Kristin J. Stuempfle, Martin D. Hoffman and Tamara Hew-Butler
Gastrointestinal (GI) distress is common during ultrarunning.
To determine if race diet is related to GI distress in a 161-km ultramarathon.
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.
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.
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.
Martin D. Hoffman, Kristin J. Stuempfle, Ian R. Rogers, Louise B. Weschler and Tamara Hew-Butler
To determine the incidence of exercise-associated hyponatremia (EAH), the associated biochemical measurements and risk factors for EAH, and whether there is an association between postrace blood sodium concentration ([Na+]) and changes in body mass among participants in the 2009 Western States Endurance Run, a 161-km mountain trail run.
Change in body mass, postrace [Na+], and blood creatine phosphokinase (CPK) concentration, and selected runner characteristics were evaluated among consenting competitors.
Of the 47 study participants, 14 (30%) had EAH as defined by a postrace [Na+] <135 mmol/L. Postrace [Na+] and percent change in body mass were directly related (r = .30, P = .044), and 50% of those with EAH had body mass losses of 3–6%. EAH was unrelated to age, sex, finish time, or use of nonsteroidal anti-inflammatory drugs during the run, but those with EAH had completed a smaller (P = .03) number of 161-km ultramarathons. The relationship of CPK levels to postrace [Na+] did not reach statistical significance (r = –.25, P = .097).
EAH was common (30%) among finishers of this 161-km ultramarathon and it was not unusual for those with EAH to be dehydrated. As such, changes in body mass should not be relied upon in the assessment for EAH during 161-km ultramarathons.
James M. Winger, Martin D. Hoffman, Tamara D. Hew-Butler, Kristin J. Stuempfle, Jonathan P. Dugas, Kevin Fogard and Lara R. Dugas
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).
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+]).
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).
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.