A Placebo-Controlled Trial of Riboflavin for Enhancement of Ultramarathon Recovery.

BACKGROUND: Riboflavin is known to protect tissue from oxidative damage but, to our knowledge, has not been explored as a means to control exercise-related muscle soreness. This study investigated whether acute ingestion of riboflavin reduces muscle pain and soreness during and after completion of a 161-km ultramarathon and improves functional recovery after the event. METHODS: In this double-blind, placebo-controlled trial, participants of the 2016 161-km Western States Endurance Run were assigned to receive a riboflavin or placebo capsule shortly before the race start and when reaching 90 km. Capsules contained either 100 mg of riboflavin or 95 mg of maltodextrin and 5 mg of 10% ß-carotene. Subjects provided muscle pain and soreness ratings before, during, and immediately after the race and for the 10 subsequent days. Subjects also completed 400-m runs at maximum speed on days 3, 5, and 10 after the race. RESULTS: For the 32 (18 in the riboflavin group, 14 in the placebo group) race finishers completing the study, muscle pain and soreness ratings during and immediately after the race were found to be significantly lower (p = .043) for the riboflavin group. Analysis of the 400-m run times also showed significantly faster (p < .05) times for the riboflavin group than the placebo group at post-race days 3 and 5. Both groups showed that muscle pain and soreness had returned to pre-race levels by 5 days after the race and that 400-m run times had returned to pre-race performance levels by 10 days after the race. CONCLUSIONS: This preliminary work suggests that riboflavin supplementation before and during prolonged running might reduce muscle pain and soreness during and at the completion of the exercise and may enhance early functional recovery after the exercise.

Determinants of recovery from a 161-km ultramarathon.

The primary study objective was to identify determinants of short-term recovery from a 161-km ultramarathon. Participants completed 400 m runs at maximum speed before the race and on days 3 and 5 post-race, provided a post-race blood sample for plasma creatine kinase (CK) concentration, and provided lower body muscle pain and soreness ratings (soreness, 10-point scale) and overall muscular fatigue scores (fatigue, 100-point scale) pre-race and for 7 days post-race. Among 72 race finishers, soreness and fatigue had statistically returned to pre-race levels by 5 days post-race; and 400 m times at days 3 and 5 remained 26% (P = 0.001) and 12% (P = 0.01) slower compared with pre-race, respectively. CK best modelled soreness, fatigue and per cent change in post-race 400 m time. Runners with the highest CKs had 1.5 points higher (P < 0.001) soreness and 11.2 points higher (P = 0.006) fatigue than runners with the lowest CKs. For the model of 400 m time, a significant interaction of time with CK (P < 0.001) indicates that higher CKs were linked with a slower rate of return to pre-race 400 m time. Since post-race CK was the main modifiable determinant of recovery following the ultramarathon, appropriate training appears to be the optimal approach to enhance ultramarathon recovery.

The influence of hydration state on thermoregulation during a 161-km ultramarathon.

It is advised that individuals should avoid losing >2% of their body mass during exercise in order to prevent hyperthermia. This study sought to assess whether a loss of >2% body mass leads to elevations in core temperature during an ultramarathon. Thirty runners agreed to take part in the study. Body mass and core temperature were measured at the start, at three locations during the race and the finish. Core temperature was not correlated with percent body mass change (p = 0.19) or finish time (p = 0.11). Percent body mass change was directly associated with finish time (r = 0.58, p < 0.01), such that the fastest runners lost the most mass (~3.5-4.0%). It appears that a loss of >3% body mass does not contribute to rises in core temperature. An emphasis on fluid replacement for body mass losses of this magnitude during prolonged exercise is not justified as a preventative measure for heat-related illnesses.

A Randomized Controlled Trial of Massage and Pneumatic Compression for Ultramarathon Recovery.

Study Design Randomized controlled trial. Background Postexercise recovery techniques are widely used, but little research has examined their effectiveness. Objectives To examine the effectiveness of massage and pneumatic compression on recovery from a 161-km ultramarathon. Methods Participants in the 2015 161-km Western States Endurance Run were randomized to a 20-minute postrace intervention of massage, intermittent sequential pneumatic compression, or supine rest. Each subject completed two 400-m runs at maximum speed before the race and on days 3 and 5 after the race, and also provided muscle pain and soreness ratings and overall muscular fatigue scores before and for 7 days after the race. Results Among the 72 runners who finished the race and completed the study, comparison among intervention groups revealed no significant group or interaction effect on 400-m run time, but there was a significant (P<.0001) time effect. Immediately posttreatment, massage resulted in lower muscle pain and soreness ratings compared with the supine-rest control condition (P<.0001), while both massage (P<.0001) and pneumatic compression (P<.01) resulted in lower overall muscular fatigue scores compared with the control group. There were no significant differences between groups in any outcome 1 to 7 days after the race. Conclusion Single 20-minute sessions of postrace massage and intermittent sequential pneumatic compression provide some immediate subjective benefit. There is no evidence, however, that such treatments provide extended subjective or functional benefits of clinical importance. The trial was registered at www.clinicaltrials.gov (NCT02530190). Level of Evidence Therapy, level 1b. J Orthop Sports Phys Ther 2016;46(5):320-326. Epub 23 Mar 2016. doi:10.2519/jospt.2016.6455.

Does oral buffered sodium supplementation reduce nausea and vomiting during an ultramarathon?

This work examines whether nausea or vomiting during an ultramarathon are due to a fluid or electrolyte imbalance, and if these symptoms can be reduced through the use of buffered sodium supplements. Starters (n = 376) of a 161.3-km ultramarathon underwent body weight measurements, 74.5% completed a post-race questionnaire, and 53.0% also underwent a post-race blood draw. The incidence of nausea or vomiting progressively increased during the race, and affected 60% of runners overall. Weight change and rate of sodium intake in supplements or in buffered sodium supplements did not differ between those with and without nausea or vomiting. Post-race serum sodium concentration also did not differ between those with and without symptoms in the last race segment. We conclude that weight change, the rate of sodium intake in supplements or in buffered sodium supplements, and serum sodium concentration are not related to symptoms of nausea or vomiting during a 161-km ultramarathon.

Is Sodium Supplementation Necessary to Avoid Dehydration During Prolonged Exercise in the Heat?

The primary purpose of this work was to gain further insight into the need for sodium supplementation for maintenance of appropriate hydration during prolonged exercise under hot conditions. Participants of a 161-km ultramarathon (ambient temperature reaching 39° C) underwent body weight measurements immediately before, during, and after the race, and completed a postrace questionnaire about supplemental sodium intake and drinking strategies during 4 race segments. The postrace questionnaire was completed by 233 (78.7%) race finishers. Significant direct relationships were found for percentage weight change during the race with intake rate (r = 0.18, p = 0.0058) and total amount (r = 0.24, p = 0.0002) of sodium in supplements. Comparing those using no sodium supplements throughout the race (n = 15) with those using sodium supplements each race segment (n = 138), body weight change across the course showed significant group (p = 0.022), course location (p < 0.0001), and interaction (p = 0.0098) effects. Posttests revealed greater weight loss at 90 km (p = 0.016, -3.2 ± 1.6% vs. -2.2 ± 1.5%, mean ± SD) and the finish (p = 0.014, -3.2 ± 1.5% vs. -1.9 ± 1.9%) for those using no sodium supplements compared with those using sodium supplements each segment. Six runners who used no sodium supplements, drank to thirst, and only drank water or a mixture of mostly water with some electrolyte-containing drink finished with mean weight change of -3.4%. Although the use of supplemental sodium enhanced body weight maintenance, those not using sodium supplements maintained a more appropriate weight than those consistently using sodium supplements. Therefore, we conclude that the supplemental sodium is unnecessary to maintain appropriate hydration during prolonged exercise in the heat.

Nausea is associated with endotoxemia during a 161-km ultramarathon.

This study explored possible contributing factors to gastrointestinal distress, including endotoxemia, hyperthermia, dehydration and nutrition, during a 161-km ultramarathon. Thirty runners participated in the study and 20 finished the race. At three checkpoints and the finish, runners were interviewed to assess the incidence and severity of 12 gastrointestinal symptoms and to determine dietary intake. Core temperature was measured at the same locations. Runners were weighed pre-race, at the three checkpoints and the finish to monitor hydration status. Blood markers for endotoxemia (sCD14) and inflammation (interleukin-6 and C-reactive protein) were measured pre- and post-race. Gastrointestinal symptoms were experienced by most runners (80%), with nausea being the most common complaint (60%). Runners with nausea experienced significantly greater (P = 0.02) endotoxemia than those without nausea (sCD14 mean increase 0.7 versus 0.5 µg · mL(-1)). There was a significant positive correlation (r = 0.652, P = 0.005) between nausea severity and endotoxemia level. Inflammatory response, core temperature, hydration level and race diet were similar between runners with and without nausea. This study links endotoxemia to nausea in ultramarathon runners. Other possible contributing factors to nausea such as hyperthermia, dehydration and nutrition did not appear to play a role in the symptomatic runners in this study.

Sodium Intake During an Ultramarathon Does Not Prevent Muscle Cramping, Dehydration, Hyponatremia, or Nausea.

BACKGROUND: Ultramarathon runners commonly believe that sodium replacement is important for prevention of muscle cramping, dehydration, hyponatremia, and nausea during prolonged continuous exercise. The purpose of this study was to measure total sodium intake to determine if these beliefs are supported. METHODS: Participants of a 161-km ultramarathon (air temperature reaching 39 °C) provided full dietary information during the race, underwent body weight measurements before and after the race, completed a post-race questionnaire about muscle cramping and nausea or vomiting during the race, and had post-race plasma sodium concentration measured. RESULTS: Among 20 finishers providing dietary data, mean (±SD) total sodium intake was 13,651 ± 8444 mg (range 2541-38,338 mg), and sodium in food and drink accounted for 66 % of the sodium when averaged across subjects (range 34-100 %). Sodium intake rates were similar when comparing the 10 % of subjects who were hyponatremic with those who were not hyponatremic, the 39 % with muscle cramping or near cramping with those without cramping, and the 57 % who reported having symptoms of nausea or vomiting with those without these symptoms. Weight change between race start and finish was significantly related to rate of sodium intake (r = 0.49, p = 0.030) and total sodium intake (r = 0.53, p = 0.016), but the maximum weight loss among those taking the least total sodium (<4400 mg total sodium during the race) was 4-5 % below the weight measured immediately pre-race. CONCLUSIONS: Exercise-associated muscle cramping, dehydration, hyponatremia, and nausea or vomiting during exercise up to 30 h in hot environments are unrelated to total sodium intake, despite a common belief among ultramarathon runners that sodium is important for the prevention of these problems.

Muscle Cramping During a 161-km Ultramarathon: Comparison of Characteristics of Those With and Without Cramping.

BACKGROUND: This work sought to identify characteristics differing between those with and without muscle cramping during a 161-km ultramarathon. METHODS: In this observational study, race participants underwent body weight measurements before, during, and after the race; completed a post-race questionnaire about muscle cramping and "near" cramping (controllable, not reaching full-blown cramping), drinking strategies, and use of sodium supplementation during four race segments; and underwent a post-race blood draw for determination of serum sodium and blood creatine kinase (CK) concentrations. RESULTS: The post-race questionnaire was completed by 280 (74.5 %) of the 376 starters. A post-race blood sample was provided by 181 (61.1 %) of the 296 finishers, and 157 (53.0 %) of finishers completed the post-race survey and also provided a post-race blood sample. Among those who completed the survey, the prevalence of cramping and near cramping was 14.3 and 26.8 %, respectively, with greatest involvement being in the calf (54 %), quadriceps (44 %), and hamstring (33 %) muscles. Those with cramping or near cramping were more likely to have a prior history of muscle cramping during an ultramarathon (p < 0.0001) and had higher blood CK concentrations (p = 0.001) than those without cramping. Weight change during the race, use of sodium supplements, intake rate of sodium in supplements, and post-race serum sodium concentration did not differ between those with and without cramping. CONCLUSIONS: Muscle cramping is most common in those with a prior history of cramping and greater muscle damage during an ultramarathon, suggesting an association with relative muscular demand. Impaired fluid and sodium balance did not appear to be an etiology of muscle cramping during an ultramarathon.

Sodium Supplementation and Exercise-Associated Hyponatremia during Prolonged Exercise.

PURPOSE: This work examines whether sodium supplementation is important in prevention of hyponatremia during continuous exercise up to 30 h and whether any distinguishing characteristics of those developing hyponatremia could be identified. METHODS: Participants of the 161-km Western States Endurance Run underwent body weight measurements before, during, and after the race, completed a postrace questionnaire about drinking strategies and use of sodium supplementation during four race segments, and underwent analysis of postrace serum sodium concentration. RESULTS: The postrace questionnaire was completed by 74.5% of the 376 starters, a postrace blood sample was provided by 61.1% of the 296 finishers, and 53.0% of finishers completed the postrace survey and also provided a postrace blood sample. Among this population, the incidence of hyponatremia among finishers was 6.6% and sodium supplements were used by 93.9% of the runners. Postrace serum sodium concentration was found to be directly related to the rate of sodium intake in supplements (r = 0.24, P = 0.0027) and indirectly related to the percentage change in body weight from immediately before the race start (r = -0.19, P = 0.010). There was no difference in rate of sodium intake in supplements between the hyponatremic and normonatremic finishers, and none of the hyponatremic finishers lost >4.3% body weight. Hyponatremic finishers were not distinguished from normonatremic or hypernatremic finishers by other runner characteristics considered, drinking strategies, or gastrointestinal symptoms of nausea and vomiting. CONCLUSIONS: We conclude that a low sodium intake in supplements has minimal responsibility for development of hyponatremia during continuous exercise up to 30 h, whereas overhydration is the primary characteristic of those developing hyponatremia. Therefore, avoiding overhydration seems to be the most important means for preventing hyponatremia under these conditions.

Exercise-associated hyponatremia with exertional rhabdomyolysis: importance of proper treatment.

BACKGROUND: Proper acute management of exercise-associated hyponatremia (EAH) has been known for decades, yet this information has not been uniformly implemented. Since treatment of EAH with isotonic fluids can result in delayed recovery and death, it is important that proper acute management in the field and hospital be utilized. CASE REPORT: We describe a participant of the 161-km Western States Endurance Run (WSER) who presented with seizure after dropping out at 145 km. He had gained 2.2% of his initial weight by 126 km from using sodium supplements and drinking copious volumes of fluids. He was treated promptly in the field for presumed EAH with two intravenous boluses of 100 mL of 3% hypertonic saline and showed rapid improvement in neurologic status. His recovery was then delayed with the use of high volumes of intravenous isotonic fluids, apparently for concern over his mild exertional rhabdomyolysis. CONCLUSIONS: Symptomatic EAH should be acutely managed with hypertonic saline, whereas treatment with high volumes of isotonic fluids may delay recovery and has even resulted in deaths from cerebral edema. Concern over central pontine myelinolysis from rapid correction of hyponatremia in EAH is unsupported. Furthermore, the exertional rhabdomyolysis often associated with EAH, and the concern over progression to acute kidney failure, should not dictate initial treatment.

Hydration strategies, weight change and performance in a 161 km ultramarathon.

To examine controversies about hydration strategies, participants (383 starters) of a 161 km ultramarathon (maximum temperature 39.0°C) underwent body weight measurements before, during and after the race; and completed a post-race questionnaire on drinking strategies and sodium supplementation use during 4 race segments. Drinking to thirst was the most common (p < 0.01) drinking strategy (used by 67.0% during at least one segment) and most runners (95.6%) used sodium supplementation during at least one segment. There was no difference in the extent of weight loss (mean 2.0-3.1%) or the weight change pattern when comparing groups using different hydration strategies. Among top-10 finishers, half had lost more than 2% of starting body weight by 90 km. We conclude that weight loss greater than 2% does not necessarily have adverse consequences on performance, and use of sodium supplements or drinking beyond thirst is not required to maintain hydration during ultra-endurance events with high thermal stress.

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.

Efficacy of oral versus intravenous hypertonic saline in runners with hyponatremia.

OBJECTIVES: To determine more conclusively whether intravenous (IV) administration of 3% saline is more efficacious than oral administration in reversing below normal blood sodium concentrations in runners with biochemical hyponatremia. DESIGN: Randomized controlled trial. METHODS: 26 hyponatremic race finishers participating in the 161-km Western States Endurance Run were randomized to receive either an oral (n=11) or IV (n=15) 100mL bolus of 3% saline. Blood sodium concentration (Na(+)), plasma protein (to assess %plasma volume change), arginine vasopressin (AVP), blood urea nitrogen (BUN) and urine (Na(+)) were measured before and 60 min following the 3% saline intervention. RESULTS: No significant differences were noted with respect to pre- to post-intervention blood [Na(+)] change between intervention groups, although blood [Na(+)] increased over time in both intervention groups (+2 mmol/L; p<0.0001). Subjects receiving the IV bolus had a greater mean (± SD) plasma volume increase (+8.6 ± 4.5% versus 1.4% ± 5.7%; p<0.01) without significant change in [AVP] (-0.2 ± 2.6 versus 0.0 ± 0.5 pg/mL; p=0.49). 69% of subjects completing the intervention trial were able to produce urine at race finish with a mean (± SD) pre-intervention urine [Na(+)] of 15.2 ± 8.5 mmol/L (range 0-35; NS between groups). [BUN] of the entire cohort pre-intervention was 30.7 ± 10.5mg/dL (range 13-50). CONCLUSIONS: No group difference was noted in the primary outcome measure of change in blood [Na(+)] over 60 min of observation following a 100mL bolus of either oral or IV 3% saline. Administration of an oral hypertonic saline solution can be efficacious in reversing low blood sodium levels in runners with mild EAH.

Characteristics of 161-km ultramarathon finishers developing exercise-associated hyponatremia.

This study sought to identify runner characteristics or symptoms that could distinguish those finishers developing exercise-associated hyponatremia (EAH) from those not developing EAH in a 161-km ultramarathon. Of 310 finishers, 207 (67%) underwent postrace blood studies. Twelve (6%) finishers had EAH (blood sodium range 131-134 mmol/L). Experience at 161-km ultramarathons was lower (p = 0.01) and blood creatine kinase (CK) concentration was higher (p = 0.04) among those with EAH than those not developing EAH. Blood sodium and CK concentration were negatively correlated (p = 0.0015, r = -0.22). There were no group differences in age, sex, regular running experience, weekly training distance, use of sodium supplements during training, immediately postrace sodium palatability and thirst ratings, body mass change, urination frequency, nonsteroidal anti-inflammatory drugs (NSAIDs) use, and various symptoms experienced during the race. These findings indicate that a clinical suspicion and measurement of blood sodium concentration remain the only viable means for determining when an ultramarathon runner has EAH.

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.

The effects of an acute dose of Rhodiola rosea on endurance exercise performance.

The purpose of this study was to determine the effects of an acute oral dose of 3 mg·kg(-1) of Rhodiola rosea on endurance exercise performance, perceived exertion, mood, and cognitive function. Subjects (n = 18) ingested either R. rosea or a carbohydrate placebo 1 hour before testing in a double-blind, random crossover manner. Exercise testing consisted of a standardized 10-minute warm-up followed by a 6-mile time trial (TT) on a bicycle ergometer. Rating of perceived exertion (RPE) was measured every 5 minutes during the TT using a 10-point Borg scale. Blood lactate concentration, salivary cortisol, and salivary alpha amylase were measured before warm-up, 2 minutes after warm-up, and 2 minutes after TT (n = 15). A Profile of Mood States questionnaire and a Stroop Color Test were completed before warm-up and after TT. Testing was repeated 2-7 days later with the other condition. Rhodiola rosea ingestion significantly decreased heart rate during the standardized warm-up (R. rosea = 136 ± 17 b·min(-1); placebo = 140 ± 17 b·min(-1); mean ± SD; p = 0.001). Subjects completed the TT significantly faster after R. rosea ingestion (R. rosea = 25.4 ± 2.7 minutes; placebo = 25.8 ± 3.0 minutes; p = 0.037). The mean RPE was lower in the R. rosea trial (R. rosea = 6.0 ± 0.9; placebo = 6.6 ± 1.0; p = 0.04). This difference was even more pronounced when a ratio of the RPE relative to the workload was calculated (R. rosea = 0.048 ± 0.01; placebo = 0.057 ± 0.02; p = 0.007). No other statistically significant differences were observed. Acute R. rosea ingestion decreases heart rate response to submaximal exercise and appears to improve endurance exercise performance by decreasing the perception of effort.

Association of gastrointestinal distress in ultramarathoners with race diet.

CONTEXT: Gastrointestinal (GI) distress is common during ultrarunning. PURPOSE: To determine if race diet is related to GI distress in a 161-km ultramarathon. METHODS: Fifteen (10 male, 5 female) consenting runners in the Javelina Jundred (6.5 loops on a desert trail) participated. Body mass was measured immediately prerace and after each loop. Runners reported if they had nausea, vomiting, abdominal cramps, and/or diarrhea after each loop. Subjects were interviewed after each loop to record food, fluid, and electrolyte consumption. Race diets were analyzed using Nutritionist Pro. RESULTS: Nine (8 male, 1 female) of 15 runners experienced GI distress including nausea (89%), abdominal cramps (44%), diarrhea (44%), and vomiting (22%). Fluid consumption rate was higher (p = .001) in runners without GI distress (10.9 ± 3.2 ml · kg-1 · hr-1) than in those with GI distress (5.9 ± 1.6 ml · kg-1 · hr-1). Runners without GI distress consumed a higher percentage fat (p = .03) than runners with GI distress (16.5 ± 2.6 vs. 11.1 ± 5.0). In addition, fat intake rate was higher (p = .01) in runners without GI distress (0.06 ± 0.03 g · kg-1 · hr-1) than in runners with GI distress (0.03 ± 0.01 g · kg-1 ·hr-1). Lower fluid and fat intake rates were evident in those developing GI distress before the onset of symptoms. CONCLUSIONS: A race diet with higher percentage fat and higher intake rates of fat and fluid may protect ultramarathoners from GI distress. However, these associations do not indicate cause and effect, and factors other than race diet may have contributed to GI distress.