| Summary: | It is becoming accepted that exercise increases gastrointestinal (GI) symptomology and permeability potentially effecting performance and recovery. This thesis addresses the issues of how exercise intensity, modality and pattern of exercise will impact upon GI permeability, damage and symptomology expression. Further it will examine how these factors may be modified by the environmental conditions under which they take place and by the use of pharmacological agents. In study 1 chapter 4, six male soccer players undertook both a 90-min rest or soccer specific intermittent exercise protocol (SSIE) under two environmental conditions (Hot 32°C or Cold 12°C) to evaluate how GI permeability and symptomology was affected by simulated soccer match play activity. SSIE elevated GI permeability relative to rest in both hot and cold conditions but these changes were only significant in the protocols undertaken in the heat. Such differences potentially reflecting the attenuated exercise intensity elicited by the protocol. However, exercise and rest in the heat relative to cold was associated with significantly higher GI permeability and wider array of subjective gastrointestinal symptomology. In study 2 chapter 5 the activity patterns typically experienced in soccer i.e. continuous and intermittent running were compared when 10 male participants undertook a series of protocol (s); rest, continuous steady state and intermittent exercise performed at the same ‘relative intensity’ of 70% V̇O 2 peak. Interaction with environmental stressors in the Hot 32°C or Cold 12°C on GI permeability and subjective GI symptomology was determined. GI permeability increased under both continuous and intermittent exercise compared to rest. No differences between continuous and intermittent exercise patterns were observed when undertaken in the cold. However, a stepwise increase in permeability was noted in the heat: Rest < SS < HIIT. Minimal expression of GI symptoms was noted and these were unrelated to the objective GI permeability markers. When relative exercise intensity is controlled for at 70% of a velocity associated with V̇O 2 peak no difference in GI permeability occur between HIIT and steady state exercise when this is undertaken in the cold. This response is abolished when exercise is undertaken in under HOT conditions but does not attain significance. Study 3 chapter 6 using a double blind repeated measures design examined the effects of HIIT exercise and the co-administration of Non-Steroidal Anti Inflammatory Drugs (NSAIDs) upon GI permeability and symptomology. Twelve trained intermittent games players participated. It was observed that HIIT exercise consisting off, repeated sprint activity [4 sets x 6 x 35 m (< 6s)] does not increase GI permeability relative to rest. Further when NSAIDS (2 x 400 mg Ibuprofen) are added to this model no further changes in gut permeability and symptoms are observed above that off the relevant control. These data suggest that following the present dosing regimen in trained male games players GI permeability and symptoms are unaffected by a single bout of HIIT exercise. Taken together the HIIT exercise model undertaken here and the co administration of Ibuprofen do not increase GI permeability seen with longer duration exercise. Finally, study 4 chapter 7 addressed whether exercise modality running vs cycling may be important in the development of GI disturbances give the epidemiological data that reports higher GI symptomology during and after running. Six male triathletes undertook three separate trials; a steady state 1000 kilojoule (KJ) cycling work test at 70% V̇O2 peak, an equivalent treadmill running protocol matched on total energy expenditure and equivalent period of non-exercise. Under these conditions GI permeability, as expressed by L:R ratio and GI symptoms were examined. Data indicate relative to rest an increase in GI permeability but indicate no modality specific differences in GI permeability and symptom expression between running and cycling. Running relative to cycling is associated with higher albeit still relatively limited subjective GI symptoms contrasting the equivalence seen in GI permeability L:R ratios. This disassociation in subjective symptoms and objective GI permeability in triathletes requires further consideration as regards mechanism of action and causality between these markers. This thesis has considered the effect of exercise intensity, modality and exercise patterning and their interactions with environmental stress upon objective and subjective markers of GI Function. Data suggest that exercise induced increases in GI permeability relative to rest occur when the exercise intensity and duration exceed a critical threshold of ~70 % peak aerobic capacity for at least 50 minutes. Manipulation of exercise patterning i.e. HIIT vs continuous undertaken at the same relative intensity shows no difference in GI permeability when under taken in the cold relative to the heat. Undertaking exercise in a Hot (32°C) environment accentuates permeability. Subjective GI symptomology does not mirror changes in the objective GI permeability markers with all subjective data indicating registering limited symptomology. It was further observed that HIIT exercise consisting of supra-maximal, short duration repeated sprints (<6s) performed on a repeated basis does not alter GI permeability. When NSAIDS are co-ingested with this model no further changes in gut permeability and symptoms are observed. Finally, exercise modality does not impact alter GI permeability and the relationship to GI symptomology.
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