Mitochondria and Marathon Running: Build More Mitochondria

Do you know what is actually happening inside your body when you do tempo runs or interval sessions? If you are serious about marathon performance, you have likely heard terms like lactate threshold and VO2max — but understanding the cellular mechanism behind them can change how you think about training.

That mechanism is driven by mitochondria. This article explains why mitochondria are so critical for marathon performance, and what you need to understand about increasing mitochondrial content and improving mitochondrial function to make the most of your training.

What Are Mitochondria?

Mitochondria are organelles found in virtually every cell in the human body. Their primary role is to metabolize (consume) carbohydrates and fats to produce energy — they are the body’s “energy production factories.”

Mitochondria can generate energy from both carbohydrates and fat, making them the central engine of aerobic metabolism.

Amino acids (proteins) can also serve as fuel once the nitrogen group is removed, but they are a minor energy source and will be omitted here.

In the carbohydrate metabolism pathway, lactate is produced as a byproduct. Mitochondria consume lactate as one of their energy substrates, but at high exercise intensities, lactate is produced faster than mitochondria can process it — causing blood lactate concentration to rise.

In summary, mitochondria metabolize carbohydrates, fat, lactate, and (to a lesser extent) amino acids to produce energy.

Why Mitochondria Are Essential for Marathon Running

The human body stores approximately 1,500–2,000 kcal of carbohydrates (in the liver, blood, and muscles), but a full marathon burns roughly 3,000 kcal — far exceeding those stores.

A marathon demands sustaining a fast pace over a long distance. To do that, you need to produce a large amount of energy in a short time. Increasing mitochondrial content (= number and size) and function directly increases how much energy you can produce per unit of time.

More energy produced more quickly means you can sustain a fast pace for longer. Improved mitochondrial function also enhances fat utilization: when more of your energy comes from fat at a given pace, muscle glycogen depletes more slowly — helping you hold your race pace through the final miles.

Most runners don’t think about their mitochondria when designing training, but understanding mitochondrial adaptations before deciding on training volume and intensity will make those decisions much clearer.

How Mitochondrial Content and Function Increase with Training

The following sections explain how training drives increases in mitochondrial content and improvements in mitochondrial function.

What “Mitochondrial Content” and “Mitochondrial Function” Actually Mean

Mitochondrial content refers to two distinct changes: individual mitochondria growing larger in volume, and the total number of mitochondria increasing.

Mitochondria inside the body are said to be completely renewed roughly once a month — old mitochondria are replaced by new ones. When that renewal occurs, the new mitochondria are larger or more numerous depending on the training load experienced up to that point (Figure 2).

When researchers compared the mitochondria located between myofibrils in two subjects with different VO2max values, they observed a clear difference in both the number and size of mitochondria (Figure 3).

Mitochondrial function refers to the surface area of the inner membrane. Research shows that elite athletes’ mitochondria have denser inner membranes and a greater total surface area compared to recreational-level athletes (Figure 4).

Even with mitochondria of identical size, those capable of producing more energy per unit time have higher function. That functional capacity is determined by the surface area of the inner membrane.

This is because ATP production in mitochondria is a reaction mediated by the inner membrane — the larger the inner membrane surface area, the higher the ATP production efficiency. Therefore, the more mitochondria you have with a well-developed inner membrane, the greater your energy metabolism capacity.

Exercise Triggers Mitochondrial Biogenesis

Exercise increases the signal molecules responsible for mitochondrial synthesis inside your muscles, triggering mitochondrial biogenesis (Figure 5).

The data in Figure 6 shows how much mitochondrial biogenesis was stimulated by training at a low exercise intensity (40% VO2max, LO) versus a high exercise intensity (80% VO2max, HI). Total caloric expenditure was matched between the two conditions to isolate the effect of intensity.

Three hours after exercise, the high-intensity condition showed more than twice the mitochondrial transcriptional activation of the low-intensity condition. Importantly, low-intensity training also promoted mitochondrial biogenesis — just to a smaller degree.

However, this experiment only shows an activation marker. It does not tell us whether mitochondrial content actually increased or whether mitochondrial function improved. The sections below address how specific types of training drive each type of adaptation.

Total Training Load Drives Mitochondrial Content

Based on multiple studies, the prevailing view is that the adaptation in mitochondrial number and size depends primarily on total training load (Granata et al., 2018 ※3). Total training load means “how much training you have accumulated, and at what intensity.”

The following study investigated VO2max and skeletal muscle mitochondrial content in two groups trained under different protocols.

Think of Group A as interval training and Group B as easy jogging.

Figure 7 compares the effects of Group A and Group B training on whole-body endurance (VO2peak) and skeletal muscle mitochondrial content. Both VO2max and skeletal muscle mitochondrial content showed virtually no difference between the two groups — suggesting that total training load, not intensity distribution, determines mitochondrial content.

This supports the view that mitochondrial content (= number and size) is determined primarily by total training load (intensity × volume).

Training Intensity Drives Mitochondrial Function

Mitochondrial function — specifically, the increase in inner membrane surface area — is more strongly driven by training intensity than by volume alone.

Running training spans a wide range of intensities, from easy jogging to efforts exceeding VO2max, and evidence shows that higher intensities promote greater expansion of the inner membrane surface area. The exact intensity threshold for optimal adaptation cannot be precisely defined, but some studies report significant adaptation at intensities at or above VO2max — consistent with standard running training theory.

Putting these findings together: training intensity strongly affects both mitochondrial content and function, while training volume primarily affects content. Sustaining the highest intensity you can manage within a volume you can consistently maintain is likely the most effective strategy for driving mitochondrial adaptation.

Running Training for Mitochondrial Growth

When applying these principles to real-world training, two additional factors become important: continuity and time constraints.

The Continuity Factor

High-intensity training like interval sessions is mentally and physically demanding. If someone told you to do intervals every day, most runners — myself included — would find that unsustainable. The suffering accumulates, and the stress becomes a barrier to showing up.

On the physical side, higher intensity means greater injury risk, which can disrupt training continuity entirely. Low-intensity training, by contrast, carries very little suffering or injury risk. When it comes to long-term continuity, easy running has a clear advantage.

The Time Constraint Factor

This factor applies especially to recreational runners, who face real limits on training time due to work, family, and other commitments. When time is limited, training efficiency becomes critical — and high-intensity sessions pack more adaptation per minute than easy runs.

However, because daily high-intensity sessions are not sustainable due to fatigue and injury risk, low-intensity easy runs fill the gaps and accumulate total training volume. Ultimately, combining high- and low-intensity training is what makes long-term training continuity possible.

How to Optimize Your Easy Runs for Mitochondrial Adaptation

Because high-intensity training drives greater mitochondrial adaptation but is difficult to sustain daily, incorporating easy jogging as filler runs is the practical approach. Many recreational runners already follow a structure of “two key sessions per week plus jogging in between” — and from a mitochondrial standpoint, this is well-reasoned training.

From a mitochondrial perspective, a higher-intensity jog is always better for adaptation — even among your easy runs. For that reason, it is worth varying your jogging intensity based on when and why you are running.

When jogging the day after a hard key session, keep the intensity low. This “post-key-session easy jog” is well-supported by mitochondrial science. Running with partially depleted glycogen stores activates molecular signals for mitochondrial biogenesis — including PGC-1α — more strongly than running in a fully fueled state.

Yeo et al. (2008) ※4 found that subjects who trained consistently with low glycogen stores showed statistically significant increases in mitochondrial enzyme activity and fat oxidation rates. That said, this is a supplementary technique — never begin a high-intensity session with depleted glycogen stores.

The practical approach is simple: fuel up fully before key sessions, and keep carbohydrate intake lower before the next day’s recovery jog. On days when you only have an easy run planned and the following day is flexible, picking up the pace slightly is a worthwhile option.

Consistency Is the Most Important Factor

Training drives mitochondrial adaptation, but stopping training causes mitochondrial content and function to decline rapidly. Mitochondrial content takes time to build, so the decline is relatively gradual — but metabolic adaptations such as fat-burning capacity and lactate clearance begin to deteriorate after as little as 10 days of inactivity (Mujika & Padilla, 2001 ※5).

Therefore, the single most important factor for continuously improving mitochondrial content and function is keeping your training going. Pushing to your absolute limit may accelerate adaptation in the short term, but it increases injury risk — which can ultimately break your training continuity for weeks or months.

Manage your training intensity and volume appropriately so you can sustain training long-term without getting injured. That consistency, more than any single hard workout, is what drives lasting mitochondrial adaptation.

Summary

Here are the key takeaways from this article.

I hope this article helps you improve your marathon performance.

References

※1 Larsen S, Nielsen J, Hansen CN et al. (2012) “Biomarkers of mitochondrial content in skeletal muscle of healthy young human subjects.” J Physiol 590(14):3349-3360.

※2 Nielsen J, Gejl KD, Hey-Mogensen M et al. (2017) “Plasticity in mitochondrial cristae density allows metabolic capacity modulation in human skeletal muscle.” J Physiol 595(9):2839-2847.

※3 Granata C, Jamnick NA, Bishop DJ (2018) “Training-Induced Changes in Mitochondrial Content and Respiratory Function in Human Skeletal Muscle.” Sports Medicine 48(8):1809-1828.

※4 Yeo WK, Paton CD, Garnham AP et al. (2008) “Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens.” J Appl Physiol 105(5):1462-1470.

※5 Mujika I, Padilla S (2001) “Cardiorespiratory and metabolic characteristics of detraining in humans.” Med Sci Sports Exerc 33(3):413-421.