Gastritis in athletes: causes and their link to exercise load and pharmacology

Heartburn, pain under the pit of the stomach, and nausea after training are often blamed on 'eating the wrong thing.' Yet behind these symptoms may lie gastritis — inflammation of the gastric mucosa. In athletes, specific causes are added to the classic ones: reduced blood flow in the stomach during exercise, a habit of anti-inflammatory pills, and a large number of supplements. Our editors examine what of this has an evidence base.

What gastritis is and how it differs from dyspepsia

Gastritis is inflammation of the gastric mucosa, which in the strict sense is confirmed histologically, that is, by examining a piece of tissue under a microscope. In everyday use, however, 'gastritis' is the name for almost any discomfort in the upper abdomen, which leads to confusion.

Doctors distinguish gastritis as a morphological diagnosis and dyspepsia as a set of symptoms: pain or burning in the epigastrium, early satiety, fullness after eating. Dyspepsia can be caused by gastritis, an ulcer, reflux, or be functional — without visible changes in the mucosa.

Gastritis is divided into acute (sudden onset, often after alcohol, drugs, or stress) and chronic (most often associated with Helicobacter pylori). Erosive gastritis is distinguished separately, in which superficial defects appear on the mucosa — a typical picture when taking nonsteroidal anti-inflammatory drugs.

For an athlete this difference is important in practice: identical symptoms can have different causes and therefore different treatments. Taking 'something for the stomach' on one's own without clarifying the cause can mask the problem.

The main causes: from Helicobacter pylori to stress

The most common cause of chronic gastritis in the world is Helicobacter pylori infection. The Kyoto consensus (2015) recognized gastritis caused by this bacterium as an infectious disease subject to treatment even without symptoms. The infection increases the risk of peptic ulcer disease and stomach cancer.

The second large group is chemical (reactive) gastropathies associated with NSAIDs, aspirin, alcohol, and bile reflux. The third is autoimmune gastritis, in which the immune system attacks the stomach cells, which over time leads to a deficiency of vitamin B12 and iron. For endurance athletes this is separately important, because both deficiencies reduce performance.

Stress by itself is rarely a direct cause of chronic gastritis, but acute physiological stress (severe trauma, burns, critical conditions) is known as a cause of stress erosions. Psychological stress is capable of aggravating dyspepsia symptoms and changing eating behavior.

How exercise affects the stomach

During intense work, blood is redistributed to the muscles, heart, and skin, while blood flow in the abdominal organs decreases. This so-called splanchnic hypoperfusion can be significant during prolonged high-intensity work, especially in the heat and against a background of dehydration.

A systematic review by Costa et al. (2017) described 'exercise-induced gastrointestinal syndrome': a complex of changes covering mucosal ischemia, increased permeability, motility disturbances, and a systemic inflammatory response. Although most of the research concerns the intestine, the stomach also suffers.

In marathon runners, cases of occult gastrointestinal bleeding after competitions have been described, including with signs of erosive gastritis. A mechanical factor — repeated jolts during running — probably also plays a role, so runners have more symptoms than cyclists at a similar intensity.

Intra-abdominal pressure also matters. During strength exercises with straining and in forward-bent positions, reflux — the backflow of acid into the esophagus — occurs more often. A person feels heartburn and may mistake it for gastritis, although the mechanism is different.

These changes are usually transient, but with regular exhausting training, dehydration, and combination with NSAIDs they can intensify damage to the mucosa.

Drugs and supplements that irritate the mucosa

NSAIDs — ibuprofen, diclofenac, naproxen, aspirin — are the most important pharmacological factor in gastritis in athletes. They block the enzyme cyclooxygenase-1, which reduces the synthesis of the prostaglandins that maintain protective mucus and blood flow in the mucosa. The risk of erosions, ulcers, and bleeding rises with the dose, duration of use, age, and combination with glucocorticoids or anticoagulants.

In the sporting environment, 'prophylactic' use of NSAIDs before training or a start is widespread. Warden's review (2010) concluded that this practice has dubious benefit and real risks — for the stomach, the kidneys, and even the processes of tissue adaptation.

• NSAIDs and aspirin:erosive gastritis, ulcers, bleeding.
• Glucocorticoids:less aggressive on their own, but sharply increase the risk in combination with NSAIDs.
• Oral iron and potassium preparations:can irritate the mucosa, especially on an empty stomach.
• Zinc, vitamin C in large doses:often cause nausea and discomfort.
• Stimulants and high doses of caffeine:increase acid secretion and dyspepsia symptoms.

Pre-workout formulas with significant amounts of caffeine, synephrine, and yohimbine are often taken on an empty stomach. There is little direct evidence that they cause gastritis, but they stimulate acidity and intensify reflux and nausea. Combining several stimulants on one's own also increases other risks — for the heart and blood pressure.

As for anabolic steroids and oral hormonal drugs, the main target organ is the liver, not the stomach. However, in people who use them, a combination of factors is often observed: NSAIDs for joint pain, alcohol, stimulants, a disrupted eating pattern.

An athlete's nutrition as a risk factor

Nutrition is rarely the sole cause of gastritis, but it substantially affects symptoms. Large portions before training, fatty food that lingers in the stomach, carbonated drinks, and spicy dishes intensify discomfort during exercise.

Concentrated carbohydrate solutions and gels with high osmolarity, taken without water, can slow gastric emptying and provoke nausea. This is not gastritis, but the sensations are similar, and so athletes often confuse these conditions.

A 'cutting' regime with long intervals between meals, a large amount of coffee, and stimulants on an empty stomach is another typical scenario. An empty stomach tolerates irritating substances worse.

Finally, alcohol after competitions combined with NSAIDs for muscle pain is one of the riskiest combinations for the mucosa. Our editors advise avoiding it especially carefully.

Editorial conclusions

Gastritis in athletes has the same main causes as in the general population — above all Helicobacter pylori and NSAIDs. However, sport adds its own factors: reduced blood flow in the stomach during prolonged exercise, mechanical effects, and the habit of 'treating oneself' with pills.

The most important pharmacological factor that can be influenced is the unsupervised and prolonged use of NSAIDs, especially in combination with alcohol, glucocorticoids, or stimulants on an empty stomach.

Dyspepsia symptoms do not always mean gastritis, so persistent stomach discomfort is a reason for examination, not for experiments.

We also recommend reading our materials on the prevention and diagnosis of gastritis, on irritable bowel syndrome in athletes, and on the safe use of painkillers.

References

1. Sugano K, Tack J, Kuipers EJ, et al. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015;64(9):1353–1367.
2. Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. Gut. 2022;71(9):1724–1762.
3. Costa RJS, Snipe RMJ, Kitic CM, Gibson PR. Systematic review: exercise-induced gastrointestinal syndrome — implications for health and intervention. Aliment Pharmacol Ther. 2017;46(3):246–265.
4. de Oliveira EP, Burini RC, Jeukendrup A. Gastrointestinal complaints during exercise: prevalence, etiology, and nutritional recommendations. Sports Med. 2014;44(Suppl 1):S79–S85.
5. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613–624.
6. Warden SJ. Prophylactic use of NSAIDs by athletes: a risk/benefit assessment. Phys Sportsmed. 2010;38(1):132–138.