Gastrointestinal Medicine in the Athlete

Gastrointestinal (GI) conditions in athletes and active individuals are common and are seen frequently by sports medicine care providers. Although there are many well-defined benefits that result from high-level physical activity, exercise places significant stress on the GI tract, which in turn may result in a number of characteristic GI disorders. Collectively, GI problems are perhaps the most common cause of underperformance in endurance sports and may also impact on subsequent recovery. The appreciation of this relationship is important for both care providers and athletes who must team together to minimize distressing GI symptoms and to prevent subsequent impairment in performance.

GI disorders in athletes often mimic those seen in the general population but may also present as unique entities seen primarily in those who exercise at a high level. This chapter will address a number of these common conditions, with a focus on their recognition and appropriate management in athletes.

Pathophysiology

Frequent, high-intensity exercise may cause a number of undesirable GI symptoms, such as heartburn, chest pain, bloating, belching, nausea, vomiting, abdominal cramps, frequent urge to defecate, diarrhea, and GI bleeding. Historically, these symptoms have been reported by up to 50% of endurance athletes and are more common in women and younger athletes. Body position and movement appear to play a role because the forward positioning of cyclists appears to protect them from GI tract issues as opposed to the higher-impact, jostling abdominal movements of runners. Other suggested mechanisms for increased GI distress include a number of neuro-immuno-endocrine adaptations to exercise. Increased catecholamines and several GI peptides including gastrin, motilin, secretin, peptide histidine-methionine, and vasoactive intestinal peptide result in increased gut transit time with negative effects on digestion and absorption.

Gastrointestinal Tract Ischemia

GI tract ischemia secondary to attenuated GI blood flow is a well-defined exercise adaptation that results from the redirection of blood flow to active muscles and the pulmonary vasculature. Vigorous exertion, hyperthermia, dehydration, hypoglycemia, mental stress, and fatigue all increase sympathetic nervous system activity, which in turn shunts blood away from the GI viscera to provide increased blood and oxygen supply to working muscles. Exercising moderately at up to 70% of maximum oxygen uptake (VO _{2 max} ) reduces blood flow to the GI tract by 60% to 70%, and higher-intensity exercise may result in GI blood flow reductions exceeding 80%. Subsequent impairment in oxygen delivery to GI tract structures may result in mucosal injury, increased gut mucosal permeability, increased risk for occult blood loss, translocation of protective bacterial flora, and generation of endotoxins. These changes contribute to ischemia-associated GI symptoms, including nausea, vomiting, abdominal pain, and bloody diarrhea. It has been postulated that GI complaints relating to gut ischemia are the result of a reperfusion injury after exercise has ceased. Reperfusion after ischemia may result in a number of chemical and vascular changes that result in “leaky mucosa.” When this occurs, the GI tract partially loses its barrier ability to protect itself from inherently irritating intraluminal substances such as endotoxins, food antigens, digestive enzymes, and bile.

Impact of Nutrition and Hydration

The overall fluid status of athletes has been shown to play an important role in the relative GI toxicity of high-level activity. Dehydration contributes significantly to GI tract dysfunction because it further accentuates the intrinsic blood flow changes associated with exercise, as noted previously. Research has shown that 80% of runners who lose at least 4% of their body weight from fluid losses during exercise experience lower GI tract symptoms. Exercise-related fluid and electrolyte shifts result in intracellular electrolyte imbalances and cell dysfunction, which may lead to colonic smooth muscle and mucosal irritation. In runners with restricted water intake, GI symptoms are more likely to arise due to increases in upper GI tract and intestinal permeability relative to resting individuals. In a study of nutritional intake patterns in endurance athletes, it was shown that high rates of carbohydrate intake (up to 90 g/h) were associated with an increased risk for nausea and flatulence. In contrast, ingestion of a lower-carbohydrate liquid meal before exercise is generally well tolerated, may help to maintain GI tract perfusion, and may prevent gut ischemia related to decreased splanchnic blood flow.

Upper Gastrointestinal Tract Conditions

Upper GI tract complaints are experienced by 30% to 70% of athletes, with the prevailing conditions being gastroesophageal reflux disease (GERD) and dyspepsia. When assessing the pathophysiology behind the high rate of upper GI tract symptoms in athletes, three primary mechanisms have been postulated: (1) mechanical forces, (2) alterations in GI tract blood flow, as noted previously, and (3) neuroendocrine changes that influence overall GI tract function. Mechanical forces include increased abdominal pressure from straining in high-exertion activities such as weightlifting, mechanical trauma to the GI tract from repetitive motion of the abdomen during exercise, and the impact of body position during exercise such as the flexed/compressed position of cyclists. GI mucosal activity and alterations in absorption may result from mechanical factors or neuroendocrine changes. Neural activity changes, as referenced previously, have all been documented to negatively influence GI tract function in athletes.

Exercise also greatly affects esophageal motility. Relaxation of the lower esophageal sphincter (LES), increased pressure gradient between the stomach and esophagus, and decreased esophageal clearance of food all have been associated with high-level physical exertion, and all appear to be potentially important in the development of GERD symptoms. As exercise intensity reaches peak levels exceeding 90% of VO _{2 max} , the frequency and duration of esophageal reflux episodes increase. Exercise type also influences esophageal motility. Running has been found to decrease upper GI tract motility more than cycling, and the highest rate of heartburn and esophageal reflux has been seen in weightlifters, with correspondingly lower rates found in runners and cyclists.

Gastroesophageal Reflux Disease

GERD is the most common cause of upper GI tract symptoms in athletes and results from the irritating effects of acidic gastric secretions as they reflux up into the esophagus due to loss of competence of the LES. The incidence of GERD increases with intensity of exercise, is more common in endurance sports, and is exacerbated by postprandial exercise. Runners demonstrate a threefold increase in GERD symptoms when running 45 minutes after completing a meal as compared with running in a fasting state. Activities with large increases in intra-abdominal pressure, most notably weightlifting and cycling when in the “aero” position, contribute to higher rates of symptomatic GERD as the LES is overwhelmed by the external pressure applied to the stomach.

Cardinal features of GERD include heartburn, retrosternal burning, and regurgitation with a sense of refluxed gastric contents arising into the mouth or hypopharynx. The majority of athletes with true exertional GERD actually have GERD at rest as well ; thus the greatest risk factor for GERD symptoms during exercise is the presence of GERD symptoms at rest.

Gastroesophageal Reflux Disease Pathophysiology

Although precise GERD mechanisms are not well defined, suggested mechanisms include inappropriate relaxation of the LES, gastric dysmotility, enhanced pressure gradient between the stomach and esophagus in sports such as football, weightlifting, and cycling, gastric distension, delayed gastric emptying, and increased mechanical stress by bouncing of organs.

Normal peristaltic motions of the esophagus, which aid in ensuring that the acidic contents of the stomach remain in the stomach and do not migrate superiorly into the neutral environment of the esophagus, decrease in the setting of higher levels of activity. Thus any food or fluid intake that fails to pass through the stomach prior to exercise predisposes the athlete to reflux. Food choice is important because high-fat foods (fried foods, creamy sauces, and gravy), coffee, caffeine, chocolate, peppermint, alcohol, acidic foods such as tomatoes and onions, and tobacco products are well known to decrease LES pressure. In exercising individuals, the widespread use of nonsteroidal antiinflammatory drugs (NSAIDs) may also impact negatively on the proximal GI tract due to inherent GI tract irritation from suppression of protective prostaglandins.

Gastroesophageal Reflux Disease, Asthma, and Other Related Conditions

GERD may present with a number of less typical symptoms, including cough, sore throat, hoarseness, asthma, bronchitis, recurrent pneumonia, intermittent choking, or chest pain. Athletes presenting with any of these symptoms or complaints should be considered potential GERD sufferers. Many of these individuals have “silent” reflux that fails to generate classic GI manifestations. GERD can provoke or exacerbate asthma by either silent aspiration into the tracheobronchial tree or by stimulating an acid-mediated esophagobronchial reflex that provokes dyspnea and wheezing. It is estimated that up to 90% of asthmatics have GERD and that up to 40% of asthmatics have esophagitis. However, to date only those with nocturnal GERD symptoms have demonstrated improvements in their asthma from aggressive GERD treatment. It is always important to consider GERD as the potential primary pathology in an athlete who has new or unusual asthmatic symptoms.

Several clinical variants of GERD are also recognized. Laryngopharyngeal reflux disease (LPRD) is typically manifest by hoarseness, voice change, and chronic cough. It is believed to result from an esophageal reflux mechanism with secondary inflammation and damage of the proximal airway and laryngeal area. Duodenogastroesophageal reflux (DGER) results from reflux of duodenal, rather than gastric, contents, including biliary secretions, pancreatic enzymes, and bicarbonate. DGER is often responsible for refractory GERD symptoms despite appropriate management with maximal dose medications. Finally, a number of proposed extraesophageal manifestations of GERD include recurrent pharyngitis, otitis media, sinusitis, and pulmonary fibrosis.

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