Effects of exercise and hyperthermia on gastrointestinal dysfunction and symptoms in recreational athletes

Exercise leads to disturbances in the gastrointestinal (GI) tract, which have been suggested to contribute towards the appearance of symptoms such as bloating, vomiting, and diarrhoea. The mechanisms underlying the appearance of GI symptoms aren’t fully understood and there is large variations in the individual susceptibility to symptoms (Karhu et al., 2017). Understanding this relationship is somewhat constrained by the methodological approaches applied in the field. The methods used to quantify the response in intestinal permeability and injury are subject to wide variations in response to a similar exertional and environmental stresses which would appear to be population independent. Whilst splanchnic hypoperfusion and hyperthermia have both been identified as key mechanism(s) contributing towards an increase in intestinal permeability, it is less clear which of these factors is most dominant. Furthermore, it is not yet clear whether these factors (hyperthermia and hypoperfusion) exist on a continuum, where one factor may dominate under certain conditions, and whether other factors such as psychological stress influence this relationship (van Wijck et al., 2011a; Pires et al., 2017). The aim of this thesis is to investigate the relationship between GI dysfunction (permeability and injury), subjective GI symptoms, hyperthermia and exercise. However, given the broad range of methods used in previous literature, a secondary aim of this thesis is to address methodological clarity about the timing of L/R test solution ingestion. The original contribution to knowledge from this work suggests, methodologically, the timing of dual-sugar probe test solution ingestion in relation to exercise does not significantly affect the subsequent serum Lactulose/L-Rhamnose ratio expressed (Chapter 4). Furthermore, GI permeability displays a dose-response relationship with exercise intensity, but this does not correlate with the expression of GI symptoms. The appearance of GI symptoms is likely due to a multitude of factors including physiological strain and exercise intensity, yet is highly individualistic (Chapter 5). Further, in Chapter 6 it is observed for the first time that hyperthermia implemented during resting conditions, in absence of exercise-induced mesenteric hypoperfusion, but does not augment GI permeability or markers of GI distress. Moreover, hyperthermia in absence of exercise-induced hypoperfusion results in the appearance of symptoms of heat illness, and core temperature is strongly correlated to nausea. Research has previously demonstrated that supplementation with glutamine can ameliorate intestinal permeability and core temperature. However, in Chapter 7, acute glutamine supplementation returned no protective effects on GI damage, permeability, core temperature or heat-illness symptoms in response to exposure of passive hyperthermia. Collectively, exercise causes an increase in GI permeability, a response not observed when similar levels of core temperature are induced by passive hyperthermia. In summary, the increase in GI permeability observed during exercise is likely to be caused by intestinal ischemia, rather than an increase in core temperature. Furthermore, no association between intestinal permeability and GI symptoms appears to exist. Passive heat stress results in a rise in core temperature, GI damage and heat-illness symptoms, with glutamine supplementation demonstrating no protective effect on these outcomes