The Exercise Mistake Which Makes You Age Faster

What I am going to share with you in this article most likely will fly in the face of nearly everything you have been taught about exercise and nutrition. It is a radically new concept that is first being introduced to you on Dr. Mercola’s site. It’s a slap in the face of everything you know or have been taught in this area.

Nearly every expert will tell you that your fitness goal is to build muscle and lose fat. But I’m here to tell you that there is an even BETTER goal.

If you follow conventional wisdom regarding fitness guidelines- train hard and eat many protein meals throughout the day- there’s a good chance you’ll gain muscle size and strength.

There is only one problem: As you get older, most likely you’ll lose all these hard gains.

The reason: Conventional fitness is not set to keep your muscle biologically young. Physical rejuvenation requires a different strategy than that of the common fitness/bodybuilding approach. And that strategy might seem a extreme contradiction to all current fitness concepts.

So how do you rejuvenate your muscle? And can you really keep your body biologically young?

Innovative Revolutionary Program to Keep Your Body Biologically Young

Why not force your body to break down and recycle your old damaged muscle and brain tissues and actually keep them biologically young?

Why not do that and lose fat at the same time?

You see, unless you are a seriously competitive athlete or body builder and use supplements from somewhere like Fusion, the best source in canada for steroids, increasing your muscle mass (which you’ll likely lose) will not provide you with any major long-term benefits. In fact, as you’ll soon read, a big muscle can be a liability as it’s prone to premature aging.

This is a radically new, revolutionary concept that most experts are not even aware of. But I have scoured the science and uncovered the latest research and evidence to show you in great detail how to turn back the biological clock in your muscle and brain by simple targeting nutrition and exercise principles.

How Can You Keep Your Body Biologically Young?

Physical aging begins in your genes. Scientists identified multiple genes that regulate your physical strength and biological age. Most notable among them are those involved in the sustainability of your muscle. Apparently it’s the decrease in these genes’ expression that causes your muscle to deteriorate and age.

So when does the aging process start?

Chronological aging starts from the minute you’re born. You can’t possibly stop the clock from ticking. It’s certainly an inevitable process. But there’s also biological aging and growing evidence indicates that that kind of aging can be slowed and even reversed, particularly in the muscle tissue.

The reason: muscle aging isn’t necessarily chronological.

A 60-year old can have a muscular gene profile similar to a person 30 years old. And a 30-year old person can already be expressing genes of a 60-year old. The purpose of this article is to present the primary reasons leading to physical aging and reveal biological mechanisms and methods that block these causes and help reverse age related physical decline.

But first let’s address some questions that need clarification.

Can Muscle Aging Start at a Young Age?

Muscle aging may start at a young age; as early as the third decade of life. Many young adults unknowingly suffer from symptoms of muscle aging due to physical inactivity, poor diet, or chronic substance abuse, and these become more and more notable as time goes by. Typically as a muscle ages, it loses its aerobic capacity and strength, and it also loses size. This is how the vast majority of people today experience physical aging.

But is it possible to stop this process?

In many respects, yes. But you need to know what to do. You need to learn what mechanisms enable your muscle to resist aging and you need to know how to trigger them.

And note that your daily activities are essential in this process. How you eat, how you exercise and even how you rest, translate into gene activities that turn on mechanisms that dictate whether you age or stay young.

But first you need to understand what muscle degradation means.

How Your Muscles Actually Prematurely Degrade

Muscle degradation is a major blow to your body. It’s associated with more than just loss of muscle size and strength…it can actually lead to a total metabolic decline.

Skeletal muscles’ biological role goes far beyond locomotion. Your muscle is your largest energy facility responsible for keeping your metabolic system intact. It essentially protects you against metabolic and hormonal decline, obesity, diabetes, and cardiovascular disease. It also enhances your cognitive function and keeps your body young.

Given this, muscle degradation can lead to a major health crisis on a scale far beyond what’s commonly believed. The loss of muscle means loss of energy, a tendency to gain excess weight, vulnerability to disease and accelerated aging. Muscle degradation seems to be a major contributing factor behind the current epidemic of obesity, diabetes and related diseases. It’s becoming evidently clear that the benefits you get from your muscular system are essential to your health. Keeping your body in shape not only makes you feel younger and stronger, it might just save your life.

So What Causes Your Muscles to Degrade?

There are many causes of muscle degradation. These include muscle misuse, insulin resistance, hormonal disorders, inflammatory disease, dietary abuse, nutritional deficiencies and chemical toxicity. Physical aging is typically associated with some of the above. But while each of these causes play a role in physical degradation, there is growing evidence that they all relate to one underlying cause: oxidative damage by free radicals.

Oxidative Damage by Free Radicals

Free radicals, known as reactive oxygen species (ROS), are toxic by-products of metabolism. They also invade your body in the form of chemical toxins or rancid food substances. Free radicals lack subatomic particles and are consequently highly reactive as they seek to bind and destroy your cells and tissues.

To defend against these destructive particles, your body uses its endogenous antioxidants such as glutathione and SOD along with dietary antioxidants. But when the cumulative concentrations of free radicals overwhelm your body’s defenses, oxidative damage to cells and tissues starts taking its toll destroying cellular proteins, lipids and DNA.

It is the accumulated oxidative damage in your muscle that leads to three detrimental changes:
•Loss of mitochondrial function
•Loss of fast neuro motors
•Loss of fast muscle fibers

Loss of Mitochondrial Function

The mitochondria is the energy chamber of your cell. It’s a cellular organelle with its own enzymes proteins and DNA responsible for the utilization of energy for all metabolic functions. Oxidative damage in your mitochondria can be caused by a number of factors including chronic infection, chronic inflammatory disease, chemical toxicity, rancid fat and excessive sugar or fructose intake. Other contributing factors to mitochondrial impairment are muscle disuse and chronic overtraining.

One of the most common causes of mitochondrial damage is aerobic overtraining.

When done chronically, it causes accumulated oxidative stress in the mitochondria with increased risk of oxidative damage. And when chronic aerobic overtraining comes along with inadequate nutrition (such as with those dieters who obsessively run on a treadmill to burn excess calories they get from a bad diet) the results could be even worse…

The combined effect of bad nutrition with bad training can be extremely destructive, and may lead over time to irreversible damage in the mitochondria along with a total metabolic decline.

The consequences include:

•Impaired ability to utilize carbohydrates and fat for energy
•Insulin resistance
•Lower threshold for physical exercise
•Excessive weight gain
•Accelerated aging

How You Lose Your Fast Muscle Nerves

Your muscle is wired with a magnificent network of neurons called the neuromuscular system which controls all of your physical activities. But when exposed to chronic accumulated oxidative stress it tends to deteriorate. Consequently your muscle is rendered dysfunctional like an engine without an ignition.

Neuro-muscular deterioration seems to be the most notable symptom of physical aging. It involves gradual disintegration of the junctions between the nerve and muscle which leads primarily to the loss of nerve motor units particularly the fast ones.

The loss of fast neuro-motors is highly devastating. It means loss of capacity for you to perform intense physical activities.

A nerve motor unit (neuro-motor) is the most basic element of your neuro-muscular system – it’s a single neural fix responsible for activating one of many muscle fibers. The more intense your physical exercise is the more motor units you need to recruit. And the more motor units you lose the weaker and slower you become.

But it’s the fast motor units that you need most. The fast motor units allow you to perform intense physical tasks…and unfortunately these are the first casualties of physical aging.

Your fast motor units are wired to your fast muscle fibers. Apparently, the highly geared neuro-wiring infrastructure of the fast neuro-motors is particularly prone to age-related damage…which explains why aging typically involves loss of strength and speed. And as people lose their fast neuro-motors they lose their fast muscle fibers along with the capacity to do intense daily functions (such as climbing stairs, carrying heavy grocery bags or fast crossing the street.)

How You Lose Your Fast Muscle Fibers

The loss of your fast muscle fibers leads to debilitating weakening of the body. Fast muscle fibers are on the top of the muscle fibers’ hierarchy. They’re critically needed in times of danger or survival necessity which require swift and strong reactions. Without fast muscle fibers you simply can’t survive physical adversity.

The deterioration of fast muscle fibers is the reason why older people typically suffer from muscle waste and metabolic decline.

Pound for pound your fast muscle fibers have the greatest capacity to gain mass and they generate three times more energy than your slow muscle fibers. They’re the key to keeping your physique strong and metabolic rate intact. Yes, as you get older your fast muscle fibers become increasingly essential to your vitality.

So what can you do to prevent these losses?

Can you stop the aging process before it takes its toll?

Can You Actually Stop or Reverse Physical Aging?

Since oxidative stress has been found to be the main cause of aging, it gives that preventing oxidative stress will stop the aging process. But apparently that’s not the case in real life.

In reality your body is designed to actually thrive under oxidative stress. Yes, this seems a bit tricky…but that’s what’s fascinating about biology; it’s full of contradictions.

Apparently, there are two kinds of oxidative stress, chronic and acute…and they have opposite effects on your aging

Chronic Oxidative Stress vs. Acute Oxidative Stress

The impact of oxidative stress on your body depends on whether it’s chronic (continuous) or acute (short), whether it applies in large or small amounts.

Chronic oxidative stress such as due to chronic infection, chronic overtraining or chronic dietary abuse has shown to overwhelm the muscles’ defenses and increase the risk of damage to the mitochondria, neuro-motors and muscle fibers. This type of oxidative stress obviously contributes to muscle degradation and aging. But this is not the case with acute oxidative stress.

Acute oxidative stress such as due to short intense exercise or periodic fasting, actually benefits your muscle. In fact, it’s essential for keeping your muscle machinery tuned. Technically, acute oxidative stress makes your muscle increasingly resilient to oxidative stress; it stimulates glutathione and SOD production in your mitochondria along with increased muscular capacity to utilize energy, generate force and resist fatigue.

Simply put, exercise and fasting yield acute oxidative stress, which keeps your muscles’ mitochondria, neuro-motors and fibers intact.

Hence, exercise and fasting help counteract all the main determinants of muscle aging. But there is something else about exercise and fasting. When combined, they trigger a mechanism that recycles and rejuvenates your brain and muscle tissues.

The Mechanism that Rejuvenates Your Brain- and Muscle Tissue

Growing evidence indicates that fasting and exercise trigger genes and growth factors which recycles and rejuvenates your brain and muscle tissues. These growth factors include brain derived neurotropic factor (BDNF) and muscle regulatory factors (MRFs); they signal brain stem cells and muscle satellite cells to convert into new neurons and new muscle cells respectively. Incredibly, BDNF also expresses itself in the neuro-muscular system where it protects neuro-motors from degradation.

This means that exercise while fasting signal your body to keep your brain, neuro-motors and muscle fibers biologically young.

You have to Make a Choice – Do You Want Big Muscles, or a Younger Brain and Muscles?

There are actually two distinct approaches you can take that have different protocols and you will not be able to achieve both goals. You will need to decide if you want large muscles or a younger brain and healthier muscles.

Obviously is it your choice but it is my strong recommendation that unless you are a competitive athlete or bodybuilder that you choose the latter. I believe ultimately we all need to choose the latter but many will want to pursue athletic goals that prioritize muscle mass over young rejuvenated and repaired muscles

But what’s behind this tissue recycling mechanism? What actually triggers this?

The main trigger of this recycling mechanism is tissue breakdown. Fasting, muscle injury and short intense exercise are all catabolic events which force your body to break down its tissues’ protein and move it towards recycling.

When your body is forced to break its tissues, it always prefers to sacrifice first its damaged proteins and old or sick cells. Technically all damaged proteins and old, sick and cancerous cells are tagged by immune cells to be digested by the body’s ubiquitine enzymes and the nitrogen byproducts are then recycled back into new cells and tissues. Ubiquitine enzymes are your body’s demolition force …when called to act they search and destroy broken, damaged or sick cells to keep your tissues’ integrity and protect against abnormal growth and tumor formation.

That’s how this tissue rejuvenating mechanism works. But to trigger it you need to use a different strategy than that of muscle buildup. Let’s review the differences between these strategies.

How to Build Your Muscles Up

Most people believe that, to gain muscle you need to feed it frequently throughout the day. It has been speculated that the minimum protein intake required to promote muscle gain is about 1g/per pound body weight. Bodybuilders often consume 2g/per pound body weight per day. This means that a 150lb bodybuilder may consume 300g protein (equivalent to three pounds of meat or 50 eggs) per day. That’s a lot of protein to shove in…

The combination of intense strength training with frequent meals and a high protein and calorie intake seems to grant muscle gain. Nonetheless, this regimen may come with a price… Inferior muscle fiber quality.

Yes, a big muscle isn’t necessarily a better muscle.

A big muscle can be a liability—that’s if it’s made with inferior fibers. One of the most determinants of your muscle quality is your muscles’ biological age. When your muscle gives up to the aging process, it gradually loses its fiber quality. And as time goes by it gets increasingly dysfunctional.

So here is the point:

Conventional fitness and bodybuilding are set to build your muscles but they fail to keep them biologically young. The consequences: you gain muscles with inferior quality and a physique which is highly susceptible to premature aging.

How to Rejuvenate Your Muscle

To trigger muscle rejuvenation, you need to initiate muscle breakdown and turn on the mechanism that signals satellite cells in your muscle to commit and convert into new muscle cells. This can be done by combining intermittent fasting with short intense exercise. But to fully take advantage of this strategy you need to know what your options are.

Intermittent Fasting/Options

Intermittent fasting [from morning to evening followed by a large evening meal (not including post exercise recovery meal)] can be done in three ways: fasting, undereating or pulse feeding.

Fasting

If you choose to fast you can do water fating or vegetable juice fasting (have one up to a few vegetable juices daily). Exercise while fasting, have your recovery meal right after and your main meal at night.

Undereating

If you choose to undereat rather than fast, minimize your food intake during the day to small servings of light, low glycemic mostly raw foods such as fruits, vegetables, whey protein (which is seen as one of the best supplements for weight loss) or lightly poached eggs every 4-6 hours. Do your workout while fasting (30 minutes after your latest snack) followed by recovery meal and have your main meal at night. Undereating is less extreme than fasting; this is your most viable strategy for rejuvenating your muscles and brain.

Pulse feeding

Pulse feeding involves frequent use of small whey protein meals with no sugar added every 3-5 hours throughout the day. Do your workout while fasting (30 minutes after your latest whey meal) followed by recovery meal and have your main meal at night. This regimen is geared towards athletes; we’ll cover it in more detail soon.

As a general rule, have 1-2 recovery meals (whey protein) after your workout. Intermittent fasting by itself has been recognized as a proven effective strategy to help negate physical and cognitive aging. Adding exercise to this routine will “seal the deal” and shoot the anti-aging impact of this regimen to another level.

Exercising while Fasting Can Produce Enormous Benefits IF Carefully Done

Fasting promotes muscle breakdown along with the removal of broken proteins and damaged cells towards recycling. Nonetheless, to fully rejuvenate your muscle, you need to grant regeneration of new muscle cells. And that’s where the short intense exercise comes into play. It turns on the mechanism that converts muscle satellite cells into new muscle fibers. And it targets your fast neuro-motors and helps keep your fast muscle fibers intact.

But that’s only the first step…

The second step is to stop the catabolic process in your muscle and promote recovery. For this you need to feed your muscle with fast assimilating protein right after exercise.

Quality whey protein is your best bet.

Right after exercise there is a two hours period called “window of opportunity” in which your muscle is most recipient to assimilate protein and nutrients towards recovery and growth. To take advantage of this opportunity you must feed your muscle right then with fast assimilating protein such as from quality whey. Slow assimilating proteins won’t do the job. Meat, poultry and fish are too slow assimilating and therefore don’t fit post exercise recovery.

If you miss this window and simply forget to eat or for whatever reasons chose not to you may actually waste and even damage your muscle tissue.

WARNING: Do NOT Do this Program Unless You Read VERY CAREFULLY

The principles I am discussing will produce VERY dramatic results if you apply them properly. They utilize very powerful physiologic principles but if you use them incorrectly, let me very confidently tell you that there is a high chance you WILL hurt yourself and cause more harm than good.

When you implement intermittent fasting you put your body into a strong catabolic state. Your body is literally eating up and destroying damaged and injured brain and muscle cells. You rapidly accelerate this process when you exercise in this state. It’s this very powerful synergy that will allow you to effectively rejuvenate your muscle and brain. This is the radical new approach that very few know about and even few have implemented.

The MAJOR danger though is that you will need to rescue your muscle tissue out of this catabolic state and supply it with the proper nutrients to stimulate repair and rejuvenation. If you fail to supply these nutrients at the proper time you will hurt yourself.

Your post exercise recovery meal is critically important. It’s needed to stop the catabolic process in your muscle and shift the recycling process towards repair and growth. If you fail to feed your muscle at the right time after exercise, you won’t just miss this window of opportunity to restore and build your muscle, you’ll actually let the catabolic process go too far and potentially waste and damage your muscle.

So you MUST EAT within 30 minutes after your workout. And you must feed your muscle with fast assimilating proteins. If, for whatever reason, your fail to supply your body with the protein it needs you may actually accelerate the damage you are seeking to repair. Let me STRONGLY warn you that you are playing with fire here. You need to be ultra-careful and use this program as described or you will pay the consequences.

Other Benefits Your Receive from this Strategy

The combined effect of intermittent fasting and short intense exercise yield additional benefits.

These include:•Boosting growth hormone: Both fasting and short intense exercise have been shown to boost growth hormone. Fasting increases expression of ghrelin, a hunger peptide which binds to growth hormone secretagogue receptors (GHSs) and increase growth hormone release by up to six fold. Short intense exercise increases muscle IGF-1 expression which then mediates growth hormones’ repair and growth actions in your muscle.
•Boosting testosterone: Both intermittent fasting and short intense exercise have shown to boost testosterone. Short intense exercise has a proven positive effect on increasing testosterone levels and preventing its decline. That’s unlike aerobics or prolonged moderate exercise which have shown to have negative or no effect on testosterone levels.

Intermittent fasting boosts testosterone by increasing the expression of satiety hormones including insulin,leptin, adiponectin, glucagon-like peptide-1 (GLP-1), colecystokinin (CKK) and melanocortins, all of which are known to potentiate healthy testosterone actions, increase libido and prevent age-related testosterone decline. Having whey protein meal after exercise can further enhance the satiety/testosterone boosting impact. Whey protein is a potent satiety food known to increase CCK and GLP-1 activities.

Note that hunger hormones cause the opposite effect on your testosterone and libido.

•Improving body composition: The increase in satiety hormone activity has been shown to substantially improve body composition. There is growing evidence to the metabolic boosting effects of satiety peptides such as leptin, adiponectin and GLP. These have shown to increase the body’s metabolic rate, reduce body fat, improve insulin sensitivity and increase the percentage of lean muscle mass.
•Boosting cognitive function and preventing depression: Exercising while fasting maximizes the expression of brain derived neuro-factor (BDNF) which has shown to induce neuro-protective, cognitive boosting and anti-depressant effects.

Exercise while on intermittent fasting is your most effective physical rejuvenating strategy: It won’t necessarily make you bigger but it will certainly keep you biologically younger. But as mentioned previously, there is yet another version to this tissue rejuvenating strategy. Called pulse feeding, it’s designed to accommodate athletic purposes.

What is Pulse Feeding and How Can it Help You?

It you are a competitive athlete and want larger masses than this is your program. The pulse feeding regimen involves frequent use of small whey protein meals throughout the day followed by a large evening meal. This regimen is still classified intermittent fasting as long as you minimize your food intake during the day to small whey protein meals about 20g net protein (This would be two scoops of Miracle Whey) with no sugar added every 3-5 hours.

What’s special about this feeding strategy is that it keeps your body in a negative energy balance similar to fasting.

This is how it technically works…

Whey protein, with its fastest assimilating rate, allows your body to quickly shift from a feeding to a fasting state – within only 15-30 minutes of small meal ingestion. This means that you can have a few small whey protein meals throughout the day and still keep your body in a fasting state for most of this time.

Hence, this regimen yields a double advantage: you can achieve both muscle rejuvenation and muscular development at the same time.

But note that pulse feeding is less catabolic than regular intermittent fasting. Given this, it probably has a lower tissue recycling effect but a stronger restoring effect; which seems like a toss.

Can Pulse Feeding Help You Build Big Muscles?

One of the most attractive properties of pulse feeding is its flexibility; so yes, pulse feeding can be adjusted to accommodate bodybuilding. All you need is to increase the frequency of your whey protein meals. 6 small whey protein meals (every 2 hours throughout the day) followed by a large healthy evening meal can grant maximum protein utilization in the muscle…but again, if you choose to incorporate such a high meal frequency, you WILL lose the rejuvenation effect.

Pulse feeding of this type has a proven record of success. It has shown to be the most effective nutritional regimen for gaining muscle mass.

Here is how it technically works…

The incorporation of small whey protein meals throughout the day grants complete protein utilization from each meal. 20g net protein is the threshold needed to grant max utilization efficiency. So when combining 6 whey meals (20g net protein each) you get a minimum 100-120g net protein utilization before you even started your evening meal.

Let’s set the record straight, the typical utilization efficiency from “normal” meals is less than 40 percent. Yes, we waste at least 60 percent of the protein we normally get from our food. That’s a known fact. So as I previously mentioned, in order to get 120g net protein utilization you need to eat about three pounds of meat or fifty eggs per day.

To sum it up, as an athlete, pulse feeding can be your most effective regimen for either building your muscle or rejuvenating your muscle. Whatever your goal is, you need to adjust the frequency of your whey meals accordingly:
•For muscle buildup – a higher meal frequency (every 2 hours)
•For muscle rejuvenation – a lower meal frequency (every 3-5 hours)

Here’s What to Do if You Want Younger Muscles and Brain

Your rejuvenating strategy should accommodate your personal priorities. For instance, if your main goal is therapeutic, such as anti-inflammatory or anti-cancerous, use extreme intermittent fasting, i.e. water or vegetable juice fasting during the day, exercise while fasting, have your recovery meal right after and your main meal at night. You could also use cbd 1000mg in order to aid the recovery process even further.

However, if your goal is to sustain a healthy rejuvenation strategy for your muscle and brain, use undereating instead. Eat small servings of low glycemic fruits, vegetables, whey protein or poached eggs throughout the day, exercise while fasting followed by recovery meal, and have your main meal at night.

Then, for athletic purposes, use pulse feeding. Eat small whey protein meals every 3-5 hours throughout the day, have 1-2 recovery meals at night.

Note that your post exercise whey meal must be fast assimilating with no sugar, fructose casein or any slow assimilating ingredient added.

Final Note

The most notable difference between the muscle rejuvenation and muscle buildup strategies is in the initiation phase. For muscle rejuvenation you need to initiate muscle breakdown via intermittent fasting and exercise. Whereas, for muscle buildup, you need to inhibit muscle breakdown and aim at gaining maximum muscle mass via frequent feeding throughout the day including pre and post exercise meals.

You should seriously ask yourself what’s your main fitness goal…getting big or getting young? Apparently, you can’t have both…

The purpose of this article is to present you with the strategy to rejuvenate your physique. It’s an option most people haven’t been aware of…and it isn’t an easy one.

The idea of giving up on breakfast and lunch and then training while fasting would probably seem too extreme to the average person. But in view of the fact that today’s average person’s health has been shattered by excess body fat, metabolic disorders and disease of premature aging…it’s worth questioning the viability of the so called “normal” or “average” diet and lifestyle.

In real life there is always a trade-off…you can’t have something for nothing. Your body is programmed to thrive under hardship and deteriorate by indulgence.

Which of these are you ready to trade?

References
Tiidus, P. M. “Radical Species in Inflammation and Overtraining.” Can. J. Physiol. Pharmacol. 76, no. 5 (1998): 533–38.
Miguel, J., and J. Fleming. “Theoretical and Experimental Support for an ‘Oxygen Radical Mitochondrial Injury’ Hypothesis of Cell Aging.” In Biology of Aging, edited by J. Johnson, R. Walford, D. Harman, and J. Miquel, 51–76. New York: Liss, 1993.
Mattson. M. “The Need for Controlled Studies of the Effects of Meal Frequency on Health.” Lancet 365 (2005): 1978–80.
Lexell, J. “Human Aging, Muscle Mass, and Fiber Type Composition.” J. Gerontol A. Biol Sci. Med. Sci. 50A (1995): 11–16.
Lexell, J., and D. Downham. “What Is the Effect of Ageing on Type 2 Muscle Fibres?” J. Neurol. Sci. 107 (1992): 250–1.
Lee, C. K., R. C. Klopp, R. Weindruch, and T. A. Prolla. “Gene Expression Profile of Aging and Its Retardation by Calorie Restriction.” Science 285 (1999): 1390–3.
Hannan D. “Free Radical Theory of Aging: Role of Free Radicals in the Origination and Evolution of Life, Aging and Disease Process.” In Biology of Aging, edited by J. Johnson, R. Walford, D. Hannan, and J. Miguel, 3–50. New York: Liss, 1986.
Sale, D. G. “Influence of Exercise and Training on Motor Unit Activation.” Exercise and Sports Science Reviews 15 (1987): 95–151.
Short, K. R., J. L. Vittone, M. L. Bigelow, D. N. Proctor, and K. S. Nair. “Age and Aerobic Exercise Training Effects on Whole Body and Muscle Protein Metabolism.” Am. J. Physiol. Endocrinol. Metab. 286, no. 1 (2004): E92–101.
Staron, R. S., E. S. Malicky, M. J. Leonardi, et al. “Muscle Hypertrophy and Fast Fiber Type Conversions in Heavy Resistance-Trained Women.” Eur. J. Appl. Physiol. Occup. Physiol. 60 (1990): 71–79.
Bottinelli, R. “Functional Heterogeneity of Mammalian Single Muscle Fibres: Do Myosin Isoforms Tell the Whole Story?” Pflugers Archiv. Euro. Jour. of Physiology 443 (2001): 6–17.
Boutrif, E. “Recent Developments in Protein Quality Evaluation.” Food, Nutrition and Agriculture 2, no. 3 (1991): 36–40.
Charge, S. B., and M. A. Rudnicki. “Cellular and Molecular Regulation of Muscle Regeneration.” Physiol Rev 84 (2004): 209–38.
Makrdies, L., J. G. Heigenhauser, N. McCartney, and N. L. Jones. “Maximal Short-Term Exercise Capacity in Healthy Subjects Aged 13–70 Years.” Clin. Sci. Lond. 69 (1996): 197–205.
Arnal, M. A., L. Mosoni, Y. Boirie, M. L. Houlier, L. Morin, E. Verdier, P. Ritz, J. M. Antoine, J. Prugnaud, B. Beaufrere, et al. “Protein Pulse Feeding Improves Protein Retention in Elderly Women.” Am. J. Clinical Nutrition 69, no. 6 (1999): 1202–8.
Baum, J. I., D. K. Layman, G. G. Freund, K. A. Rahn, M. T. Nakamura, and B. E. Yudell. “A Reduced Carbohydrate, Increased Protein Diet Stabilizes Glycemic Control and Minimizes Adipose Tissue Glucose Disposal in Rats.” J. Nutr. 136, no. 7 (2006): 1855–61.
Bekinschtein, P., M. Cammarola, C. Katche, L. Slipczuk, J. I. Rossato, A. Goldin, I. Izquierdo, and J. H. Medina. “BDNF Is Essential to Promote Persistence of Long-Term Memory Storage.” Proc. Natl. Acad. Sci. U.S.A. 105, no. 7 (2008): 2711–6.
Binder, D. K., and H. E. Scharfman. “Brain-Derived Neurotrophic Factor.” Growth Factors 22, no. 3 (2004): 123–31.
Boirie, Y., M. Dangin, P. Gachon, M.-P. Vasson, J.-L. Maubois, and B. Beaufrere. “Slow and Fast Dietary Proteins Differently Modulate Postprandial Protein Accretion.” Laboratoire de Nutrition Humaine, University Clermont Auvergne, Centre de Recherche en Nutrition Humaine, BP 321 (1997): 6.
Chevrel, G., R. Hohlfeld, and M. Sendtner. “The Role of Neurotrophins in Muscle under Physiological and Pathopsychological Conditions.” Muscle Nerve 33 (2006): 462–76.
Clow, C., and B. J. Jasmin. “Brain-Derived Neurotrophic Factor Regulates Satellite Cell Differentiation and Skeletal Muscle Regeneration.” Cell Physiology 21, no. 13 (2010): 2182–90.
Cotman, C. W., and N. C. Berchtold. “Exercise: A Behavioral Intervention to Enhance Brain Health and Plasticity.” Trends Neurosci. 25, no. 6 (2002): 295–301.
Deponti, D., et al. “The Low Affinity Receptor for Neurotrophins p75NTR Plays a Key Role for Satellite Cell Function in Muscle Repair Acting via RhoA.” Cell 20 (2009): 3620–27.
Doherty, T. J. “Invited Review: Aging and Sarcopenia.” J. Appl Physiol 95, no. 4 (2003): 1717–27.
Dwivedi, Y. “Brain-Derived Neurotrophic Factor: Role in Depression and Suicide.” Neuropsychiatr. Dis. Treat. 5 (2009): 433–49.
Fitts, R. H., and J. J. Widrick. “Muscle Mechanics: Adaptations with Exercise Training.” Exerc. Sport Sci. Rev. 24 (1996): 427–73.
Gordon, T. “The Role of Neurotrophic Factors in Nerve Regeneration.” Neurosurg. Focus 26 (2009): E3.
Grand, T. I. “Body Weight: Its Relation to Tissue Composition, Segment Distribution and Motor Function: I. Interspecific Comparisons.” Am. Jour. Phys. Anthrop. 47 (1977): 241–48.
Griesbeck, O., A. S. Parsadanian, M. Sendtner, and H. Thoenen. “Expression of Neurotrophins in Skeletal Muscle: Quantitative Comparison and Significance of Motorneuron Survival and Maintenance of Function.” J. Neurosci. Res. 42 (1995): 21–33.
Hasten, D. L., J. Pak-Loduca, K. A. Obert, and K. E. Yarasheski. “Resistance Exercise Acutely Increases MHC and Mixed Muscle Protein Synthesis Rates in 78–84 and 23–32 Yr Olds.” Am. J. Physiol Endocrinol Metab. 278, no. 4 (2000): 5620–26.
Henneman, E. “The Size Principle: A Deterministic Output Emerges from a Set of Probabilistic Connections.” Journal of Experimental Biology 115 (1985): 105–12.
Howell, F. C. “Recent Advances in Human Evolutionary Studies.” Quart. Rev. Biol. 42 (1967): 471–513.
Jin, X., et al. “Opposite Roles of MRF4 and MyoD in Cell Proliferation and Mygenic Differentiation.” Biochem. Biophys. Res. Commun. 364 (2007): 476–82.
Jostarndt-Fogen, K., A. Puntschart, H. Hoppeler, and R. Billeter. “Fibre-Type Specific Expression of Fast and Slow Essential Myosin Light Chain mRNAs in Trained Human Skeletal Muscles.” Acta. Physiol. Scand. 164 (1998): 299–308.
Jubrias, S. A., P. C. Esselman, L. B. Price, M. E. Cress, and K. E. Conley. “Large Energetic Adaptations of Elderly Muscle to Resistance and Endurance Training.” J. Appl Physiol. 90, no. 5 (2001): 1663–70.
Kablar, B., and A. C. Belliveau. “Presence of Neurotrophic Factors in Skeletal Muscle Correlates with Survival of Spinal Cord Motor Neurons.” Dev. Dyn. 234 (2005): 659–60.
Kaplan, A. S., R. S. Levitan, Z. Yilmaz, C. Davis, S. Tharmalingam, and J. L. Kennedy. “A DRD4/BDNF Gene-Gene Interaction Associated with Maximum BMI in Women with Bulimia Nervosa.” Int. J. Eat. Disord. 41, no. 1 (2008): 22–28.
Karlsson J. “Exercise, Muscle Metabolism and the Antioxidant Defense.” World Rev. Nutr. Diet. 82 (1997): 81–100.
Kermani, P., and B. Hempstead. “Brain-Derived Neurotrophic Factor: A Newly Described Mediator of Angiogenesis.” Trends Cardiovasc. Med. 17 (2007): 140–143.
Koopman, R., and L. J. van Loon. “Aging, Exercise, and Muscle Protein Metabolism.” J Appl Physiol. 106 (2009): 2040–48.
Larsson, L., G. Grimby, and J. Karlsson. “Muscle Strength and Speed of Movement in Relation to Age and Muscle Morphology.” J. Appl. Physiol. 46 (1979): 451–56.
———. “The Emerging Role of Dairy Proteins and Bioactive Peptides in Nutrition and Health: The American Society for Nutritional Sciences.” J. Nutr. 134 (2004): S968–73.
Layman, D. K., R. A. Boileau, D. J. Erickson, J. E. Painter, H. Shiue, C. Sather, and D. D. Christou. “A Reduced Ratio of Dietary Carbohydrate to Protein Improves Body Composition and Blood Lipid Profiles during Weight Loss in Men.” J. Nutr. 133 (2003): 411–17.
Leewenburgh, C., R. Fiebig, R. Chandwancy, and L. L. Ji. “Aging and Exercise Training in Skeletal Muscle: Responses of Glutathione and Antioxidant Enzyme Systems.” Am. J. Physiol. 267 (1994): R439–45.
Lipton, B. R., and E. Schultz. “Developmental Fate of Skeletal Muscle Satellite Cells.” Science 205 (1979): 1292–94.
Mattson, M. P. “Glutamate and Neurotrophic Factors in Neuronal Plasticity and Disease.” Annals of the New York Academy of Sciences 1144 (2008): 97–90.
Mousavi, K., D. J. Parry, and B. J. Jasmin. “BDNF Rescues Myosin Heavy Chain IIB Muscle Fibers after Neonatal Nerve Injury.” Am. J. Physiol. Cell Physiol. 287 (2004): C22–29.
Paddon-Jones, D., E. Westman, R. D. Mattes, R. R. Wolfe, A. Astrup, and M. Westerterp-Phantenga. “Protein, Weight Management, and Satiety.” Am. J. Clinical Nutrition 87, no. 5 (2008): S1558–61.
Pitteloud, N., M. Hardin, A. A. Dwyer, E. Valassi, M. Yialamas, D. Elahi, and F. J. Hayes. “Increasing Insulin Resistance Is Associated with a Decrease in Leydig Cell Testosterone Secretion in Men.” Journal of Clinical Endocrinology and Metabolism 90, no. 5 (2005): 2636–41.
Rennie, M. J, and K. D. Tipton. “Protein and Amino Acid Metabolism during and after Exercise and the Effects of Nutrition.” Annu. Rev. Nutr. 20 (2000): 457–83.
Reynolds, G. “Phys Ed: The Benefits of Exercising Before Breakfast.” http://well.blogs.nytimes.com/2010/12/15/phys-ed-the-benefits-of-exercising-before-breakfast/?ref=gretchenreynolds, December 15, 2010.
Rios, M., G. Fan, C. Fekete, J. Kelly, B. Bates, R. Kuehn, R. M. Lechan, and R. Jaenisch. “Conditional Deletion of Brain-Derived Neurotrophic Factor in the Postnatal Brain Leads to Obesity and Hyperactivity.” Mol. Endocrinol. 15 (2001): 1748–57.
Roubenoff, R. “Sarcopenia: Effects on Body Composition and Function.” J. Gerontol. A. Biol. Sci. Med. Sci. 58, no. 11 (2003): M1012–17.
Tidball, J. G. “Inflammatory Processes in Muscle Injury and Repair.” Am. J. Physiol. Regul. Integr. Comp. Physiol. 288 (2005): R345–53.
Van Proeyen, K., K. Szlufcik, H. Nielens, K. Pelgrim, L. Deldicque, M. Hesselink, P. P. Van Veldhoven, and P. Hespel. “Training in the Fasted State Improves Glucose Tolerance during Fat-Rich Diet.” J. Physiol. 588, pt. 21 (2010): 4289–302.
Xu, Y., B. Ku, L. Tie, H. Yao, W. Jiang, X. Ma, and X. Li. “Curcumin Reverses the Effects of Chronic Stress on Behavior, the HPA Axis, BDNF Expression and Phosphorylation of CREB.” Brain Research 1122, no. 1 (2006): 56.
Crawley, J. N., and R. L. Corwin. “Biological Actions of Cholecystokinin.” Peptides 15 (1994): 731–55.
Ellacott, K. L., and R. D. Cone. “The Central Melanocortin System and the Integration of Short- and Long-Term Regulators of Energy Homeostasis.” Recent Progress in Hormone Research 59 (2004): 395–408.
Fulton, S., B. Woodside, and P. Shizgal. “Modulation of Brain Reward Circuitry by Leptin.” Science 287 (2000): 125–28.
Hermann, C., R. Goke, G. Richter, H. C. Fehmann, R. Arnold, and B. Goke. “Glucagon-like Peptide-1 and Glucose-Dependent Insulin-Releasing Polypeptide Plasma Levels in Response to Nutrients.” British Journal of Pharmacology 93 (1995): 79–84.
Heymsfield, S. B., A. S. Greenber, K. Fujioka, R. M. Dixon, R. Kushner, T. Hunt, J. A. Lubina, J. Patane, B. Self, P. Hunt, and M. McCamish. “Recombinant Leptin for Weight Loss in Obese and Lean Adults: A Randomized, Controlled, Dose-Escalation Trial.” Journal of the American Medical Association 282 (1999): 1568–75.
Livingstone, C., and M. Collison. “Sex Steroids and Insulin Resistance.” Clinical Science 102 (2002): 151–66.
Lord, G. M., G. Matarese, J. K. Howard, R. J. Baker, S. R. Bloom, and R. I. Lechler. “Leptin Modulates the T-Cell Immune Response and Reverses Starvation-Induced Immunosuppression.” Nature 394 (1998): 897–901.
Makimura, H., T. M. Mizuno, J. W. Mastaitis, R. Agami, and C. V. Mobbs. “Reducing Hypothalamic AGRP by RNA Interference Increases Metabolic Rate and Decreases Body Weight without Influencing Food Intake.” BMC Neuroscience 3 (2002): 18.
Menendez, J. A., and D. M. Atrens. “Insulin and the Paraventricular Hypothalamus: Modulation of Energy Balance.” Brain Research 555 (1991): 193–201.
Nauck, M. A., N. Kleine, C. Orskov, J. J. Holst, B. Willms, and W. Creutzfeldt. “Normalization of Fasting Hyperglycaemia by Exogenous Glucagon-Like Peptide 1 (7-36 Amide) in Type 2 (Non-Insulin-Dependent) Diabetic Patients.” Diabetologia 36 (1993): 741–44.
Pasquali, R., F. Casimirri, R. De Iasio, P. Mesini, S. Boschi, R. Chierici, R. Flamia, M. Biscotti, and V. Vicennati. “Insulin Regulates Testosterone and Sex Hormone-Binding Globulin Concentrations in Adult Normal Weight and Obese Men.” Journal of Clinical Endocrinology and Metabolism 80 (1995): 654–58.
Porte, D., Jr., D. G. Baskin, and M. W. Schwartz. “Leptin and Insulin Action in the Central Nervous System.” Nutritional Reviews 60 (2002): S20–29.
Strobel, A., T. Issad, L. Camoin, M. Ozata, and A. D. Strosberg. “A Leptin Missense Mutation Associated with Hypogonadism and Morbid Obesity.” Nature Genetics 18 (1998): 213–15.
Sun, Y., P. Wang, H. Zheng, and R. G. Smith. “Ghrelin Stimulation of Growth Hormone Release and Appetite Is Mediated through the Growth Hormone Secretagogue Receptor.” PNAS 101 (2004): 4679–84.
Traish, A. M., F. Saad, and A. Guay. “The Dark Side of Testosterone Deficiency: II. Type 2 Diabetes and Insulin Resistance.” J. Androl. 30, no. 1 (2009): 23–32.
Wynne, K., S. Stanley, B. McGowan, and S. Bloom. “Appetite Control.” Journal of Endocrinology 184 (2005): 291–318.
Date, Y., M. Kojima, H. Hosoda, A. Sawaguchi, M. S. Mondal, T. Sugamuma, S. Marsukura, K. Kangawa, and M. Nakazato. “Ghrelin, a Novel Growth Hormone-Releasing Acylated Peptide, Is Synthesized in a Distinct Endocrine Cell Type in the Gastrointestinal Tracts of Rats and Humans.” Endocrinology 141 (2000): 4255–61.

DR. MERCOLA

MERCOLA’S HEALTH BLOG

A Celebration of Women