What Mitochondria Actually Do — and Why It Matters
How the powerhouses of your cells keep you alive and how to keep them strong with daily habits, better sleep, and the right support.

You’ve probably heard it before: mitochondria are the powerhouse of the cell. It’s that one biology fact that stuck with most of us from school — and it turns out to be profoundly true in ways that affect our daily lives.
But behind that catchphrase is a much bigger story. These tiny structures don’t just power your cells — they shape how you feel, how you age, how quickly you recover, and how resilient your body is to stress.[1]
Every heartbeat, every breath, every spark of thought in your brain relies on mitochondrial energy. These tiny structures are constantly turning the food you eat and the oxygen you breathe into adenosine triphosphate (ATP) — the fuel that keeps your body going.[2] But when mitochondria start to struggle, the effects can ripple outward and influence your energy, mood, and overall health.[3]
In this article, we’ll explore what mitochondria actually do — far beyond the textbook definition — and how their health influences your metabolism, cognition, endurance, and even your biological age.
Because here’s the truth we’re only beginning to grasp: if there’s a master switch for energy, longevity, and metabolic resilience, it just might live inside your mitochondria. And supporting them may be one of the most powerful ways to age well — from the inside out.
How mitochondria shape your health
If mitochondria only made energy, they’d still be some of the most important structures in your body. But they do much more — and the deeper researchers look, the more central mitochondria appear to nearly every process that keeps you alive and thriving.
But first, let’s look at how they generate the energy that fuels everything else.
Mitochondria produce most of your body’s ATP — the molecule your cells use to power nearly every function. They do it through a process called oxidative phosphorylation, breaking down nutrients like glucose and fatty acids and using oxygen to generate ATP efficiently.[2]
In fact, mitochondria are responsible for producing about 90% of the ATP in your cells, driving everything from muscle contractions and hormone synthesis to neural signaling. This happens inside the mitochondria’s inner membrane, where a series of proteins called the electron transport chain shuttles electrons and pumps protons to build an electrical gradient — like a mini battery.[4] That gradient then drives the production of ATP, molecule by molecule, around the clock.
But mitochondria do far more than generate energy. Among their other essential roles:
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Calcium regulation: Mitochondria help manage calcium levels in your cells, especially in the brain, heart, and muscles.[5] Calcium acts like a messenger for nerve signals, muscle movements, and a steady heartbeat. When it's out of balance, things can go awry — and mitochondria play a key role in keeping it stable.
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Steroid hormone production: Certain cells use mitochondria to synthesize steroid hormones — like cortisol, estrogen, and testosterone — from cholesterol.[6] This process happens in tissues such as the adrenal glands, ovaries, and testes, and it’s one reason why mitochondrial dysfunction can influence hormone imbalances and age-related hormonal decline.
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Heat generation: Some mitochondria — particularly those in brown fat — can uncouple their ATP production process and release energy as heat instead.[7] This helps maintain body temperature in cold environments, particularly in infants and lean adults. It’s a process called non-shivering thermogenesis — one of the many adaptive roles mitochondria play beyond just making energy.
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Immune system signaling: Mitochondria play a key role in innate immunity. They help detect cellular stress and infection, sending out danger signals that activate immune defenses.[8] In this way, they’re not just responding to damage — they’re helping the body decide how to respond.
- Programmed cell death: Mitochondria are also gatekeepers of apoptosis, or programmed cell death. When a cell is damaged beyond repair or infected, mitochondria can release signaling proteins that trigger that cell’s self-destruction.[9] This process is vital for preventing cancer, controlling inflammation, and making way for new, healthy cells.
Taken together, mitochondria act as command centers — not just energy factories. They monitor and manage key processes across your body: energy production, metabolic signaling, calcium balance, heat regulation, immune defense, and controlled cell death.
That’s why mitochondrial health is so tightly connected to overall systemic health — including your brain, muscles, heart, and immune system. And why researchers increasingly see mitochondrial decline as a driver of fatigue, brain fog, slower recovery, and early aging.
Where mitochondria came from
For all that mitochondria do today, they likely didn’t start out as part of us.
According to the leading explanation — known as the endosymbiotic theory — mitochondria evolved from free-living bacteria that were engulfed by ancestral cells more than a billion years ago.[10] Instead of being digested, those bacteria formed a mutually beneficial relationship with their host — one that became permanent over time.
And the clues are still visible:[10] [11] [12]
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They have their own circular DNA, separate from the cell’s nucleus — a hallmark of their bacterial ancestry.
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They’re enclosed by a double membrane, consistent with an engulfed bacterium surrounded by its host’s internal membrane.
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They reproduce by binary fission, just like bacteria — growing and splitting independently of the host cell cycle.
- They contain bacterial-style ribosomes, which are sensitive to antibiotics that don’t affect human ribosomes.
This origin story helps explain why mitochondria are so unique — part of our cells, yet still semi-autonomous. It also helps explain why they’re unusually sensitive to toxins, inflammation, and nutrient deficits — relics of their bacterial ancestry that still shape how they function today.[26]
What damages mitochondria?
When mitochondria struggle, the effects ripple through every part of the body. These organelles power nearly every cellular process — so when they stop performing well, you tend to feel it.
Low mitochondrial function has been linked to common symptoms like fatigue, brain fog, poor endurance, and metabolic slowdown.[13] Over time, researchers have connected mitochondrial dysfunction to a growing list of chronic conditions, including type 2 diabetes, Alzheimer’s disease, Parkinson’s disease, and cardiovascular disease.[14]
So what causes these cellular power plants to decline?
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Oxidative stress from pollution, alcohol, and even normal metabolism can damage mitochondrial DNA over time.[15]
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Nutrient depletion, especially of key cofactors like B vitamins and magnesium, slows down energy production.[16]
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Chronic inflammation can impair mitochondrial signaling and make energy production less efficient.[15]
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Environmental toxins, including heavy metals and pesticides, are known to directly damage mitochondrial membranes and DNA.[15]
- Disrupted sleep and circadian rhythms can interfere with mitochondrial repair cycles and reduce energy efficiency over time.[15]
The result is often a vicious cycle: damaged mitochondria create more oxidative stress, which leads to further damage — contributing to both aging and disease progression at the cellular level.
How to support your mitochondria
While aging and genetics play a role in mitochondrial health, everyday choices make a big difference. These five habits can help your mitochondria stay efficient, resilient, and ready to meet your body’s energy demands.[15]
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Move often: Exercise — especially endurance and interval training — signals your cells to create more mitochondria. This process, called mitochondrial biogenesis, is driven by PGC-1α, a master regulator of energy metabolism.
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Eat for energy: Diets rich in omega-3 fats, fiber, and plant polyphenols — like the Mediterranean diet — help protect mitochondrial membranes and reduce oxidative stress. Colorful fruits and vegetables offer additional support through antioxidants and micronutrients.
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Don’t overfeed your cells: Calorie moderation and intermittent fasting have been shown to improve mitochondrial efficiency and activate autophagy — a cellular renewal process that clears out damaged components and supports long-term health.[17]
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Protect your sleep, manage your stress: Both poor sleep and chronic stress can impair mitochondrial repair and increase oxidative damage over time. Supporting circadian rhythms helps maintain their natural recovery cycles.
- Avoid toxins when you can: Excess alcohol, cigarette smoke, heavy metals, and some pesticides are known to damage mitochondrial DNA and membranes, accelerating functional decline.
Even when you’re doing everything right — moving your body, eating well, sleeping deeply — your mitochondria are still under pressure. They work hard, and over time, some wear out.
That’s where mitophagy comes in.
Mitophagy: your cells’ built-in cleanup crew
Think of mitophagy as your body’s internal quality-control system. It’s how your cells identify and remove damaged or dysfunctional mitochondria — making space for new, healthy ones to take their place.
This cellular “recycling” helps keep your mitochondrial network efficient and responsive, especially in energy-hungry tissues like muscle, brain, and heart. When mitophagy is working well, you’re more likely to feel focused, resilient, and energized.
Mitophagy is triggered by certain types of stress that signal renewal, including:[15] [17]
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Fasting or calorie restriction
- Exercise, especially endurance and resistance training
But as we age, mitophagy slows down — and damaged mitochondria start to pile up. This can lead to slower metabolism, increased fatigue, and greater vulnerability to oxidative stress and inflammation.[18]
The good news: supporting mitophagy is possible. And in addition to lifestyle strategies, certain supplements can help nudge those cellular cleanup systems back online — especially the ones that restore nicotinamide adenine dinucleotide (NAD+) — a molecule your cells rely on for energy production and repair.
That brings us to one of the most important players in mitochondrial health.
The NAD+ connection
If mitochondria are your body’s power plants, NAD+ is the fuel line and the maintenance crew. It plays a central role not only in generating energy, but also in powering enzymes that drive mitophagy and cellular repair.
Inside your mitochondria, NAD+ acts like a currency exchange, shuttling electrons between metabolic pathways so your body can make ATP.[4] It also fuels enzymes that regulate stress responses, DNA repair, the creation of new mitochondria, and mitophagy — helping your cells clear out damaged ones for better overall function.[27]
The problem? NAD+ levels decline naturally with age — often starting in your 30s or 40s. By midlife, studies show that your NAD+ levels may be nearly half of what they were in youth.[19] That drop makes it harder for your mitochondria to keep up, contributing to lower energy, slower recovery, and increased vulnerability to stress.
In recent years, researchers have found that restoring NAD+ levels — especially with precursor compounds like nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) — can improve mitochondrial function, endurance, metabolic health, and even mitophagy in both animals and humans.[20] [21] [28] These compounds help refill the body’s NAD+ pool, giving mitochondria what they need to perform at a higher capacity and efficiently recycle damaged ones.
That’s why supporting NAD+ may be one of the most direct ways to recharge your mitochondria — and protect your energy as you age.
How supplementation supports mitochondrial health
If NAD+ is so important, why not just supplement with it directly?
It’s a fair question — but oral NAD+ doesn’t absorb well.[22] Very little reaches your cells intact, which is why research has focused instead on NAD+ precursors: compounds your body can convert into NAD+ more efficiently.
That’s where Innerbody Labs NAD+ Support comes in.
Our formula starts with two of the most widely studied NAD⁺ precursors — NMN and NR — and pairs them with additional nutrients that support methylation, cellular cleanup, and absorption:
- 700mg NMN
- 400mg NR
- 500mg Trimethylglycine (TMG)
- 15mg Spermidine
- 10mg BioPerine black pepper
Studies show that NMN and NR can raise NAD⁺ levels in the blood, and our 1,100mg precursor blend delivers a dual-action foundation that’s stronger and more comprehensive than many other options.[20] [21]
To understand why we include TMG and spermidine alongside these precursors, it helps to know how your body recycles NAD⁺ through a system called the salvage pathway.
Understanding the salvage pathway
This pathway acts like a cellular recycling loop, turning the byproducts left over when your body uses NAD+ (especially nicotinamide, or NAM) back into a fresh supply of NAD+.[23]

As shown in the diagram:
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When your cells use NAD+, it leaves behind NAM, which the salvage pathway converts back into NMN — and then new NAD+.
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NMN supplements provide that building block directly, while NR converts into NMN first.
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TMG donates methyl groups essential for these reactions, helping keep NAD⁺ recycling efficient over time.[24]
- Spermidine helps preserve NAM for reuse, preventing wasteful side reactions that would lower NAD+ availability.[25]
By combining NR, NMN, TMG, and spermidine, Innerbody Labs NAD⁺ Support promotes not just a quick NAD+ boost, but a sustained improvement in energy production, mitochondrial efficiency, and long-term cellular resilience.
Supporting your mitochondria, so they can support you
Mitochondria are more than just your body’s power plants — they’re the descendants of ancient bacteria that now fuel every heartbeat, breath, and thought.
Their health shapes everything from your energy and focus to how well you age and recover. Supporting them isn’t about chasing youth — it’s about protecting the systems that keep you strong, clear-minded, and resilient.
With the right habits — movement, nourishment, rest, and NAD+ support — your mitochondria can keep doing what they’ve done since before you were born: powering the life ahead of you.
Sources
-
National Institutes of Health. (2025, July 22). Mitochondria and health. NIH Research Matters.
-
Wen, H., Deng, H., Li, B., Chen, J., Zhu, J., Zhang, X., Yoshida, S., & Zhou, Y. (2025). Mitochondrial diseases: from molecular mechanisms to therapeutic advances. Signal Transduction and Targeted Therapy, 10, 9.
-
Cleveland Clinic. (n.d.). Mitochondrial Diseases. In Health Library.
-
Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). The Mitochondrion. In Molecular Biology of the Cell (4th ed.). National Center for Biotechnology Information.
-
Duchen, M. R. (2000). Mitochondria and calcium: From cell signalling to cell death. The Journal of Physiology, 529(Pt 1), 57–68.
-
Bassi, G., Sidhu, S. K., & Mishra, S. (2021). The Expanding Role of Mitochondria, Autophagy and Lipophagy in Steroidogenesis. Cells, 10(8), 1851.
-
Nam, M., & Cooper, M. P. (2015). Role of Energy Metabolism in the Brown Fat Gene Program. Frontiers in Endocrinology, 6, 104.
-
Angajala, A., Lim, S., Phillips, J. B., Kim, J.-H., Yates, C., You, Z., & Tan, M. (2018). Diverse Roles of Mitochondria in Immune Responses: Novel Insights Into Immuno-Metabolism. Frontiers in Immunology, 9, 1605.
-
Li, A., Gao, M., Liu, B., Qin, Y., Chen, L., Liu, H., Wu, H., & Gong, G. (2022). Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease. Cell Death & Disease, 13, 444.
-
Martin, W., & Mentel, M. (2010). The Origin of Mitochondria. Nature Education, 3(9), 58.
-
University of California, Berkeley. (n.d.). Evidence for endosymbiosis. In Understanding Evolution. University of California Museum of Paleontology.
-
Chatzispyrou, I. A., Held, N. M., Mouchiroud, L., Auwerx, J., & Houtkooper, R. H. (2015). Tetracycline Antibiotics Impair Mitochondrial Function and Its Experimental Use Confounds Research. Cancer Research, 75(21), 4446–4449.
-
Kelly, C., Junker, A., Englestad, K., Hirano, M., Trumpff, C., & Picard, M. (2024). Perceived association of mood and symptom severity in adults with mitochondrial diseases. medRxiv [Preprint].
-
Wallace, D. C. (2013). A mitochondrial bioenergetic etiology of disease. Journal of Clinical Investigation, 123(4), 1405–1412.
-
Casanova, A., Wevers, A., Navarro-Ledesma, S., & Pruimboom, L. (2023). Mitochondria: It is all about energy. Frontiers in Physiology, 14, 1114231.
-
Kiani, A. K., Dhuli, K., Donato, K., Aquilanti, B., Velluti, V., Matera, G., Iaconelli, A., Connelly, S. T., Bellinato, F., Gisondi, P., & Bertelli, M. (2022). Main nutritional deficiencies. Journal of Preventive Medicine and Hygiene, 63(2 Suppl 3), E93–E101.
-
Mehrabani, S., Bagherniya, M., Askari, G., Read, M. I., & Sahebkar, A. (2020). The effect of fasting or calorie restriction on mitophagy induction: a literature review. Journal of Cachexia, Sarcopenia and Muscle, 11(6), 1447–1458.
-
Xu, X., Pang, Y., & Fan, X. (2025). Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances. Signal Transduction and Targeted Therapy, 10, 190.
-
Zhang, X., Gao, Y., Zhang, S., Wang, Y., Pei, X., Chen, Y., Zhang, J., Zhang, Y., Du, Y., Hao, S., Wang, Y., & Ni, T. (2025). Mitochondrial dysfunction in the regulation of aging and aging-related diseases. Cell Communication and Signaling, 23, 290.
-
Conze, D., Brenner, C., & Kruger, C. L. (2019). Safety and metabolism of long-term administration of NIAGEN (Nicotinamide riboside chloride) in a randomized, double-blind, placebo-controlled clinical trial of healthy overweight adults. Scientific Reports, 9, 9772.
-
Huang, H. (2022). A multicentre, randomised, double blind, parallel design, placebo controlled study to evaluate the efficacy and safety of Uthever (NMN supplement), an orally administered supplementation in middle aged and older adults. Frontiers in Aging, 3, 851698.
-
She, J., Sheng, R., & Qin, H. (2021). Pharmacology and potential implications of nicotinamide adenine dinucleotide precursors. Aging and Disease, 12(8), 1879-1897.
-
Su, M., Qiu, F., Li, Y., Che, T., Li, N., & Zhang, S. (2024). Mechanisms of the NAD+ salvage pathway in enhancing skeletal muscle function. Frontiers in Cell and Developmental Biology, 12, 1464815.
-
Sharma, A., Chabloz, S., Lapides, R. A., Roider, E., & Ewald, C. Y. (2023). Potential synergistic supplementation of NAD+ promoting compounds as a strategy for increasing healthspan. Nutrients, 15(2), 445.
-
Bonhoure, N., Byrnes, A., Moir, R. D., Hodroj, W., Preitner, F., Praz, V., Marcelin, G., Martinez-Lopez, N., Singh, R., Moullan, N., Auwerx, J., Willemin, G., Shah, H., Hartil, K., Vaitheesvaran, B., Kurland, I., Hernandez, N., & Willis, I. M. (2015). Loss of the RNA polymerase III repressor MAF1 confers obesity resistance. Genes & Development, 29(9), 934-947.
-
Nunnari, J., & Suomalainen, A. (2012). Mitochondria: In Sickness and in Health. Cell, 148(6), 1145–1159.
-
Fang, E. F. (2019). Mitophagy and NAD+ inhibit Alzheimer disease. Autophagy, 15(6), 1112–1114.
- Yang, B., Dan, X., Hou, Y., Lee, J.-H., Wechter, N., Krishnamurthy, S., Kimura, R., Babbar, M., Demarest, T., McDevitt, R., Zhang, S., Zhang, Y., Mattson, M. P., Croteau, D. L., & Bohr, V. A. (2021). NAD+ supplementation prevents STING‐induced senescence in ataxia telangiectasia by improving mitophagy. Aging Cell, 20(4), e13329.