Hyponatremia

Hyponatremia has received attention in the media as a result of its occurrence in popular road running races [28]. Hyponatremia is a serious complication of low plasma sodium levels (<130 mEq/L) [29]. The exact cause is likely multi-faceted and circumstantial [30]. Hyponatremia has been observed in exercising individuals who became dehydrated [31,32], maintained hydration [32], and became overhydrated [31,32]. Asymptomatic hyponatremia is the most common type of hyponatremia [32] and is defined as a decrease in sodium level (<130 mEq/L) that occurs in the absence of life-threatening symptoms [33]. Asymptomatic hyponatremia per se is not harmful or detrimental to performance [34]. When plasma sodium decreases to less than 125 mEq/L, hypona-tremic illness may occur. Hyponatremic illness is a medical emergency that is symptomatic and requires immediate medical treatment [32,33,35].

Overdrinking, identified as an increase in body mass, significantly increases one's risk for developing hyponatremia and should be avoided [32,35,36]. Some observational studies have found that increased dehydration results in higher sodium levels [31,32,37], but this does not mean that dehydration prevents hyponatremia. The increased risk of heat illnesses associated with dehydration does not warrant dehydration as a method for preventing hyponatre-mia. High sweat rates or sodium-concentrated sweat may lead to large losses of sodium and put one at risk for hyponatremia, especially in events lasting more than 3 hours [38]. It is recommended that one should ingest fluid at a rate that closely matches fluid loss (ie, <2% body weight loss) [39].

Replacing large fluid losses with equal amounts of pure water may dilute the plasma sodium level [36], so it has been suggested that replacement of electrolytes can be achieved through sports drinks or salt tablets [30,34]. Mathematical modeling has shown that in a variety of conditions the ingestion of sodium may attenuate the decline of serum sodium over time (Fig. 3) [40]. However, recent

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Fig. 2. Controlled consumption of caffeine at a level of 3 mg/kg/d for 6 days and then decreased to 0 mg/kg/d (C0), maintained at 3 mg/kg/d (C3), or increased to 6 mg/kg/d (C6); none of these conditions altered hydration status. Urine osmolality (top graph) and volume (data not shown) during repeated 24-hour collection periods did not change over the course of the investigation. Acute urine (middle graph) and serum (bottom graph) osmolality also did not differ as a result of the level of caffeine consumption. (Data from Armstrong LE, Pumerantz AC, Roti MW, et al. Fluid, electrolyte, and renal indices of hydration during 11 days of controlled caffeine consumption. IntJ Sport Nutr Exerc Metab 2005;15(3):252-65.)

Fig. 2. Controlled consumption of caffeine at a level of 3 mg/kg/d for 6 days and then decreased to 0 mg/kg/d (C0), maintained at 3 mg/kg/d (C3), or increased to 6 mg/kg/d (C6); none of these conditions altered hydration status. Urine osmolality (top graph) and volume (data not shown) during repeated 24-hour collection periods did not change over the course of the investigation. Acute urine (middle graph) and serum (bottom graph) osmolality also did not differ as a result of the level of caffeine consumption. (Data from Armstrong LE, Pumerantz AC, Roti MW, et al. Fluid, electrolyte, and renal indices of hydration during 11 days of controlled caffeine consumption. IntJ Sport Nutr Exerc Metab 2005;15(3):252-65.)

  1. 3. Predicted effectiveness of a carbohydrate-electrolyte sports drink (CHO-E) containing 17 mEq/L of sodium and 5 mEq/L of potassium for attenuating the decline in plasma sodium concentration (mEq/L) expected for a 70-kg person drinking water at 800 mL/h when running 10 km/h in cool (18°C; upper panel) and warm (28°C; lower panel) environments. The solid shaded areas depict water loss that would be sufficient to diminish performance modestly and substantially. The hatched shaded area indicates the presence of hyponatremia. M indicates the finishing time for the marathon run. IT indicates the approximate finishing time for an iron-man triathlon. For the sodium figures, the solid lines reflect the effect of drinking water only, and hatched lines illustrate the effect of consuming the same volume of a sports drink. The pair of lines of similar type represent the predicated outcomes when total body water accounts for 50% and 63% of body mass. BML, body mass loss. (From Montain SJ, Cheuvront SN, Sawka MN. Exercise associated hyponatraemia: quantitative analysis to understand the etiology. Br J Sports Med 2006;40(2):98-105; with permission.)
  2. 3. Predicted effectiveness of a carbohydrate-electrolyte sports drink (CHO-E) containing 17 mEq/L of sodium and 5 mEq/L of potassium for attenuating the decline in plasma sodium concentration (mEq/L) expected for a 70-kg person drinking water at 800 mL/h when running 10 km/h in cool (18°C; upper panel) and warm (28°C; lower panel) environments. The solid shaded areas depict water loss that would be sufficient to diminish performance modestly and substantially. The hatched shaded area indicates the presence of hyponatremia. M indicates the finishing time for the marathon run. IT indicates the approximate finishing time for an iron-man triathlon. For the sodium figures, the solid lines reflect the effect of drinking water only, and hatched lines illustrate the effect of consuming the same volume of a sports drink. The pair of lines of similar type represent the predicated outcomes when total body water accounts for 50% and 63% of body mass. BML, body mass loss. (From Montain SJ, Cheuvront SN, Sawka MN. Exercise associated hyponatraemia: quantitative analysis to understand the etiology. Br J Sports Med 2006;40(2):98-105; with permission.)

studies involving consumption of sodium through sports drinks and salt tablets have confirmed [30,34,41] and refuted [37,42,43] this relationship (Fig. 4). Some of these differences in results may lie in methodologic differences, [30] assumptions, and conflicting conclusions [44].

Understanding the etiology and cause of hyponatremia may help to understand its prevention better. It is well agreed that overconsumption of fluids is the primary, but not the only, cause [35,40]. Whether replacement of sweat losses with equal volumes of sodium-containing beverages would prevent or

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Fig. 4. Ingestion of a carbohydrate-electrolyte beverage (CE) slightly attenuated the decline of plasma sodium observed with ingestion of plain water (W) over 180 minutes of exercise at a moderate intensity in a hot environment (34°C). (Adapted from Vrijens DM, Rehrer NJ. Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat. J Appl Physiol 1999;86(6): 1847-51; with permission.)

attenuate hyponatremia is still debated [35]. More studies that look at varying environmental conditions, sweat rates, and body masses may help shed light on this complex picture. Some authorities have suggested that allowing dehydration would prevent hyponatremia because the contraction of extracellular fluid would increase sodium concentration. Until further studies are conducted, promoting dehydration (ie, >2% of pre-exercise weight) is not warranted and may put some individuals at greater risk for exertional heat illnesses and could compromise performance [2].

CREATINE

Creatine is one of the most popular nutritional supplements on the market. Athletes of all levels and varieties of sports are using it in hopes of gaining a competitive edge. During creatine supplementation, 90% of the increase in body weight (0.7-2.0 kg) is accounted for by increases of total body water (TBW) [45]. The increase of TBW during the ''loading phase'' results from increases of intracellular water stores [46], but prolonged use of creatine results in TBW increases in all body fluid compartments [45]. Some authors speculate that creatine use while exercising in the heat impairs heat tolerance and may be a contributing factor for heatstroke [47,48]. Those authors propose that creatine increases one's risk for heat injury because the increases of intracellular water stores deplete intravascular volume [49]. Before any published conclusive studies concerning creatine's effect on hydration status and use in the heat, the American College of Sports Medicine published a consensus statement stating that ''high-dose creatine supplementation should be avoided during periods of increased thermal stress ... there are concerns about the possibility of altered fluid balance, and impaired sweating and thermoregulation ...'' [48].

Paradoxically, studies using short-term and long-term creatine supplementation have shown that subjects exercising in the heat (30-37°C) for 80 minutes have either no change or an advantageous lower heart rate and Tc [46,50-52]. Work from our laboratory also has shown that creatine supplementation does not alter exercise heat tolerance, even when subjects begin exercise in a dehydrated state (Fig. 5) [51]. One study that found lower Tc with creatine use during exercise in heat suggests that the increases of TBW with supplementation may hyperhydrate the body and lower Tc [46]. Despite early concerns about creatine supplementation and exercise in the heat [48], more recent studies have shown conclusively that heat storage does not increase as a result of creatine use [46,50-52]. There is no evidence to support restriction of creatine use during exercise in the heat.

EXERCISE-ASSOCIATED CRAMPS

Although the exact mechanism is unknown, skeletal muscle cramps are associated with numerous congenital and acquired conditions, including hereditary

  1. 5. The use of creatine monohydrate (CrM) does not compromise exercise heat tolerance. After becoming dehydrated, rectal temperature and mean weighted skin temperature (MWST) had similar responses in CrM and placebo treatments when subjects exercised in the heat and recovered in a cool environment. (From Watson G, Casa D, Fiala KA, et al. Creatine use and exercise heat tolerance in dehydrated men. J Athl Train 2006;41(1):18-29; with permission.)
  2. 5. The use of creatine monohydrate (CrM) does not compromise exercise heat tolerance. After becoming dehydrated, rectal temperature and mean weighted skin temperature (MWST) had similar responses in CrM and placebo treatments when subjects exercised in the heat and recovered in a cool environment. (From Watson G, Casa D, Fiala KA, et al. Creatine use and exercise heat tolerance in dehydrated men. J Athl Train 2006;41(1):18-29; with permission.)

disorders of carbohydrate and lipid metabolism, diseases of neuromuscular and endocrine origins, fluid and electrolyte deficits (ie, owing to diarrhea or vomiting), pharmacologic agents (ie, p-agonists, ethanol, diuretics), and toxins [53]. The medical treatments for these various forms of muscle cramps are as varied as their etiologies. McGee [54] specifically classified leg muscle cramps as contractures (ie, electrically silent cramps caused by myopathy or disease), tetany (ie, sensory plus motor unit hyperactivity), dystonia (ie, simultaneous contraction of agonist and antagonist muscles), or true cramps (ie, motor unit hyper-activity). The last category includes skeletal muscle cramps that are due to heat, fluid-electrolyte disturbances, hemodialysis, and medications.

The International Classification of Diseases [55] defines heat cramps, a form of motor unit hyperactivity, as painful involuntary contractions that are associated with large sweat (ie, water and sodium) losses. Heat cramps occur most often in active muscles (ie, thigh, calf, and abdominal) that have been challenged by a single prolonged event (ie, >2-4 hours) or during consecutive days of physical exertion. A high incidence of heat cramps occurs among tennis players [56], American football players [57], steel mill workers [58], and soldiers who deploy to hot environments [59,60]. These activities result in a large sweat loss, consumption of hypotonic fluid or pure water, and a whole-body sodium and water imbalance [59,61]. The distinctions between heat cramps and other forms of exercise-associated cramps are subtle [54,59,62], but sodium replacement usually resolves heat cramps effectively [56,59,61-63]; successful treatment via sodium administration confirms a preliminary diagnosis of heat cramps.

Bergeron [62] described a tennis player who was plagued by recurring heat cramps. This athlete secreted sweat at a rate of 2.5 L/h and had a sweat sodium (Na+) concentration of 83 mEq/L. This sweat Na+ concentration is high, in that most heat-acclimatized athletes exhibit 20 to 40 mEq Na+/L of sweat (ie, heat acclimatization reduces sweat Na+ concentration), but occurs naturally in a small percentage of humans. During 4 hours of tennis match play, this young athlete lost 10 L of sweat and a large quantity of electrolytes (ie, 830 mEq of Na+; 19,090 mg of Na+; 48.6 g of sodium chloride). Given that the average sodium chloride intake of adults in the United States is 8.7 g (3.4 g Na+) per day, it is not difficult to see how this athlete could experience a whole-body Na+ deficit. To offset his 4-hour sodium chloride loss in sweat, this athlete would require 1.6 L of normal saline, 7.8 to 9.8 cans of canned soup (85-107 mEq per can), 12.6 servings of tomato juice (66 mEq of Na+ per serving), or 39.5 to 127.7 L of a sport drink (6.5-21 mEq Na+/L). These options are unreasonable. A long history of heat cramps ended when this tennis player began consuming supplemental salt during meals. Other tennis players have been successfully treated using a similar course of action [63].

In 2004, the authors' research team evaluated a female varsity basketball player (body mass 78.5 kg, height 187 cm) who experienced exercise-induced cramps during the winter months in New England, with signs and symptoms identical to heat cramps. The authors measured her sweat rate as 1.16 L/h, her sweat sodium concentration (ie, via whole-body washdown) as 42 mEq/L, and her daily consumption of sodium. These values were normal and typical of winter sport athletes. Three days of observations indicated that her dietary intake of Na+ per day was similar to her daily sweat Na+ loss (ie, both 3200-3600 mg). Because she did not train or compete in a hot environment, the authors hesitated to diagnose her malady as heat cramps. When she began ingesting supplemental sodium (ie, by liberally salting each meal at midsea-son), however, the skeletal muscle cramps resolved permanently. This case suggests that a history of skeletal muscle cramps, with a large daily Na+ turnover owing to a high sweat rate, indicates the need for an evaluation of whole-body Na+ balance. It further suggests that heat cramps may have been named because they usually occur in hot environments, but they also may occur in mild environments when sweat Na+ concentration and sweat losses are large.

A study by Stofan and colleagues [57] examined the link between sweat sodium losses and heat cramps. Sweat rate, sodium content, and percent body weight loss were measured on a single day of a ''two-a-day'' practice in subjects who had a history (episode within the last year) of severe heat cramps. Although heat cramps were not observed, football players with a history of heat cramps had sweat sodium losses two times greater than matched controls. Although the exact etiology of heat cramps may be unknown, sodium deficits seem to contribute to their development. In most cases, restoration and compensation of sodium losses seems to prevent further heat cramps.

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