Dehydration is how you define it: comparison of 318 blood and urine athlete spot checks.

Clinical medicine defines dehydration using blood markers that confirm hypertonicity (serum sodium concentration ([Na+])>145 mmol/L) and intracellular dehydration. Sports medicine equates dehydration with a concentrated urine as defined by any urine osmolality (UOsm) ≥700 mOsmol/kgH2O or urine specific gravity (USG) ≥1.020. OBJECTIVE: To compare blood versus urine indices of dehydration in a cohort of athletes undergoing routine screenings. METHODS: 318 collegiate athletes (193 female) provided blood and urine samples and asked to rate how thirsty they were on a 10-point visual analogue scale. Serum was analysed for [Na+], while serum and UOsm were measured using an osmometer. USG was measured using a Chemstrip. Data were categorised into dehydrated versus hydrated groupings based on these UOsm and USG thresholds. RESULTS: Using UOsm ≥700 mOsmol/kgH2O to define dehydration, 55% of athletes were classified as dehydrated. Using any USG ≥1.020 to define dehydration, 27% of these same athletes were classified as dehydrated. No athlete met the clinical definition for dehydration (hypertonicity; serum [Na+]>145 mmol/L). Normonatremia (serum [Na+] between 135 mmol/L and 145 mmol/L) was maintained in 99.7% of athletes despite wide variation in UOsm (110-1298 mOsmol/kgH2O). A significant correlation was confirmed between serum [Na+] versus UOsm (r=0.18; P<0.01), although urine concentration extremes did not reflect derangement in serum markers or thirst rating. CONCLUSION: Urine concentration thresholds classified 27%-55% of collegiate athletes as dehydrated, while no athlete was dehydrated according to blood [Na+] measurement. Practitioners should caution against using urine indices to diagnose or monitor dehydration, because urinary output is a response rather than a reflection of (tightly regulated) blood tonicity.

Effect of compression stockings on physiological responses and running performance in division III collegiate cross-country runners during a maximal treadmill test.

There is a growing trend for runners to use compression stockings (CS) to improve performance. The purpose of this study was to determine the effect of CS on physiological variables associated with running performance. Participants were 10 NCAA division III cross-country runners. The study used a randomized, crossover design with 2 conditions (with CS and without CS). Both conditions consisted of a maximal treadmill test that involved 3-minute stages of increasing speed and incline, separated by a minute and one-half walking recovery stage. Seven days later, the participants repeated the maximal test but switched CS condition. Heart rate, blood lactate (BLa), blood lactate threshold, maximal oxygen consumption (VO2max), respiratory exchange ratio, rating of perceived exertion, and time to fatigue were measured. Before and during the maximal treadmill tests, the variables showed no significant difference (p ≤ 0.05) between the CS conditions. Blood lactate was lower while wearing CS when measured during recovery at the 1-minute (CS = 13.3 ± 2.9 mmol · L(-1), non-CS = 14.8 ± 2.8 mmol · L(-1), p = 0.03) and the 5-minute (CS = 11.0 ± 2.7 mmol · L(-1), non-CS = 12.8 ± 2.8 mmol · L(-1), p = 0.02) periods. Time to fatigue was longer without CS (CS = 23.570 ± 2.39 minutes, non-CS = 23.93 ± 2.49 minutes, p = 0.04). These findings suggest that CS may not improve running performance, but could lend credence to certain manufacturers' claims of improved recovery through lower BLa values after exercise.

The need for salt: does a relationship exist between cystic fibrosis and exercise-associated hyponatremia?

Salt replacement is often recommended to prevent exercise-associated hyponatremia (EAH) despite a lack of evidence to support such practice. Exercise-associated hyponatremia is known to be a complex process resulting from the interplay of hydration, arginine vasopressin, and sodium balance. Although evidence suggests overhydration is the dominant pathophysiologic factor in most cases, the contributions of sweat sodium losses remain unclear. A theoretical genetic mechanism producing exuberant sweat sodium loss in athletes is the presence of cystic fibrosis (CF) gene. Individuals with CF develop hypovolemic hyponatremia by sodium loss via sweat through a defective chloride ion transport channel, the CF transmembrane conductance regulator (CFTR). Elevated sweat sodium concentrations in CF single heterozygotes suggest that athletes developing EAH may be CFTR carriers. We targeted the 2010 and 2011 Western States Endurance Run ultramarathon, an event where athletes with EAH regularly present in a hypovolemic state, for a cohort maximizing the potential to document such a relationship. A total of 798 runners started the 2010 (n = 423) and 2011 (n = 375) races. Of the 638 finishers, 373 were screened for EAH by blood draw, 60 (16%) were found to have EAH, and 31 (alpha = 0.05 for n = 9) reported their CF result from a saliva-based genetic testing kit. Neither the 31 EAH-positive athletes nor the 25 EAH-negative comparison cohort athletes tested positive for a CF mutation. This null relationship suggests that CFTR mutations are not associated with the development of EAH and that salt supplementation is unnecessary for such a reason.

The effect of physiology and hydration beliefs on race behavior and postrace sodium in 161-km ultramarathon finishers.

PURPOSE: To determine if beliefs about physiology and rehydration affect ultramarathon runners' hydration behaviors or if these beliefs increase the risk for exercise-associated hyponatremia (EAH). METHODS: Participants of the 2011 161-km Western States Endurance Run completed a prerace questionnaire, prerace and postrace body-mass measurements, and postrace assessment of serum sodium ([Na⁺]). RESULTS: Of 310 finishers, 309 (99.7%) completed the prerace questionnaire and 207 (67%) underwent postrace blood studies. Twelve (5.8%) finishers had asymptomatic EAH ([Na⁺] range 131-134 mmol/L). The most common hydration plan (43.1%) was drinking according to schedule, and these runners did so to replace fluid lost when sweating (100%) and to avoid dehydration (81.2%). Prerace drinking plan was not associated with postrace [Na⁺] or the development of postrace hyponatremia. There also were no group differences between those with and those without EAH for any other variables including planned energy intake or knowledge of fluid balance. Runners not planning to drink to thirst trended toward more influence from advertisements (P = .056) and were significantly more influenced by scientific organizations (P = .043) than runners with other drinking plans. Finally, runners who believe that EAH is caused by excessive drinking adopted a lower-volume drinking plan (P = .005), while runners who believe that EAH is caused by sodium loss via sweating reported more common use of sodium supplementation during the race (P = .017). CONCLUSIONS: Beliefs regarding the causes of EAH alter race behaviors including drinking plan and sodium supplementation but do not appear to affect the likelihood of developing EAH during a 161-km ultramarathon.