Build muscle

Here is a short summary:

1. Increase the number of mitochondria in your muscle cells and increase your strength and strength endurance
2. By maintaining the health of your mitochondria, you can potentially control metabolic disease and heart disease, as well as lower your risk of prostate cancer, diabetes and hundreds of other diseases.
3. By increasing your mitochondrial density, you can potentially live much longer and increase your chances of never seeing the inside of a hospital.
4. You can easily influence your mitochondrial health and density through exercise and dietary manipulation.

You are electric

Every millisecond, hundreds of thousands of tiny cellular components called mitochondria pump protons across a membrane to generate electrical charges equivalent to the force of a lightning strike over a distance of a few micrometers.

And if you look at energy in general, gram for gram your body generates 10,000 times more energy than the sun - even when you're sitting still. Each cell contains an average of 300 to 400 of these often-ignored energy-producing cellular organs - about 10 million billion in your entire body. If you somehow managed to stack all your mitochondria and put them on a scale, these mitochondria would make up roughly 10% of your body weight. The whole thing is even more amazing when you consider that these mitochondria have their own DNA and reproduce independently. That's right, they are not part of you. They are in fact alien life forms, free-living bacteria that adapted to live in larger cells about two billion years ago.

But they are not parasitic in any way. Biologically, they are symbionts and without them you could hardly move a muscle and without them none of the thousands of biological functions in your body could take place. In a broader sense, mitochondria have shaped human existence. Not only do they play a huge role in energy production, sex and fertility, but also in ageing and death.

If you could somehow influence your mitochondria, you could theoretically double your lifespan without contracting any of the diseases typically associated with old age. You could avoid metabolic diseases like Syndrome X, which affects about 47 million Americans, while maintaining the energy of your youth into old age.

From an athletic perspective, controlling the vitality and number of mitochondria in your muscles could lead to tremendous improvements in strength and endurance that would not diminish in the years to come.

Fortunately, I'm not tempting you with things that might happen at some point in the future. Controlling your mitochondria is within your reach - right now. But before we talk about how mitochondria affect muscle strength and endurance, we need to take a look at some really mind-blowing stuff that will be the crux of tons of scientific research and innovation in the coming years.

Mitochondria, sex and Eve

Mitochondria are tiny organelles which, as the name suggests, are kind of like tiny organs - and like organs, they have specific functions, which in this case is the production of energy in the form of ATP - the energy currency of cells. They do this by metabolizing sugars, fats and other chemicals with the assistance of oxygen. (Every time you consume creatine, you are in a sense "feeding" your mitochondria. Creatine is transported directly into the cell, where it is combined with a phosphate group to form phosphocreatine, which is stored for later use. When energy is needed, the phosphocreatine releases its phosphate group, which combines with an ADP molecule to form ATP).

A cell may contain a single mitochondrion or hundreds of thousands of mitochondria, depending on its energy requirements. Metabolically active cells such as the cells of the liver, kidneys, heart, brain and muscles have so many mitochondria that they make up 40% of the cell, while other, lazier cells such as blood and skin cells contain very few mitochondria.

Even sperm cells contain mitochondria, but these are located in the flagellar tail of the sperm. As soon as the sperm cell hits its target - the egg - the tail breaks off and disappears into the deep ocean of prostatic fluid. This means that only the mother's mitochondria are passed on to the offspring. This happens with such unerring precision that we can trace mitochondrial genes back almost 190,000 years to a woman in Africa affectionately known as "mitochondrial Eve".

Biologists have even suggested that this phenomenon is the reason why there are two sexes instead of just one. One sex must specialize in passing on mitochondria with the egg cell, while the other must specialize in not passing them on.

Mitochondria and a long, long life

The popular idea of ageing is that as the years go by, we become more and more frail until eventually one or more parts break down beyond repair and we die.

The popular reasons for this include wear and tear or breakdown of telomeres - the nucleotide sequences at the ends of genes that are said to determine how often a cell can divide. In the case of genetic attrition, this does not seem to stand up to closer scrutiny, as such attrition accumulates at different rates in different species, and as far as the telomere theory is concerned, the decay of telomeres in different species simply shows too much divergence to pass the smell test.

Others say it's due to a drop in growth hormone production or a decline in immune system function, but why the hell is there such a decline in the first place?

What we need to do is look at the individuals or species that don't seem to suffer from the normal signs of aging. The oldest among us, those rare centenarians who appear on talk shows and brag about eating bacon every morning and drinking alcohol every day, seem to be less prone to degenerative diseases than the rest of us. They end up dying of muscle wasting rather than specific diseases. Birds also rarely suffer from degenerative diseases as they age. Mostly they fly around as they always have until one day their flying power fades and they crash-land in a sewage ditch.

The answer to the centenarians and the long, disease-free life of birds seems to lie in the mitochondria. In both cases, the mitochondria release fewer free radicals. And this is important because mitochondria often determine whether a cell lives or dies and this is dependent on the position of a single molecule - cytochrome C. Various factors including UV radiation, toxins, heat, cold, infection or pollution can cause a cell to commit suicide - or apoptosis - but the unrestricted flow of free radicals is what we are concerned with here. The underlying principle is this: depolarization of the inner mitochondrial membrane - by some kind of stress, which can be either external or internal - triggers a production of free radicals. These free radicals release cytochrome C into the cell fluid, which initiates a cascade of enzymatic reactions that fragment and dispose of the cell.

This observation led to the popular theory of mitochondrial ageing, which appeared on the scene in 1972. Dr. Denham Harman, the "father" of free radicals, observed that mitochondria are the main source of free radicals and that they are destructive and attack different components of the cell. If enough cells commit apoptosis often enough, it's like a butcher slicing up a pound of salami. The liver, kidneys, brain, immune system cells and even the heart lose mass and effectiveness slice by slice. This is thought to be the cause of the diseases associated with ageing. Dr. Harman is the reason why all kinds of foods on the market are advertised as having antioxidant power.

The problem here, however, is that Dr. Harman appears to have been wrong with his theory - at least in part. For one thing, it is difficult to target the mitochondria with antioxidant foods. It could be the wrong dosage, the wrong timing or even the wrong antioxidant. In addition, it seems that if you completely shut down the leakage of free radicals from the mitochondria, a cell commits suicide. That's not really the effect we're looking for. (This is not to say that eating antioxidants isn't good for you, but it's important to realize that this endless, single-minded pursuit of foods with higher and higher levels of antioxidants probably won't do much to prolong life).

Free radicals, in addition to telling cells to commit suicide, also appear to be responsible for fine-tuning respiration - which is also known as the production of ATP. They are involved in a delicate feedback loop that signals the mitochondria to make compensatory changes to their activities. If you completely eliminate or slow down the production of free radicals by external methods such as an extremely antioxidant-rich diet or medication, the membrane potential of the mitochondria collapses and apoptotic proteins are swept into the cell. If a large number of mitochondria do this, the cell dies. If a large number of cells do this, then the health of that organ or the overall health of the individual is compromised. In the case of free radical control, you seem to be damned if you do and damned if you don't.

So again we have to look at the old codgers and the birds. There seems to be a gene in certain Japanese men who are over a hundred years old that leads to a slight reduction in the release of free radicals. If you have this gene, then your chance of living to be 100 years old is 50% higher. At the same time, your chance of ending up in hospital for any reason is 50% lower. As for the birds, there are two things that help them. First, they can separate their electron flow from ATP production - a process known as uncoupling. This results in limiting the release of free radicals.

Secondly, birds have more mitochondria in their cells. Because they have more mitochondria, they also have more extra capacity at rest, which lowers the rate of reduction and release of free radicals.

This leads us to the following conclusion: an increase in mitochondrial density combined with a slowdown in free radical release would lead to a longer life free of most diseases typically associated with aging.

Mitochondria and a disease-free life

Because mitochondria have their own genes, they are subject to mutations that affect their health and function. If enough of these mutations come together, then this will also affect the function of the cell. And if enough cells are affected, it will also affect the organ/system of which they are a part. The organs most affected are those that are generally rich in mitochondria. These include muscles, the brain, the liver and the kidneys. Specific diseases associated with mitochondria include Parkinson's, Alzheimer's, diabetes, various vaguely diagnosed muscle weakness diseases and even Syndrome X. Look at heart patients, for example. In general, they show a reduction in mitochondrial DNA of about 40%.

And as an indication that mitochondrial deficiencies may be passed down from generation to generation, insulin-resistant children who suffer from type II diabetes, despite being young and lean, have 38% fewer mitochondria in their muscle cells. Mitochondrial dysfunction has even been identified as a marker for prostate cancer progression in patients treated with surgery. Some of these mitochondrial diseases may not become apparent until a person with altered mitochondria reaches a certain age. A youthful muscle cell, for example, has a high population of mitochondria (about 85%) that are free of mutations and can fulfill all the energy demands placed on them. However, as the number of mitochondria decreases with age, the energy demands on the remaining mitochondria increase.

At some point, a point is reached where the mitochondria can no longer produce enough energy, with the result that the affected organ begins to exhibit diminishing capacity.

Certainly, mitochondria play a critical role in the development of a variety of diseases, and maintaining a high level of normal, healthy mitochondria could likely eliminate many of these diseases.

Mitochondria and bigger, stronger muscles

You can guess that muscle cells have a lot of mitochondria and furthermore, you can easily see that the more mitochondria you have in your muscle cells, the higher your performance capacity will be. The more mitochondria you have, the more energy you can produce during training. Examples of this are mallards and pigeons, both of which are known for their endurance and have a large number of mitochondria in their breast tissue. In contrast, chickens, which don't fly very much, have very few mitochondria in their breast tissue.

However, if you were to decide to train a chicken for a bird version of a marathon, you could easily increase the number of mitochondria in that animal - but only up to a point, as the number of mitochondria is also influenced by species-specific genetics.

Fortunately, you can also increase the number of mitochondria in humans. Chronic exercise can increase mitochondrial density and the more intense the exercise, the more mitochondria are produced. If you know a delusional runner who runs over 50 miles a week, tell them that 10 to 15 minutes of running at a tight 8 mph might do more for their ultimate energy production and efficiency than increasing their weekly distance.

The high-intensity race of short duration will increase mitochondrial density to a higher degree than long-distance running, which, although it may sound somewhat ironic, will lead to better times in long-distance runs.

Training with weights also increases mitochondrial density

Type I muscle fibers, which are often referred to as slow-contracting muscle fibers or endurance muscle fibers, contain a high number of mitochondria, while the different types of fast-contracting muscle fibers - type IIa, type IIx and type IIb - are progressively less rich in mitochondria, in that order. And while it is true that heavy resistance training can convert slow-contracting muscle fibers into fast-contracting muscle fibers, the relative number and efficiency of mitochondria in each type of muscle fiber must be maintained at maximum levels or the exerciser will experience a loss of muscle quality. This is what happens as strength athletes age. An aging individual may be able to maintain most or even all of their muscle mass through intelligent training, but a loss of mitochondrial efficiency could lead to a loss of strength. A study conducted on aging men concluded that muscle strength decreases three times faster than muscle mass.

Maintaining the efficiency of mitochondria while maintaining or increasing their population would therefore have a positive effect on strength and performance regardless of age.

Take care of your mitochondria and "feed" them

Fortunately, there are a lot of ways you can improve your mitochondrial health and efficiency. There are even some ways to increase the number of mitochondria. Since the main problem with a decline in mitochondrial health associated with age seems to be related to the release of free radicals, we need to figure out how to reduce this release over a lifetime. We could probably do this through genetic modification, but given society's fear of genetic modification of all kinds, we need to put the idea of introducing new genes into our bodies on the back burner. The least controversial way seems to be good old aerobic exercise. Exercise increases the rate of electron flow, which makes the mitochondria less reactive and thereby (it seems) slows down the release of free radicals.

In addition, aerobic exercise also reduces the rate at which free radicals are released by increasing the number of mitochondria. The more mitochondria there are, the greater the free capacity at rest, which lowers the rate of reduction and reduces the production of free radicals - ultimately resulting in a longer life. Birds give us further clues. They "uncouple" their respiratory chain, which means that they separate the electron flow from ATP production. Energy is then released in the form of heat. By allowing a constant flow of electrons along the respiratory chain, the release of free radicals is limited.

As it turns out, there are several compounds that, when consumed by humans, do the same thing. One of these is the infamous insecticide/fire-retardant fat loss agent called DNP. Bodybuilders are big fans of this chemical as it causes a breakdown of fat. Users of this compound are easy to spot as they would still secrete rivulets of sweat even in a cold room. The problem here, however, is that DNP is highly toxic.

The party drug ecstasy also works well as a decoupling agent. But aside from causing serious dehydration and making the mitochondria listen to techno music while having uninhibited sex, this drug has all kinds of ethical/sociological implications that make its use problematic. Also, aspirin is a mild respiratory decoupler, which might help explain some of the strange benefits of this drug.

Another way in which we may be able to increase the number of mitochondria (which appears to have the added benefit of resulting in reduced free radical release) is through the use of supplements such as Pyrroloquinoline Quinone (PQQ).

Although PQQ is not currently considered a vitamin, its involvement in cellular signaling pathways - particularly those related to mitochondrial biogenesis - may eventually lead to it being considered essential for life. It's been shown that taking PQQ can increase the number of mitochondria, which is pretty damn exciting. Other compounds that seem to work in the same way are the diabetes drug cyanidin-3 glucoside, as it has similar metabolic properties. In fact, cyanidin-3 glucoside has been shown in laboratory studies to be very helpful in correcting or preventing mitochondrial dysfunction.

In addition to increasing the number of mitochondria, there are a number of other nutritional strategies that can improve mitochondrial function.

• Coenzyme Q10 supports mitochondrial function.
• Creatine provides "fuel" to the mitochondria and may also protect the mitochondria from age-related mutations.
• Carnitine supports mitochondrial function.
• Lipoic acid supports mitochondrial function.
• In addition to its anti-estrogen/pro-testosterone properties, resveratrol increases the size of mitochondria and also leads to higher mitochondrial density.
• Nitrates, found in spinach and beetroot, improve mitochondrial efficiency.
• Calorie restriction has been shown to lead to mitochondrial genesis, which may explain how it allows certain species to live longer.
• Vitamin D improves the oxidative function of mitochondria.

The action plan

The solutions just mentioned mean you have a lot to swallow - literally.

After thinking long and hard about this topic, I've developed a strategy based on pragmatism and the idea of potentially overlapping supplements. In other words, I've taken many of the things I've listed, but almost everything I take has additional implications than simply protecting and "feeding" the mitochondria. And if these things have the added benefit of prolonging the life of my mitochondria or increasing their efficiency, then I'm on the safe side.

Here's what I use:

• Baby aspirin: 1 or 2 per day
• Coenzyme Q10: 150 mg per day
• Cyanidin-3 Glucoside: 6 capsules per day
• Resveratrol: 3 capsules per day
• Creatine: 5 grams per day
• PQQ: 30 mg per day

In addition to this, I have added a healthy dose of aerobic and semi-aerobic activity to my training.

The 100-year-old strength athlete

Will "nurturing" your mitochondria really build muscle, end disease and allow you to live forever? To be as precise as the current science allows me to be, the answers are probably "sort of" and "in some ways." Increased mitochondrial efficiency and density would allow your muscles to generate more power over a longer period of time, which should be a surefire recipe for more muscle.

Since many of the diseases that plague us can be directly or indirectly linked to mitochondrial function, there is a good chance that mitochondrial support could eliminate or alleviate many of these diseases. And last but not least, it seems that a long-term reduction in the release of free radicals could theoretically extend the human lifespan by around 10 to 20%. Is it worth the effort? That's your call, of course, but the whole story is too tantalizing and potentially too rewarding to ignore.

References:

1. Berneburg, M, et al, "Creatine supplementation normalizes mutagenesis of mitochondrial DNA as well as functional consequences," J Invest Dermal, 2005 Aug:125(2):213-20.
2. Chilibeck, PD, "The effect of strength training on estimates of mitochondrial density and distribution throughout muscle fibers," Eur J Appl Physiol Occup Physiol, 1999 Nov-Dec;80(6):604-9.
3. Chowanadisai, W., et al, "Pyrroquinoline quinone stimulates mitochondrial biogenesis through cAMP response element-binding protein phoshphorylation and increased PGC-1 alpha expression," J Biol Chem, 2010, Jan 1;285(1):142-52.
4. Faloon, William, "Our Aging Mitochondria," Life Extension, February 2011, pp. 7-13.
5. Lagouge, Marie, "Resveratrol Improves Mitochondrial Function and Protects against Metabolic Disease by Activating SIRT1 and PGC-1," Cell 127, 1109-1122, December 15, 2006.
6. Lane, Nick, "Power, Sex, and Suicide - Mitochondria and the Meaning of Life," Oxford University Press, New York, 2005.
7. Luoma, TC, "Luoma's Big Damn Book of Knowledge," Punjab Publishers, Lahore, 2011.
8. Mortensen SA, et al, "Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure," Int J Tissue React. 1990;12(3):155-62.
9. Petersen, Courtney M., et al, "Skeletal Muscle Mitochondria and Aging: A Review," Journal of Aging Research Volume 2012 (2012), Article ID 194821.
10. Rucker, Robert, "Potential Physiological Importance of Pyrroloquinoline Quinone," Alternative Medicine Review, Volume 14, Number 3, 2009.
11. Sinha, A, et al, "Improving vitamin D status of vitamin D deficient adults is associated with improved mitochondrial function in skeletal muscle," J Clin Endocrinol Metab. 2013 Mar;98(3):E509-13.
12. Tanaka H, Swensen T, "Impact of resistance training on endurance performance. A new form of cross-training?" Sports Med. 1998 Mar;25(3):191-200.
13. Tesch PA, "Skeletal muscle adaptations consequent to long-term heavy resistance exercise," Medicine and Science in Sports and Exercise [1988, 20(5 Suppl):S132-4].
14. Yu JJ, et al, "Mitochondrial function score combined with Gleason score for predicting the progression of prostate cancer," Zhonghua Nan Ke Xue, 2010 Mar;16(3):220-2.
15. Zorov, DB, et al, "The Mitochondrion as Janus Bifrons, Biochemistry (Moscow), Vol. 72, No. 10, 2007.

From TC Luoma
Source: https://www.t-nation.com/supplements/grow-muscle-end-disease-live-longer