You are electric.
Every millisecond hundreds of thousands of tiny cellular constituents called mitochondria are pumping protons across a membrane to generate electric charges that are each equivalent to the power, over a few nanometers, of a bolt of lighting.
And when you consider energy in general, your body, gram for gram, is generating 10,000 times more energy than the sun, even when you're sitting comfortably.
There's an average of 300 to 400 of these often ignored energy-producing cellular "organs" in every cell – roughly 10 million billion in your body. If you were to somehow pile them together and put them on a scale, these mitochondria would constitute roughly 10% of your bodyweight.
It's even more remarkable when you consider that they have their own DNA and reproduce independently. That's right, they're not even part of you. They're actually alien life forms, free-living bacteria that adapted to life inside larger cells some two billion years ago.
But they're not parasitic by any means. Biologically speaking, they're symbionts, and in their absence, you could hardly move a muscle or undergo any of thousands of biological functions.
In a broad sense, mitochondria have shaped human existence. Not only do they play a huge role in energy production, sex and fertility, but also in aging and death.
If you could somehow influence them, you could theoretically double your lifespan without any of the diseases typically associated with old age. You could avoid metabolic diseases like syndrome X that afflict some 47 million Americans and simultaneously retain the energy of youth well into codger-dom.
From an athletic perspective, controlling the vitality and number of mitochondria in your muscle cells could lead to huge improvements in strength endurance that didn't decline with the passing of years.
Luckily, I'm not just teasing you with things that might someday happen. Controlling mitochondria is within our grasp, right now.
But before we discuss how they affect muscle strength and endurance, we need to look at some really mind-blowing stuff that will be the crux of tons of scientific research and innovation in the years to come.
Mitochondria are tiny organelles, which, as you can tell by the word, are kind of like teeny-tiny organs and like organs, they each have specific functions, in this case the production of energy in the form of ATP, the energy currency of the cell. They do this by metabolizing sugars, fats, and other chemicals with the assistance of oxygen.
(Every time you take creatine, you're in a sense "feeding" your mitochondria. Creatine is transported directly into the cell where it's combined with a phosphate group to form phosphocreatine, which is stored for later use. When energy is required, the phosphocreatine molecule lets go of it phosphate group and it combines with an ADP molecule to form ATP.)
A cell can have one lonely mitochondria or as many as hundreds of thousands, depending on its energy needs.
Metabolically active cells like liver, kidney, heart, brain, and muscle have so many that they may make up 40% of the cell, whereas other slacker cells like blood and skin have very few.
Even sperm cells have mitochondria, but they're all stored in the flagellating tail. As soon as the sperm cell hits its target, the egg cell, the tail plunks off into the deep ocean of prostatic fluid. That means that only the mother's mitochondria are passed on to offspring. This is done with such unfailing precision that we can track mitochondrial genes back almost 190,000 years to one woman in Africa who's been affectionately named "Mitochondrial Eve."
Biologists have even postulated that this particular phenomenon is the reason why there are two sexes instead of just one. One sex must specialize to pass on mitochondria in the egg whereas the other must specialize in not passing them on.
The commonly held assumption of aging is that as the years go by, we get more and more rickety until, finally, some part or parts break down beyond repair and we up and die.
The popular reasons include wear and tear or the unraveling of telomeres – those nucleotide sequences at the end of genes that are said to determine how many times a cell can replicate. In the case of generic wear and tear, it doesn't seem to bear up to scrutiny because different species accumulate wear and tear at different rates, and as far as telomere theory, their degradation among different species displays just too much divergence to pass the smell test.
Others say it's because of a drop in GH or a decline in the abilities of the immune system, but why the heck do they drop in the first place?
What we need to do is look at those individuals or species that don't seem to suffer from the normal signs of aging. The oldest among us, those rare centenarians that appear on morning talk shows every so often boasting about eating bacon and liquoring it up every day, seem to be less prone to degenerative disease than the rest of us. They end up dying from muscle wastage rather than any specific illness.
Similarly, birds rarely suffer from any degenerative diseases as they age. More often, they fly around as they always have until one day their power of flight fails and they crash land ignominiously into a drainage ditch.
The answer to both the centenarians' and the birds' long, disease-free life seems to lie with the mitochondria. In both cases, their mitochondria leak fewer free radicals.
This is important because mitochondria often determine whether a cell lives or dies, and this is dependent on the location of a single molecule – cytochrome C.
Any one of a number of factors, including UV radiation, toxins, heat, cold, infections, or pollutants can compel a cell to commit suicide, or apoptosis, but the unrestricted flow of free radicals is what we're concerned with here.
The underlying principle is this: depolarization of the mitochondrial inner membrane – through some sort of stress, either external or internal – causes free radicals to be generated. These free radicals release cytochrome C into the cellular fluid, which sets into motion a cascade of enzymes that slice up and dispose of the cell.
This observation led to the popular theory of mitochondrial aging that surfaced in 1972. Dr. Denham Harman, the "father" of free radicals, observed that mitochondria are the main source of free radicals and that they're destructive and attack various components of the cell.
If enough cells commit apoptosis enough times, it's like a butcher slicing up a pound of salami. The liver, the kidneys, the brain, immune system cells, even the heart, lose mass and effectiveness slice by slice. Hence the diseases of aging.
Dr. Harman is why practically every food on the market today boasts about its antioxidant power.
The trouble is, Dr. Harman appears to have been wrong, at least partially.
For one thing, it's hard to target the mitochondria with antioxidant foods. It might be the wrong dosage, the wrong timing, or even the wrong antioxidant. Moreover, it seems that if you completely turn off free radical leakage in the mitochondria, the cell commits suicide. Hardly the effect we're looking for.
(That's not to say that ingesting antioxidants isn't good for you, but it's important to realize that this endless, single-minded pursuit of higher and higher antioxidant-containing foods might not do much to prolong life.)
Free radicals, it seems, in addition to telling the cell when to commit suicide, also fine tune respiration, otherwise known as the production of ATP. They're involved in a sensitive feedback loop, telling the mitochondria to make compensatory changes in performance.
However, if you completely shut off or slow down free radical production too much through external methods like an antioxidant diet or drugs, the membrane potential of the mitochondria collapses and it spills apoptotic proteins into the cell. If a larger number of mitochondria do this, the cell dies. If a large number of cells do this, the organ and overall health of the individual is affected.
In the case of controlling free radicals, it seems you're damned if you do and damned if you don't.
So again, we need to look at old codgers and the birds. It so happens there's a gene in certain Japanese men who are well over a hundred years old that leads to a tiny reduction in free radical leakage. If you have this gene, you're 50% more likely to live to be a hundred. You're also half as likely to end up in a hospital for any reason.
As far as birds, they've got two things going for them. One, they disassociate their electron flow from ATP production, a process known as uncoupling. This, in effect, restricts leakage of free radicals.
Secondly, birds have more mitochondria in their cells. Since they have more, it leads to a greater spare capacity at rest, and thus lowers the reduction rate and free radical release is lowered.
So we're left with this: increasing mitochondrial density, along with slowing free radical leakage, would likely lead to a longer life, free from most of the diseases typically attributed to old age.
Since mitochondria have their own genes, they're subject to mutations that affect their health and function. Acquire enough of these mutations, and you affect the way the cell functions. Affect enough cells, and you affect the organ/system they're a part of.
The hardest hit organs are those that are generally mitochondria-rich, like muscles, the brain, liver, and kidneys. Specific mitochondria-associated diseases range from Parkinson's, Alzheimer's, diabetes, various vaguely diagnosed muscle weakness disorders, and even Syndrome X.
Take a look at heart patients, for instance. Generally, they have about a 40% decrease in mitochondrial DNA.
And, as evidence that mitochondrial deficiency might be passed down from generation to generation, the insulin-resistant children of Type II diabetics, despite being young and still lean, had 38% fewer mitochondria in their muscle cells.
Mitochondria dysfunction has even been shown to predict prostate cancer progression in patients who were treated with surgery.
Some of these mitochondrial diseases might not become apparent until the person with the funky mitochondria reaches a certain age. A youthful muscle cell, for example, has a large population (approximately 85%) of mitochondria that are mutation free and it can handle all of the energy demands placed on it. However, as the number of mitochondria decline with age, the energy demands placed on the remaining mitochondria rise.
It ultimately reaches a point where the mitochondria can't produce enough energy and the affected organ or organs start to display diminished capacity.
Clearly, mitochondria play a pivotal role in the genesis of a host of maladies, and maintaining a high degree of normal, healthy mitochondria could well eliminate many of them.
You can intuit that muscle cells have a lot of mitochondria, and furthermore, you can easily realize that the more you have, the better your performance capacity. The more mitochondria, the more energy you can generate during exercise.
As an example, pigeons and mallards, which are both species known for their endurance, have lots and lots mitochondria in their breast tissue. In contrast, chickens, which don't fly much at all, have very few mitochondria in their breast tissue.
However, if you were to decide to train a chicken for a fowl version of a marathon, you could easily increase the number of mitochondria he had, but only to a point since the number is also governed to a point by species-dependent genetics.
Luckily, you can also increase the number of mitochondria in humans. Chronic exercise can increase mitochondrial density and apparently, the more vigorous the exercise, the more mitochondria formed. In fact, if you know any delusional runners that tally upwards of 50 miles a week, tell them that 10 to 15 minutes of running at a brisk 5K pace could do much more for their ultimate energy production and efficiency than an upturn in total mileage.
The short duration, high-intensity running will increase mitochondrial density to a much greater degree than long distance running, which, kind of ironically, will lead to better times in their long distance races.
Weight training also increases mitochondrial density.
Type I muscle fibers, often referred to as slow-twitch or endurance fibers, have lots of mitochondria, whereas the various type of fast-twitch fibers – Type IIa, Type IIx, and Type IIb – are each progressively less rich in mitochondria.
And while it's true that heavy resistance training converts slow-twitch fibers to fast-twitch fibers, the relative number and efficiency of the mitochondria in each type needs to be kept at peak levels, lest the lifter start to experience a loss in muscle quality.
This is what happens as lifters age. An aging human may be able to retain most or even all of his muscle mass through smart training, but loss of mitochondrial efficiency might lead to a loss of strength. One supportive study of aging males showed that this muscle strength declined three times faster than muscle mass.
Clearly, maintaining mitochondrial efficiency while also maintaining or increasing their population would pay big dividends in strength and performance, regardless of age.
Luckily, there are a lot of ways in which you can improve mitochondrial health and efficiency. There are even a couple of ways you can make more of them.
Since the main problem in age-related decline of mitochondrial health overall seems to be free-radical leakage, we need to figure out how to slow this leakage over a lifetime.
We could probably do this by genetic modification (GM), but given the public's horrific fear of genetic modification of any kind, the idea of inserting new genes into our make-up will have to be put aside for a while.
The least controversial way seems to be through plain old aerobic exercise. Exercise speeds up the rate of electron flow, which makes the mitochondria less reactive, thus lowering (or so it seems) the speed of free radical leakage.
Likewise, aerobic exercise, by increasing the number of mitochondria, again reduces the speed of free radical leakage. The more there are, the greater spare capacity at rest, which lowers the reduction rate and lessens the production of free radicals, hence longer life.
The birds give us more clues. They "uncouple" their respiratory chains, which means they disassociate electron flow from the production of ATP. Respiration then dissipates as heat. By allowing a constant electron flow down the respiratory chain, free radical leakage is restricted.
It turns out there are a few compounds that, when ingested by human, do the same thing. One is the notorious bug killer/weight loss drug known as DNP. Bodybuilders were big fans of this drug as it worked well in shredding fat. Users were easy to spot as they sported a sheen of sweat even when sitting in a meat locker. The trouble is, DNP is toxic.
The party drug ecstasy works well, too, as an uncoupling agent. However, aside from causing severe dehydration and making mitochondria listen to techno music while having uninhibited sex, the drug poses all kinds of ethical/sociological implications that make its use problematical.
Aspirin is also a mild respiratory uncoupler, which might help explain some of its weird beneficial effects.
Another way we might be able to increase the number of mitochondria (which seemingly has the added benefit of resulting in less free radical leakage) is through the use of dietary compounds like pyrroloquinoline quinone (PQQ), a supposed component of interstellar dust.
While PQQ isn't currently viewed as a vitamin, its involvement in cellular signaling pathways – especially those having to do with mitochondrial biogenesis – might eventually cause it to be regarded as essential to life.
Taking PQQ has been shown to increase the number of mitochondria, which is exciting as hell. Other compounds that seem like they might work the same way are the diabetic drug Metformin and perhaps, since it shares some of the same metabolic effects as Metformin, cyanidin-3 glucoside.
Indeed, cyanidin-3 glucoside has been shown in lab experiments to be highly beneficial in preventing or fixing mitochondrial dysfunction.
Aside from increasing the number of mitochondria, there are also a number of other dietary strategies that can enhance mitochondrial function or increase their number:
- Coenzyme Q10. Supports mitochondrial function.
- Creatine. Provides fuel to mitochondria, in addition to possibly protecting mitochondria from age-related mutations.
- Carnitine. Supports mitochondrial function.
- Lipoic Acid. Supports mitochondrial function.
- Resveratrol. In addition to its anti estrogen/pro Testosterone properties, also increases the size of mitochondria, plus leads to higher mitochondrial density.
- Nitrates. (found in spinach and beet roots ) – Improves mitochondrial efficiency.
- Calorie restriction. While not eminently practical, it's been shown to lead to mitochondrial genesis, which might explain how it makes certain species live longer.
- Vitamin D. Improves oxidative function in mitochondria.
The aforementioned "fixes" are a lot to swallow... literally.
After thinking about it a lot, I've taken up a strategy that's based on pragmatism and the idea of potentially overlapping supplements.
In other words, I take many of these things I listed, but almost everything I take has applications other than the care and feeding of my mitochondria. And if they have the added benefit of increasing mitochondrial life or efficiency, I'm sitting pretty.
Specifically, I take the following:
- Baby aspirin. 1 or 2 daily
- Coenzyme Q10. 150 mg. daily
- Cyanidin-3 glucoside. 6 capsules daily
- Resveratrol. 3 capsules daily
- Creatine. 5 grams a day
- PQQ. 30 mg. daily
Lastly, I augment my lifting with a healthy dose of aerobic or semi-aerobic activity.
Will feeding and nurturing your mitochondria really build muscle, end disease, and allow you to live forever? To be as precise as current science allows me to be, the answers are probably, kinda', and sort of.
Increased mitochondrial efficiency and density would make your muscles more capable of generating power for longer amounts of time, which is pretty much a surefire recipe for more muscle, provided you're a decent muscle chef.
Since many of the diseases that plague us can directly or indirectly be tied to mitochondrial function, there's a good chance that aiding and abetting them could eliminate or ameliorate many of them.
And lastly, a slight, long-time reduction in free radical leakage seems like it could, theoretically, increase human lifespan by about 10 to 20%.
Is it worth the trouble, given that we're operating on at least a few hunches? That's of course your call, but the story is too compelling and too potentially rewarding to ignore.
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