What happens to the gut during training?

There’s lots of evidence to show that exercise is good for us, leading to many bodily adaptions that lead to better health. But there’s one bodily system that receives a bit of a hard time during exercise – the gut. Lots goes on in the gut during exercise and, in some cases, this leads to some athletes experiencing GI symptoms alike to those experienced in IBS patients, which can have a negative effect on their performance. So, the focus of this article is to focus on some of the underlying physiological mechanisms which may explain why some athletes experience these symptoms.

If you’re an endurance athlete, particularly a runner, ultra-athlete, or long-course triathlete, chances are you will have experienced some sort of gastrointestinal trouble during training or racing. If so, you’re not alone, with some research indicating that 90% of athletes have experienced GI trouble at some point. When speaking to elite and recreational athletes, as well as listening to ultra-running podcasts, it’s generally accepted that GI discomfort is just part of the sport, but what is happening in the gut which causes these symptoms?

When we train, blood is redirected away from the gut region towards to the muscle to help deliver nutrients as well as remove heat. This happens pretty quickly, with as much as an 20% decrease in gut blood flow within 10 minutes and 80% within an hour. Along side this drop in blood flow, there is an increase in sympathetic nervous system activity, causing, amongst other things, a contraction of the blood vessels within the gut. Together, these effects result in damage to the cells which line the intestinal tract and reduce the overall function of the gut. This damage can increase gut ‘leakiness’, allowing larger nutrient particles to pass through areas of the intestine which they normally cannot, as well as allowing toxins within the gut to enter the bloodstream.

Research has shown that the majority of people experience some degree of (increased) leakiness and damage during exercise, but often doesn’t lead to the appearance of any GI symptoms. Unfortunately for long distance athletes, the risk of these side-effects increases during longer training sessions, as the intestinal region receives less oxygen for a longer period of time. This can also happen during shorter but higher intensity sessions such as 400m repeats. Other factors, such as hot environments and dehydration can also increase the likelihood of increased ‘leakiness’, and athletes often report experiencing more GI symptoms on hot days. Heat, specifically the rise in core temperature which occurs with exercise, has also been proposed as another theory as to why we see increased gut leakiness and damage during exercise. At the moment, we’re not sure if heat (i.e. core temperature) or the reduced blood flow is more to blame for increased leakiness, but data from my PhD will (hopefully) add some information to the puzzle!

Although there is plenty of research showing the gut becomes more ‘leaky’ during training, these effects don’t correlate to the appearance of the symptoms which athletes report when racing. Symptoms such as nausea, heart-burn, the need to go to the toilet or vomit, don’t seem to appear in lab during research studies, even though blood analysis showed the participants experienced an increase in leakiness. Also, some athletes don’t experience GI symptoms during normal daily life, but do during training. This leaves a lot of questions remaining, and suggests that the psychological stress of racing may play a part in the appearance of symptoms.

One difference between lab studies and the real-world of training, is lab studies are commonly done fasted. Athletes don’t often complete the types of sessions (or racing) which more commonly cause GI symptoms, such as long runs or rides, or high-intensity repeats, without some sort of pre-exercise meal. Studies ask participants to fast because what you eat can have an effect on the biomarkers you are attempting to measure. This obviously brings questions regarding the applicability of (fasted) research studies to the real-world of training, but arguments aside, there is little research investigating how pre-exercise meals affect GI symptoms. Yet, as a nutritionist, this (pre-exercise feeding) is one of the first areas I examine when working with an athlete who is experiencing GI symptoms during training/racing.

What can you do about it?

The aim of this article was to provide you with some insight into the physiological changes that happen within the gut – which may be leading to the appearance of GI symptoms. Whilst I will go into greater detail, explaining some strategies you can implement into your nutrition programme to prevent symptoms appearing, below are some simple take-away points you can try:

  • Firstly, look for patterns in your daily activity and training that seem to cause symptoms. Do they occur during certain sessions or after a certain type of pre-exercise meal?
  • Make sure you are hydrated before and during exercise. A simple way to test this is to look at the colour of your urine. A light yellow, straw-like colour is ideal. Adding a small amount of salt or an electrolyte tablet to your pre-exercise drink can help with fluid retention.
  • Reduce the amount of fat, protein and fibre in your pre-exercise meal, as these nutrients take longer to digest.
  • Consume carbohydrate during exercise, ideally through a drink, as this helps increase blood flow back to the gut. This doesn’t necessarily have to be a carb powder, fruit juice is sufficient.
  • Avoid anti-inflammatories such as aspirin and ibuprofen before exercise.
  • On hot days, or if you are more susceptible to symptoms, try adding ice to your workout drink to offset some of the rise in core temperature.
  • Certain supplements may be beneficial, such as glutamine, anti-oxidants and probiotics may help, and I will dive into these in greater detail in a later article.


Costa et al (2017). Systematic review: exercise-induced gastrointestinal syndrome-implications for health and intestinal disease. Aliment Pharmacol Ther. 46(3):246-265.

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