How Does Exercise Build More Mitochondria, and Why Does It Matter at Any Age?

Picture two 70-year-olds. One has been sedentary for decades; the other runs, or only started training a few years ago. Muscle biopsies tell the story. The first shows what we expect from age: fewer mitochondria, weaker oxidative enzymes, accumulated damage to mitochondrial DNA. The second often looks like someone decades younger.

That case vignette sits near the end of The Mitochondrion and Bioenergetics, and it sums up why I wrote the book. Mitochondria and exercise are tied together more tightly than most people realize: the mitochondrion is not a fixed battery, it is a living engine that grows when you ask more of it and shrinks when you stop. Here is what the book explains about that engine, and what it means for how you train, fuel and age.

What do mitochondria actually do for your energy?

Every movement, heartbeat and thought is paid for with one molecule: ATP, the cell's energy currency. The surprising part is how little of it you hold. The body contains only about 50 g of ATP at any moment, yet at rest it recycles roughly its own body weight in ATP every day (Berg et al., 2019; Nelson & Cox, 2021). Muscle stores enough ATP for only one or two seconds of maximal contraction.

So "having energy" never means having a big stock of ATP. It means being able to remake ATP fast enough. In the book, I describe three systems that do this:

• The phosphagen system recharges ATP almost instantly from phosphocreatine. It gives the highest power but runs out in about 5 to 10 seconds of all-out effort.
• The glycolytic system breaks down glycogen quickly, without oxygen, and dominates hard efforts from roughly 10 seconds to 2 minutes.
• The oxidative system, inside the mitochondria, burns carbohydrate and fat with oxygen. It is the slowest, but its capacity is close to unlimited, and it supplies about 90% of the ATP your cells make.

These systems blend rather than take turns. The oxidative system is also what recharges the other two between efforts. That is why aerobic fitness matters even for sprinters, lifters and team-sport athletes.

How does exercise increase mitochondria?

The headline adaptation to endurance training was first described by John Holloszy in 1967: a large rise in muscle mitochondria. Regular endurance training increases mitochondrial content and oxidative enzyme activity by roughly 40 to 100% over weeks to months (Holloszy & Coyle, 1984; MacInnis & Gibala, 2017).

The mechanism, called mitochondrial biogenesis, works like this:

1. Each training session raises calcium inside the muscle cell and lowers its energy charge.
2. The drop in energy activates AMPK, the cell's low-energy sensor.
3. AMPK and calcium switch on PGC-1α, the master regulator that coordinates the genes needed to build new mitochondria.
4. One session raises PGC-1α briefly; consistent training turns those signals into lasting gains.

Two points from the book are worth keeping in mind. First, both moderate continuous training and high-intensity interval training work, and intervals reach comparable mitochondrial adaptations in less total time. Second, the gains appear fast, within one to two weeks of consistent training, and they reverse with inactivity over weeks. Use it or lose it. People who trained before do re-adapt faster.

More mitochondria is only part of the picture. Training also adds capillaries around muscle fibres, raises myoglobin, increases the capacity to burn fat at a given pace (sparing glycogen) and lifts the lactate threshold, the intensity you can hold before lactate starts to pile up.

Does lactic acid cause muscle fatigue?

This is one of the myths the book corrects. Lactate is a fuel and a marker, not the direct cause of fatigue. Lactate made by fast fibres is taken up by other muscle fibres, the heart and the liver, and either burned for energy or turned back into glucose (Brooks, 2018).

In hard efforts, fatigue comes mainly from the build-up of inorganic phosphate, disturbed ion gradients and, in a secondary role, acidosis from high ATP turnover (Allen et al., 2008). In long efforts, glycogen depletion ("hitting the wall") and the nervous system also play a part.

The practical point: the lactate threshold is often a better predictor of endurance performance than VO₂max, and it is largely a mitochondrial story. Two athletes with the same VO₂max can perform very differently if one can work at a higher fraction of it. Training raises that threshold by building the machinery that burns and clears lactate.

Should you take antioxidants after training?

Here is the most counterintuitive idea in the book. The electron transport chain inside mitochondria leaks small amounts of reactive oxygen species (ROS). In excess, they damage lipids, proteins and mitochondrial DNA. But at low, brief levels, as during exercise, they act as signals that drive the very adaptations you train for: more mitochondria, stronger antioxidant defences and better insulin sensitivity. This is called mitohormesis.

The consequence is direct. Large doses of antioxidant supplements, such as high-dose vitamin C and E taken routinely around training, can blunt some of those adaptations by muting the signal. Several controlled trials have shown this, though not all, and the effect depends on dose and context (Ristow et al., 2009; Merry & Ristow, 2016). The book's practical consensus is to get antioxidants mainly from a varied diet and to avoid routine high-dose antioxidant supplements around training, unless there is a specific medical reason. If you are considering any supplement, talk to a qualified health professional first, especially if you take medication or have a health condition.

Can you keep your mitochondria healthy as you age?

Declining mitochondrial quantity and quality is recognized as one of the hallmarks of aging (López-Otín et al., 2013). It contributes to lower aerobic capacity and to sarcopenia, the age-related loss of muscle mass and function. Reduced muscle mitochondrial function is also associated with insulin resistance and type 2 diabetes. Whether it is cause or consequence is still debated, but the association is robust.

The encouraging part is that this decline is not fixed. Exercise stimulates mitochondrial biogenesis and the recycling of worn-out mitochondria even in old age, partly reversing the decline. The same PGC-1α program that builds a young athlete's mitochondria still works at 70. That is the 70-year-old from the opening, and in my view it is the most hopeful conclusion of the book.

The levers the book identifies are simple:

• Exercise, both endurance and intervals: the strongest lever by far.
• Adequate micronutrients, not megadoses: iron, copper and B vitamins for the energy machinery; selenium, zinc, manganese and vitamins C and E for the antioxidant defences. Correct genuine deficiencies, ideally with a health professional.
• No chronic energy surplus: overnutrition and inactivity impair mitochondrial function.
• Enough sleep, which supports mitochondrial quality and hormonal regulation.

Go deeper into the cell's energy engine

In The Mitochondrion and Bioenergetics, Book A2 of The Performance & Human Physiology Encyclopedia, a 93-book collection from Netritious, I take you from the laws of thermodynamics to ATP, glycolysis, the citric acid cycle, oxidative phosphorylation, fat and ketone metabolism, the energy systems of exercise and the practical side: VO₂max, the fat-to-carbohydrate crossover, fueling, and supplements judged by the pathway they target. Each chapter includes worked calculations, evidence levels and a section for coaches. You can find the book here: The Mitochondrion and Bioenergetics.

Frequently asked questions

How long does it take to build more mitochondria?

According to the book, measurable increases appear within one to two weeks of consistent training and keep building over months. They fade within weeks if you stop.

Is interval training or steady cardio better for mitochondria?

Both are effective. High-intensity intervals reach comparable mitochondrial adaptations in less total time, while longer moderate sessions also build fat-burning capacity and the aerobic base.

Is lactate bad for performance?

No. Lactate is a fuel that other tissues reuse and a marker of effort, not the main cause of fatigue. Training raises the lactate threshold, which lets you hold a faster pace.

Where can I find The Mitochondrion and Bioenergetics?

The book is available on Amazon in Kindle format, in English.