.

	RESULTS

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All runners completed the race. Finish times were 2.6 to 5.8 hours. Plasma and urinary choline concentrations are found in Table 1. Both plasma free and phospholipid-bound choline concentrations, as well as urinary free choline concentration, decreased immediately following the race (p=0.005, 0.068, 0.042 for plasma free, phospholipid-bound and urinary free choline, respectively) and, except for the phospholipid-bound choline which continued to decrease, rebounded towards baseline after 48 hours, although plasma concentrations remained significantly below baseline. Plasma free and phospholipid-bound choline concentrations were significantly correlated (r=0.46, p=0.0001), although urinary free choline concentration was not correlated with either. There was no correlation between plasma free, phospholipid-bound or urinary free choline concentration and actual finish time or the ratio of predicted to actual finish time. However, the percent of decrease in urinary free choline concentration was significantly correlated with the ratio of predicted to actual time (r=0.47, p=0.036). No relationship was seen between this ratio and the percent of decrease in either plasma free or phospholipid-bound choline concentrations immediately after the race.

	DISCUSSION

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We have extended both reports. Phospholipid-bound choline concentrations have not previously been reported on in marathon runners. Our finding of a significant decrease in both free and phospholipid-bound choline suggests the decrease in choline status is related accelerated choline metabolism or enhanced choline uptake by tissues, rather than decreased hepatic choline release. This assessment is consistent with previous investigation in the guinea pig [9]. Our conclusion is further supported by the decreased urinary choline excretion which indicates body conservation of choline. The 24% decrease in plasma free choline concentration immediately following the race was significantly greater than has been previously reported [2,10]. This may be related to the more prolonged running time of our participants. The further decline in plasma phospholipid-bound choline two days after the race may be related to requirements during cell growth and repair, since phospholipid-bound choline is a constituent of cell membranes, although the concentration remained what is considered normal for non-runners [11]. It appears plasma free choline concentration may be partially restored via metabolism of phospholipid-bound choline as well.

The lack of an association between urinary and plasma choline is consistent with the fact that very little choline excretion relative to an ingested dose of choline occurs [12]. However, the decrease in urinary choline excretion reflects the renal tubular choline homeostasic mechanism described by Acara and Rennick whereby most choline filtered by glomeruli is reabsorbed when plasma choline concentration decreases in order to conserve choline [13,14]. Our data suggest choline depletion may occur during the 26-mile marathon run. We cannot explain why the plasma free choline concentration was significantly greater in our runners than that described previously or in normal healthy volunteers in our laboratory (11.4±3.7 nmol/mL), although the phospholipid-bound choline concentration was normal. The reservoir of phospholipid-bound choline is considerable, although there is some variation from subject to subject. This may account for the fact that the plasma concentration remained in the normal range despite a significant decline. No subject took choline or lecithin supplements. It is also unlikely that dietary intake played a role since most long distance runners are significant carbohydrate consumers and choline is found in greatest concentration in eggs, liver and other organ meats. Studies have not shown intake of these foods to be increased in marathon runners [15].

The runners studied in our investigation, while not elite, were all accomplished marathoners. Each had run many previous marathons and could accurately predict his or her finish time. Therefore, we assumed that any improvement or decrement in performance over that predicted by the runners themselves would indicate a possible treatment effect. Our observation, that those runners who had the least choline losses also had the best finish time relative to what they had predicted, was consistent with a role for choline in performance.

It is known that choline is the precursor for the neurotransmitter acetylcholine. Decreased choline and the resultant decrease in acetylcholine [16] have been associated with delayed transmission of muscle contraction impulses [8]. This could represent a mechanism by which choline deficiency could adversely affect performance. Although we failed to find a correlation between the decrease in either plasma free or phospholipid-bound choline and performance, the association between the percent decrease in urinary choline excretion and performance suggests a possible role for choline depletion in poorer than expected performance. That association suggests the possibility of a role for choline supplementation in long distance runners. Von Allworden et al. found that 90% pure lecithin (approximately 12% choline), when supplemented to adolescents at a dose of 0.2 g/kg body weight one hour prior to a 30 to 60 minute cross country run, maintained plasma free choline concentration at baseline level, while runners who received a placebo experienced a mean 17% decrease (p<0.01) [10]. Performance data was not reported. Sandage et al. reported the preliminary results of choline citrate supplementation in ten long distance runners [3]. These investigators found that a small choline supplement (2.8 g of choline citrate) ingested one hour before the run was associated with faster finish time than was a placebo, although finish times were not reported. In addition, this supplement reportedly maintained plasma free choline concentrations, although data was not reported. The role of choline supplementation in long distance runners requires further investigation.

	ACKNOWLEDGMENTS

 
The authors wish to thank Healix Home Care (Houston, TX) for their help in providing phlebotomists and supplies for the study, as well as the phlebotomists themselves (Ms. Verbest Brown and Phlebotomy Services).

Received May 1, 1999. Accepted September 1, 1999.

	REFERENCES

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