Low Endurance on Runs and Rides? Support Your Stamina

Reviewed by SOMA HEALTH's Medical Research Team

You know the feeling: the first hour of a long run or ride goes fine, then the wheels come off. Your legs turn heavy, your pace drifts, and the effort that felt sustainable now feels like a grind. That late-session fade is one of the most common frustrations in endurance sport, and it usually has less to do with willpower than with what is happening inside your muscle cells.

This guide looks at the physiology behind endurance fade, why the mitochondria in your muscles sit at the center of it, and where a gut-derived compound called urolithin A fits into the conversation. We will keep the science honest: separating what has been shown in humans from what is still early or preclinical, and being clear about what a supplement can and cannot do.

Why endurance fades before your motivation does

Endurance performance is, at its core, a question of energy supply. To hold a pace for an hour or more, your working muscles need a steady stream of ATP, the molecule that powers every contraction. Most of that ATP is produced aerobically inside mitochondria, the small structures often described as the cell's power plants. The more mitochondrial capacity a muscle has, and the better that capacity is maintained, the longer it can keep producing energy at a given intensity before fatigue sets in.

Exercise physiologists have long linked endurance capacity to mitochondrial density and function in skeletal muscle. A large body of human research shows that endurance training increases both the number and the size of mitochondria in trained muscle, alongside growth of the tiny capillaries that deliver oxygen. Higher mitochondrial content is associated with greater aerobic capacity, better fat oxidation at submaximal efforts, and a higher intensity you can sustain before lactate accumulates. In practical terms, more and healthier mitochondria tend to mean a run or ride that stays smoother, later.

The flip side matters too. Heavy training blocks, poor recovery, aging, and simple wear-and-tear can leave some mitochondria damaged or inefficient. When worn-out mitochondria are not cleared and replaced quickly enough, the muscle's energy machinery becomes less reliable, which can show up as exactly the kind of second-half fade endurance athletes complain about. Maintaining mitochondrial quality, not just quantity, is part of the endurance equation.

Mitophagy: the quality-control step behind mitochondrial health

Your cells have a built-in recycling program for mitochondria called mitophagy. When a mitochondrion becomes damaged or inefficient, mitophagy tags it, breaks it down, and clears the components so fresher, better-functioning mitochondria can take over. Think of it as maintenance for your cellular power plants: keeping the fleet healthy rather than letting broken units drag down the whole system. If you want the deeper mechanism, we cover it in what is mitophagy and in our overview of mitochondrial health.

Mitophagy is a normal, continuous process, but its efficiency can decline with age and can be stressed by demanding training. That is where urolithin A enters the picture, because in laboratory research it has been studied specifically for its ability to support this recycling step.

What urolithin A actually is

Urolithin A is not something you eat directly. It is a postbiotic, meaning your gut bacteria make it. When you consume ellagitannins, the polyphenols found in pomegranates, walnuts, and certain berries, some gut microbes convert them into urolithin A. The catch is that not everyone's microbiome can do this efficiently; studies suggest only a subset of people produce meaningful amounts from food alone. That variability is a big reason direct supplementation has been researched, since it delivers a standardized dose regardless of your gut ecology. For the food angle, see foods high in urolithin A, and for the fuller picture start with our urolithin A guide.

Mechanistically, the interest in urolithin A centers on mitophagy. By supporting the clearance of worn mitochondria, the theory goes, it may help muscle maintain a healthier mitochondrial pool over time. That is a plausible and actively studied idea, but the strength of the evidence depends heavily on whether we are talking about animals or humans, so let us take those in order.

The human evidence, from strongest to newest

Proven-safe and biologically active in people

The first-in-human study of urolithin A, published by Andreux and colleagues in Nature Metabolism in 2019, established two important things. First, it was safe and well tolerated at doses up to 1,000 mg per day. Second, it produced a measurable mitochondrial gene-expression signature in participants, meaning the compound was doing something biologically relevant at the level of muscle cell energy machinery, not just passing through inertly. This is the foundation the rest of the human work builds on.

Human trials in muscle function and exercise

Several randomized trials have since looked at muscle and performance outcomes. In a 2022 study by Liu, D'Amico and colleagues (JAMA Network Open), older adults taking urolithin A over roughly four months showed improvements in muscle endurance. A separate 2022 trial by Singh and colleagues (Cell Reports Medicine) in middle-aged adults, using 500 mg and 1,000 mg daily arms over four months, reported benefits in muscle strength and aspects of exercise performance. More recently, a 2024 randomized controlled trial in the Journal of the International Society of Sports Nutrition ran an eight-week protocol in resistance-trained men, and a 2025 trial examined distance runners, extending the research into trained, athletic populations rather than only sedentary or older groups.

For endurance athletes, the relevant takeaway is measured. The human data most directly support muscle endurance and strength outcomes, and the athletic-population trials are encouraging but still few in number. A 2024 systematic review in Ageing Research Reviews summarized the field fairly: the evidence for targeting aging processes with urolithin A in humans is genuinely promising but still emerging. You can dig into the specific trials in our roundup of urolithin A clinical studies, and see how it maps to training in urolithin A for muscle.

Newer human signals: immune-cell mitochondria

A 2025 randomized controlled trial published in Nature Aging (roughly a 28-day protocol) reported that urolithin A supported the mitochondrial health of immune cells in midlife adults, a finding tied to the concept of inflammaging, the low-grade inflammation that tends to accumulate with age. This is an interesting expansion of the story beyond muscle, though it is a single short trial and should be read as an early, if promising, signal rather than a settled conclusion.

What is still preclinical (and should be labeled that way)

Much of the excitement around urolithin A traces back to animal and cell research, and it is important to keep that clearly separated from the human evidence. The landmark 2016 study by Ryu and colleagues in Nature Medicine demonstrated that urolithin A induced mitophagy, extended lifespan in the roundworm C. elegans, and improved muscle function in rodents. Those are compelling mechanistic results, but they are preclinical: worms and rodents are not people, and effects on lifespan or muscle in animals do not automatically translate to endurance gains in a human athlete. Similarly, work on joints and cartilage (D'Amico and colleagues, Aging Cell, 2022) has been conducted in osteoarthritis models, and areas like skin, gut, brain, and heart remain in early or preclinical stages of exploration. Treat those as directions researchers are investigating, not as established benefits.

Practical guidance for runners and riders

If you are considering urolithin A as part of an endurance routine, a few grounded points apply. The doses studied in humans range from 500 to 1,000 mg per day, with 1,000 mg being the upper end used in the trials; our urolithin A dosage page walks through the specifics. Consistency matters more than timing: the human trials ran over weeks to months, not single sessions, so a supplement is best thought of as a background support taken daily, not a pre-race booster. And no supplement replaces the fundamentals that actually build endurance, namely progressive aerobic training, adequate fueling, sleep, and recovery. Urolithin A is best framed as a way to support the mitochondrial quality-control processes that training already stresses, not as a shortcut around the training itself.

One more honest note: because urolithin A works over time and interacts with your existing fitness, expectations should be realistic. If you want a sense of the timeline, we address it in how long does urolithin A take to work. Persistent, unexplained drops in endurance or energy can also have medical causes, from iron deficiency to thyroid or cardiac issues, so this content is educational and structure-function only. It is not a treatment for any condition; if your stamina loss is new, severe, or does not fit your training load, see your doctor rather than reaching for a supplement.

Explore SOMA HEALTH Urolithin A Gummies

For a fuller view of the science and how to choose a product, see our urolithin A guide and our comparison of the best urolithin A gummies.

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. This guide is educational and is not a substitute for advice from a qualified healthcare provider.