Athletes, coaches, athletic trainers, and physicians can benefit from knowing how sweat sodium concentration or content impacts sports performance and sports medicine. Athletes with "salty sweat" are prone to sodium deficits, heat cramping, plasma volume contraction, and notably in endurance events, hypovolemic hyponatremia, sometimes called "hyponatremic dehydration." No easy, practical method exists to gauge sweat sodium concentration in athletes. Yet sweat sodium concentration is influenced by genetics, diet, heat acclimatization, sweat rate, and even by age and gender. This review covers relevant scientific and clinical information in this field, along with the practical implications for athletes. Sweat collection methods are not detailed here, but are covered nicely elsewhere; sweat sodium concentration normally ranges from a low of about 20 mmol·L-1 to a high of about 80 mmol·L-1 (1). Renal handling of sodium also is important for athletes, of course, but is beyond the scope of this article.
Probing the genetics of sweat sodium begins with cystic fibrosis (CF). In sweat glands, sweat is secreted in the glandular coil at the base of the gland and then passes through a narrow duct in which resorption of salt occurs. Normally, sodium is avidly resorbed from the ductular lumen, mainly via an epithelial sodium channel, and the counter-ion chloride is resorbed via another channel, the cystic fibrosis transmembrane conductance regulator (CFTR). In CF, because of the genetic absence of a functioning CFTR, sweat ducts are impermeable to chloride. In other words, patients with CF are unable to resorb sweat chloride before sweat emerges on the skin. The absence of functioning CFTR, normally situated in the luminal plasma membrane of the mucosal cells lining the duct, limits the amount of salt that can be reclaimed. Sodium is also poorly absorbed, and sweat emerging on the skin has a salt concentration some 3-5 times above normal (2,3). The poor absorption of sodium also stems from the functional interaction of CFTR and the sweat-gland epithelial sodium channel (ENaC), because it is known that CFTR is also a conductance regulator (4). In fact, research shows that CFTR and ENaC are activated together in sweat duct salt absorption, and that ENaC activation depends upon functioning CFTR. In the CF duct, salt is absorbed poorly because loss of CFTR activity imposes a loss of ENaC activity as well (5).
The CFTR gene comprises 180,000 base pairs on the long arm of chromosome 7. The CFTR protein has 1480 amino acids. Activation relies upon phosphorylation of CFTR subunits, mainly via protein kinase A. More than 1300 mutations of CTFR are grouped into six classes. The most common mutation, deletion of a phenylalanine residue at codon 508 (Delta F508), occurs in 70% of defective CFTR alleles and in 90% of patients with CF in the United States. It is a class II defect; the protein is misfolded and so degraded early. A class I defect, no synthesis of CFTR, occurs in 5%-10% of mutations. Because of a founder effect (effect of establishing a new population by a few persons carrying only a small fraction of the parent population's genetic variation), a class I defect from premature truncation is common in Ashkenazi Jews. Other defects include disordered functions of the chloride channel, a low number of CFTR transcripts, or accelerated loss of CFTR from the cell surface (2,3).
Classical CF is an autosomal recessive disorder with typical pathology in the respiratory tract, gastrointestinal tract, male reproductive tract, and sweat glands, caused by loss-of-function mutations in the CFTR gene. The observation that patients have salty sweat led to a milestone in diagnosis, the sweat test. This test also enabled diagnosis of older children and adults who have milder forms of CF. Some nonclassical forms are tied to milder defects in CFTR, and others apparently have no tie to mutations in the CFTR gene (2,3,6).
One defective gene for CFTR is common among white individuals. The incidence of CF (two defective genes) is about 1 in 3200 white live births. This means, for example, that 4%-5% of northern European adults are heterozygotic for the classic form of CF. In other words, up to one white person in 20 has one abnormal CFTR gene. Limited studies suggest these heterozygotes lose elevated amounts of salt in sweat. For example, in an early study of adults, CF heterozygotes had sweat chloride levels nearly twice those of normal control subjects, and in a study of infants, heterozygotes had levels about 50% higher than normal control subjects (7).
Among black individuals, one defective gene for CFTR is less common. The incidence of CF is about 1 in 15,000 black live births. Some CFTR mutations in black individuals are unique. Clinical differences between black and white patients with CF were noted in early studies, including a greater prevalence of hyponatremic "dehydration" in blacks, but in a recent study, sweat sodium levels and clinical manifestations generally were similar in both racial groups (8). In Sardinia, however, a specific CF mutation (T338I) was tied to "hypotonic" (including hyponatremic) dehydration in eight children who had no other features of CF. The authors suggest this genotype confers a mild phenotype that, via heavy and salty sweating in Sardinia's hot climate, predisposes mainly to hypotonic (hyponatremic) dehydration (9). Another group, from Spain, reports hyponatremic dehydration as the presentation of CF in 13 children, all during the summer months, all with gastroenteritis, fever, and sweating (10).
IMPLICATIONS FOR ATHLETES
Hyponatremic dehydration in heterozygotes for CF surely has implications for endurance athletes in the heat. If up to 1 in 20 white adults is a heterozygote for CF, that means that in a marathon with 20,000 white runners, up to 1000 runners may be genetically programmed for "salty sweating." These runners may risk hyponatremic dehydration during the event.
Hyponatremic dehydration clearly occurs in CF, as in the 24-year-old soldier who collapsed with hyponatremic dehydration (sodium 116 mEq·L-1) after running 3 miles in Saudi Arabia (11). When three adolescents with CF ran a marathon, serum sodium fell and aldosterone rose more than in control subjects who ran with them (12). During exercise in the heat, eight patients with CF, versus controls, lost more than twice the sodium and had a fall in serum sodium (13). When 11 young subjects with CF exercised in the heat and drank water, mean serum sodium fell slightly, and one boy had a fall of 11 points, from 142 to 131 mEq·L-1. When they drank a sports drink with 50 mmol·L-1 sodium, their fluid intake increased and the fall in serum sodium was lesser (14). Lisa Bentley, a top Canadian triathlete, has CF, and according to an online profile (Inside Triathlon, 2004), struggled with salt depletion, cramping, and heat exhaustion. She learned to consume more sodium and fluid, and then placed higher in Ironman and other triathlons.
Salty sweating is also a culprit in heat cramping in tennis and football players, although a link to CF is not established. Bergeron studied top male tennis players who were fit and acclimatized but had a history of heat cramping. During a hot, humid singles match, among 17 players, average sweat rate was 2.6 L·h-1 and sweat sodium loss was 2.7 g·h-1. One player lost 12 g of salt in 1 h. Bergeron argues that cramping may occur when loss of sodium and fluid contracts interstitial volume to deform mechanically nerve endings and increase ionic and neurotransmitter concentrations. He concludes that appropriate salt and fluid intake can avert heat cramping in tennis (15).
Heat cramping is common in summer football training. We studied sweat and sodium losses in NCAA Division I college football players in action on-field during summer training. Five players with a history of heat cramping were matched (weight, age, race, position) with five teammates who had never heat cramped. Change in body weight (adjusted for fluid intake) determined gross sweat loss. Ad libitum fluid intake was gauged from pre- and post-practice bottle weights. Sweat samples (absorbent patch on forearm) were analyzed for sodium and potassium. Gross sweat loss was slightly but not significantly greater in crampers. Sweat potassium was similar between groups, but sweat sodium was more than twice as high in crampers as non-crampers (55 mmol·L-1 vs 25 mmol·L-1). Average sweat sodium loss over 1 d (two practices of 2.5 h each) was 10.4 g in crampers. This equates to losing about 5 tsp of salt in sweat in 1 d of summer football training. One cramper lost 9 tsp of salt in 1 d. We conclude that large acute sodium and fluid loss in sweat may be typical of football players prone to heat cramping (16). Like Bergeron, we find that increasing salt in the diet and in sports drinks can help avert heat cramping in football.
We also measured 24-h fluid turnover (FTO) during 6 d of preseason training in similar football players. Players, training in full gear in moderate heat stress, ingested deuterium oxide and donated urine daily for analysis. Mean FTO was 10.3 ± 2.2 L·d-1. Sweat rates were also high. We did not gauge sodium balance, but assuming 40%-45% of total body water is extracellular fluid and turnover of total body water is proportional to that of extracellular fluid, an FTO this high may in theory deplete up to 15 g of sodium a day (17).
High sweat rates may also contribute to high sodium losses in football players. In an unpublished study, we tracked core temperature (via an ingestible temperature sensor) and gauged fluid intake and sweat loss in eight players, in T-shirts and shorts, during an intense 95-min June workout: field drills, then weight lifting, then sprinting. During the drill, mean core temperature rose sharply early, to 101°F by 10-20 min, and peaked at 103-104°F. One player, known to have a high sweat sodium level, peaked at 104°F, dehydrated 1.4%, and developed major heat cramping late in the drill.
Consensus holds that sweat sodium increases as sweat rate increases. This has been shown repeatedly, most recently in a study of 11 young men who exercised at two intensities in a hot room. Sweat rate and sweat sodium were higher at 60% V˙O2max than at 40%, and in each man, sweat sodium increased significantly as sweat rate increased (18).
IMPLICATIONS FOR ATHLETES
Sweat sodium rises as sweat rate rises because as sweat traverses the gland ever faster, there is less time for sodium resorption. This suggests the possibility that, independent of sweat genetics, athletes who are the most intense in football drills, for example, may heat up faster, sweat faster, and lose more sodium than their less intense counterparts.
A paradox of heat acclimatization is that the higher sweat rates it confers can lead to greater loss of sodium at maximal work output and sweat rates, even as acclimatization evokes lower concentrations of sweat sodium. This concept is shown in Table 1, adapted from Knochel (19).
The result is the heat-acclimatized athlete working at peak performance and sweating maximally may be able to stay on-field longer and eventually lose more salt in sweating than his unacclimatized counterpart. This may be one reason why, in football, overweight, unfit, unacclimatized linemen are prone to heatstroke, whereas lean, fit, acclimatized wide receivers or cornerbacks are prone to sodium depletion and heat cramping (20-22). Military research also finds that recruits most prone to heatstroke are the largest and least fit, judged by body mass index and 1.5-mile run time (23).
State of acclimatization to heat also affects sweat sodium level. A key part of heat-acclimatization is salt-saving in sweat. This adaptation was suggested in 1912 and demonstrated by Dill in 1933. An unacclimatized person may secrete sweat with sodium as high as 60 mmol·L-1 or more, and with heavy sweating can lose large amounts of salt. With acclimatization, sweat sodium may be as low as 10 mmol·L-1. This sweat salt-saving stems from aldosterone, secreted in response to exercise, heat, and sodium deficits; with acclimatization, the sweat gland may also be more responsive to aldosterone (19,24). For example, when 10 subjects exercised in the heat daily for 10 d, sweat sodium level fell, but the ratio of sweat sodium reabsorbed to plasma aldosterone level rose. So exercise and heat acclimation may augment sweat gland responsiveness to aldosterone (25). As covered later in this article in the section on dietary sodium, aldosterone also plays a role in differences in sweat sodium level on high- or low-sodium diets.
Salt-saving in sweat is among the many physiological adaptations of heat acclimatization. Sweating adaptations in heat acclimatization are in Table 2, which includes other features, adapted from Sawka and Young (24).
Degree of acclimatization hinges on intensity, duration, and frequency of heat exposures. Exercise works best to achieve these adaptations, but just resting in the heat confers some benefit. Salt-saving in sweat begins within a day or two and - like other thermoregulatory adaptations - is thought to level off or be complete in about 7-14 d. Military field studies suggest, however, that peak physiologic tolerance to heat may take longer than just a week or two (24).
When heat exposure ends, salt-saving in sweat wanes. The few studies available on loss of heat acclimatization suggest that it begins to wane by 1 wk after the end of heat exposure, and by 3 wk is 75% gone (24). Exactly when sweat sodium concentration is back to baseline is unclear, but it likely is just a few weeks.
IMPLICATIONS FOR ATHLETES
College football training exemplifies how heat acclimatization can wax and wane. During training in June and July, many players work out for an hour or so in the heat and so likely acclimatize somewhat. Depending on dietary sodium, this might lower their sweat sodium content. But they get a week off before August preseason ("2-a-days") training. If they spend this time relaxing in air conditioning, they lose some heat acclimatization and sweat sodium level rises. Then they face grueling August practices. Despite recent NCAA regulations that make the first week safer, it seems likely that, on the first hard day back in the heat, practicing 2.5 h, many of them heat up and sweat fast. Even if they are partly heat-acclimatized and "salt-saving," this high sweat rate would likely increase sweat sodium level and so foster a salt deficit and sequelae. Indeed, most major heat cramping in football, a multi-factorial problem, occurs during the first week of August practice.
A practical "dipstick" to gauge sweat sodium would be a boon for athletes who want to fathom their salt needs. Until such is invented, clinical clues to salty sweating include sweat that burns the eyes, stings abrasions, or tastes salty when it trickles into the mouth, along with white residue (salt) visible on caps, clothes, or skin. Orthostatic hypotension, reflecting hypovolemia, also can be a clue.
AGE AND GENDER EFFECTS
Some age and gender differences exist in sweating and sweat sodium. The sweat rate of boys, expressed per unit body surface area, is lower than in men (26). In contrast, there is little difference in sweat rate between girls and women (27). In children and adults, sweat sodium concentration rises with sweat rate. Yet at any given sweat rate, sweat sodium (or chloride) is lower in children (26).
Gender differences in sweat sodium in adults are inconsistent. Young women have lower sweat concentrations of chloride or sodium than young men in some but not all studies, and large intragroup variability is a confounder. As a group, females have a lower sweating rate than males (27).
In the elderly exercising in the heat, skin blood flow and peak sweat rates may be lower than in the young (28), but variability exists, fitness is key, and when the effects of disease are minimized, heat tolerance is compromised little by age. Older men, whether highly or normally fit, can acclimate well to the heat (29). Little is known about sweat sodium concentrations in the elderly.
IMPLICATIONS FOR ATHLETES
Age and gender differences in sweat sodium level are fairly minor and have little practical implication for athletes. In general, boys and women seem to have lower sweat rates and sweat sodium than men. This has theoretical implications for the composition of sports drinks or the threat of heat stress. Yet in sports, grave heat illness is more common in men. Exertional heatstroke deaths, for example, are rare in children and women. The warrior mentality may be the final enemy, as competitive men ignore warning signs and push beyond their limits (20-22).
Researchers long ago noted that, during heat acclimatization, salt-saving in sweat followed soon after a salt deficit via sweating and that men with no fall in sweat chloride (or sodium) were consuming enough salt to avoid a deficit. The sweat salt-saving was tied to increased activity of the adrenal cortex (30). Recent research agrees.
In a cross-over study, nine young men heat-acclimated via two 8-d regimens (daily 90-min walk, 40°C), on a high- (9.2 g·d-1) versus low- (2.3 g·d-1) sodium diet. Sweat electrolyte loss during the walk was gauged on d 1, 4, and 8 via whole body wash down. From d 1 to 8, sweat sodium fell about 40% (63 to 38 mmol) on low-sodium diet, but rose about 40% (61 to 87 mmol) on high-sodium diet (31).
If sweat sodium level rises on a high-sodium diet, how so? On the high-sodium diet in this study, subjects retained a mean excess of 21 g of sodium. Part of the excess was accounted for by a rise in both plasma volume and plasma sodium concentration. Possibly these changes inhibited aldosterone (not measured in the study) and so increased sweat sodium level on the high-sodium diet (31).
Two other studies of young men tie differences in dietary and sweat sodium to differences in aldosterone. In one, men heat-acclimated on a low-sodium diet (1.5 g·d-1 sodium), moderate-sodium diet (4 g·d-1), or high-sodium diet (8 g·d-1). During acclimation, sweat sodium fell in all three groups. In the 3-d lead-in phase, plasma aldosterone rose on the low-sodium diet but fell on the high-sodium diet (32). In the second study, after 2 wk on a low-sodium (50 mmol·d-1) or moderate-sodium (150 mmol·d-1) diet, sweat sodium level was 32% higher on the moderate-sodium diet (50 vs 38 mmol·L-1), and plasma aldosterone level was lower (33). These studies suggest that aldosterone suppression accounts for higher sweat sodium levels seen on diets higher in sodium.
IMPLICATIONS FOR ATHLETES
Differences in dietary sodium may account for some of the differences in sweat sodium levels in, for example, football players who cramp or not. Also, high-sodium diets can blunt or reverse the expected fall in sweat sodium during heat-acclimatization. In everyday life, especially in temperate climates with minimal sweating, the kidney is more critical than the sweat gland in maintaining sodium balance in the face of high- or low-sodium diets.
Salt-losing genes can predispose athletes to clinical problems because of sodium deficits from heavy sweating. These problems include heat cramping, plasma volume contraction, and hyponatremic dehydration (hypovolemia). Sweat salt concentration tends to rise in concert with sweat rate. Differences in dietary sodium can shape differences in sweat sodium level at baseline and during heat-acclimatization; these differences may occur largely by suppressing or enhancing the secretion of aldosterone or its action upon the sweat gland. Age and gender effects upon sweat sodium content seem fairly minor. Athletes can learn to increase salt in diet and sports drinks to help avoid performance and clinical consequences of "salty sweating." Inventing a "dipstick" to gauge sweat sodium concentration would be a boon to help fathom individual sodium needs among athletes.
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