Epidemiological data report increased symptomology of gastrointestinal disturbance in both the upper and lower GI tract (nausea, regurgitation, wind, vomiting, diarrhoea, cramps, abdominal pain and bloating) in both male and female athletes (Haaf et al., 2014b; Lambert et al., 1999; Peters et al., 1999b; Riddoch & Trinick, 1988; ter Steege et al., 2008; 2012). In particular endurance athletes seem susceptible to this symptomology and frequently express gastrointestinal symptoms ( Costa et al., 2017; Haaf et al., 2014; ter Steege et al., 2008). Gastrointestinal symptom severity presented across the studies ranged from mild (wind, bloating) to severe/clinically significant (acute colitis, faecal occult blood, chronic ischemia) the latter symptoms being expressed particularly at the extreme endurance event end of the scale (Cohen et al., 2009; Costa et al., 2016; Grames & Berry-Cabán, 2012; Jeukendrup et al., 2000; Pfeiffer et al., 2012; Roberts et al., 2016; Stuempfle et al., 2016; Stuempfle & Hoffman, 2015). In examining this literature association have seen sought between objective and subjective symptoms to provide explanation as to possible factors that contribute to the expression of these symptoms (Costa et al., 2017; Lambert et al., 2008). GI permeability and GI damage which although used interchangeably represent different patho-physiology; the former leading to translocation of molecules from luminal to systemic circulation whilst the later provide an indicator of loss of distal villus integrity (Grootjans et al., 2016; Grootjans et al., 2013). The central driving mechanism around these changes in gastrointestinal permeability, damage and symptomology are factors related exercise intensity, exercise pattern, modality and environment in which they are performed. A central theme in literature indicates that 70 % V̇O 2 max/peak may be a critical threshold for permeability changes to occur (Pires et al., 2016). It is important to note that GI permeability in this thesis is considered relative to rest (within treatment effect) and relative to alternative treatment. In line with this model, the exercise intensity applied across the studies was designed to achieve approximately 70 % V̇O 2 peak (chapter 4,5,&7) or to exceed it (chapter 6). In chapter 4 the impact of a SSIE protocol which can be classified as aerobic combined with periods of high intensity intermittent exercise was assessed for it impact on GI permeability. It was determined that performance of the SSIE protocol did not significantly increase GI permeability relative to rest; which may reflect the protocol not exceeding the 70% V̇O 2 peak ‘critical threshold’ under cold conditions. However, when environment was considered as an additional stressor the SSIE in the heat achieved (>70 % V̇O 2 peak) relative to the cold with increased GI permeability and symptoms also observed. Whilst we note increased GI
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Figure 8.0 Schematic representation of the effects of exercise intensity, exercise pattern modality and pharmacological upon GI permeability and damage.
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permeability in the heat the significance of this needs to be ascertained particularly in the context of soccer games played in hot environments (>32°C) and especially when the co- expressed symptomology scores are mild. Where permeability and heat stress are co- expressed there seems from present data to be a synergistic/additive effect present that elevates GI permeability without translating effectively to increased symptomology. It may be this GI permeability could lead to an increased risk of heat illness and heat stroke secondary to systemic inflammatory responses as a result of luminal antigen translocation from the gut (Selkirk et al., 2008; Selkirk et al., 2009). In studies 5 and 7 this theme of ‘exercise intensity’ being critical to GI permeability response was further explored. In chapter 5 relative exercise intensity was held at 70% V̇O 2 peak during the performance of two separate protocols designed to determine how the exercise pattern i.e. continuous steady state vs intermittent exercise effects GI permeability and symptomology. Across both studies permeability was again increased relative to rest, with no change in symptom expression. In treadmill HIIT programmed at a 90%-50% work to active recovery ratio (~70 % V̇O 2 peak) and steady state exercise as well as cycling performed at 70 % V̇O 2 peak for minimum of 50 min will increase GI permeability. Importantly the magnitude of the increase in permeability does not appear to differ when undertaken in the cold for steady state exercise. However, as noted in chapter 4 the addition of heat stress to the HIIT protocol accentuated GI permeability; in this case relative to the cold. Based upon the observations from study 1 (chapter 4) and study 2 (chapter 5), exercise in the heat (32°C) is an important factor that provides an additive stress upon the GI tract contributing to increased GI permeability. In relation to how the exercise is patterned t is interesting to note that comparison of chapter 5 HIIT exercise consisting of long interval(s) (180 s) relative to study 3 (chapter 6) supra maximal sprint HIIT (short intervals <6 s x 6 [~36 sec]) indicates that supramaximal HIIT does not increase permeability (no environmental thermoregulatory challenge presented). The factors contributing to these differences can’t be resolved within the current data set as no data on core temperature in the HIIT short intervals was determined. It is likely the short intensity bouts and long rest will attenuate heat load accumulation which would seem to have been an important factor elevating permeability in studies 1 and 2 (chapters 4 and 5). Further, when Non-Steroidal Anti-Inflammatory Drugs (NSAIDS) are added to this HIIT model contrary to initial the hypothesis no further changes in GI permeability and symptoms are observed. These data are contrary to that reported in steady state exercise studies (Audet et al., 2016; van Wijck et al., 2012) and may thus differentiate HIIT from steady state NSAID effects observed in literature. In study 4 (chapter 7) maintaining the ‘critical exercise intensity threshold’ concept the first direct comparison of permeability after running and cycling was determined. It had been postulated that differences in GI symptomology between running and cycling could be explained largely by differences in mechanical/loading characteristics
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applied to the GI tract (Gil et al., 1998). The direct comparison of running to cycling when closely matched indicates no difference in permeability as a result of mode of exercise during short term exposure (< 90 min).
In aligning a possible series of mechanism to explain the diverse results outlined above, GI permeability will be impacted by several key factors resulting from the protocols undertaken i.e. splanchnic hypo-perfusion, GI hyperthermia, perfusion-reperfusion related tissue hypoxia and oxidative stress (Costa et al., 2017; Lambert et al., 2002b; ter Steege et al., 2008; Ward et al., 2014). The onset of exercise is likely to bring about a redistribution of cardiac output from the splanchnic organs with reductions in splanchnic blood flow of up 80% dependent upon the exercise protocol applied and pattern of activity (Crandall & Gonzalez-Alonso, 2010; Knight et al., 2017; van Wijck et al., 2012b). In particular comparison of steady state activity and intermittent activity will result in different blood flow patterns with the former seeing a reduction and maintenance of that reduction in blood flow until exercise cessation. Conversely with HIIT exercise an oscillatory pattern of splanchnic blood flow will result as exercise intensity increases and decreases during progression through the protocol. This difference in splanchnic perfusion places significant stress on the gastrointestinal system in relation to managing thermal load and oxidative stress (Hayashi et al., 2012; Knight et al., 2017; Lambert et al., 2002; Perko et al., 1998). However, a sense of the likely impact of these pattern differences can be observed from the lack of difference in GI permeability responses under the HIIT vs steady state model in the cold (Chapter 5). Where exercise was under taken under different environmental conditions i.e. hot conditions heat accentuates permeability at rest (chapter 4) and with exercise (chapter 4 and 5). Figure 8.1 summarises the impact of the 4 individual studies upon GI permeability.