Can the gut microbiota be trained?

Athletes that follow an exercise and dietary regimen usually expect to see a performance benefit for their efforts. Also impacted by these factors are the microbes harbored in the gut, called the gut microbiota. In Part I of this series, we covered how this community of microbes responds to exercise and diet. This is part 2: Here we explore how such stimuli might modify this community in a way to support athletic performance. A sort of “training” if you will.

The gut-muscle axis

The impact of exercise

There is evidence that exercise promotes changes in the structure of the gut, though this appears to vary greatly depending on the exercise intensity, mode, and time (1). While longitudinal data is generally limited in humans, some very intriguing work has been conducted using rodents. For example, mice undergoing moderate-intensity treadmill exercise for several months had a significant alteration in their core microbiota and associated metabolic activity, paralleling increased exercise performance (2). There was a notable increase in the bacterial genera Bifidobacteria, often used in probiotics, in the exercised mice. Interestingly this was correlated with enhanced metabolic activities related to exercise, including glucose metabolism.


To better determine a causal link and explore the importance of the gut microbiota, several research groups have used antibiotics to effectively kill off a significant portion of gut bacteria and then subjected animals to exercise. In comparison to baseline exercise performance, where mice had an intact gut microbiota, heavy antibiotic treatment resulted in large decreases in running capacity and muscle function (3, 4). Such work showcases an emerging concept, termed the ‘gut-muscle axis’, that highlights the bi-directional relationship between muscle tissue and the gut microbiota (5). Demonstrating that this relationship is in fact a two-way street, one of the researcher groups took it one step further and also restored the gut bacteria of the antibiotically treated mice. Restoration of the gut flora reversed the decrements in endurance capacity and muscle function (3). Clearly, the gut microbiota can impact performance, but what about humans?


There is evidence from rodent studies of a bi-directional relationship between muscle tissue and the gut microbiota, termed the 'gut-muscle axis'.

In one of the more interesting and recent investigations, Barton and colleagues used a case-study approach, tracking the gut microbiotas of two sedentary male humans as they embarked on a 6-month training program for either a marathon or an Olympic-distance triathlon (6). As the training progressed, so did the participant’s body composition and fitness parameters. Increases in gut microbiota diversity (a health-associated feature) occurred with sustained training. The participants exhibited increased abundance of microbial species that have been shown to influence short-chain fatty acid (SCFA) production. SCFAs act as fuel substrates that have been shown previously to be taken up by the body and used in muscle tissue (7). Yet the increase in these SCFA-producing microbes was not reflected in actual SCFA levels. The authors stated it may take time for the metabolic alterations to emerge or the microbes were not getting enough nutrients via the participants’ diets.


Exercise or diet? Not so easy to distinguish

Exercise has the potential to modify the gut microbiota, but it is rather difficult to separate out other confounding factors like dietary intake. In relation to comparing differences in gut microbiotas, this has been highlighted in professional rugby athletes vs. sedentary controls (8). While these two groups were approximately the same body mass, the athletes consumed about 1,500 more calories and 140 grams more protein! Whether it be greater energy intake, high-carb, low-carb, increased protein, feeding strategies during exercise, etc., all can influence the composition and, ultimately, the function of the gut microbiome.


As noted in Part I, gut bacteria can break down complex carbohydrates, like dietary fiber, through fermentation processes ultimately producing SCFAs. This includes, acetate, propionate, and important for our discussion, butyrate. This SCFA is one of the primary sources of fuel for the cells that line our gastrointestinal tract. Forming the gut barrier, these cells have a short life cycle of a few days and need a substantial amount of energy and nutrients (9). By providing them with energy and nutrients, it follows that they may do their job better, and maintain better gastrointestinal health.