Evaluation and Treatment of Injury and Illness in the Ultramarathon Athlete

Ultramarathon runners commonly endure musculoskeletal pain during endurance events. However, the effect of pain coping skills on performance has not been examined.

A prospective observational study during three 250 km (155 mi), 6 stage ultramarathons was conducted. Finish line surveys were completed after each of the four 40 km (25 mi) and one 80 km (50 mi) stages of racing. Variables gathered included pain intensity, pain coping strategy use, pain interference, finishing position (quintile), and successful race completion.

A total of 204 participants (age 41.4±10.3 y; 73% male) reported average pain intensity of 3.9 (±2.0 SD) and worst pain intensity of 5.3 (±2.3) on a 0 to 10 scale. They used greater adaptive pain coping strategies (3.0±1.3) relative to maladaptive strategies (1.3±1.1). Worst pain and pain interference increased over each stage of the race for all runners (P<0.001), with worst pain being significantly different by finishing status (P=0.02). Although all runners endured increased pain and interference, the nonfinishers (28 [14%]) had significantly greater differences in changes in pain intensity (P<0.01) and pain interference (P<0.001). Maladaptive pain coping strategies were more common in nonfinishers; with each 1-point increase (0–6 scale), there was a 3 times increase in odds of not finishing the race.

Although increased pain intensity and pain interference was found in all multistage ultramarathon runners, successful event completion was significantly associated with less maladaptive pain coping. Training in coping with pain may be a beneficial part of ultramarathon preparation.

Ultramarathon races represent any foot race longer than 42 km and can occur over single or multiple days. The popularity of ultramarathon races continues to grow with increased participation and races throughout the world. Ultramarathons have unique challenges, commonly involving more extreme environments and variable terrain versus marathon races. Athletes, as well as care providers, ill prepared for such challenges will be at risk for injury, illness, and impaired performance. The goal of this chapter is to provide education and care guidance on musculoskeletal, integumentary, medical, and environmental illnesses to enhance safe and successful completion in ultramarathon participation.

Dysnatremia and altered hydration status are potentially serious conditions that have not been well studied in multistage ultramarathons. The purpose of this study was to assess the incidence and prevalence of exercise-associated hyponatremia (EAH) (Na⁺ <135 mmol·L^-1) and hypernatremia (Na⁺ >145 mmol·L^-1) and hydration status during a multistage ultramarathon.

This study involved a prospective observational cohort study of runners competing in a 250-km (155-mile) multistage ultramarathon (in the Jordan, Atacama, or Gobi Desert). Prerace body weight and poststage (stage [S] 1 [42 km], S3 [126 km], and S5 [250 km]) body weight and serum sodium concentration levels were obtained from 128 runners.

The prevalence of EAH per stage was 1.6% (S1), 4.8% (S3), and 10.1% (S5) with a cumulative incidence of 14.8%. Per-stage prevalence of hypernatremia was 35.2% (S1), 20.2% (S3), and 19.3% (S5) with a cumulative incidence of 52.3%. Runners became more dehydrated (weight change <–3%) throughout the race (S1=22.1%; S3=51.2%; S5=53.5%). Body weight gain correlated with EAH (r=–0.21, P = .02). Nonfinishers of S3 were significantly more likely to have EAH compared with finishers (75% vs 5%, P = .001), but there was no difference in either EAH or hypernatremia between nonfinishers and finishers of S5.

The incidence of EAH in multistage ultramarathons was similar to marathons and single-stage ultramarathons, but the cumulative incidence of hypernatremia was 3 times greater than that of EAH. EAH was associated with increased weight gain (overhydration) in early stage nonfinishers and postrace finishers.

Exercise-associated hyponatremia (EAH) is one of the most common causes of exercise-associated collapse. The primary pathogenesis of EAH is largely the result of excessive fluid intake but is influenced by other factors, including hormonal abnormalities (ie, inappropriate arginine vasopressin secretion), renal abnormalities, and mobilization of sodium stores. Early recognition of EAH is crucial to appropriate treatment, because symptoms are varied and may be confused with other causes of exercise-associated collapse. Onsite testing of [Na+] will confirm the diagnosis but is not always available. Rapid treatment of EAH will depend upon the type and severity of symptoms. Treatment protocols range from fluid restriction or oral hypertonic fluids for mild symptoms to intravenous hypertonic fluids for more severe symptoms. Preventative strategies should emphasize fluid consumption based on thirst and athlete/coach/staff education regarding proper hydration practices.