Med Sci Sports Exerc. 1990 Apr;22(2):165-70.
The incidence of hyponatremia during prolonged ultraendurance exercise.
Noakes TD, Norman RJ, Buck RH, Godlonton J, Stevenson K, Pittaway D.
Department of Physiology, University of Cape Town Medical School, South Africa.

Recent studies have shown that potentially fatal hyponatremia can develop during prolonged exercise. To determine the incidence of hyponatremia in athletes competing in ultradistance events, we measured serum sodium levels in 315 of 626 (50%) runners who were treated for collapse after two 90 km ultramarathon footraces (total starters 20,335; total finishers 18,031) and in 101 of 147 (69%) finishers in a 186 km ultratriathlon. In both races the athletes drank fluids with low sodium chloride content (less than 6.8 mmol.l-1). Hyponatremia (serum sodium level less than 130 mmol.l-1) was identified in 27 of 315 (9%) collapsed runners in the 90 km races and in none of the triathletes. In response to diuretic therapy, the runner with the most severe hyponatremia (serum sodium level = 112 mmol.l-1) excreted in excess of 7.5 l dilute urine during the first 17 h of hospitalization. These data suggest that, although symptomatic hyponatremia occurs in less than 0.3% of competitors during prolonged exercise even when they ingest little sodium chloride, it is found in a significant proportion (9%) of collapsed runners. A regulated contraction of the extracellular fluid volume would explain why the majority of athletes maintain normal serum sodium levels even though they develop a significant sodium chloride deficit during prolonged exercise. Alternatively, sodium chloride losses during prolonged exercise may be substantially less than are currently believed. Physicians treating collapsed ultradistance athletes need to be aware that as many as 10% or more of such patients may be hyponatremic.

J Hum Hypertens. 2005 Dec;19 Suppl 3:S10-9.

Why and how to implement sodium, potassium, calcium, and magnesium changes in food items and diets?
Karppanen H, Karppanen P, Mervaala E.
Institute of Biomedicine, Pharmacology, University of Helsinki, Helsinki, Finland.

The present average sodium intakes, approximately 3000-4500 mg/day in various industrialized populations, are very high, that is, 2-3-fold in comparison with the current Dietary Reference Intake (DRI) of 1500 mg. The sodium intakes markedly exceed even the level of 2500 mg, which has been recently given as the maximum level of daily intake that is likely to pose no risk of adverse effects on blood pressure or otherwise. By contrast, the present average potassium, calcium, and magnesium intakes are remarkably lower than the recommended intake levels (DRI). In USA, for example, the average intake of these mineral nutrients is only 35-50% of the recommended intakes. There is convincing evidence, which indicates that this imbalance, that is, the high intake of sodium on one hand and the low intakes of potassium, calcium, and magnesium on the other hand, produce and maintain elevated blood pressure in a big proportion of the population. Decreased intakes of sodium alone, and increased intakes of potassium, calcium, and magnesium each alone decrease elevated blood pressure. A combination of all these factors, that is, decrease of sodium, and increase of potassium, calcium, and magnesium intakes, which are characteristic of the so-called Dietary Approaches to Stop Hypertension diets, has an excellent blood pressure lowering effect. For the prevention and basic treatment of elevated blood pressure, various methods to decrease the intake of sodium and to increase the intakes of potassium, calcium, and magnesium should be comprehensively applied in the communities. The so-called 'functional food/nutraceutical/food-ceutical' approach, which corrects the mineral nutrient composition of extensively used processed foods, is likely to be particularly effective in producing immediate beneficial effects. The European Union and various governments should promote the availability and use of such healthier food compositions by tax reductions and other policies, which make the healthier choices cheaper than the conventional ones. They should also introduce and promote the use of tempting nutrition and health claims on the packages of healthier food choices, which have an increased content of potassium, calcium, and/or magnesium and a lowered content of sodium. Such pricing and claim methods would help the consumers to choose healthier food alternatives, and make composition improvements tempting also for the food industry.

The consequences of low electrolytes can sometimes be severe:
    
Ann Intern Med. 2000 May 2;132(9):711-4.
Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners.
Ayus JC, Varon J, Arieff AI.
Baylor College of Medicine, Houston, Texas 77024, USA.

BACKGROUND: Non-cardiogenic pulmonary edema is often associated with increased intracranial pressure and can be the initial manifestation of hyponatremic encephalopathy. Marathon runners tend to develop conditions that lead to hyponatremia. OBJECTIVE: To describe the development and treatment of noncardiogenic pulmonary edema in marathon runners that was associated with hyponatremic encephalopathy. DESIGN: Case series. SETTING: One university hospital and two community hospitals. PATIENTS: Seven healthy marathon runners who had a history of nonsteroidal anti-inflammatory drug use. The runners collapsed after competing in a marathon and were hospitalized with pulmonary edema. MEASUREMENTS: Plasma sodium levels, chest radiograph, electrocardiogram, cardiac enzyme levels, and magnetic resonance imaging or computed tomographic scans of the brain. RESULTS: Patients had nausea, emesis, and obtundation. The mean (+/-SD) plasma sodium level was 121 +/- 3 mmol/L, and oxygen saturation was less than 70%. Electrocardiograms and echocardiograms were normal. Chest radiographs showed pulmonary edema with a normal heart. Creatine phosphokinase-MB bands, troponin levels, and pulmonary wedge pressure were not elevated. Scanning of the brain showed cerebral edema. All patients were intubated and mechanically ventilated. Treatment with intravenous NaCl, 514 mmol/L, increased plasma sodium levels by 10 mmol/L in 12 hours. Pulmonary and cerebral edema resolved as the sodium level increased. One patient had unsuspected hyponatremic encephalopathy and died of cardiopulmonary arrest caused by brainstem herniation. All six treated patients recovered and were well after 1 year of follow-up. CONCLUSIONS: In healthy marathon runners, noncardiogenic pulmonary edema can be associated with hyponatremic encephalopathy. The condition may be fatal if undiagnosed and can be successfully treated with hypertonic NaCl.

Arch Pathol Lab Med. 2005 Feb;129(2):227-30.

Sodium status of collapsed marathon runners.
Kratz A, Siegel AJ, Verbalis JG, Adner MM, Shirey T, Lee-Lewandrowski E, Lewandrowski KB.
Division of Laboratory Medicine, Department of Pathology, Massachusetts General Hospital, Boston, MA 02114, USA.

CONTEXT: Recommendations for prevention and treatment of medical emergencies in participants in marathon races center on maintenance of adequate hydration status and administration of fluids. Recently, new recommendations for fluid replacement for marathon runners were promulgated by medical and athletic societies. These new guidelines encourage runners to drink ad libitum between 400 and 800 mL/h as opposed to the previous "as much as possible" advice. OBJECTIVE: To assess the sodium and hydration (plasma osmolality) status of collapsed marathon runners after the promulgation of new hydration guidelines. DESIGN: Plasma sodium and osmolality values of runners who presented to the medical tent at the finish line of the 2003 Boston Marathon were measured. RESULTS: Using reference ranges derived from the general population, of 140 collapsed runners, 35 (25%) were hypernatremic (sodium, >146 mEq/L) and 6 (12%) were hyperosmolar (osmolality, >296 mOsm/kg H(2)O), whereas 9 (6%) were hyponatremic (sodium, <135 mEq/L) and 8 (16%) were hypo-osmolar (osmolality, <280 mOsm/kg H(2)O). Compared with a population of marathon runners who had experienced no medical difficulties, 9% of the runners were hypernatremic, 5% were hyponatremic, 8% were hypo-osmolar, and none were hyperosmolar. CONCLUSIONS: Our findings indicate a significant incidence of hypernatremia with hyperosmolality and hyponatremia with hypo-osmolality among collapsed runners despite the new fluid intake recommendations, suggesting that either further educational measures are required or that the new guidelines are not entirely adequate to prevent abnormalities in fluid balance. Furthermore, the immediate medical management of hypernatremia and hyponatremia is different. Administration of fluids to severely hyponatremic patients may result in fatal cerebral edema. Our findings caution against institution of treatment until laboratory tests determine the patient's sodium status.

South Med J. 2005 Dec;98(12):1212-5.
Unusual cause of hypokalemic paralysis in aged men: Sjogren syndrome.
Cheng CJ, Chiu JS, Chen CC, Lin SH.
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.

Hypokalemic paralysis is a less recognized but reversible disorder in elderly patients. This report describes two elderly Chinese males (age 74 and 78 years) who had progressive muscle weakness and eventually paralysis. Physical examination showed symmetrical flaccid paralysis of extremities. Both had the major biochemical abnormality of profound hypokalemia (1.4 and 1.8 mmol/L) accompanied by high urine K+ excretion and hyperchloremic metabolic acidosis. A positive urine anion gap and alkaline urine pointed to the diagnosis of distal renal tubular acidosis. Large doses of potassium chloride supplementation were required to restore muscle strength. Pertinent investigations, including elevated titers of antinuclear antibody and rheumatoid factor, positive anti-Ro antibody, low serum C3 and C4 levels, and delayed saliva excretion on salivary scintigraphy suggested Sjogren syndrome. Despite the lack of sicca syndrome at the initial presentation, both had development of typical sicca syndrome and positive Schirmer test at the 5-month and 1-year follow-up, respectively. Potassium citrate supplement and prednisolone therapy completely corrected the hypokalemia and metabolic acidosis. Extraglandular involvement with distal renal tubular acidosis preceding the typical sicca syndrome may induce hypokalemic paralysis and unveil Sjogren syndrome in elderly males.

Hypertension. 2004 Dec;44(6):969-73.

Potassium chloride supplementation diminishes platelet reactivity in humans.
Kimura M, Lu X, Skurnick J, Awad G, Bogden J, Kemp F, Aviv A.
Hypertension Research Center, Cardiovascular Research Institute, University of Medicine and Dentistry of New Jersey, Newark 07103, USA.

The prevalence of occlusive stroke is inversely correlated with potassium intake. We explored the hypothesis that a high potassium intake attenuates platelet reactivity, as expressed in ADP-evoked platelet aggregation. We studied healthy men (n=31) and women (n=42), blacks (n=33) and whites (n=40). In this cohort, we supplemented the habitual intake of 17 men and 21 women with 60 mmol KCl/70 kg body weight per day for 3 days and maintained 14 men and 21 women on their habitual intake. We then compared the change in ADP concentration causing 50% of the maximal initial rate (EC50) of platelet aggregation in the potassium-supplemented versus control groups. Potassium supplementation attenuated platelet reactivity, expressed by an increase in EC50 of platelet aggregation (P=0.0005), which was primarily attributable to an increase in EC50 in whites (P=0.0004). Urinary potassium excretion was significantly lower in blacks than in whites under basal conditions and after potassium supplementation. We conclude that potassium supplementation diminishes platelet reactivity, a phenomenon that provides a link between platelet biology and occlusive stroke.

Med Sci Sports Exerc. 2000 Sep;32(9):1549-55.

A 12-yr profile of medical injury and illness for the Twin Cities Marathon.
Roberts WO.
MinnHealth SportsCare, White Bear Lake, MN 55110, USA.

OBJECTIVE: To summarize the medical encounters (injury/illness) for runners and the meteorologic data collected in the medical area of a large marathon race. DESIGN: Prospectively transcribed medical records were analyzed for encounter rate, injury/illness type, treatment rendered, and outcomes. The environmental conditions for each race day are compared with injury/illness rates and types. SETTING: An urban 42-km marathon located at 44 degrees 53' N latitude and 93 degrees 13' W longitude, scheduled on the first Sunday of October with an early morning start time. PARTICIPANTS: 81,277 entrants in the Twin Cities Marathon from 1982 to 1994. MAIN RESULTS: The start temperature range was -4 to 16 degrees C and the 4-h temperature range was 5-20 degrees C. The average dew point was 3 degrees C at the start and 4 degrees C at 4 h. The finish area medical encounter rates for marathon runners were 18.9 per 1000 entrants and 25.3 per 1000 finishers. Mild injury/illness accounted for 90% of finish line medical encounters. Runners presented with exercise-associated collapse (59%), skin problems (21%), musculoskeletal problems (17%), and other medical problems (3%). Only 112 runners received intravenous fluids and 30 runners were transferred to emergency medical facilities. One death occurred in 1989. CONCLUSIONS: Marathon racing in cool conditions is a safe activity and most of the medical encounters are of minor severity. An early morning start time contributes to a cool racing environment and a low injury rate. More than 99.9% of runners who finish this race leave the finish area without hospital or emergency room care. The injury/illness profile can be used to tailor medical care at the finish area of marathons.
 

Med Sci Sports Exerc. 2002 Feb;34(2):185-9.

Hyponatremia in runners requiring on-site medical treatment at a single marathon.
Hsieh M, Roth R, Davis DL, Larrabee H, Callaway CW.
Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

STUDY OBJECTIVE: Literature reports indicate an increasing number of cases of hyponatremia in athletes participating in moderate endurance events such as standard marathons. In this study, we evaluated the incidence of hyponatremia in marathon finishers requiring medical treatment on-site and attempted to assess the contribution of fluid type ingested and nonsteroidal antiinflammatory drug (NSAID) use to the development of hyponatremia. METHODS: We examined a prospective, convenience sample of runners requiring intravenous hydration at the final medical tent of a standard marathon course and a comparison group of finishers who did not require intravenous hydration. After giving informed consent, subjects had blood drawn and answered a questionnaire regarding fluid intake on the course and NSAID use before the race. Blood samples were analyzed on-site for serum sodium values as well as other hematologic parameters. RESULTS: Fifty-one subjects requiring intravenous hydration as well as 11 subjects who did not were enrolled. Three subjects (5.6%; 95% CI, 0-11.9%; missing = 8) in the intravenous hydration group had serum sodium less than 130 mEq/L. None of the three runners suffered neurologic or pulmonary consequences and only one required overnight hospital admission for hydration. The small number of hyponatremic subjects precluded the analysis of the role of fluid type or NSAID use in the development of hyponatremia or the development of a model for prediction. CONCLUSION: This study found a 5.6% incidence of hyponatremia in marathon runners requiring medical treatment.

N Engl J Med. 2005 Apr 14;352(15):1550-6.
Hyponatremia among runners in the Boston Marathon.
Almond CS, Shin AY, Fortescue EB, Mannix RC, Wypij D, Binstadt BA, Duncan CN, Olson DP, Salerno AE, Newburger JW, Greenes DS.
Department of Medicine, Children's Hospital, Boston, MA 02115, USA.

BACKGROUND: Hyponatremia has emerged as an important cause of race-related death and life-threatening illness among marathon runners. We studied a cohort of marathon runners to estimate the incidence of hyponatremia and to identify the principal risk factors. METHODS: Participants in the 2002 Boston Marathon were recruited one or two days before the race. Subjects completed a survey describing demographic information and training history. After the race, runners provided a blood sample and completed a questionnaire detailing their fluid consumption and urine output during the race. Prerace and postrace weights were recorded. Multivariate regression analyses were performed to identify risk factors associated with hyponatremia. RESULTS: Of 766 runners enrolled, 488 runners (64 percent) provided a usable blood sample at the finish line. Thirteen percent had hyponatremia (a serum sodium concentration of 135 mmol per liter or less); 0.6 percent had critical hyponatremia (120 mmol per liter or less). On univariate analyses, hyponatremia was associated with substantial weight gain, consumption of more than 3 liters of fluids during the race, consumption of fluids every mile, a racing time of >4:00 hours, female sex, and low body-mass index. On multivariate analysis, hyponatremia was associated with weight gain (odds ratio, 4.2; 95 percent confidence interval, 2.2 to 8.2), a racing time of >4:00 hours (odds ratio for the comparison with a time of <3:30 hours, 7.4; 95 percent confidence interval, 2.9 to 23.1), and body-mass-index extremes. CONCLUSIONS: Hyponatremia occurs in a substantial fraction of nonelite marathon runners and can be severe. Considerable weight gain while running, a long racing time, and body-mass-index extremes were associated with hyponatremia, whereas female sex, composition of fluids ingested, and use of nonsteroidal antiinflammatory drugs were not.

J Am Coll Nutr. 2002 Dec;21(6):553-9.

Food intake and electrolyte status of ultramarathoners competing in extreme heat.
Glace BW, Murphy CA, McHugh MP.
Nicholas Institute of Sports Medicine and Athletic Trauma, New York, New York 10021, USA.

OBJECTIVE: To relate changes in laboratory indices to dietary intake during extremely prolonged running and to determine if dietary intake influences the ability of runners to finish an 160 km trail race. METHODS: We monitored intake and serum chemistries of 26 runners competing in an 160 km foot race in temperatures which peaked at 38 degrees C. Blood was drawn pre-, mid- and post-race. Dietary intake and incidence of gastrointestinal distress or changes in mental status were determined by interview with runners approximately every 13 km. Twenty-three runners completed at least 88 kms and, of these 23 runners, 13 finished 160 km in a mean time of 26.2 +/- 3.6 hours. RESULTS: Finishers ingested nearly 30,000 J, 19.4 +/- 8.1 L of fluid and 16.4 +/- 9.5 g of sodium (Na). Sodium and fluid intake per hour was estimated to be 0.6 g/hour and 0.7 L/hour, respectively. Electrolyte intake during the first half of the race was similar between those that finished the race and those that did not. Finishers ingested fluid at a greater rate than non-finishers (p = 0.01) and tended to meet their caloric needs more closely than did non-finishers (p = 0.09). Body weight was unchanged over time (ANOVA, p = 0.52). Serum Na concentration tended to fall from 143 to 140 mEq/L during the race (p = 0.06), and was inversely correlated with weight loss (p = 0.009). Serum Na concentration was lower mid-race in runners experiencing changes in mental status than in runners without changes (p = 0.04). Fluid intake was inversely correlated with serum Na concentrations (p = 0.04). Most of the runners experienced nausea or vomiting; these symptoms were not related to serum sodium concentration. Hyponatremia (<135 mEq/L) was seen in one runner at 88 kms, but resolved by 160 km. Urinary sodium excretion decreased (p = 0.002) as serum aldosterone concentration increased pre- to post-race (p < 0.001). From start to finish of the race plasma volume increased by 12%. CONCLUSIONS: Food and fluid was ingested at a greater rate than described previously. Runners consumed adequate fluid to maintain body weight although dietary sodium fell far short of the recommended 1 g/hour. The rate of fluid intake was greater in finishers than in non-finishers, and finishers tended to more nearly meet their energy needs. Maintenance of body mass despite large exercise energy expenditures in extreme heat is consistent with fluid overload during a running event lasting more than 24 hours in hot and humid conditions.

Clin J Sport Med. 2005 May;15(3):148-53.
Women hydrate more than men during a marathon race: hyponatremia in the Houston marathon: a report on 60 cases.
Hew TD.
MRC/UCT Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town Sport Science Institute of South Africa, Newlands, South Africa.

OBJECTIVE: To examine the relationship between gender and the development of hyponatremia in marathon runners. DESIGN: A retrospective analysis of prerace and postrace data collected on 117 runners completing the Houston Marathon from 2000 to 2003. SETTING: The Houston Marathon. PARTICIPANTS: A total of 117 marathon runners (63 male and 54 female) who consented to participate in hyponatremia research. MAIN OUTCOME MEASURES: Prerace and postrace body weight and serum sodium ([Na+]) concentrations were measured. Total fluid intake was self-reported immediately following the race. RESULTS:: Of the runners tested, 28% developed hyponatremia ([Na+] < or = 135 mmol/L). Hyponatremic runners (n = 33) drank significantly more fluid (31.70 versus 18.90 cups; P < 0.001), lost the least weight (-0.14 versus -1.61 kg; P < 0.001), and dropped serum [Na+] levels further (-7.48 versus -1.92; P < 0.001) compared with nonhyponatremic runners. Female runners (n = 54) were significantly lighter (62.46 versus 80.73 kg; P < 0.001), ran slower (303.02 versus 269.06 minutes; P < 0.001), lost the least weight (-0.62 versus -1.68 kg; P < 0.001), dropped serum [Na+] levels further (-4.44 versus -2.67; P < 0.01), and had lower post-race serum [Na+] values (136.87 versus 138.50; P < 0.01) compared with male runners while consuming the same total amount of fluid during the race (22.87 versus 22.30 cups; P = 0.83, NS). There were significant inverse relationships between serum [Na+] change versus body weight change (r = -0.65; P < 0.001) and between post-race [Na+] versus body weight change (r = -0.60; P < 0.001), with significant sex differences noted only between nonhyponatremic female and male runners (-0.91 versus -0.2.05 kg; P < 0.001) and between hyponatremic and nonhyponatremic male runners (-0.11 versus -2.05 kg; P < 0.001). CONCLUSIONS: Female marathon runners drink more fluid than male runners in proportion to body size. A loss of 3 kg body weight corresponds to a 0 change in serum [Na+] from prerace to postrace, suggesting that a loss of 3 kg during a marathon represents euhydration and not dehydration. All cases of hyponatremia reported in this study are a result of overhydration based on this convention.

Clin J Sport Med. 2003 Jan;13(1):41-7.
The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners.
Hew TD, Chorley JN, Cianca JC, Divine JG.
 
OBJECTIVE: To report on the incidence, identify the risk factors, and clarify the clinical manifestations of acute hyponatremia in marathon runners. DESIGN: An observational and retrospective case-controlled series. SETTING: The medical care area of the 2000 Houston Marathon. PATIENTS: Marathon finishers treated in medical area receiving intravenous fluids (N=55), including a more detailed analysis of 39 runners completing a retrospective questionnaire. MAIN OUTCOME MEASURES: Vital signs, serum electrolytes, and finish time were analyzed via ANOVA studies between all non-hyponatremic (NH: N=34)) and hyponatremic (H: N=21)) runners. Fluid intake, training variables, NSAID use, and Symptomatology were further analyzed to delineate all significant differences between groups. RESULTS: There were no significant differences in vital signs, training variables, or NSAID use between H and NH groups, although there was a trend towards the less experienced runners presenting with lower post-race sodium levels. H runners had lower potassium [K] (p=.04), chloride [Cl] (p<.001), and blood urea nitrogen [BUN] (p=.004) levels than NH runners. There was a significant inverse linear relationship between both finish time versus [Na] (r2 =.51) and total amount of fluid ingested versus [Na] (r2 =.39). The total cups of water (p=.004), electrolyte/carbohydrate solution (p=.005) and total amount of fluid ingested (p<.001) were significantly higher in H compared to NH runners and the degree of hyponatremia was related in a dose dependent manner. Vomiting was observed more frequently in H than NH runners (p=.03). CONCLUSION: 21 runners presented to the medical area of the Houston Marathon with hyponatremia (.31% of entrants). Excessive fluid consumption and longer finishing times were the primary risk factors for developing this condition. Vomiting was the only clinical sign differentiating hyponatremia from other conditions that induce exercise-associated collapse.

Med Sci Sports Exerc. 1999 Oct;31(10):1406-13.

Plasma-electrolytes in natives to hypoxia after marathon races at different altitudes.
Schmidt W, Rojas J, Boning D, Bernal H, Garcia S, Garcia O.
Department of Sports Medicine and Sports Physiology, Universitat Bayreuth, Germany.

PURPOSE: It is well known that altitude natives differ from sea level natives in aspects of fluid and electrolyte homeostasis. METHODS: To evaluate exercise and environmental influences on the electrolyte and water status in hypoxia adapted subjects, we investigated 11 well-trained marathon runners (33.7 +/- 0.7 yr, 60.5 +/- 1.9 kg), native to an altitude above 2600 m, before and after two marathon races. One competition was held at moderate altitude (AM, 2650 m, 14 degrees C, 55% RH, running time 3 h 6 min +/- 22 min) and another under tropical conditions (HM, 470 m, 28 degrees C, 70% RH, running time 2 h 54 min +/- 30 min). Blood samples were taken 3 d before, immediately after, 1 h after, and 24 h after the races. RESULTS: The loss in body fluid was calculated to be 2.15 L during AM and 5.05 L during HM, respectively. It was compensated mostly by ingested fluids without electrolyte content and by metabolically produced water, which led to hyponatremia during AM (plasma [Na+] from 144.3 +/- 0.7 to 131.7 +/- 2.1 mmol x L(-1)). Severe dehydration without significant changes in plasma [Na+] could be detected after HM. Serum antidiuretic hormone concentrations and serum aldosterone concentrations significantly increased during both races and remained at a high level for at least 1h after both competitions. Serum atrial natriuretic peptide (ANP) concentrations were at a high level at rest, increasing during HM, and decreasing during AM. CONCLUSION: Under tropical conditions, we found a severe state of dehydration characterized by an extended ANP-response, which was not prevented by water intake during the race. Under hypoxic conditions, however, we found that hyponatremia had developed. This can be partly explained by pure water intake and metabolically produced water, and also, possibly, by a special hypoxia-induced effect.

Med Sci Sports Exerc. 2005 May;37(5):759-67.

Effects of induced metabolic alkalosis on prolonged intermittent-sprint performance.
Bishop D, Claudius B.
Team Sport Research Group, School of Human Movement and Exercise Science, The University of Western Australia, Crawley, WA, Australia.

PURPOSE: Previous studies have shown that induced metabolic alkalosis, via sodium bicarbonate (NaHCO3) ingestion, can improve short-term, repeated-sprint ability. The purpose of this study was to assess the effects of NaHCO3 ingestion on a prolonged, intermittent-sprint test (IST). METHODS: Seven female team-sport athletes (mean +/- SD: age = 19 +/- 1 yr, VO2peak = 45.3 +/- 3.1 mL x kg(-1) x min(-1)) volunteered for the study, which had received ethics clearance. The athletes ingested two doses of either 0.2 g x kg(-1) of NaHCO3 or 0.138 g x kg(-1) of NaCl (placebo), in a double-blind, random, counterbalanced order, 90 and 20 min before performing the IST on a cycle ergometer (two 36-min "halves" of repeated approximately 2-min blocks: all-out 4-s sprint, 100 s of active recovery at 35% VO2peak, and 20 s of rest). Capillary blood samples were drawn from the ear lobe before ingestion, and before, during, and after each half of the IST. VO2 was also recorded at regular intervals throughout the IST. RESULTS: Resting plasma bicarbonate concentration ([HCO3-]) averaged 22.6 +/- 0.9 mmol x L(-1), and at 90 min post-ingestion was 21.4 +/- 1.5 and 28.9 +/- 2.8 mmol x L-1 for the placebo and NaHCO3 conditions, respectively (P < 0.05). Plasma [HCO3-] during the NaHCO3 condition remained significantly higher throughout the IST compared with both placebo and pre-ingestion. There was a trend toward improved total work in the second (P = 0.08), but not first, half of the IST after the ingestion of NaHCO3. Furthermore, subjects completed significantly more work in 7 of 18 second-half, 4-s sprints after NaHCO3 ingestion. CONCLUSIONS: The results of this study suggest that NaHCO3 ingestion can improve intermittent-sprint performance and may be a useful supplement for team-sport athletes.

Nutrition. 2004 Jul-Aug;20(7-8):651-6.

Fluids and hydration in prolonged endurance performance.
Von Duvillard SP, Braun WA, Markofski M, Beneke R, Leithauser R.
Human Performance Laboratory, Department of Health, Kinesiology and Sports Studies, Texas A and M University--Commerce, Commerce, Texas 75429, USA.

 
Numerous studies have confirmed that performance can be impaired when athletes are dehydrated. Endurance athletes should drink beverages containing carbohydrate and electrolyte during and after training or competition. Carbohydrates (sugars) favor consumption and Na(+) favors retention of water. Drinking during competition is desirable compared with fluid ingestion after or before training or competition only. Athletes seldom replace fluids fully due to sweat loss. Proper hydration during training or competition will enhance performance, avoid ensuing thermal stress, maintain plasma volume, delay fatigue, and prevent injuries associated with dehydration and sweat loss. In contrast, hyperhydration or overdrinking before, during, and after endurance events may cause Na(+) depletion and may lead to hyponatremia. It is imperative that endurance athletes replace sweat loss via fluid intake containing about 4% to 8% of carbohydrate solution and electrolytes during training or competition. It is recommended that athletes drink about 500 mL of fluid solution 1 to 2 h before an event and continue to consume cool or cold drinks in regular intervals to replace fluid loss due to sweat. For intense prolonged exercise lasting longer than 1 h, athletes should consume between 30 and 60 g/h and drink between 600 and 1200 mL/h of a solution containing carbohydrate and Na(+) (0.5 to 0.7 g/L of fluid). Maintaining proper hydration before, during, and after training and competition will help reduce fluid loss, maintain performance, lower submaximal exercise heart rate, maintain plasma volume, and reduce heat stress, heat exhaustion, and possibly heat stroke.

Harefuah. 2004 May;143(5):342-7, 391.
[Exercise induced hyponatremia]      [Article in Hebrew]
Hadad E, Rosen E, Heled Y, Moran DS, Schindel Y.
Heller Institute of Medical Research, Chaim Sheba Medical Center, Tel Hashomer, Israel.

A normal water-electrolyte balance is essential for normal function of body systems during physical activity. During recent years, awareness of the importance of drinking amongst athletes and Israeli Defense Force (IDF) soldiers, in particular, has been highlighted. A large number of athletes tend to drink prior to, during and after their exercise in order to enhance physical abilities and to prevent heat casualties and dehydration. However, excessive water consumption combined with sweat induced electrolytes loss during physical activity, may cause hyponatremia in extreme cases. Recently, several cases of exercise induced hyponatremia were reported in the IDF, resulting from improper water consumption. In this article, we describe a clinical case of exercise-induced hyponatremia in a soldier and a review of the literature, including the etiology, clinical characterization and recommended treatment. Moreover, water consumption recommendations with regard to physical activity are presented. The application of such recommendations may prevent future events of exercise-induced hyponatremia.

Calcif Tissue Int. 2004 May;74(5):407-14. Epub 2004 Jan 23.

Acute effects of an oral calcium load on markers of bone metabolism during endurance cycling exercise in male athletes.
Guillemant J, Accarie C, Peres G, Guillemant S.
Faculte de Medecine Pitie-Salpetriere, Service de Biochimie, Paris, France.

Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.

Acta Astronaut. 1995 Aug;36(3):183-9.
Effect of potassium and calcium loading on healthy subjects under hypokinesia and physical exercise with fluid and salt supplements.
Zorbas YG, Naexu KA, Federenko YF.
Hypokinetic Physiology Laboratory, European Institute of Environmental Cybernetics, Athens, Greece.

The objective of this investigation was to determine the acute responses to the electrolyte challenges under hypokinesia and physical exercise (PE) of different intensities with fluid and salt supplementation (FSS). The studies were performed on 12 physically healthy male volunteers aged 19-24 years under 364 days of hypokinesia (decreased number of steps per day) with a set of PE with FSS. The volunteers were divided into two equal groups. The first group was subjected to a set of intensive PE and the second group was submitted to a set of moderate PE. Both groups of subjects consumed daily water and salt supplements that aimed to increase the body hydration level. For simulation of the hypokinetic effect all subjects were kept under an average of 3000 steps per day. Functional tests with a potassium chloride (KCl) and calcium lactate (Cal) load were performed during the hypokinetic period of 364 days and the 60-day, prehypokinetic period that served as control, while both groups of subjects consumed daily calcium and potassium supplements. The concentration of electrolyte and hormone levels in the blood and their excretion rate in urine were determined. Renal excretion of calcium and potassium and the blood concentration thereof increased markedly in both groups of subjects. With the potassium chloride load tests the increased potassium excretion was accompanied by higher aldosterone and insulin blood levels, and with the calcium lactate load tests the increased calcium excretion was accompanied by a decreased parathyroid content in the blood. FSS and PE, regardless of intensity, failed to attenuate calcium and potassium losses. Additional intake of KCl and Cal also failed to normalize potassium and calcium abnormalities. It was concluded that during the KCl and Cal loading tests, the increased losses of potassium and calcium in the hypokinetic subjects were due to the inability of their bodies to retain these electrolytes, and that electrolyte abnormalities could not be reversed by PE or rehydration in individuals subjected to prolonged restriction of motor activity.

Br J Sports Med 2004;38:292-294

Effects of prolonged strenuous exercise (marathon running) on biochemical and haematological markers used in the investigation of patients in the emergency department

J E Smith¹, G Garbutt², P Lopes² and D Tunstall Pedoe^{3 1} Academic Department of Sports Medicine, Royal London Hospital, London E1, UK ²,  School of Health Sciences, University of East London, Dagenham, Essex, UK ³,  Department of Cardiology, Homerton Hospital, London E9, UK

Objectives: To investigate the effects of strenuous exercise on commonly used biochemical and haematological variables in subjects running the 2002 London marathon.

Methods: 34 healthy volunteers (7 female, 27 male) were recruited for the study. Blood was taken before the start (at registration) and immediately after completion of the marathon. Samples were analysed for urea and electrolytes, liver function tests, creatine kinase (CK), CK-MB isoenzyme, myoglobin, troponin I, full blood count, a clotting screen, and D-dimers. The results before and after exercise were compared. Pearson’s correlation coefficients were calculated for all variables.

Results: Significant increases were found in CK, CK-MB, aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and myoglobin following the marathon. However, there was no significant change in the level of troponin I. There was also evidence of activation of the coagulation and fibrinolytic cascades following the marathon, with a reduction in activated partial thromboplastin time, a reduction in fibrinogen, and an increase in D-dimers.

Conclusions: The results confirm previous individual studies on marathon running and the biochemical and haematological tests routinely carried out in hospital. These are affected by prolonged exercise, and "abnormal" results in these tests may be normal after prolonged exercise and therefore not diagnostic of a disease process. The results of investigations in patients who have been exercising should be interpreted with caution. Biochemical and haematological measurements form the basis of the initial investigation of several clinical problems in patients who may have undertaken recent exercise, including cardiac chest pain, exertional heat stroke, and thromboembolic disease. The traditional markers of cardiac damage are the enzymes creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), but recently, more specific markers of myocardial damage have been identified. These include the CK-MB isoenzyme, myoglobin, and cardiac troponins. Many emergency departments and chest pain assessment units use measurement of these variables to rule out or rule in myocardial infarction.¹ In patients with suspected thromboembolic disease in the form of pulmonary embolism or deep vein thrombosis, clinical risk stratification occurs in conjunction with investigation. Many protocols for the investigation and treatment of patients with possible deep vein thrombosis or pulmonary embolism include measurement of D-dimers as part of the investigative process.^2,3 It has been shown that exercise may influence the results of these investigations in asymptomatic healthy subjects, particularly if the exercise is prolonged or strenuous.^4,5 Many of the studies in this area have used laboratory based subjects. In the present study, we aimed to quantify these effects in a group of runners completing the Flora London marathon on 14 April 2002.