Lactate Beyond the Locomotor Muscle: The Gut and Energy Intake

This is part one of a series of articles looking at the role of lactate in areas beyond the locomotor muscles. Despite the focus of this article being away from this area, as this is the first article of the series it’s important to briefly discuss the roles of lactate in relation to the locomotor muscles (the reason the term ‘locomotor muscle’ is being used is because the role of lactate in relation to other muscles, like the heart or even respiratory muscles, may be discussed within this series at some point). The notion that lactate has a direct role in harming performance is a myth, and contrary to the (unfortunate) common belief, lactate is extremely beneficial to performance. Following a conversion from pyruvate to lactate at the end of anaerobic Glycolytic metabolism, lactate can be converted back to pyruvate and shuttled intra or inter cellularly where it’s oxidised for further adenosine triphosphate production (a vital molecule in muscle contraction and thus maintaining a certain exercise intensity), and even to other organs where it can either be directly regenerated into ATP or converted to fuel that can be used for ATP regeneration.

Although interesting and extremely important in allowing athletes to sustain given intensities, this article (and the series of articles to follow) will not focus on lactate’s role within the locomotor muscle, but instead on its many roles beyond the locomotor muscle, starting with a discussion on its link with the gut and energy intake following different exercise intensities.

The Gut

As briefly discussed above, lactate can be shuttled into a vast amount of different areas once produced, with one of those areas being the gut. There’s a small amount of robust research looking into the role of the gut microbiome (a collection of microbes/bacteria within the gut) in lactate metabolism. Although there are numerous types of bacteria that may metabolise lactate, the particular research focus is on veillonella atypica due to its potential positive effect on endurance performance. Scheiman et al. (2019) contains a variety of research on the link between veillonella and lactate. In their research post the 2015 Boston Marathon, they found race finishers to have higher levels of veillonella at rest (compared to sedentary individuals) and a much larger increase following completion lf the marathon.

This is significant due to veillonella’s role in improved performance (in a study of rats, ingestion of veillonella was linked to increased time to exhaustion, about a 13% increase in favour of the rats who were gavaged with veillonella) through mechanisms relating to lactate metabolism. It’s known that lactate travels throughout the body once it’s produced, and the lumen of the gut is one of many destinations. Once entered into the gut, lactate can be converted into propionate, a short chain fatty acid. The most obvious benefit to this process is that a new fuel source for further ATP production is made available (a process that’s much simpler and thus quicker to act than the standard process of glycolysis). A benefit of this process that may be slightly undervalued is the role of propionate in pro-inflammatory cytokine inhibition (Vinolo et al. 2011). This inhibition may impact the level of inflammation an athlete faces following exercise, which could have an impact on rates of recovery further down the line. For example, an athlete with a larger inflammatory response to exercise may require a longer recovery period or a smaller total training volume in order to reduce the risk of overtraining, illness or injury (Novick and Chong, 2023).

The mechanisms behind the increase in veillonella aren’t fully researched, but a plausible theory is that an increase in this bacteria among athletes (compared to sedentary humans) is related to counteracting the frequent “lactic” environment that an athlete exposes themselves to through daily training.

In summary, the gut is one of many locations in which lactate can be transported to in order to fuel further exercise performance. In the case of the gut, lactate is converted to propionate which not only provides an additional fuel source for ATP reproduction but also inhibits pro-inflammatory cytokines which will positively affect rates of recovery, potentially allowing for an increased training volume.

Energy Intake

This next section is less relating to the transporting of lactate, but the effect of lactate on appetite and subsequent energy intake.

It’s known that with an increase in exercise intensity there’s also an increase in lactate through increased Glycolytic flux. From a number of different studies, it’s possible to estimate that perception of hunger decreases approximately 5-10% for every 1 millimole increase in lactate per litre of blood. The effects of this decreased appetite (and thus potentially reduced energy intake) could contribute to an accidental energy deficiency, which could affect numerous physical and mental aspects relating to endurance performance.

Ghrelin is a very important hormone due to its role in hunger. Levels of ghrelin can vary depending on hunger, for example a human’s ghrelin levels may peak during hungry moments before consuming a meal. Decreased levels of ghrelin align with feelings of “fullness” and decreased appetite. Large amounts of research supports lactate as a molecule that suppresses ghrelin. This was tested in a study by Vanderheyden et al. (1985), who compared ghrelin levels following intense exercise between a group that ingested sodium bicarbonate (which has more recently been popularised by Maurten) and a placebo group. With bicarbonate being a lactate buffer (and forcing more lactate into the bloodstream), they found those who ingested the bicarbonate pre-exercise had 25% ghrelin levels in comparison to the placebo group, which would’ve very likely effected energy intake in the following hours. Whether ghrelin suppression related to the actual decreased release of ghrelin or an altered processing of ghrelin from the hypothalamus, a region of the brain that plays a role in hunger is still debated. In the case of the latter, it would suggest that lactate crosses the blood-brain barrier, hinting at lactate playing a role in other neurobiological processes.

As touched on above, this process is unlikely to effect acute performance, but may effect chronic performance by initiating under-fuelling. The fact that increased lactate levels may affect energy intake through decreased perceptions of hunger (even if the body still needs food) may provide another rationale for training below the “lactate threshold” in non-specific training cycles. In this case, training below the threshold (and thus producing less lactate) may be a safer long-term option by ensuring sufficient fuelling can be completed to allow for consistent training and the decreased risk of developing calorie related issues (like relative energy deficiency).

In summary, the above article looks into the role of lactate metabolism within the gut microbiome (and subsequent roles in additional fuel/decrease in pro-inflammatory cytokines) and the role of lactate in adjusting appetite (and potentially energy intake) following intense exercise. As mentioned, the goal of this article (and the articles to follow) is to emphasize the importance of lactate in almost all bodily processes, not just those relating to the locomotor muscles.