The Role of NAD+ in Muscle Health, Aging, and Physical Performance

Key Takeaways

• NAD+ is central to how muscles make energy and repair themselves, influencing strength, endurance, and recovery.
• NAD+ levels decline with age in skeletal muscle, especially in inactive or physically impaired adults, and are linked to weaker muscle function.
• Research shows disuse suppresses key genes in muscle NAD+ production, suggesting that inactivity may undermine the machinery muscles need to maintain their NAD+ supply.
• Regular exercise is the most reliable way to support muscle NAD+ biology, with NAD+ precursors best used as complements, not replacements.
• Combining exercise with NAD+ supplementation may offer extra benefits for muscle health, but human data on this synergy are still emerging.
  

Maintaining muscle health is not only important for strength and physique—it also plays a vital role in metabolism, movement, posture, and longevity.¹ Skeletal muscles make up approximately 40% of total body mass,² and measures of muscle health, such as grip strength, have emerged as independent predictors of mortality,³ highlighting how muscle health is a core pillar of well-being rather than just athletic performance.

The body contains three main types of muscle: skeletal muscle, which attaches to bones and powers voluntary movement; cardiac muscle, which forms the heart and drives circulation; and smooth muscle, which lines vessels and organs. Among these, skeletal muscle is the largest and most metabolically active²—and the type we most often associate with “muscle”—and it is particularly relevant to longevity because it responds dynamically to changes in daily activity, aging, and nutrition.

From pushups to putting on your shoes, skeletal muscles are constantly contracting, maintaining posture, and recovering after activity—all of which require a steady supply of energy in the form of ATP.⁴ As this energy production becomes less efficient with age, inactivity, or disease, muscle performance and repair capacity can decline.⁵

At the center of these processes is nicotinamide adenine dinucleotide (NAD+), a coenzyme that supports mitochondrial ATP production and fuels enzymes involved in DNA repair, cellular stress responses, and the signaling pathways that help muscles adapt to exercise.⁶ Because of its role in energy production and cellular maintenance, NAD+ has become a growing focus of research in muscle health.⁷ In the sections that follow, we will explore why muscles depend on NAD+, why it declines with age, and what current evidence suggests about its relationship to muscle health and exercise—including what you can do about it.

Why NAD+ Is Essential for Muscle Health and Function

NAD+ is a coenzyme found in every cell that helps turn the food we eat into usable energy and powers the body’s repair systems. It participates in more than 500 enzymatic reactions, with energy production and cellular repair standing out as two of the most important—and both are especially critical for keeping muscles healthy, strong, and able to recover from everyday wear and tear.

NAD+ and Energy Production

NAD+ sits at the center of how muscles make and use energy.⁸ It helps convert nutrients into ATP through both oxygen‑dependent (aerobic) pathways and faster, oxygen-independent (anaerobic) routes. Every muscle movement, from a single rep to a marathon run, depends on ATP, which means each contraction, set, and recovery window is NAD-dependent.⁸ Skeletal muscle also has extraordinary energy demands,⁹ so its cells are densely packed with mitochondria—often thousands per cell—to keep up with continuous ATP production. Because NAD+ is present in every cell and feeds these energy‑producing pathways, it acts as a fuel enabler for muscle tissue throughout the body. 

NAD+ and Muscle Repair

After intense exercise, muscles are not just fatigued and achy—they are actively repairing and rebuilding, and that recovery is also NAD-intensive.⁸ Muscle growth (hypertrophy) involves synthesizing new proteins, which increases ATP demand,¹⁰ while intense contractions deplete ATP and phosphocreatine that must be resynthesized post‑exercise.¹¹ These energy stores are restored by ATP produced through NAD‑dependent metabolic pathways.¹¹

Both muscle repair and growth rely on dynamic shifts in NAD+ levels as the tissue moves from exertion into recovery. Downstream, NAD+ also helps activate key enzymes like sirtuins (especially SIRT1 and SIRT3) and poly(ADP-ribose) polymerases (PARPs), which together influence muscle protein synthesis, mitochondrial health, and DNA repair, ultimately supporting muscles as they repair, adapt, and become more resilient over time.¹²'¹³

How NAD+ Levels Decline With Age—And What That Costs Your Muscles

NAD+ levels decline with age across multiple tissues—including skeletal muscles. Research shows that NAD+ is one of the most prominently reduced metabolites in the muscles of older adults, with the lowest levels seen in those with physical impairments.¹⁴ In contrast, exercise‑trained older adults had muscle NAD+ levels much closer to those of younger people, and higher NAD+ abundance correlated with daily step count, mitochondrial function, and overall muscle performance, suggesting that this decline is strongly shaped by lifestyle and may not be inevitable.

As muscles lose NAD+, they also lose some of their ability to produce energy efficiently, repair damage, and maintain strength, underscoring the importance of keeping this pathway supported across the entire lifespan. With age, mitochondrial function in muscle tends to decline,¹⁵ so these “cellular powerhouses“ can struggle to generate ATP as efficiently, and aging muscle often shifts toward a more glycolytic, less efficient metabolic state that is less capable of regenerating after stress.

Preclinical models help illustrate this, with studies in aging mice showing that lower NAD+ in skeletal muscles is accompanied by reduced ATP production, diminished exercise capacity, loss of muscle stem cell function, and mitochondrial dysfunction—a pattern that closely mirrors what is seen in aging human muscle.¹⁵ One influential mouse study found that deleting NAMPT—an enzyme needed to recycle NAD+ in skeletal muscle—led to a depletion of intramuscular NAD+ by about 85%, along with losses in muscle mass, strength, and treadmill endurance.¹⁶ These animal studies underscore how critical healthy NAD+ stores and intact NAD+ biosynthesis are for maintaining muscle function.

In humans, these dysfunctional processes can cascade into sarcopenia—the age‑related loss of muscle mass and strength. Research in older men with sarcopenia found a strong signature of mitochondrial dysfunction in skeletal muscle, along with reduced NAD+ biosynthesis and lower NAD+ levels that were associated with lower muscle mass, weaker grip strength, and slower gait speed.¹⁷ 

Recent research adds an important layer to this picture: inactivity itself directly shuts down the muscle’s ability to process NAD+. A 2026 study found that when young adults had one leg immobilized for just two weeks, NMRK2 (also known as NRK2)—the gene responsible for converting the NAD+ precursor nicotinamide riboside (NR)—was the single most suppressed gene in the entire muscle transcriptome.¹⁸ This suggests that disuse doesn’t just reduce NAD+ demand, it actively dismantles one of the key molecular tools muscles use to maintain their NAD+ supply.

This sets up a vicious cycle, where reduced activity leads to muscle loss, followed by further mitochondrial impairment and NAD+ loss, thereby accelerating muscle decline. At the same time, other work suggests a more hopeful picture: those who remain physically active tend to show muscle NAD+ profiles and mitochondrial health that more closely resemble younger individuals, hinting that supporting NAD+ through movement and other lifestyle strategies may help preserve muscle health with age.¹⁴

Boosting NAD+ Naturally: What Exercise Does to Muscle NAD+ Levels

If staying active can help protect NAD+ levels in muscle, what does the research actually show about using exercise as an intervention? Emerging evidence points to physical activity as one of the most direct, evidence-based levers we have for influencing NAD+ biology in skeletal muscle, providing an empowering and actionable step for supporting muscle health with age. 

Across many of these studies, researchers track NAMPT, which is the rate‑limiting step in the NAD+ salvage pathway that acts as a reliable proxy for the muscle’s capacity to make and maintain NAD+. In younger adults, endurance-type exercise has been shown to increase NAMPT expression in skeletal muscle,¹⁹ suggesting that repeated bouts of exercise “teach” the muscles to recycle more NAD+ to meet higher energy demands. Similar patterns have been observed in trained athletes, who show higher NAMPT levels in muscle tissue compared to sedentary individuals,²⁰ suggesting a more robust NAD+ salvage system. Resistance training tells a similar story, with structured strength programs raising skeletal muscle NAMPT in middle-aged and overweight adults.²¹

Across multiple age groups and activity levels, physical activity has been shown to restore the NAD+ machinery in skeletal muscle—and the good news is that the body responds faster than most people expect. Often over just weeks or months, muscle tissue adapts to upregulate NAMPT and improve mitochondrial capacity.²¹ This means that consistent movement routines are not only good for strength and endurance, but also for supporting the underlying NAD+ systems that keep muscles energized and resilient over time.

That said, while exercise is a powerful lifestyle tool, maintaining regular activity is not always realistic—particularly for older adults experiencing mobility limitations, fatigue, or early sarcopenia. For these individuals, lifestyle changes alone may not fully address muscle NAD+ declines, which is where other strategies, including NAD+ precursors, are being explored as potential complements to physical activity.

NAD+ Supplementation and Muscle Health: What the Research Shows 

The science around NAD+ supplementation and muscle health is promising and consistent, although the evidence base is still evolving. Both animal models and early human trials contribute different, complementary pieces of the picture, with preclinical studies clarifying what happens inside muscle cells when NAD+ is depleted versus restored, while human data is beginning to show how those mechanisms translate into real-world function. 

In mice, some of the clearest signals come from experiments that turn off or disrupt the muscle’s ability to make NAD+.²² In the same NAMPT‑knockout model described above, severe NAD+ depletion caused pronounced losses in muscle mass, strength, and endurance, but restoring NAD+ with the precursor nicotinamide riboside (NR) partially reversed these deficits—animals showed measurable gains in exercise capacity after just one week of treatment. 

Building on these findings, a short-term study took a closer look at muscle stem cells, finding that NR supplementation improved muscle performance and fiber size in middle-aged mice, while parallel lab experiments showed that NR boosted both aerobic and anaerobic respiration in mouse and human muscle stem cells in vitro.²³ This is the first study to demonstrate that NR directly influences human muscle stem cell differentiation, suggesting important implications for age-related muscle regeneration.

This effect appears to extend to human muscle stem cells recovering from disuse. In the 2026 immobilization study discussed earlier, treating muscle stem cells from atrophied human muscle with NR increased myotube size, suggesting that muscles emerging from a period of disuse may be responsive to NR support.¹⁸

In human trials, the evidence becomes more nuanced, with small early studies in older and obese adults showing that NR supplementation did not substantially raise NAD+ levels in muscle tissue.²⁴'²⁵ However, NR did increase NAD+ flux—the rate at which cells are making and using NAD+—which suggests that the pathway is becoming more active rather than simply accumulating more NAD+ at rest. That pattern is consistent with the idea that, in human muscle, NAD+ precursors may be improving the turnover and utilization of NAD+ in response to cellular demands rather than dramatically elevating baseline levels.

Beyond changes in NAD+ flux, a growing body of work links NAD+ precursors with shifts in muscle health and physical performance. In several small studies, NAD+ precursor compounds like niacin²⁶ and NR²⁷ have been shown to increase muscle mass, stimulate mitochondrial biogenesis, restore aspects of muscle stem cell function, and raise muscle acetylcarnitine levels—a marker of metabolic flexibility. 

Recent trials in older adults and people with limited mobility also report improvements in walking speed, grip strength, walking distance, or exercise efficiency after periods of NR or nicotinamide mononucleotide (NMN) supplementation, typically with modest but meaningful gains.²⁸'²⁹ Furthermore, an ongoing trial in the U.S. Special Forces is looking at NMN to explore whether NAD-based strategies can support performance and resilience under extreme conditions, underscoring how much interest there is across the spectrum from age‑related decline to high‑performance training.

Together, the current evidence suggests that NAD+ precursors like NR and NMN may be most useful when NAD+ pathways are already under strain, such as older adults with sarcopenia or metabolic disease. Studies in healthy, active individuals remain limited, positioning NAD+ precursor supplements as potential complements to exercise and healthy lifestyle. 

NAD+ and Exercise: A Combination Greater Than the Sum of Its Parts

Exercise and NAD+ supplementation appear to work best together, operating through complementary parts of the same system. While studies suggest that each can support muscle health on its own, combining them may produce benefits that are at least additive and possibly synergistic by simultaneously increasing NAD+ demand and ensuring that the building blocks to synthesize are readily available. 

In preclinical work, this synergy shows up clearly: NR on its own did not significantly improve aerobic performance in mice, but when NR was combined with aerobic training, the animals outperformed those who only trained, showing greater running distance, higher peak power, more oxidative (type I) fibers, and higher levels of mitochondrial proteins.³⁰ Newly published clinical evidence paints a similar picture, as NR supplementation paired with exercise improved peak VO₂—a gold‑standard measure of how much oxygen the body can use during intense effort, and a key indicator of aerobic fitness and cardiovascular health.

Mechanistically, exercise upregulates enzymes like NAMPT and increases NAD+ demand in muscle, while supplementation supplies additional precursors to meet that demand. Together, these effects may enhance sirtuin activation, mitochondrial biogenesis, and repair signaling more than either strategy alone, which is why many researchers, including those at the recent NAD for Health Conference in Copenhagen, now view the exercise‑plus‑NR supplementation combination as one of the most promising ways to support muscle NAD+ biology over time.

Conclusion: What NAD+ Means for the Future of Muscle Health

NAD+ sits at the heart of how muscles make energy and repair themselves, and it appears to decline with age in ways that may contribute to muscle loss and reduced function. Emerging evidence shows that both exercise and NAD+ precursors can influence this pathway, helping to restore NAD+ biology and muscle performance, especially when NAD+ metabolism is already under strain. 

Overall, the research suggests that NAD+ is not a peripheral wellness buzzword, but increasingly recognized as a key contributor to how muscles age—and how that process can be meaningfully influenced to support muscle health. Although more research in humans is needed, the practical hierarchy is clear: prioritize regular exercise as the foundation for supporting muscle health and NAD+ homeostasis, while considering NAD+ precursor supplementation as a complement—not a replacement—for movement. A combination of the two may represent the most potent strategy, though the science is still emerging.

As larger clinical studies on the pairing of exercise and NAD+ precursors report results, NAD-informed protocols may become more common in both longevity medicine and sports performance settings. For now, the encouraging signal is that muscles do respond—often faster than expected—when given the right inputs: consistent activity, adequate recovery, and thoughtful support of the NAD+ systems that help keep them resilient with age.

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