Supercharge Your Mitochondria for Energy, Endurance, And Longevity

You are not singular.

You are legion.

You are not alone.

You are symbiote.

Living inside your cells are mitochondria. Tiny fuel cells that evolved endosymbiotically from alphaproteobacteria.

That’s right: the mitochondria that provide us with ALL of our energy began life as an entirely separate species from our own biological ancestors. This is why our mitochondria actually has its own DNA.

And by protecting them and nourishing them, we empower them to do their job better and to fuel us with even more power. For running, lifting, climbing, even healing and thinking.

Origins of Mitochondria

All life on Earth can be classified as one of two groups: eukaryote and prokaryote. Prokaryotes are simple, single celled organisms. Their DNA is ring shaped and actually floats freely within the cell.

Being so simple has its advantages: some prokaryotes are capable of entering a dormant state that allows them to exist in suspended animation for millions of years. We have successfully reanimated individual bacterium that lived during the time of the Dinosaurs!

Eukaryotes, like you and me, have larger and more complex cells with DNA housed within a nucleus. Eukaryotes can be multicellular but they aren’t always. See: yeast.

But this complexity is what is able to give rise to the huge variety of life we see today.

While we don’t know this with 100% certainty, the prevailing theory is that, at some point, smaller cells started making their way into larger ones. These cells enjoyed a mutually beneficial relationship, to the point where they eventually became a single organism. The first eukaryotes.

We think this happened around 2.4 billion years ago. So, a while back.

And it is thought that the mitochondria within our very own cells are the descendants of just such a bacterial guest. While they serve as organelles today – tiny organs that live within our cells – they began life as entirely separate bacteria.

Today, they provide us with adenosine triphosphate (ATP) which is the fuel source required for every process within our bodies. That’s not the only way we get it, but it is by far the predominant way.

Similarly, chloroplasts in plants are thought to have a similar role: helping plants to turn energy from sunlight into sugar using chlorophyll. This process may actually rely on quantum processes by the way. Life is amazing.

Owing to this unique history, mitochondria actually behave like living things in many ways. For example, they can only reproduce by splitting into two. That’s right: the cell isn’t able to produce its own mitochondria. This isn’t a problem for our other organelles.

Likewise, mitochondria are bound in membranes, just like bacteria.

It’s been observed that mitochondria actually resemble an infectious kind of bacteria called rickettsia. Not only aesthetically but also in terms of their DNA.

Roles of Mitochondria

For these reasons, we need to think of our mitochondria as pets… or maybe weird guests. Like a guest that sits at your table for you to endlessly feed. Then their vomit powers your washing machine.

Maybe tending to a garden is the nicest analogy.

We can’t produce more mitochondria, we can only create the conditions favourable for them to reproduce.

And it’s important that we do create these favourable conditions. I’ve already told you that mitochondria are required for most processes in the human body. That should probably be enough.

Saying that mitochondria play an important role in your health is a bit like saying oxygen plays an important role in your health. Which is to say it’s accurate… but maybe an understatement.

But they actually do more than that, too. A lot more. I’m going to recommend you check out a YouTube channel called Physionic for more on this, as he is by far the expert. But, for example, mitochondria actually play an important role in signalling – that is to say that they help tell the body when certain tasks need to be carried out. They do this by releasing free-radicals (reactive oxygen species or ROS). While that might sound like a bad thing, we actually need a small amount for this kind of communication.

In fact, mitochondria actually modulate the amount of these free radicals and can also help to reduce the amount via the glutathione pathway, among others. This, of course, can prevent damage to the cells.

Mitochondria play an important role in cell death – helping to trigger apoptosis by effectively starving the cell of energy. Again, this is important for preventing the unwanted proliferation of damaged cells.

They also provide energy in forms other than ATP, such as “GTP.” This can be used as an equivalent to adenosine triphosphate to power the cell. Interestingly, it is sometimes described as an ancient “molecular fossil.” Not literally, of course, but rather that it may have been preserved from a time when the Earth had less atmosphere and, therefore, less available oxygen and CO2. Back then, it may have been the primary energy source for early cells!

And, seeing as they have their own DNA, they also need to be able to create protein. Mitochondrial protein synthesis is responsible for thirteen different peptides via the mitoribosome (reference). Fun fact: mitochondrial DNA is passed down on the maternal side, meaning we directly inherit our mitochondrial function from our parents!

Mitochondrial DNA is actually far more mutable than our nuclear DNA, meaning it’s more susceptible to damage and mutation. For that reason, it’s important that it is regularly maintained.

One way this can happen is via fusion and fission – the process of combining and dividing mitochondria, respectively. Combining two mitochondria into a single mitochondrion may improve efficiency, but may also help to “dilute” errors in DNA.

Fission, conversely, may be used to isolate damaged parts of the mitochondria – allowing cells to effectively target and destroy those broken components. It can also facilitate general mitophagy – breaking down mitochondria so that they may be more easily broken down and destroyed.

And, of course, these processes can be used to control the number of mitochondria – responding to the needs of the cell. And, of course, fission is needed during cell division (mitosis) to ensure both new cells get their own mitochondria.

A healthy cell should exhibit a somewhat equal balance of fusion and fission events to optimise mitochondrial function. This is referred to as “mitochondrial dynamics”.

Mitochondria can even move around within the cell to meet demand and to become more evenly distributed.

Again: the human body is incredible, right?

Mitochondria and Energy

But let’s focus on the primary function first: that being the production of energy. After all, they are the power plants of the cells!

Specifically, mitochondria provide energy via phosphorylation. Here, oxygen is used to convert energy from nutrients like glucose and fatty into ATP. This process is responsible for something like 95% of the energy in the human body and is the most efficient way for us to fuel our actions.

Because phosphorylation requires oxygen, that means it is limited by how quickly we can get oxygen around the body. This is why we start panting if we exert ourselves.

When we think of energy, we tend to focus on moving. Lifting our arms or running or lifting weights. But energy is also necessary for our heart beating. For our thoughts. For our digestion and immune system and our healing. Without mitochondria, we simply could not function.

Another way we make energy is through glycolysis. This is an anaerobic process that occurs within the cytoplasm itself (the fluid inside the cell). Here, glucose is broken down into pyruvate which yields a small amount of ATP. This provide a faster supply of energy but it is inefficient and finite. It also leads to a build up of lactate, hydrogen, and other waste products that eventually cause what we experience as “the burn.”

If you start sprinting, you will will first use cytoplasmic ATP. Specifically, you will use the ATP-Creatine Phosphate system. This utilises locally stored ATP and creatine phosphate but can only last for 10-15 seconds before the supply is used up. After that, the body needs to start producing its own energy. At this point, glycolysis begins and you’ll start to utilise glucose. This can last about two minutes before the build up of waste products causes muscle fatigue.

Now the body must switch to the third energy system: phosphorylation. That’s where the mitochondria kicks in. This provides a theoretically limitless energy supply, meaning that you can run for hours if you so wish. But you will need to reduce the pace. Why? Because your body needs to wait for the blood to get to the muscles.

One way you can immediately see your performance improve drastically is to learn to perform more efficiently. Grant can spar for much longer than me without getting tired out. The reason for this is that his movements are more efficient. He is not co-contracting unwanted muscles. He is not tense. And when he punches he recruits only the necessary muscle fibres.

In other words, he can achieve more with less energy. He can still perform martial arts incredible well while utilising his aerobic energy system. I cannot.

Where people oversimplify this process is when they tell you that you “switch” to this energy system or that. The reality is that you are usually using multiple energy systems all at once.

For example, while you might be sprinting, you are still also thinking and healing. Some of the muscles in your body will be relaxed or playing a more supporting role. Therefore, you’ll be using BOTH aerobic and anaerobic energy systems.

Beyond this, the muscles primarily responsible for the movement itself will be using multiple energy systems.

To understand this, we need to think again about Henchman’s Size Principle. I talk about this all the time but that’s because it’s such a misunderstood concept that sheds so much light on the way our muscles work.

Mitochondria and Performance

Our muscles, as you no-doubt know, are made up of lots of tiny fibres. These are grouped into motor units. Fibres can be categorised into type 1 (slow twitch), type 2a (fast twitch), and type 2x (super fast twitch). That said, it’s really more accurate to think of this as a spectrum rather than distinctly different types of fibre.

Type 2b is actually only present in some animals, like squirrels, and it’s what allows those animals to move to with those twitchy jerky movements.

Side note: I fucking love squirrels.

I always thought a human with type 2b fibres would be a really cool mutant superpower…

While type 1 fibres contain lots of mitochondria and rely primarily on phosphorylation for their energy, type 2x fibres contain far fewer and rely primarily on cytoplasmic ATP production. Motor units – those bundles of muscle fibres – only contain fibres of one type. And each motor unit within a muscle is controlled by a separate nerve, connected to a separate neuron within the brain. When you contract gently to pick up a spoon, a weak signal activates just a few of the smaller, slow-twitch motor units and therefore a very small percentage of your muscle fibre. This is how you might lift your spoon to your mouth while eating, for example.

When you contract powerfully, you send a much more powerful signal from the brain that engages the faster twitch fibres grouped in the much bigger motor units.

Here’s the thing: you actually can’t activate your type 2x fibres without also activating your type 1 and type 2a fibres. That’s because the motor units are recruited once the signal reaches a certain threshold. In other words: if you send a strong enough signal to engage the largest motor units, this must by definition ALSO be strong enough to engage all the smaller ones. This is Henchman’s Size Principle. We always engage motor units from the smallest to the largest.

(I wonder if a hypothetical superhuman could get around this by simply having efficient enough movement to call upon individual motor units?)

The point is: when you sprint BOTH your fast twitch AND your slow twitch motor units are contributing to your forward momentum. This is why it’s important to train your slow twitch fibres as well as your large twitch fibres if you want to maximise your performance. You want to make those slow twitch fibres stronger via resistance training and you want to increase their efficiency by increasing mitochondrial density and health.

However, what’s also important to recognise, is that training that focusses entirely on fast twitch fibre won’t provide a huge stimulus for the slow twitch fibre. Why? Because you won’t be taking that slower twitch muscle to a point of failure – you won’t be challenging it. That’s another reason it’s so important to to combine fast and slow cadences in your workouts. And to combine both aerobic and resistance training.

And while you might not think about resistance training for mitochondria or endurance more generally; the truth is that resistance training is actually a great option when it comes to improving mitochondrial function. Not number as much, but health and efficiency.

Endurance training is still the most valuable for mitochondrial health, though, and will improve the number of mitochondria to meet demand – on top of health and efficiency.

Interestingly, though, the mechanisms at place are slightly different. And so, your best bet is likely to combine both approaches.

Many of the signals for hypertrophy will encourage mitochondrial adaptations. For example, IGF-1increases mitochondrial survival (reference) and may help reduce the production of reactive oxygen species (study).

Mitochondrial Dynamics and Hybrid Training

Generally, fission is a response to stress: oxidative stress, metabolic changes, etc. Resistance training is particularly effective at triggering this process and thereby helping to ensure mitochondria are distributed where they are needed and that damaged mitochondria are degraded.

Post resistance training sees the activation of the mTOR pathway. This, too, is important for the health and function of mitochondria. mTOR directly encourages mitochondrial fusion via mTORC1, by synthesising proteins necessary for the process, such as MFN1, MFN2, and OPA1.

Mechanical tension and metabolic stress also create signals for mitochondrial biogenesis. And there are many additional benefits and adaptations that support mitochondrial function indirectly. For example: resistance training can increase oxygen capacity in the muscle.

Note that it is also possible to add mitochondria to type 2 fiber without converting fiber types.

However, if you want to maximise the number of mitochondria then you, of course, need to incorporate endurance training. It should make sense that increasing your energy demand would result in more energy factories in the cells. Because aerobic exercise most greatly increases the demand for ATP, this alters the AMP/ATP ratio, activating AMPK. Increases in calcium also lead to increased AMPK. In other words, AMPK kicks in when energy is low to increase glucose uptake and other catabolic processes. AMPK is known to bodybuilders for its role in inhibiting protein synthesis by inhibiting the mTOR pathway. It’s what makes us more catabolic, rather than anabolic.

However, AMPK activation also directly induces PGC-1a – which regulates mitochondrial biogenesis – creates more mitochondria. It does this by enhancing expression of the mitochondrial genes within the nuclear DNA (activating transcription factors). In other words: the recognition that the cells needs more energy results in signals that encourage the birth of more mitochondria. AMPK also influences fusion and fission and promotes mitophagy – the removal of mitochondria – as needed.

Note that mTOR, the counterpoint to AMPK, ALSO increases PGC-1a, but more indirectly.

This is all getting pretty heady and it’s an impossibly deep rabbit hole to go down. But the takeaway point I’m trying to make? Once again, it’s that hybrid training results in the best outcome: helping to ensure both the number of mitochondria and their health and efficiency through a number of different ways.

Those muscle heads saying they don’t need to do any endurance training should take note: healthy mitochondria means slower aging, more energy, and even a longer lifespan. Unhealthy, inefficient mitochondria means more free radicals and more cell damage.

You can scoff about cardio destroying your gains, but you may wish you’d taken a more moderate approach when you start seeing yourself age prematurely.

Can I also just take this moment to address the small but growing number of people that think exercise is bad and may shorten your life span? This all further disproves that notion. The overwhelming evidence suggests that exercise extends lifespan, precisely by facilitating these sorts of processes.

What may be damaging, however, is consistent overtraining and some studies do suggest this may lead to mitochondrial dysfunction (reference). More research is needed… but consider this your license to not completely destroy your body every time you do a workout – it’s overall not conducive.

And I think a lot of this is just common sense, right?

If you put demand on your body to produce more energy, more efficiently, then it will do so. If you place too much demand and stress, then you will cause damage as you degrade the body faster than it can recover.

Looking After Your Mitochondria: It’s Common Sense

The same common sense approach proves to be useful when considering diet and lifestyle. For example, we know that being in a huge calorie surplus leads to mitochondrial dysfunction. If you bombard your cells with sugar, according to Dr. Martin Picard, you literally see the mitochondria become more fragmented and dysfunctional within minutes (reference).

This might seem alarming, but the truth is that this is simply a way for the mitochondria to become less efficient at utilising energy. After all: there is a surplus. It also helps to protect the mitochondria against cellular stress, isolating damaged mitochondria among other things. Excess glucose increases the production of ROS, creating oxidative stress.

Over time, though, prolonged fragmentation can lead to damaged or dysfunctional cells.

We shouldn’t stress about every little over-indulgence, then. But we should certainly aim to be roughly calorie and nutrient neutral on average. That is to say that consistent over-eating is not good. But you could have guessed that, right?

It may be that being in calorie deficit – being hungry sometimes – is also good for mitochondria. After all: this requires greater efficiency. Fasting may well be useful in this regard, too, then. But both Dr Picard and Physionic both point out that we don’t know enough to prescribe specific eating windows for optimal mitochondrial health and efficiency.

This is why I really respect Physionic: because he doesn’t take a few studies and then use that to start suggesting protocols or hacks. I did some deep research for this post (I have a headache) but if you want to hear this from the expert and in FAR more depth, then I highly recommend his channel. Link will be in the description.

Likewise, we know that many supplements like coenzyme Q10, omega 3 fatty acid, PQQ, etc. are all good for mitochondrial health and function. This is where some content creators might recommend you take these supplements and possibly even sell you a bottle called “Energy++” or something.

But look: while they might appear to be somewhat useful, the truth is that they are also pretty expensive. And the benefits you get are nebulous, hard to measure, likely individual… And if you took all those things you’d also need to take supplements for countless other aspects of your health. Mitochondria is just one piece of the puzzle. It’s reductive and exhausting to suggest you take a billion different supplements.

So, you know what? Just eat as well as you can. You’ll get omega 3 from fish. You’ll get CoQ10 from meats and fish. Just look for nutrient dense foods and get a good variety. Trust your body to do the rest.

The rest is also what you’d expect. Sleep is very important for mitochondrial health. So, as a Dad of two I’m fucked then. Also: stress levels. In fact, Dr Picard talks about another study he conducted where he found a correlation between mood and mitochondrial function. This makes sense when you consider the negative impact of stress broadly.

Be healthy and your mitochondria will be healthy – who would have thought! That might seem a little anticlimactic after all this talk of ancient protobacteria and endosymbioses and molecular fossils… but I don’t view it that way. I view it as another reminder of the holistic nature of health. If you’re neglecting your mental health, this will have an impact on your performance and maybe even your longevity.

And train, dammit!

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One Comment

1. Martín says:

   July 25, 2024 at 8:46 am

   Thanks for this post Adam, I really enjoyed it!!! I like this kind of in depth dives into very niche aspects of the human body and how the can be exploited through training to achieve a superhuman results, even though in the end we always come back to the basics, which in the end becomes encouraging, don’t think too much about what you’re doing, just do it. It’s only once you’ve done it that you can look back at it and try to find a scientific explanation for the outcome, it’s better to explain the outcome than to theorize about it. Once again thanks a lot Adam, it felt like a really authentic post as well.

   Reply