Athletic Development

All athletes benefit from strength training for one simple reason: they need to produce varying degrees of force from multiple angles at any given moment.

Increasing an athlete's absolute strength, or the maximum amount of force a muscle can produce during a single contraction, will lead to an increase in his ability to demonstrate explosive power. But finding the right exercises to overload the specific force vector has been a bit harder to nail down.

Some strength coaches believe developing absolute strength by training a muscle through a full range of motion will translate to greater degrees of general strength and neural development. Others lean more toward using specific strength protocols designed to overload various portions of a movement pattern similar to what an athlete uses during competition.

So who's right? Well, there hasn't been much clear-cut evidence to support either approach, but a recent study is shedding some light.

This study looked at the effect of full, half, and quarter-rep range squats on sprinting speed and vertical jump ability.

Researchers took 28 trained male college athletes and split them into three groups. Before beginning the study each athlete's full squat, half squat, quarter squat, 40 yard dash time, and vertical jump were tested.

Each group did four strength training workouts per week: two for upper body and two for lower body, utilizing progressive overload and periodized loading techniques for each exercise in the 2-8 rep range.

On lower body training days, group one did full range of motion squats, group two did half squats, and group three did quarter rep squats. At the end of the 16 week period each group was reassessed to determine how, or if, their training protocols translated to performance increases.

Each group increased strength in their specialized squats (full range, half, and quarter reps), but it's the impact on forty yard dash times and vertical jump that are interesting.

The group that did full-range squats did see improvements in strength by upwards of 16%, but their strength gains didn't do much for their athletic performance. In fact, the full range squat group showed less improvement than the half and quarter rep groups, boosting vertical jump height by less than 1% and only decreasing forty yard dash time by .09 seconds.

The half-squat group did show similar increases in strength to group one, but they also showed significantly greater improvements in sprinting speed and vertical jump than the full rep range group.

However, the most shocking findings occurred in the quarter rep group. Not only did they increase one rep max strength by nearly 12%, they also increased vertical jumping ability by over half an inch, and decreased their forty yard dash times by an average of .41 seconds.

So why are quarter squats better at improving sprint speed and jumping ability than full and half squats?

The range of motion used during quarter squats is much more similar to the natural range of motion used in a full sprint. And if increases in strength lead to greater force production and more explosive power during athletic movements, there would seem to be a likely correlation between getting stronger in an exercise that mimics the natural range of motion used during sprinting and jumping.

Athletes looking to add quarter squats to their training should do so as a part of a periodized program that uses strength-based training protocols during their off-season. Saving heavy strength training work for the off-season allows for a more targeted focus on overall improvements in performance, as opposed to in-season training which should be mostly geared toward maintenance and facilitating recovery from practice and competition.

by Corey Young | 08/23/16

Have 3-4 cups per day, regular or decaf, and you might live longer.

Coffee is a little mysterious in that we're not really sure how it does some of the things it does. One thing seems for certain, though: the more you drink, the better off you are. In fact, the more you drink, the longer you live.

In a 2012 mortality study of 400,000 people printed in The New England Journal of Medicine, coffee drinkers had between 6 and 16 percent fewer deaths. Likewise, in a Japanese study printed in The American Journal of Clinical Nutrition, coffee drinkers were 24 percent less likely to die during a 19-year follow-up.

The sweet spot seems to be three to four cups a day of regular or decaf, but one study involving six cups a day saw a 33 percent reduction in diabetes diagnoses. Other maladies positively affected by coffee include liver cancers, fatty livers, alcoholic liver disease, heart disease, stroke, depression, Alzheimer's, and Parkinson's.

Low T is associated with a higher death rate. It also makes you fat.

You know that testosterone plays a role in muscle size and strength, libido, energy, and keeping body fat low, but high testosterone is also important to just plain staying alive. Contrary to what late-night TV ambulance-chasin' lawyer commercials spout about high testosterone killing people, it's low testosterone that's the real concern.

• Higher risk of cardiovascular disease
• Narrowing of carotid arteries
• Abnormal EKG
• More frequent congestive heart failure
• Increased incidence of angina
• Increased body mass index
• Type II diabetes
• Metabolic syndrome
• Insulin resistance
• Higher death rate from all causes, including cardiac mortality

Maybe you did a double take at the last item in the list. You should've. One study involving 858 male service veterans found that low testosterone individuals had an 88 percent greater chance of dying, for any reason, even after variables like age, other illnesses, and body mass index were accounted for.

Are you immune to low testosterone because you're a big-time weight lifter? Nope. Male athletes often have lower testosterone than untrained men. One study found that weight lifters (along with rowers, cyclists, and swimmers) had testosterone levels that were 60-85 percent of untrained men.

Some of the researchers attributed that disparity in alterations of hepatic (liver) and extrahepatic (muscles, skin) metabolism of testosterone that can't be compensated for by the athletes' gonads, but I suspect it might have to do with some yet-unexplained exercise-related increase in steroid hormone binding globulin (SHBG), which makes less testosterone available to tissues. Low testosterone levels seem to be epidemic among lifters. True, testosterone levels usually go up after an intense workout, but the rise is short-lived and levels often drop to below baseline soon after.

So keep testosterone high. Use herbal testosterone boosters (we like Alpha Male®), and if your levels are seriously deficient, consider physician-monitored testosterone replacement therapy.

High estrogen can increase degenerative diseases and early death.

It's becoming increasingly evident that a number of doctors are idiot savants. Case in point, consider the big estrogen study that was reported in the Journal of the American Medical Association.

Researchers monitored the estrogen levels of a large group of men. They found that men with estradiol (a form of estrogen) in the normal range between 21.80 and 30.11 pg/ml had the fewest deaths during a three-year period. Men with the highest levels (above 37.99 pg/ml) had 133 percent more deaths during the same time period. However, men with the lowest estrogen levels (below 12.90) fared the worst as they suffered 317 percent more deaths!

What some doctors took away from this was that men need estrogen, so they don't want to give patients anything to lower estrogen. In other words, many doctors ignored the far more prevalent problem of high estrogen and as such are loathe to prescribe anti-estrogen medications. The problem is that once estrogen levels rise, the risk of degenerative diseases climbs. Atherosclerosis goes up, as does the risk of stroke. Prostates grow. And the risk of flat-out dying in general goes up.

If you're an athlete, higher levels of estrogen also affect your ability to build strength or grow muscle, and it also makes it harder to get lean. Clearly, estrogen needs to be kept in check. Consider natural estrogen-fighting supplements such as Rez-V™ or, if the problem is really severe, consult with a progressive doctor and get on an estrogen-lowering drug like Arimidex.

Too many frequent meals throughout the day keeps blood sugar high all day long leading to a variety of complications.

Subjecting meat to heat causes it to brown. It's simply the result of binding sugars to protein, called the Maillard Reaction. It's good when you do it to a pork chop, but not so good when you do it to your internal organs. Cooking yourself sounds like an unlikely scenario.

However, it's exactly what's happening when you habitually keep your blood sugar levels above 85mg/dl. Cook yourself long enough and you get kidney diseases, joint deterioration, stiffening of connective tissues, atherosclerosis, and insulin resistance, which might eventually lead to type II diabetes. You'll also get pudgy.

Scientists estimate that between one in three and one in five Americans will end up either rare, medium rare, or well done by mid-century. This is just the logical progression of our current lifestyle that includes dietary excess in general, eating too many fast-digesting carbs over too long a period, and a lack of exercise. Surprisingly, the very act of eating multiple small meals a day might itself lead to insulin resistance and problematically high blood sugar levels.

Those multiple meals, contrary to what most people think, cause multiple insulin surges throughout the day, which in turn makes cells more insulin resistant. As time goes by, more and more insulin is released to compensate for the insulin resistance, until finally it starts losing the battle. Blood sugar elevates and stays elevated.

Most docs tell you to keep fasting blood sugar below 100, as anything higher than that (up to 126 mg/dl) marks you as pre-diabetic. Once you start testing at anything much further north than 126, you're considered full-blown diabetic. However, the Maillard Reaction starts kicking in at or above 85 mg/dl.

There are a couple of courses of action to take. You can either start eating fewer daily meals (3 or 4 instead of 6), making sure the meals are glycemically correct (high in protein and healthy fats while low in carbs, or at least simple, fast-digesting carbs), or you can start using cyanidin-3 glucoside (Indigo 3G®) to increase insulin sensitivity.

C3G makes your body handle carbs better, even preferentially shuttling carbohydrates to muscle storage instead of fat storage and keeping blood sugar levels in the optimum range so that you don't cook yourself.

Curcumin is a powerful anti-inflammatory but its other effects range from pain management to benefits that affect nearly every organ system in the body.

• Enhance cardiovascular health
• Reduce body fat
• Support healthy cholesterol
• Alleviate cognitive decline
• Act as an anti-aromatase (thus increasing testosterone)
• Reduce plaque levels in arteries
• Reduce risk of diabetes

And like anything else that comes from a plant, it has antioxidant capabilities. Curcumin is found in the spice turmeric, and Indians probably use more of it, per capita, than anyone in the world. Given its seemingly endless health benefits, you'd think that Indians would be the healthiest people in the world, but that's not the case. Unfortunately, the body doesn't absorb curcumin very well. Simply ingesting it as a main constituent of curry powder, regardless of the amount eaten, isn't going to have much of an effect.

As such, you need to ingest curcumin as part of a formula that contains piperine, such as this curcumin, which enhances absorption by up to 2000 percent. Take a couple of grams a day. It's one of the few substances that you'll be consciously aware of making you feel better.

Cook and eat things that are dense in nutrition.

Most of us eat the same crap every week, so we might as well make sure that at least some of the same crap we eat contains a ton of nutrients. This chili of the nutritional gods is high in protein, has a low glycemic index, and it contains several foods that rank high on the ANDI scale (Aggregate Nutrient Density Index).

It's so nutritious that you could probably live off it and nothing else for a considerable amount of time. Oh, it also tastes incredibly good. The following recipe should make enough meals to last you most of the week.

• 3 pounds grass-fed ground beef or turkey
• 1-2 medium onions, chopped
• 2 red peppers, chopped
• 5 carrots, chopped
• 2 cups spinach
• 2 cloves garlic, minced
• 28 ounces Italian peeled tomatoes with juice
• 46 ounces Spicy Hot V8 Juice
• 16 ounces red kidney beans, drained
• 16 ounces white northern beans, drained
• 2 tsp iodized salt (to protect you from all-too-common iodine deficiencies)
• 2 tsp oregano
• 5 tsp. chili powder
• three-fourth tsp red pepper flakes
• 1 cup raw cashews, ground until almost butter
• Optional: one-fourth pound grass-fed liver, ground to itty-bitty bits (this small of an amount won't affect the taste)

1. Brown burger (and liver, if so desired) in large soup kettle and remove when cooked.
2. Brown onions, red peppers, carrots, and garlic in olive oil in the same kettle.
3. Add tomatoes, V8 juice, beans, all the spices, and the ground cashews and stir.
4. Cover and simmer for at least two hours, stirring occasionally. Add spinach about 10 minutes before eating.

Too many antioxidants is not better than too few, and may do more harm than good.

The theory offered up in 1972 was this: Free radicals affect the mitochondria of the cells, setting into motion a cascade of enzymes that slice up and kill the cells, ultimately leading to organ and possibly systemic failure. As such, you need to fortify yourself with anti-oxidants so that you're invulnerable to the ravages of chemicals, bad diet, too much sunlight, radiation, pollution, Internet trolling, and even time. That's why nearly everyone in the civilized world goes around with the blind belief that ingesting as many antioxidants as possible is a good thing.

It's quite likely they're all wrong. Yes, quenching the production of free radicals is a good thing... to a point. The problem is probably one of dosage, incorrect timing, the wrong antioxidants, or too much antioxidant. If you completely turn off free radical leakage through antioxidants, the membrane potential of the energy-producing cellular organelles known as mitochondria collapse and cell-dissolving proteins are spilled into the cell. If a bunch of mitochondria do this, the cell dies. If a bunch of them do this, organ health and overall health can suffer.

Free radicals are actually important to health because, in addition to telling the cell when or when not to commit suicide, they also fine tune cellular respiration, otherwise known as the production of ATP (the energy currency of the cell). ATP is essential to existence. Monkey around with it too much through the use of antioxidants and the center can't hold. You might not feel any different, but on a cellular level, you might be self-destructing, little by little.

You should still ingest antioxidants, but probably not individual antioxidants in pill or capsule form. What nutritional science has done, in its hubris, was cherry-pick individual antioxidants and mega-dose on them, assuming that they act alone instead of in concert with dozens, hundreds, or even thousands of other antioxidants. This is why you get reports that too much vitamin E or C can cause serious health problems.

Consider a lowly sprig of thyme. It alone contains 30 different antioxidants. Isn't it possible that maybe, just maybe, their alleged benefits are obtained when ingesting all of them together, rather than cherry-picking one or two? Therefore, it's prudent to get your antioxidants in whole fruit and vegetable form, or consider a freeze-dried fruit and vegetable antioxidant formula such as Biotest Superfood that contains thousands of antioxidants, along with countless phytochemicals in general. That way, you likely get the correct amount of free-radical control – enough to prevent premature aging or deterioration, but not so much that it would promote cell suicide.

Sprinting not only makes you look hot, it enhances mitochondrial health and performance.

If only people would start sprinting instead of using cardio machines. Think of all the space that would be left over for weights and racks and Prowler tracks.

• Preferentially burns body fat, increasing post-exercise fat oxidations by 75%.
• Builds muscle in the legs and trunk.
• Builds profound amounts of muscle in women (protein synthesis up 222% in women after sprinting, as opposed to 43% in men).
• Improves insulin sensitivity.

Furthermore, sprinting enhances mitochondrial health and performance. Intense exercise, like sprinting, increases the number of mitochondria in the cell, which is good for performance and overall systemic health (as the number of mitochondria – the higher the number the better – correlates strongly with performance, heart health, prostate health, liver health, etc.).

Aspirin can help control free radicals, improve health, extend lifespan, and potentially even burn fat.

You know about aspirin and heart attacks. Sure, for people over 50, taking a baby aspirin (83 mg.) a day leads to a 22% reduction in heart attacks and anywhere from a 25% to an 80% reduction in strokes. Likewise, there's substantial evidence that taking a baby aspirin every day leads to a substantial reduction in colon cancer.

But those might not be the best reasons to take aspirin, particularly if you're in your forties, thirties, or maybe even in your twenties. Aspirin, it turns out, is a mild respiratory uncoupler, which might explain some of its mysterious effects on health. Uncoupling is a cellular process that enables a constant flow of electrons down the respiratory chain (i.e., ATP production) in the little energy producing mitochondria. This process restricts (but doesn't shut off) the flow of free radicals, thus theoretically improving health, extending lifespan, and even burning fat.

Shutting off free radical production entirely, as you might do when "overdosing" on antioxidants, might cause the cell to die, which is kinda' against the whole point of taking anti-oxidants. So, respiratory uncoupling, as accomplished by aspirin, is good. Consider taking one baby aspirin a day – two a day if you're a big mofo – but be aware that aspirin can cause gastrointestinal bleeding in a small percentage of the population.

 by TC Luoma

1. Increase the number of mitochondria in your muscle cells and you improve strength and strength endurance.
2. If you maintain the health of your mitochondrial, you can potentially control metabolic diseases, along with heart disease, prostate cancer mortality, diabetes, and hundreds of other afflictions.
3. If you increase mitochondrial density, you can potentially live a lot longer and increase your chances of never visiting a hospital.
4. You can easily affect mitochondrial health and density through exercise and dietary manipulation.

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.

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 fibres," 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.

1. The percentage of women between the ages of 18 and 59 who are suffering from "sexual dysfunction" is somewhere around 50%. Much of this sexual dysfunction is related to testosterone deficiency.
2. Women with low testosterone often find it more difficult to gain muscle or burn fat.
3. There are several potential causes for testosterone deficiency, among them the use of birth control pills or antidepressants, drinking soy milk, a vegetarian diet, or even psychological factors.
4. While obtaining actual testosterone replacement is problematical for women in America, there are several courses of action, some pharmaceutical, some through supplements, some through diet, and some through simple lifestyle changes.

Female athletes competing at the highest levels of their sport, female trial lawyers, the women CEOs of Fortune 500 companies: all of them probably have it. Maybe you see some of the women who have it in your daily life, too. They're the ones who might dress a little boldly or even flamboyantly. In the gym, they seem to be the ones who put on muscle or lose fat a little easier than a lot of the other women and there always seems to be a guy or two or three chatting them up.

Contrast that with women who don't have it. They might lack ambition and they might prefer to let others make decisions for them. They might dress a little modestly, hoping to blend in rather than stand out. They might not understand all the fuss about sex and when they do give in (they rarely initiate), they usually don't experience much satisfaction. And when it comes to exercise, they find it difficult to lose fat or gain curvy muscle and they never seem to get the results they hope for.

The "it" I'm talking about is high, or at least normal, levels of testosterone. While testosterone replacement for men is big business, no one really pays much attention to the role testosterone plays in women, at least not in pre-menopausal or even young women.

Consider that more than a few studies report that the percentage of women between the ages of 18 and 59 who are suffering from "sexual dysfunction" is somewhere around 50%. This dysfunction is commonly diagnosed as underlying depression with quick referrals to counseling or psychotherapy, but more and more scientists and clinicians are starting to point the finger at female testosterone deficiency and perhaps rightly so, because it plays a huge role in the physiology, the psyche, and sexuality of women as well as men.

One of the reasons that testosterone gets such short shrift in discussions about women's health is that women just don't manufacture much of it, but therein lies one of the reasons the whole issue is so misunderstood.

Sure, men typically make 8 to 10 times more testosterone than women every day, but that doesn't mean the average healthy man is 8 to 10 times more masculine than the average healthy woman, especially as evidenced by some of the men walking around Whole Foods nowadays. Nope, in women, testosterone is only a part of a complicated chemical profile that results in them being far more sensitive to its effects than men. As such, a little goes a long way.

Conversely, while women are considered to be "all estrogen," the testosterone levels in healthy women are 10 times greater than their estrogen levels. Obviously, the hormonal picture is a lot more complicated than it's given credit for.

About one quarter of a woman's testosterone production comes from her ovaries while another quarter is manufactured in her adrenal glands. The remaining half is produced in peripheral tissues from various chemical precursors produced in the ovaries and adrenals. The main precursor is androstenedione, which became a household word a few years back when a reporter espied a bottle in Mark McGwire's locker. A lot of this androstenedione is converted to estrone, a form of estrogen, but some of it can and is converted to testosterone.

If you need a real-life example of the power of these chemical precursors, consider the hyena, which is a matriarchal species where females run the show. Normally, female hyenas have perfectly reasonable levels of an enzyme that converts androstenedione into estrogen. However, during pregnancy, they experience a drop in this enzyme so that lots of androstenedione is instead converted into lots of Testosterone.

The resultant high levels of testosterone affect the pups in such a way that when females are born, they have masculinized external genitalia with penis-like clitorises and empty scrotal sacks that they could probably use to store coupons, spare change, and hyena makeup. The result is a female mammal that runs roughshod over the hapless hyena males.

Obviously, that doesn't happen in us human types, but nevertheless some conversion of androstenedione to testosterone does occur. All of this is important because they're all contributing factors in a woman's health. Without proper levels of testosterone (and accordingly, its precursors), women might suffer diminished energy levels and even a loss of sense of well being, regardless of age.

Low testosterone also plays a role in weight gain and the ability to put on muscle (just as it does in men), and it can also play a big role in libido. In fact, one of the surest signs of low female testosterone is HSDD, or hypoactive sexual desire disorder, which is characterized by "persistent or recurrent deficiency or absence of sexual thoughts and fantasies and/or desire for, or receptivity for, sexual activity causing personal distress or interpersonal difficulties."

One of the earliest studies that showed an association between female sexual desire and decreased testosterone was published in 1959, but acceptance was mighty slow. I guess it's not too surprising, though, since women weren't even scientifically proven to have orgasms until Masters and Johnson starting outfitting women's private parts with electrodes. Luckily, the association between testosterone and female sex drive is pretty well established now. Studies have shown, for instance, that a woman's testosterone levels rise during ovulation and there's a corresponding rise in frequency of intercourse during this time. While ovulating women might not always initiate sex, they're at least more receptive to sexual advances. Consider too that behavioral endocrinologists have noted that women who are ovulating often dress a little more hoochily, allegedly to attract sexual partners, but it's probably done on a subconscious level.

Unfortunately, there's not much data on what really constitutes "normal" female testosterone levels, but our current best guess is that a total plasma level of under 25 ng/dl in women under 50 years old is considered deficient. The trouble is, docs don't typically measure the testosterone level of females. In fact, historically, the only time doctors bothered to even think about female testosterone levels is when they suspected a scant few women of having levels that were too high, as perhaps evidenced by excess facial hair, loss of scalp hair, infertility, or acne.

Things are starting to change, though, and it's high time as the number of women with decreased libido (and, likely, many of the other symptoms of low testosterone) is now estimated to be between 10 and 15 million, and not all of them are in their forties or beyond; many in fact are in their 20's and 30's. If true, it certainly constitutes an epidemic of low testosterone, but what could have caused this epidemic?

Running a holiday sale or weekly special? Definitely promote it here to get customers excited about getting a sweet deal.

Have you opened a new location, redesigned your shop, or added a new product or service? Don't keep it to yourself, let folks know.

Customers have questions, you have answers. Display the most frequently asked questions, so everybody benefits.