Results from the present study indicate that high-sodium (900 mg·hr-1) salt supplementation did not have a significant effect on indices of thermoregulation during long-duration, endurance exercise of moderate to vigorous intensity, as evidenced by no effect on sweat rate, perceived heat stress, or skin temperatures. Furthermore, salt supplementation did not significantly affect cardiovascular drift, rating of perceived exertion, or time to exhaustion. This research supports the findings of a field study conducted at an Ironman competition in which ad libitum salt consumption (~550 mg·hr-1) did not have a significant impact on weight change, perceived exertion or performance (Hew-Butler et al., 2006). Coles and Luetkemeier found no effect of pre-exercise sodium ingestion on measures of thermoregulation, including core body temperature and sweat rate, during a shorter duration exercise test (45-minute cycling test, followed by a 15-minute time trial) (Coles and Luetkemeier, 2005). However, findings from the present study refute two other studies, one that tested moderately trained, male runners, and the other that tested endurance trained, female cyclists. These earlier studies showed that sweat rates were significantly lower with ingestion of high-sodium fluid, although the lengths of the tests were shorter than the present study (~75-98 minutes at 70% VO2peak), and the intervention fluids were administered pre-exercise (Sims et al., 2007a; 2007b). As mentioned previously, the participants in the present study were required to be trained endurance athletes. However, a range of training levels still existed, with some participants being more endurance-trained than others. It is known that training results in certain physiological adaptations, including changes in response to heat stress with acclimatization. One such adaption is an increased sweat response and sweat rate with changes in core body temperature (Shibasaki et al., 2006). Therefore, variations in the level of training among participants may have caused some heterogeneity in responses to the intervention. Furthermore, while all participants completed the study within a 7-26 day time window (mean ± SD, 13.5 ± 6.45 days), it is possible that that changes in training status and the degree of acclimatization between study trials might have confounded the results. Lastly, the time course of the study spanned from spring to summer, and sweat rates vary with changes in environmental conditions (Torii et al., 1992). However, the likelihood of this being a confounding factor is minimal, as the study procedures were performed in a laboratory where temperature and relative humidity remained consistent throughout the study (mean 21.22°C and 36.55%, respectively). The current study assessed perceived heat stress using a thermal sensations rating scale and showed no difference in the ratings between the SS and PL trials. It might be argued that these heat stress ratings did not differ between trials because the exercise was not performed in a heat chamber. However, mean thermal ratings were 5 to 6 on a 0 to 8 scale, indicating that the participants perceived a substantial heat stress. Furthermore, mean weight losses of 2.03% in the SS trial and 2.26% in the PL trial (despite meeting water consumption recommendations), and respective sweat rates of 1.02 L·hr-1 and 1.03 L·hr-1, provide physiologic evidence of heat stress. It is noteworthy that a 2% change in body weight is reflective of significant dehydration (hyperosmolar hypohydration) and this has been shown to reduce active cutaneous vasodilation (Shibasaki et al., 2009), which preserves blood pressure but further exacerbates heat stress. Sodium supplementation is thought to alter heat stress through mechanisms involving serum osmolality. However, another factor besides sodium intake that affects osmolality is water consumption, via hemoconcentration and/or hemodilution. During dehydration, blood volume decreases to a greater extent than serum sodium levels, thereby creating hyperosmotic state and decreasing sweat rates despite increases in core temperature (Sawka et al., 1985). Furthermore, hyperosmolality after an infusion of hypertonic saline has been shown to decrease sweat rate and increase the core temperature threshold for cutaneous vasodilation during heat stress (Shibasaki et al., 2009). The high-dose sodium that was administered during the present study would have been expected to increase serum osmolality and thus decrease sweat rates. In this context, it is surprising that sweat rates did not differ between PL and SS trials. In addition to serum osmolality being a determinant of sweat rates, blood volume also affects sweat rates, albeit to a lesser extent than osmolality (Sawka et al., 1985). Isosmotic hypovolemia (volume depletion without alterations in osmolality) has been demonstrated to reduce sweat rates, which is an effect thought to be important for preserving blood volume during exercise (Fortney et al., 1981). In the present study, the ~2% weight losses during exercise suggest that hypovolemia may have occurred and this may have decreased sweat rates during the 2-hr exercise bout. However, based on the comparable changes in body weight, changes in blood volume would likely have been similar between trials and therefore would not contribute to differences in sweat rates. In contrast to isotonic hypovolemia, isotonic hypervolemia (induced with water or glycerol) does not alter sweat rates (Fortney et al., 1981; Latzka et al., 1997). In the light of significant decreases in body weight during exercise in the present study, it is highly unlikely that hypervolemia occurred. Therefore, while hypervolemia from overhydration can lead to hemodilution and hyponatremia (Rosner, 2008), which may have important health consequences, it is not an important factor in the interpretation of sweat rate results from the present study. There are several possible explanations for why the results did not reach significance or demonstrate an effect on the endurance performance parameters that were measured. One possibility is that the sample was too small. The a priori goal in our study was to determine if salt supplementation had a clinically relevant effect on sweat rate as the primary outcome variable (a clinically relevant change in sweat rate was defined as 10% or 142 ml/hr based on previous unpublished research from our laboratory). A post-hoc power analysis indicated that power for the present study was 0.85 for a 1-tailed test and 0.74 for a two-tailed test, suggesting that statistical power was adequate for detecting a clinically relevant effect, if such an effect was present. Prior to each test, participants were required to follow a sodium-restricted (<2300 mg·day-1) diet and record all food and beverage intake for 48 hours. Self-reported food diaries carry some degree of error in accuracy, and the amount of dietary sodium and fluid intake may have varied between tests. Although the food diaries were not analyzed to quantify exact nutrient intakes, they were compared on a qualitative basis, and with the exception of some small-to-modest variations in dietary intakes between trials the participants largely consumed the same diet prior to the two trials. The same limitation is true for the recorded exercise logs that participants were required to fill out for 48 hours prior to testing; again, based on qualitative review of the exercise logs, the participants reported similar activity patterns before the two study trials. Skin temperature was measured using a non-contact infrared thermometer. The measurements were taken on the biceps, calf, thigh, and chest, although temperature readings are subject to variations due to air movement, sweat on the skin, and other unknown variables. While not feasible for the current study, future studies may benefit from measuring core body temperature as a more optimal indication of changes in thermoregulation. |