Numerous theories have been proposed to explain the mechanism responsible for ETAP, however, many are based on case studies or anecdotal reports. The recent spate of investigations over the past 15 years have provided a better understanding of the characteristics of ETAP and factors relating to its provocation, allowing an evidence-based approach for appraising previously proposed theories and generating alternative explanations [1, 11, 12, 16, 20–22, 25]. Interestingly, long-held theories that have now been convincingly discredited still commonly appear in the literature [30, 32, 33]. In this section, the most prominent theories of ETAP are presented and appraised. Importantly, the consistent characteristics of ETAP reported in widely differing individuals and sporting activities suggests a single etiology [1, 32].
In 1941, Capps  proposed that ETAP was caused by ischemia of the diaphragm. In support of this theory are sensations associated with innervation of the diaphragm. The diaphragm is mostly innervated by the phrenic nerve, which refers pain to the shoulder tip region, but the peripheral portions of the diaphragm are supplied by the lower six intercostal nerves, which could account for sharp and well localized pain in the subcostal region [34, 35].
The main evidence against this theory is that ETAP can be induced by activities of low respiratory demand, such as horse, camel, and motorbike riding, where ischemia of the diaphragm is improbable [1, 2, 36]. Further, this theory does not account for ETAP in regions of the abdomen other than the subcostal border. Finally, it has been questioned whether in non-diseased individuals the diaphragm muscle would become ischemic and fatigue before the muscles of the limbs, as this would imply central fatigue precedes peripheral fatigue .
Interestingly, in a study that predated Capps’ theory, diaphragmatic movements were monitored during an episode of ETAP using a fluoroscopic technique and were found to be full and unrestricted . More recently, Morton and Callister  required subjects to perform a flow-volume loop while experiencing ETAP and found no compromise in any spirometry measures. They had hypothesized that lung function would be impaired, especially inhalation, if the diaphragm was ischemic . In conclusion, diaphragmatic ischemia is an unlikely etiology of ETAP.
Mechanical Stress on the Visceral Ligaments
Historically, the most widely accepted theory on the causation of ETAP has centred on mechanical stress being placed upon the visceral ligaments that support the abdominal viscera, especially the liver and stomach, via attachments to the diaphragm. The theory was first proposed at least as far back as the 1920s [3, 7], but was popularized by Sinclair  in 1951.
This theory explains several features of ETAP, most notably the high prevalence of ETAP in activities that are ‘jolting’ in nature yet of low respiratory demand such as horse riding [1, 2, 36]. Further, consuming food and fluid prior to exercise could provoke ETAP by the increased gastric mass loading the visceral ligaments . Plunkett and Hopkins  argued that increased gastric mass would also result when consuming hypertonic beverages [20, 21, 28] due to these fluids slowing gastric emptying and thereby maintaining a larger gastric mass. As the visceral ligaments attach to the diaphragm, the theory could also explain the experience of STP. Less well established observations that lend credibility to the visceral ligament theory include the alleged therapeutic effect of body inversion or wearing a supportive belt around the abdomen [2, 21].
While the visceral ligament theory accounts for many of the characteristics of ETAP, it has been argued that there are several aspects of the pain that the theory cannot explain . The observation of ETAP low in the abdomen is not consistent with the theory. Further, it is unclear why ETAP would be prevalent in swimming as this activity is not ‘jolting’ in nature and occurs in a prone position [1, 3]. It would be expected that increasing adipose stores within the greater and lesser omentum would contribute to an increased susceptibility to ETAP, as these structures attach via mesentery directly to the stomach , yet ETAP appears unrelated to body mass index [11, 12] or endomorphy . Finally, as the ligaments are extensions of the abdominal viscera, pain arising from them would likely be visceral in nature, which is typically dull, medial and poorly localized , in contrast to ETAP, which is mostly sharp, lateral and well localized [1, 12].
In conclusion, the visceral ligament theory explains several features of ETAP such as its high prevalence in ‘jolting’-type activities and its relation to the post-prandial state. However, the theory has shortcomings relating to the documented pain distribution and characteristics, as well as the observation that ETAP can occur in non-‘jolting’ activities.
ETAP has been commonly referred to as a gastrointestinal disturbance [4, 10, 13, 15, 27, 28, 40–42] and is commonly the most prevalent symptom reported in studies of gastrointestinal complaints during exercise [4, 15]. Despite being labeled a gastrointestinal disturbance, the etiology of the pain from a gastrointestinal perspective is poorly defined [15, 41, 43].
The few reports that have offered a gastrointestinal explanation for ETAP have focused on the pain originating from gut ischemia [13, 15, 36, 44] or distension . Supportive of an ischemic explanation for the pain, splanchnic blood flow decreases by up to 80 % during exercise [13, 41]. Indeed, gut ischemia has been observed in otherwise healthy subjects, but only during maximal exercise , unlike ETAP which can occur during lower intensity activities.
The main reason ETAP has been labeled a gastrointestinal disturbance is due to its association with the post-prandial state [1, 2, 10, 12, 21], yet the pain is commonly experienced when no food or drink is consumed for several hours before exercise [20, 21]. More importantly, the established characteristics of ETAP are dissimilar to gastrointestinal pain, which is typically described as medial, diffuse and colicky [6, 39]. Silen  observed that people with gastrointestinal discomfort tend to writhe the torso to obtain pain relief, which is unlike ETAP that is relieved by reducing movement [1, 2, 12, 21, 22].
In conclusion, while ETAP is commonly considered a gastrointestinal complaint, elements of the pain are not consistent with a gastrointestinal origin.
In the two large epidemiological studies by Morton and colleagues [1, 12] (see Table 1), approximately one in four sufferers of ETAP described the sensation of the pain as ‘cramping’. They suggested that a muscular cramp could explain several of the features of ETAP, such as the pain occurring throughout the abdomen, and suggested the theory warranted further investigation. Subsequently, Morton and Callister  measured localized electromyographic (EMG) activity while ETAP was present, as muscular cramp is associated with high levels of EMG activity [46, 47]. EMG activity was not elevated at the site of ETAP during an episode of the pain, which convincingly discredited the muscular cramp theory.
Median Arcuate Ligament Syndrome
ETAP has been referred to in the literature as median arcuate ligament syndrome [48, 49]. The median arcuate ligament is a fibrous arch that unites the crura of the diaphragm on either side of the aortic hiatus. In some people, the ligament inserts low and crosses the proximal portion of the celiac axis, which can cause compression and ischemic-related epigastric pain, especially post-prandially and during expiration . While the condition does not explain several of the characteristic of ETAP, such as its manifestation in other regions of the abdomen, the anatomical abnormality leading to the syndrome is surprisingly common, being present in approximately 16 % of individuals and 30 % of young people .
The experience of ETAP appears to be affected by poor posture, especially in the thoracic region [5, 25]. Kugelmass  was the first to make this observation and he suggested that poor posture might affect ETAP by altering the mechanics of the abdominal structures responsible for the pain. However, Morton and Aune  noted that palpating specific vertebrae in the T8–12 region, which innervates the abdominal wall, could reproduce symptoms of ETAP. ETAP could be exactly reproduced in 8 of 17 subjects assessed, and the site at which the subjects reported ETAP corresponded to the dermatome arising from the nerve root being palpated. Hence, they suggested that a neurogenic origin of ETAP should be considered.
Other reports of ETAP-like symptoms in the literature have implicated the nervous system. For example, slipping rib syndrome, in which hypermobility of the eighth, ninth and/or tenth rib results in trauma to the adjacent intercostal nerve, is a documented but often undiagnosed source of upper abdominal pain similar in nature to ETAP [52–58]. Similarly, abdominal wall nerve entrapment, in which the anterior cutaneous branch of an intercostal nerve is compressed at the site at which it reflexes sharply and pierces the abdominal musculature, can produce pain with similar features to ETAP [54, 59–62]. Finally, spinal tumors and facet joint cysts have been known to produce similar symptoms to ETAP as a result of compressive forces being placed on the intercostal nerves [63, 64].
While a neurogenic explanation does not account for all features of ETAP, such as its relation to the post-prandial state, it is notable that the intercostal nerves can be rendered vulnerable to compression as a result of a reduction in intervertebral disk height that can occur during repetitive, dynamic torso movements such as running [65, 66].
Irritation of the Parietal Peritoneum
After studying approximately 600 sufferers of ETAP, Morton and Callister  suggested that ETAP might be caused by irritation of the parietal peritoneum, which is the outer layer of the peritoneum that adheres to the abdominal wall and underside of the diaphragm. They presented the following evidence for ETAP arising from this tissue: aggravation of the portion of the parietal peritoneum that adheres to the abdominal wall causes sharp, well localized pain similar in nature to ETAP [23, 67]; the portion of the parietal peritoneum that underlays the diaphragm is innervated by the phrenic nerve and gives rise to STP when aggravated [23, 68–70]; pain arising from the parietal peritoneum is accentuated by movement ; the parietal peritoneum traverses the entire abdominal wall which could account for the widespread distribution of ETAP [34, 71]; the parietal peritoneum is most firmly adhered to the abdominal wall along the linear alba and the greatest potential for movement is therefore in the lateral aspects of the abdomen ; the tension in the parietal peritoneum is increased with the torso in an extended posture; children have a proportionally larger peritoneal surface area than that of adults which might explain the high prevalence of ETAP in the young ; and pain arising from the parietal peritoneum relieves quickly on removal of the stimulus  which is similar to that observed for ETAP when activity is ceased .
In addition to these observations, several case reports describing ETAP have implicated the parietal peritoneum [73–75]. Dimeo et al.  reported the case of a 29-year-old national class distance runner with severe, recurrent ETAP in the upper right abdominal quadrant during exertion. Laparoscopy showed congenital supernumerary ligaments binding the gallbladder to the abdominal wall. Symptoms of ETAP resolved after cholecystectomy and resection of the adhesions. Similarly, Lauder and Moses  reported adhesions between the ascending colon and anterior abdominal wall to be the cause of recurrent ETAP in a 28-year-old triathlete. The pain resolved following surgical intervention. Several authors have also suggested that ETAP is caused by a ‘cecal slap syndrome’ in which the caecum slaps against the anterior abdominal wall during repetitive jolting actions such as running [19, 76].
Morton and Callister  suggested that ETAP might result from increased friction between the parietal peritoneum attached to the abdominal wall and the visceral peritoneum that overlays the abdominal viscera. They argued that friction might be increased by the visceral and parietal layers of the peritoneum being forced more firmly together by distension of the stomach, as occurs in the postprandial state, or other abdominal organs such as the liver or large intestine. Further, they suggested that exercise-mediated changes in the quantity or viscosity of the lubricating serous fluid contained within the peritoneal cavity might increase friction. The serous fluid within the peritoneal cavity is in a constant state of flux [71, 77], being derived from splanchnic blood flow, which decreases during exercise [13, 41], and draining into the lymphatic system, which is facilitated by movement of the diaphragm [78–80]. Interestingly, the fluid in the peritoneal cavity is highly responsive to osmotic gradients between it and its vascular supply [71, 77, 81], which might explain the provocative effect of consuming hypertonic beverages on ETAP [20, 21]. Indeed, results of the study by Morton et al.  indicated that consuming hypertonic beverages provoked ETAP for reasons other than just increasing gastric mass due to slowing of gastric emptying.
Recently, Mole et al.  found that individuals symptomatic to ETAP had significantly thinner transversus abdominis and poorer functional core stability than asymptomatic individuals. The authors argued that better strength and activation of the abdominal musculature, especially the transversus abdominis, might reduce abdominal content mobility leading to lesser symptoms of ETAP. This observation may lend further support to the parietal peritoneum theory, although it would also support the visceral ligament theory as better core stability might reduce loading on the visceral ligaments.
In summary, many of the characteristics of ETAP are consistent with irritation of the parietal peritoneum, and while speculative, friction on this tissue might be a plausible explanation for ETAP.
The etiology of ETAP remains speculative, although progress has been made within the past 15 years regarding potential mechanisms. While some long-standing theories seem unlikely in the light of more recent findings, other novel theories have emerged. Indeed, determining the cause of ETAP is the first step towards developing procedures to manage the ailment, if at all possible.