Functional GI functions and exercise Flashcards
GI symptoms in endurance athletes - 4
30-90%
vomiting, nausea, abdominal angina, bloody diarrhea
musosal erosions and ischemic colitis
similar to IBS
triggers of GI symptoms in athletes - 4
mechanical- jostling splanchnic hypoperfusion (blood shunting, dehydration) - reduced nutrient absorption, impaired intestinal permeability nutritional - fibre, fat, protein, fructose
strategies to improve GI symptoms - 4
lower fibre/residue or fat intake
reduced fructose load
minimize dehydration
consume multiple transporter carbs
Fodmaps - 6
short chained carbs
Monosaccharide (fructose)
Disaccharides (lactose),
Oligosaccharides (FOS and GOS) - beans and lentils
Polyols (sorbitol and mannitol- sugar alcohols)
rapidly fermented and osmotically active with additive effects
proximal colonic gas production
supply of SCFA to mucosa
low FODMAP diet
clinical practices as potentially efficacious treatment for irritable bowel syndrome
IBS and FODMAP
malabsorption - increase colonic fluid and gas - trigger/amplify GI symptoms including bloating, flatulence, abdominal pain, loose stool or diarrhea, abdominal distension,
- hypersensitive bowl - luminal distension mediated by osmotic effects/rapid fermentation
Athletes believe _ can improve exercise induced GI issues
low residue/GFD
GFD
naturally low in fructan and GOS - may be modulating factor in symptom improvement instead of gluten but one had no improvement
2 objectives of FODMAP diet
nutritional adequacy and long term effect
strategic reintroduction of foods to figure out what specific high FODMAP triggers symptoms
suggestion of low FODMAP diet
2-3 days before events/critical training to alleviate bloating, intestinal cramps, flatulence, urge to defecate
symptoms of IBS as output from gut brain axis
how they relate to known pathophysiological abnormalities and their functional consequences.
ingestion of food can theoretically influence the gut brain axis in 3 ways
responses of the gut NS and ascending pathways in 3 ways
food volume - non specific changes in motility and gut distention (cephalic phase) - gastrocolic reflex
afferent input through stimulation of sensory receptors in the gut which compromises the mechano/stretch receptors, and the chemosensory receptors
food components may induce/modualte visceral hypersensitivity through inflammatory responses/modify receptor expression
indigestable carbs and poorly absorbed sugars and sugar alcohols (polyols such as sorbitol(gum)/mannitol(mushrooms)) most influence
intestinal sensory input and function through their delivery to the colon and subsequent lisation by bacteria
indigestable carbs can be functionally classified
with relevance to intestinal effects into 3 overlapping gps - fibre, fermentable oligo-, di-, and mono-saccharides and polyols (FODMAP) and prebiotics
oligosaccharides
cannot be hydrolyzed so >90% delivered to colon
why doesnt lactose get absorbed
lack of lactase
risks of low FODMAP - 4
low fibre - short term constipation, long term bowel cancer
reduced prebiotic - reduction of bifido 4 weeks after low FODMAP diet
psychological component
vitamins
gluten and IBS
poor evidence - anecdotal evidence
rechallenge RCT negative for specific gluten effect but may worsen symptoms
risk of low gluten diet
nutritional inadequacy
low fibre
fermentilibity of fibre from very rapid to none
FOS, GOS, innulin guar gum resistant starch psyllium wheat bran fruit and veggies fibre cellulose, sterculia
gluten -2
group of proteins found predominantly in wheat, barley and rye - cause of celiac disease - symptoms that match IBS
trigger for symptoms
is gluten responsible for IBS beyond celiac disease?
non celiac gluten sensitivity - controversial
gluten free also reduces
FODMAP
4 pathophysiological abnormalities for IBS
central processing, preception
visceral hypersensitivity
impaired motility responses
abnormal viscero-abdominal reflexes
