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INTRODUCTION Hyponatraemia by definition means low (hypo) sodium (Na) in the blood (emia), (Benardot, 2006). Mild hyponatraemia results from a serum sodium concentration below 135 mmol/L, while a serum sodium concentration below 125 mmol/L triggers severe hyponatraemia (McArdle, Katch & Katch, 2006). As serum sodium concentrations drop, fluid will leave the bloodstream by osmosis and accumulate in tissues, causing swelling i.e. cellular edema. If nerve cells swell too much they cease to function properly. Therefore, although cellular edema is well tolerated by many of the body’s tissues, it is not well tolerated by the brain (Smolin & Grosvenor, 2008; Dunford & Doyle, 2008). Consequently, the serious symptoms of hyponatraemia are mainly related to cerebral edema and include mild symptoms of headaches, confusion, nausea and cramping; to severe symptoms of seizures, coma, pulmonary edema, cardiac arrest and death (McArdle et al., 2006; Benardot, 2006). There are a number of speculated causes of hyponatraemia in athletes. One is known as the syndrome of inappropriate antidiuretic hormone response (SIADH) which causes decreased urine production and increased fluid retention during fluid overload. But by far the most common factor in hyponatraemia is excessive drinking (Murray, Stofan, & Eichner, 2003). Rates of occurrence vary from 0-0.4% of finishers in case-based publications, to as high as 1.3% of finishers in cohort study populations (Chorley, 2007). The reported incidence of hyponatraemia in ultra-endurance events lasting over 6 hours ranges from 0.3-27%. This incidence is even higher among athletes requiring medical attention, ranging from 9-60% (Hsieh, 2004). In a study of more than 18 000 ultra-endurance runners, approximately 9% of collapsed individuals presented with symptoms of hyponatraemia (Noakes et al., 1990, as cited by McArdle et al., 2005). Death is a rare occurrence with only nine cases reported worldwide since 1985 (Carter, 2008). However, there is still some debate in regards to some of the reported incidences, as some of these studies had incorporated biased subject selection into their methodologies. An example of this is the selection of subjects based on showing possible signs of hyponatraemia upon finishing their event, potentially leading to an overestimated population (Carter, 2008). The purpose of this literature review is to review recently published scientific research to evaluate the importance of the factors involved, and to possibly identify any further factors that may increase the risk of developing hyponatraemia. The strengths and weaknesses of the reviewed studies will be discussed, before conclusions are drawn and recommendations made to athletes on how to avoid or lessen the chance of developing hyponatraemia. Relevance to Sports Nutrition An understanding of hyponatraemia for athletes and others involved in sport is important because many of the symptoms may be non-specific and similar to those of dehydration and other exercise-related illnesses, which may lead to inappropriate treatment. Near-deaths from hyponatraemia during the 1985 Comrades ultra-marathon prompted the subsequent establishment of field laboratories in the medical tents of some ultra-endurance events (Hsieh, 2004). Under normal circumstances, it is very difficult for a healthy individual to develop hyponatraemia through overzealous drinking and rarely occurs outside of the mental illness domain. This is due to the kidneys ability to process and excrete excess water as well as conserve sodium. However, during exercise, urine production is decreased by between 20–60% due to a decrease in kidney blood flow leading to a reduced capacity for fluid homeostasis and therefore an increased risk of developing hyponatraemia when combined with excessive fluid intake (Achinger, Moritz & Carlos Ayus, 2006; Murray, Stofan, & Eichner, 2003; McArdle, Katch & Katch, 2005). Regardless of the ‘true’ incidence rate, the fact remains that hyponatraemia is a fairly common occurrence in the domain of ultra-endurance athletic events and therefore deserves closer scrutiny as to how this incidence may be lowered, more easily recognised and treated more effectively. SUMMARY OF THE REVIEWED LITERATURE In 1996 the American College of Sports Medicine (ACSM) proposed guidelines that athletes should ‘drink as much as tolerable’ during exercise. This recommendation has possibly led to some athletes becoming over-zealous in their drinking habits. The most recent guidelines by the International Olympic Committee (IOC) urge athletes to drink enough to replace what is lost. This latest recommendation has received both criticism and praise with Noakes (2007) suggesting that both these guidelines lack an adequate, scientifically proven evidence base, and that they have not been properly evaluated in appropriately controlled, randomized, prospective clinical trials conducted in conditions that match the exercise. Many athletes may also suffer gastrointestinal distress if consuming the recommended amounts of fluid or aiming to replace fluid that is lost. On the other hand, the notion of aiming to replace all or most of the fluid that is lost has been supported by numerous studies and publications and it is argued that this is the most personalized approach to fluid intake and takes account of the athletes actual sweat loss which may vary with different environments and exercise intensities. Although it is important that during training athletes need to learn to approximate their sweat rate under various conditions in order to plan an effective drinking strategy as well as learn what is tolerable (Sallis, 2008; Murray, Stofan, & Eichner, 2003; Jeukendrup & Gleeson, 2004). In an article by Noakes (2007), six studies were reviewed that compared the effects of ‘some’ fluid replacement with full fluid replacement during exercise (Below et al., 1997; McConnell et al., 1997; McConnell et al., 1998; Daries et al., 2000; Backx et al., 2003; Dugas et al., unpublished, as cited by Noakes, 2007) and none of the studies showed that full replacement was advantageous over ‘some’ replacement. It was also suggested that all currently published evidence shows that hyponatraemia is caused by fluid overload while any acute sodium deficiency plays only a minor role. To avoid fluid overload, it was recommended that thirst be used as the mechanism to determine fluid consumption (Noakes, 2007). In a conference paper presented by Chorley (2007), risk factors for hyponatraemia that were consistently noted in all studies reviewed included high fluid intake, insufficient weight loss and slower finishing times. Other risk factors that may contribute included low and high body mass index, lighter pre-race weight, less Marathon experience, female gender, NSAID use and higher heat stress weather conditions. It was found that runners who fail to lose 0.75 kg throughout the duration of the event were seven times more likely to be hyponatraemic than those who lose more than 0.75 kg (Chorley, 2007). In a review article by Verbalis (2007) it was found that in virtually all studies where bodyweight has been recorded before and after exercise, there has been a consistent inverse relationship between bodyweight and serum sodium concentrations, indicating fluid retention. For example, data from the New Zealand Ironman triathlon in 1997 showed that the most severe cases of hyponatraemia occurred in athletes who had gained weight during the event. In studies that have quantified fluid intake, a significant negative correlation between ingested fluid volumes and serum sodium concentrations have been shown. The trend of net weight gain suggests that fluid ingestion often exceeds the sum of fluid loss from sweating and urination (Verbalis, 2007). In two case-control studies (Irving, Noakes & Buck, 1991; Speedy, Rogers & Noakes, 2000, as cited by Verbalis, 2007), athletes who developed hyponatraemia following ultra-marathon and ironman triathlon races were matched to a subset of non-hyponatraemic competitors. It was found that in the 9-24 hour period after the race, the hyponatraemic finishers excreted 1.3-3.0 L of fluid while the non-hyponatraemic finishers ingested 0.5-2.7 L, thus indicating the development of excess fluid retention throughout the race for the hyponatraemic finishers. Also, both groups had similar levels of sodium losses and sodium retention. It was concluded that these results supported the hypothesis that it is excess fluid retention that is the primary cause of hyponatraemia (Verbalis, 2007). It was also found that in most studies in which gender differences have been examined, the incidence and severity of hyponatraemia has been found to be greater in female athletes (Verbalis, 2007). In a consensus statement issued by 12 international experts on what is currently known about hyponatraemia, it was stated that excessive sodium loss did not appear to be a contributor to hyponatraemia, although it was acknowledged that more research was needed to track sodium losses in athletes with large sweat volumes related to warm climates (Schnirring, 2005). Risk factors that were highlighted were in agreement with trends noted by medical directors at endurance events. Avoiding sports drinks, sodium supplements, and salty food does not seem to be a risk factor for events lasting less than four hours (Schnirring, 2005). To prevent hyponatraemia, it was recommended that slower participants could either allow thirst to guide fluid consumption, or calculate individual sweat loss rates and use this to limit consumption (Schnirring, 2005). However, the former of the two suggestions has been criticised by numerous studies and publications which argue that using thirst as a guide will allow a greater degree of dehydration to occur, as quite often the feeling of thirst is not felt until a significant degree of dehydration has occurred. Dehydration has been shown to adversely affect exercise performance at levels of 2% loss of body weight or more (Jeukendrup & Gleeson, 2004; Murray, Stofan, & Eichner, 2003). Weschler (2005) conducted a mathematical analysis on data from previous studies. A high correlation was found between fluid overload and hyponatraemia. It was also noted that while over-hydrated event finishers with a serum sodium concentration of 128-130 mmol/L present with hyponatraemia, thus far dehydrated finishers with the same serum sodium concentration have not yet been observed with symptoms of hyponatraemia. This supports the hypothesis that serum sodium concentrations alone are not enough to cause swelling in the cerebral nerves; fluid overload must also be present. In a mathematical analysis of studies in which pre- and post-event bodyweights are known, it was shown that the more the athlete weighed at the end of the event relative to their weight at the start, the lower their serum sodium concentration. In an identical analysis but where fluid ingestion rates were known, the same relationship with serum sodium concentration was found. Also of interest, where no weight change occurs, serum sodium concentrations tended to be either low or normal. It was concluded that while over-drinking is the primary cause of hyponatraemia, sodium losses cannot be completely discounted, especially in longer events held in warm weather (Weschler, 2005). Sports drinks were not shown to protect against hyponatraemia if consumed to excess levels although when not consumed to excess levels, a sports drink containing sodium may significantly delay or prevent exertional hyponatraemia from occurring (Weschler, 2005; Carter, 2008). In a review article by Hsieh (2004), it was stated that guidelines for fluid intake have traditionally focused on the adverse effects of dehydration, with recommendations that fluid intake should exceed the sensation of thirst satiety. Some guidelines have recommended ingestion of fluids at a rate of 1L/hr, especially during hot weather events which is extremely generalized and non-specific to the many variables involved in endurance events and competitors. It was noted that this has resulted in some competitors over-compensating, and thus ingesting too much fluid in an effort to avoid dehydration and other heat-related illnesses. As a result, these competitors become overloaded with fluid and this, combined with inappropriate physiological responses of the body, leads to excessive retention of fluid and a danger of developing hyponatraemia. Hsieh (2004) was critical of the notion of drinking to replace losses in bodyweight. In a study by Rogers (1997) (as cited by Hsieh, 2004), it was found that fluid deficit only accounted for 40% of weight loss in ultra-marathon runners. This finding suggested that the use of weight changes may over-estimate the rate of fluid depletion. Hsieh (2004) also pointed out that while the intake of excessive amounts of hypotonic fluid has been linked to hyponatraemia, no cases of hyponatraemia have been reported in those that are dehydrated. A fluid intake of 500 mL/hr or less was suggested, especially for athletes performing at lower exercise intensities (Hsieh, 2004) although this figure seems far too generalized considering the many variables involved in athletes sweat rates, exercise intensities and environments. Hsieh (2004) also stated that calculations of the amount of sodium lost through sweat based on observed sweat content and volume in endurance athletes have not matched the hypothesised sweat sodium losses required to result in hyponatraemia. High sodium (57mg/100ml) replacement fluids may be poorly tolerated. Many commercial sports drinks are sufficiently dilute, although some are too dilute. Some athletes ingested salt tablets, although laboratory and field studies have not shown these to be effective in raising serum sodium concentrations (Hsieh, 2004). STRENGTHS AND WEAKNESSES OF THE REVIEWED STUDIES In an article by Noakes (2007), the author criticises the ACSM and IOC fluid consumption guidelines because they lack an adequate, scientifically proven evidence base, and that they have not been properly evaluated in appropriately controlled, randomized, prospective clinical trials conducted in conditions that match the exercise. Yet it is unclear whether or not the six studies he reviewed met the same stringent criteria. In fact, one study has not even been published. Chorley (2007) likewise, quotes their own unpublished data to support their claims. Chorley discusses risk factors that are consistently noted in ‘all studies’, yet only offers seven stated references to support their discussion. Verbalis (2007) cites two case-control studies (Irving, Noakes & Buck, 1991; Speedy, Rogers & Noakes, 2000) where hyponatraemic athletes were matched with non-hyponatraemic athletes for comparison. Yet it is unclear how large the samples were, or whether or not the matching process overcame potentially confounding variables (such as age, bodyweight, level of training etc). Schnirring (2005) uses consensus statements not just from those in academia, but also from medical directors at endurance events. Weschler (2005) performed a mathematical review on up to 150 studies using the Nguyen-Kurtz equation. This equation has been refined and is solidly grounded in experimental observation, and is a best-fit equation with r=0.83 for serum sodium concentration and total body water. CONCLUSION Regarding the risk factors for hyponatraemia: 1) Prolonged exercise in hot weather/climates. Numerous studies have suggested that higher heat stress due to weather conditions is a risk factor, especially during prolonged physical activity greater than four hours. Exercise intensity did not necessarily have to be high. All of the studies reviewed focused on marathon or ultra-marathon-type distances (Chorley, 2007; Schnirring, 2005; Hseih, 2004; Murray, Stofan & Eichner, 2003). 2) Poorly conditioned or acclimatized individuals who experience excessive sweat loss with high sodium concentrations. Athletes who have acclimatized well to their environment typically excrete less sodium in their sweat due to an improved capacity of the sweat glands to conserve sodium (Murray, Stofan & Eichner, 2003). Noakes (2007) suggests that acute sodium deficiency only plays a minor role in hyponatraemia. 3) Frequent intake of large quantities of sodium-free fluid during prolonged exercise. Numerous studies and publications have concluded that there is a consistent link between fluid overload and hyponatraemia. Some studies have also reported that thus far no dehydrated athletes have ever presented with hyponatraemia. Further studies have also commented that certain recommendations for athletes to replace lost fluids during events have led to over-consumption of ingested fluids and subsequent incidences of hyponatraemia (Noakes, 2007; Chorley, 2007; Verbalis, 2007; Weschler, 2005). Weschler (2005) stated that even beverages containing sodium can still lead to hyponatraemia if consumed in excess. 4) Use of diuretic medication. Chorley (2007) and Hseih (2004) identified use of non-steroidal anti-inflammatory drugs (NSAIDs) as a possible risk factor. NSAIDs such as aspirin or ibuprofen, or any other substances that causes a diuretic effect, such as some hypertension medications, may alter kidney function in a way that increases the risk of hyponatraemia during long-duration events (Benardot, 2006; McArdle et al., 2006). 5) Female gender. Numerous studies have highlighted and suggested that the female gender is a possible risk factor when linked with endurance exercise. Female athletes in general tend to be at higher risk for hyponatraemia because of their smaller body masses (Chorley, 2007; Schnirring 2005; Hseih 2004). In a study review by Murray, Stofan & Eichner (2003) the authors suggest that the higher incidence of hyponatraemia in females may be due to the female gender being more vigilant drinkers compared to their male counterparts as well as more likely to heed and possibly exceed advice from experts and coaches, or general advice such as ‘optimal hydration is beneficial for performance’ which is open to misinterpretation. The following additional risk factors were also highlighted in the reviewed studies: 6) Lower body mass. This is due to the fact that those with less body mass will have lower absolute fluid requirements and it will take less fluid to dilute the extra cellular fluid (Chorley, 2007; Schnirring, 2005; Murray, Stofan & Eichner, 2003). 7) Slower finishing times. This risk factor is linked to 1) and 3), because slower finishers are competing for longer, they have a longer amount of time to ingest more fluid (Chorley, 2007; Schnirring, 2005; Hseih, 2004). 8) Race inexperience. This risk factor is likely to be linked to 7), as slower finishers are more likely to be inexperienced and may also less knowledge of safe fluid intake practices (Schnirring, 2005). Recommendations Athletes engaging in endurance events of greater than four hours duration should, if possible, compete in events held in cool weather conditions and if performing in hot conditions, acclimatization training would be beneficial. In events of more than four hours duration, a sports drink containing sodium will be beneficial. If thirst is used as an indicator of fluid intake this may potentially cause a loss in performance due to excessive dehydration. It would, in the authors opinion, be far more beneficial to create a fluid intake plan based on trialled strategies in training based on maintaining close to weight balance pre and post exercise and using amounts that the athlete can tolerate without negative side effects such as gastro-intestinal stress and discomfort. Athletes should experiment beforehand in training to determine their appropriate fluid intake and take into account and trial different exercise intensities and climates/environments in an effort to match race conditions. However, under no circumstances should they replace more fluid than what is lost. If hypotonic sports beverages containing sodium are to be ingested during the event, this should be done with the understanding that such beverages do not protect against hyponatraemia but may delay or prevent this occurrence when taken in adequate amounts. Any athlete taking medications that may alter kidney function, such as NSAIDs or diuretics, should consult with their doctor before undertaking any ultra-endurance event. Slower finishers, females and those with low body mass need to be aware that they may be at increased risk of hyponatraemia. Upon examining an athlete with hyponatraemia, blood pressure will be stable, as well as heart rate. A certain degree of confusion or altered consciousness may be noticed as well as puffiness when hyponatraemia is moderate to severe. Therefore, anyone involved in the evaluation of collapsed athletes at endurance events should assume hyponatraemia if the athlete shows signs of altered consciousness but other factors such as heart rate, blood pressure and temperature are normal (Sallis, 2008). REFERENCES Banardot, D. (2006). Advanced Sports Nutrition. Champaign, IL: Human Kinetics. Carter, R. (2008). Exertional Heat Illness and Hyponatraemia: An Epidemiological Prospective. 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McArdle, W.D., Katch, K.I., & Katch, V.L. (2006). Essentials of Exercise Physiology. (3rd ed.). Baltimore, MD: Lippincott Williams & Wilkins. Noakes, T.D. (2007). Drinking guidelines for exercise: What evidence is there that athletes should drink “as much as tolerable”, “to replace the weight lost during exercise” or “ad libitum”? Journal of Sports Sciences, 25, (7), 781-796. Sallis, R. (2008). Fluid Balance and Dysnatremias in Athletes. Current Sports Medicine Reports, 7, (4), 14-19. Schnirring, L. (2005). Experts Issue Hyponatraemia Consensus. Sports Medicine, 33, (8), 18-39. Smolin, L.A., & Grosvenor, M.B. (2008). Nutrition: Science and Applications. Hoboken, NJ: John Wiley & Sons, Inc. Verbalis, J.G. (2007). Renal Function and Vasopressin During Marathon Running. Sports Medicine, 37, (4-5), 455-458. Weschler, L.B. (2005). Exercise-Associated Hyponatraemia: A Mathematical Review. Sports Medicine, 35, (10), 899-922. Whitney, E., & Rolfes, S.R. (2008). Understanding Nutrition. (11th ed.). Belmont, CA: Thomson Higher Education. Clothing Alterations Hamilton NZ
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