Build Massive Legs with Post Exhaustion

This post-exhaustion routine is set up so that the most neurologically demanding exercise is performed first instead of last (which makes perfect sense, if you think about it). Secondly, the reps and tempo of each exercise are varied. The idea is to knock off as many motor units from the motor-unit pool as possible. Also, make certain that all your weights are pre-set so you don’t inadvertently get some extra rest by messing around with the poundages.

Post-Exhaustion Leg Growth Routine

A1. Barbell Hack Squat: 3 x 6-8, 50X0, no rest
A2. 45-Degree Leg Press: 3 x 12-15, 20X0, no rest
A3. Leg Extension: 3 x 12-15, 2012, rest 180 seconds

A1. Barbell Hack Squat
This exercise was brought to the bodybuilding world by Russian wrestler Georges Hackenschmidt. Hackenschmidt had sought to develop an isolation exercise for the quadriceps, and he succeeded. However, in Hackenschmidt’s heyday, exercise machines weren’t exactly commonplace. Hackenschmidt invented the exercise with a barbell in mind, and the so-called Hack Squat Machine wasn’t developed until years later.

A very-low-cost alternative to back squatting, the Hack Squat will promote top-level growth in the vastus medialis. Granted, using a barbell instead of a machine makes it a little uncomfortable, but its effectiveness overrides any comfort problems.

In order to perform a true barbell hack squat, you need a barbell and an adjustable rack so you can place the barbell at an optimal height for picking up and racking the bar. Your heels should be elevated by at least one and a half inches (the depth of a two-by-four) so you can squat with a straight back and your hips are under your shoulders in the bottom position. (It’s better to use a wedged board instead of a two-by-four so the exercise is more comfortable for your arches, but a two-by-four will do). Place the two-by-four or wedged board on the ground under the middle of the power rack. Set a barbell on the rack so it is about four to six inches lower than your gluteal line. Standing with your back to the bar, grab the barbell, preferably with straps (this is one of the few exceptions when you would use straps).

Walk forward until your heels rest on the board. Initiate the squatting motion by allowing your knees to travel as far forward as possible, without allowing your glutes to move back. Keep a slight arch in your lower back. Once your knees have gone as far forward as possible, lower your hips to the bottom position of the squat. Be sure to keep your back upright by pushing the bottom of your sternum up. Don’t allow your shoulders to round forward, and be certain your hips are under your shoulders in the bottom position.

After doing the prescribed number of reps, move directly to exercise A2. Don’t take any rest.

A2. 45-Degree Leg Press

The problem with using leg press machines is that they build nonfunctional strength. However, since the focus of this article is hypertrophy and not necessarily functional strength, an exception is allowable in this case. The standard 45-degree leg press machines work fine for this workout.

One point to remember when you do leg presses is that when you extend your hips and knees, make sure to keep the tension on your thighs by going to 95 percent of knee lockout. To prevent any dizziness, make sure you breathe in during the eccentric contraction and exhale on the concentric contraction. Again, the key is to keep the tension on the muscle at all times.

By the time you finish this exercise, you’ll want to rest, but not yet. It’s time to go directly to exercise A3.

A3. Leg Extension

As a general rule, leg extensions should be avoided because they expose your knees to undue stress. However, when your legs are pre-exhausted from the previous two exercises, you won’t be able to use much weight on them and the stress will be minimal. Also, this is not the type of workout you would perform year-round.

If possible, use a machine that overloads more of the middle of the strength curve, as that’s where the quadriceps are the strongest in this movement. Keep your head in a neutral position and don’t grip the handles too tightly, as that would raise your blood pressure and increase the likelihood of dizziness. Furthermore, try to follow the tempo prescribed. Often when trainees go through this excruciating routine, they start getting sloppy with the tempo by the time they get to this exercise. It’s best to guess light and complete all the reps rather than going too heavy and ending up looking like a penguin having an epileptic fit.

By the time you walk/wobble off this machine, you’ll probably feel quite nauseated. That’s quite normal because of the high lactate levels you’ll have generated. The good news is that high levels of lactate are linked to high levels of growth hormone.

Now, take a three-minute rest before repeating the tri-set. When you’ve gone through it three times, you’ve had enough. Do this routine for six workouts, working your legs once every four or five days.

This routine is very demanding physiologically and psychologically. Make sure you don’t eat anything more than a light meal within two hours before, as it’s easy to become quite nauseated from this routine.

To break through training plateaus it’s often necessary to shock your muscles into growth. Post-exhaustion tri-sets such as this one will do just that!

More Sleep Can Double Your Testosterone Levels

Older men can sometimes double their testosterone levels by getting more sleep, according to a human study that Plamen Penev of the University of Chicago.

Nearly all of us probably get too little sleep, mainly because we are seduced every day by the technology around us. It enables us to generate light at night, provides us with 24-hour entertainment and information through electronic media, and makes it possible for us to have contact with each other whenever we want. Every evening, when our body tells us that it’s time to sleep, we can also do a thousand other things instead.

Too little sleep messes up our hormone balance. It makes our body less sensitive to insulin for example. Dutch researchers recently showed that after just one night of four hours’ sleep, young men’s insulin sensitivity went down by 20 % and that of diabetics by a quarter.

In the latter case, lack of sleep is clinically relevant, so doctors could advise diabetics who react insufficiently to their medicines to get more sleep. “Sleep duration might become another therapeutic target to improve glucoregulation in type 1 diabetes”, the Dutch researchers say.

Testosterone is also affected by amount of sleep. That’s not so strange, as our bodies make much more testosterone when they’re asleep than when they’re awake. We’ve taken the figure below from the study mentioned here. It shows how much testosterone is present in the blood of 22-32 year-old men while asleep and during the rest of the day.

The better men sleep, the higher their testosterone level rises while they are asleep.

In the average male over forty, the testosterone level goes down by 1-2 % per year, but researchers occasionally come across men in their eighties with a testosterone level you’d expect in a young man. Add to that the fact that many older men – but not all men – sleep less and less deeply as they get older, then you automatically think of the idea that Plamen Penev wanted to test in his study: does the testosterone level decrease in older men because they sleep less?

More sleep can double your testosterone level

Penev based his theory on, among other things, research done by Eve Van Cauter, a sleep researcher at the University of Chicago who has celebrity status in the field of endocrinology. Van Cauter discovered early in the 21st century that men in their forties make less testosterone while sleeping than men in their twenties.

Penev measured the amount of testosterone 12 slim, healthy, non-smoking men aged between 64 and 74 had in their blood in the morning. He also got the men to wear a small gadget around their wrist, which enabled him to see how many hours per night the men slept. That varied from 4.5 to 7.5 per 24 hours. The longer the men slept, the figures below show, the more testosterone there was circulating in their blood.

The men that slept the least had a testosterone level of 200-300 ng/dl. That’s a normal amount for men of this age, but it’s on the low side. The men in the study who slept the most had a testosterone level that was twice as high: 500-700 ng/dl. That’s a level you’d expect in healthy young men.

“These findings suggest that complaints of poor or insufficient sleep in otherwise healthy older men can be associated with a more pronounced age-related androgen decline”, writes Penev. “Eliciting such sleep complaints in the physician’s office may facilitate the judicious interpretation of lower testosterone levels in the older male patient.”

Before men consider doing testosterone therapy, they might first measure the amount of sleep they get. And ‘measuring’ is different from ‘guessing’ or ‘estimating’. Most people overestimate the number of hours that they sleep. This was also the case in Penev’s study. The men thought that they slept seven and a quarter hours per day on average, but Penev’s recordings showed that they only slept six hours a day.

Muscle Growth and Vitamin D

Vitamins are typically associated with protective functions that support overall health and wellness. For example, vitamin C has antioxidant properties that mitigate the many negative effects associated with oxidative damage to biomolecules such as DNA within the human body. Vitamin D is somewhat different. Like other vitamins, it promotes overall health— but it also plays an active role in promoting muscle growth and strength.

Vitamin D is a fat-soluble, steroid-like vitamin that functions as a prohormone— aiding manydifferent processes such as the absorption and metabolism of calcium and phosphorous, promoting bone health. Furthermore, low levels of vitamin D—which are prominent in the western world— correlate with several diseases such as cancer and cardiovascular disease.

Some of the muscle-promoting properties associated with vitamin D apparently stem somewhat from the similar chemical structure between vitamin D and steroid molecules like testosterone— as studies have shown vitamin D can bind the androgen receptor, perhaps mimicking some of the muscle-building properties of testosterone. Vitamin D can also bind and activate the vitamin D receptor— which directly regulates the expression of hundred of genes, with several of the genes turned on by vitamin D directly involved in generating muscle growth and strength.

Among the genes regulated by vitamin D, a few appear to be involved in the production of testosterone. A study by Wehr et al. investigated the association of vitamin D levels with testosterone in over 2,200 men. The study showed a strong correlation between vitamin D levels and testosterone.The group with the lowest vitamin D levels had the lowest testosterone measurements, and the group with the highest amount of vitamin D possessed the highest testosterone.

Interestingly, Wehr et al. also found that higher levels of vitamin D produced lower amounts of the sex hormone binding globulin protein (SHBG). Since testosterone circulates in the bloodstream bound mostly to SHBG and only a small fraction is unbound— and thus biologically active where it can activate the androgen receptor— vitamin D's ability to lower SHBG levels will give way to greater testosterone activity.

Thus, vitamin D not only increases the production of testosterone but it also increases testosterone activity by diminishing SHBG's inhibitory influence on testosterone function.

Since the production of vitamin D can be produced in the human body by exposure to sunlight, the differences in sunlight-induced vitamin D production should vary throughout the year. Thus, in another part of this study, Wehr et al. further validated the relationship between vitamin D and testosterone production by uncovering the tight correlation between vitamin D levels and testosterone production throughout the year.The researchers demonstrated that high vitamin D production in the summer months corresponds with greater testosterone levels, and vice versa during the winter months.

Altogether, this study highlights vitamin D's capability to raise or maintain testosterone levels. The research emphasizes the importance of consuming enough dietary vitamin D—especially during the long winter months, when exposure to sunlight is diminished and the need for dietary vitamin D is the greatest— in order to stimulate or maintain testosterone production.

In addition to increasing testosterone levels, vitamin D has been shown by researchers at the Dutch company Organext Research to stimulate the expression of the androgen receptor in isolated skeletal muscle cells. The increase in androgen receptor stimulated by vitamin D promoted the proliferation of muscle satellite cells into new muscle fibers, potentially leading to increased muscle growth. In addition to the influence of vitamin D on the androgen receptor, the researchers found that the anabolic steroid nandrolone decanoate stimulated the expression of the vitamin D receptor in isolated skeletal muscle cells— and that the combination of nandrolone decanoate and vitamin D had a overwhelmingly synergistic effect on satellite cell conversion into muscle tissue in isolated skeletal muscle cells.

These results suggest that consumption of vitamin D along with anabolic steroids should be extremely influential on muscle growth. What's more, given that anabolic steroids have negative side effects that are amplified by consuming large quantities of these drugs, ingesting smaller doses of steroids supplemented with vitamin D should mitigate some of the side effects associated with steroid use while still stimulating significant increases in muscular size and strength.

All in all, vitamin D's ability to increase the amount of testosterone and androgen receptor should powerfully stimulate muscle growth— not only by initiating satellite cell proliferation, but also by cranking up protein synthesis in muscle tissue— considering that testosterone and the androgen receptor function cooperatively to stimulate muscle cell protein synthesis.Anti-Aromatase Activity

According to an investigation by Krishnan et al., vitamin D considerably decreases the expression of the aromatase enzyme— most potently in fat cells. Since aromatase activity in fat cells can decrease testosterone levels by catalyzing the conversion of testosterone into the estrogen-like compound estradiol, vitamin D's ability to decrease aromatase represents another mechanism in its arsenal for increasing testosterone.

In the above study, mice were given large quantities of the steroid molecule androstenedione— which can be converted to the estrogen-like molecules estradiol or estrone by aromatase. Some of the mice were also given a daily injection of vitamin D, while the control group received no vitamin D injections. The mice that received vitamin D showed a significant decrease in the expression levels of aromatase and a lower amount of estradiol or estrone, specifically in fat cells, compared to the control group that received no vitamin D.

In addition, the researchers in this study showed that vitamin D diminishes aromatase levels and activity in isolated human breast cancer cells, which is a cell type that typically expresses large amounts of the aromatase enzyme. This finding implies that vitamin D functions similarly in humans by diminishing the quantity and activity of aromatase. Moreover, the researchers also investigated the influence of vitamin D in combination with aromatase inhibitors such as Arimidex on aromatase activity, also in isolated human breast cancer cells. Interestingly, their results showed that vitamin D enhances the effect of aromatase inhibitors. Since some bodybuilders and athletes consume aromatase inhibitors during anabolic steroid cycles to prevent the conversion of steroids into estrogen, vitamin D in combination with aromatase inhibitors should more potently decrease aromatase's ability to convert anabolic steroids into estrogen—thus preventing some of the unpleasant side effects associated with anabolic steroid use such as the development of breast tissue, also known as gynecomastia.

In conclusion, vitamin D has the powerful ability to regulate the expression of specific genes that are intimately involved in muscle growth. Moreover, most people appear to have suboptimal amounts of vitamin D due to dietetic inadequacy and a lack of sunlight exposure. Consequently, vitamin D is evidently a necessary and influential supplement for the athlete, bodybuilder or recreational weightlifter for gaining muscle and increasing strength.

Alcohol and Steroids. Drinking While On A Cycle.

For centuries, people from various civilizations and societies have enjoyed alcohol as a way to unwind from the day and experience a slight level of bliss for a short time. In many countries, alcohol is being served with most meals. Alcohol is a uniter as well as a divider, and responsible for the conception of many of us reading this article today!

Alcohol has a place in society and in many lives and it is important to know about joining alcohol and anabolic steroids.

In bodybuilding and fitness, it’s another story. Alcohol dehydrates muscles that you are trying to hydrate when you consumpt of a lot of water. Alcohol depresses your immune system, which must be ramped up if you want to remain healthy to combat the rigors of your workouts without becoming ill. Alcohol contains a great deal of empty calories which detract from that waistline and deliver the dreaded “beer gut” that no bodybuilder wants to possess. Alcohol saps motivationand introduces a relaxed state to the bodybuilder that needs a bit of a hurried or frantic enthusiasm to wake up and go to the gym.

Bodybuilders use post-cycle therapy (PCT) drugs to help to fight the hormone imbalance that occurs following a 10 to 16 weeks cycle. Following a cycle, estrogen levels tend to be over limit, which leads to bloating and a dreaded puffiness of tissue under the nipple called Gynecomastia. Testosterone tends to be low, as do energy levels. The libido of a bodybuilder will plummet, as his body hasn’t been required to produce any natural testosterone for the past several months.

Most bodybuilders use Clomid, Tamoxifen, or other compounds to help fighting these side effects and to help restore normal and optimal hormone functionality of the body. The body is at a particularly vulnerable time for damage and disruption during that post-cycle therapy period. The use of alcohol during this time is probably more potentially damaging than at any other time in the year. Alcohol rises estrogen levels and drops down testosterone levels. This directly defeats the purpose of the PCT drugs. Additionally, the oral PCT drugs can be very toxic to the liver, as they are essentially oral anabolic steroids.

Alcohol also has a detrimental effect upon the liver. It’s not a great idea to be placing such undue stress upon the organs, particularly when the end results could be lost muscle. You’d better running two orals – an equally dangerous idea – because it would at least lead to some new muscle gains!The bottom line is that alcohol does not belong near bodybuilders and in particular, the bodybuilder in post-cycle therapy. Set your priorities and decide if being a successful healthy bodybuilder means more to you than drinking.

How to prevent age related muscle mass loss

Is a loss of strength, mobility, and functionality an inevitable part of aging? No, it’s not. It’s a consequence of disuse, suboptimal hormone levels, dietary and nutrient considerations and other variables, all of which are compounded by aging. One of the greatest threats to an aging adult’s ability to stay healthy and functional is the steady loss of lean body mass – muscle and bone in particular.

The medical term for the loss of muscle is sarcopenia, and it’s starting to get the recognition it deserves by the medical and scientific community. For decades, that community has focused on the loss of bone mass (osteoporosis), but paid little attention to the loss of muscle mass commonly seen in aging populations. Sarcopenia is a serious healthcare and social problem that affects millions of aging adults. This is no exaggeration. As one researcher recently stated:

“Even before significant muscle wasting becomes apparent, ageing is associated with a slowing of movement and a gradual decline in muscle strength, factors that increase the risk of injury from sudden falls and the reliance of the frail elderly on assistance in accomplishing even basic tasks of independent living. Sarcopenia is recognized as one of the major public health problems now facing industrialized nations, and its effects are expected to place increasing demands on public healthcare systems worldwide”

Sarcopenia and osteoporosis are directly related conditions, one often following the other. Muscles generate the mechanical stress required to keep our bones healthy; when muscle activity is reduced it exacerbates the osteoporosis problem and a vicious circle is established, which accelerates the decline in health and functionality.

What defines sarcopenia from a clinical perspective? Sarcopenia is defined as the age-related loss of muscle mass, strength and functionality. Sarcopenia generally appears after age 40 and accelerates after the age of approximately 75. Although sarcopenia is mostly seen in physically inactive individuals, it is also commonly found in individuals who remain physically active throughout their lives. Thus, it’s clear that although physical activity is essential, physical inactivity is not the only contributing factor. Just as with osteoporosis, sarcopenia is a multifactorial process that may involve decreased hormone levels (in particular, GH, IGF-1, MGF, and testosterone), a lack of adequate protein and calories in the diet, oxidative stress, inflammatory processes, chronic, low level, diet-induced metabolic acidosis, as well as a loss of motor nerve cells.

A loss of muscle mass also has far ranging effects beyond the obvious loss of strength and functionality. Muscle is a metabolic reservoir. In times of emergency it produces the proteins and metabolites required for survival after a traumatic event. In practical terms, frail elderly people with decreased muscle mass often do not survive major surgeries or traumatic accidents, as they lack the metabolic reserves to supply their immune systems and other systems critical for recovery. There is no single cause of sarcopenia, as there is no single cause for many human afflictions. To prevent and/or treat it, a multi-faceted approach must be taken, which involve hormonal factors, dietary factors, supplemental nutrients, and exercise.

Dietary considerations

The major dietary considerations that increase the risk of sarcopenia are: a lack of adequate protein, inadequate calorie intake, and low level, chronic, metabolic acidosis. Although it’s generally believed the “average” American gets more protein then they require, the diets of older adults are often deficient. Compounding that are possible reductions in digestion and absorption of protein, with several studies concluding protein requirements for older adults are higher than for their younger counterparts. These studies indicate that most older adults don’t get enough high quality protein to support and preserve their lean body mass.

There is an important caveat on increasing protein, which brings us to the topic of low level, diet-induced, metabolic acidosis. Typical Western diets are high in animal proteins and cereal grains, and low in fruits and vegetables. It’s been shown that such diets cause a low grade metabolic acidosis, which contributes to the decline in muscle and bone mass found in aging adults. One study found that by adding a buffering agent (potassium bicarbonate) to the diet of post-menopausal women the muscle wasting effects of a “normal” diet were prevented. The researchers concluded the use of the buffering agent was “… potentially sufficient to both prevent continuing age-related loss of muscle mass and restore previously accrued deficits.”

The take home lesson from this study is that – although older adults require adequate intakes of high quality proteins to maintain their muscle mass (as well as bone mass), it should come from a variety of sources and be accompanied by an increase in fruits and vegetables as well as a reduction of cereal grain-based foods. The use of supplemental buffering agents such as potassium bicarbonate, although effective, does not replace fruits and vegetables for obvious reasons, but may be incorporated into a supplement regimen.

Hormonal considerations

As most are aware, with aging comes a general decline in many hormones, in particular, anabolic hormones such as Growth Hormone (HGH), DHEA, and testosterone. In addition, researchers are looking at Insulin-like Growth factor one (IGF-1) and Mechano Growth factor (MGF) which are essential players in the hormonal milieu responsible for maintaining muscle mass as well as bone mass. Without adequate levels of these hormones, it’s essentially impossible to maintain lean body mass, regardless of diet or exercise.

It’s been shown, for example, that circulating HGH declines dramatically with age. In old age, HGH levels are only one-third of that in our teenage years. In addition, aging adults have a blunted HGH response to exercise as well as reduced output of MGF, which explains why older adults have a much more difficult time building muscle compared to their younger counterparts. However, when older adults are given HGH, and then exposed to resistance exercise, their MGF response is markedly improved, as is their muscle mass.

Another hormone essential for maintaining lean body mass is testosterone. Testosterone, especially when given to men low in this essential hormone, has a wide range of positive effects. One review looking at the use of testosterone in older men concluded:

“In healthy older men with low-normal to mildly decreased testosterone levels, testosterone supplementation increased lean body mass and decreased fat mass. Upper and lower body strength, functional performance, sexual functioning, and mood were improved or unchanged with testosterone replacement”

Contrary to popular belief, women also need testosterone! Although women produce less testosterone, it’s as essential to the health and well being of women as it is for men.

The above is a highly generalized summary and only the tip of the proverbial iceberg regarding various hormonal influences on sarcopenia. A full discussion on the role of hormones in sarcopenia is well beyond the scope of this article. Needless to state, yearly blood work after the age of 40 is essential to track your hormone levels, and if needed, to treat deficiencies via Hormone Replacement Therapy (HRT). Private organizations like the Life Extension Foundation offer comprehensive hormone testing packages, or your doctor can order the tests. However, HRT is not for everyone and may be contraindicated in some cases. Regular monitoring is required, so it’s essential to consult with a medical professional versed in the use of HRT, such as an endocrinologist.

Nutrient considerations:

There are several supplemental nutrients that should be especially helpful for combating sarcopenia, both directly and indirectly. Supplements that have shown promise for combating sarcopenia are creatine, vitamin D, whey protein, acetyl-L-carnitine, glutamine, and buffering agents such as potassium bicarbonate.

Creatine

The muscle atrophy found in older adults comes predominantly from a loss of fast twitch (FT) type II fibers which are recruited during high-intensity, anaerobic movements (e.g., weight lifting, sprinting, etc.). Interestingly, these are exactly the fibers creatine has the most profound effects on. Various studies find creatine given to older adults increases strength and lean body mass. One group concluded: - “Creatine supplementation may be a useful therapeutic strategy for older adults to attenuate loss in muscle strength and performance of functional living tasks.”

Vitamin D

It’s well established that vitamin D plays an essential role in bone health. However, recent studies suggest it’s also essential for maintaining muscle mass in aging populations. In muscle, vitamin D is essential for preserving type II muscle fibers, which, as mentioned above, are the very muscle fibers that atrophy most in aging people. Adequate vitamin D intakes could help reduce the rates of both osteoporosis and sarcopenia found in aging people  leading the author of one recent review on the topic of vitamin D’s effects on bone and muscle to conclude: “In both cases (muscle and bone tissue) vitamin D plays an important role since the low levels of this vitamin seen in senior people may be associated to a deficit in bone formation and muscle function” and  “We expect that these new considerations about the importance of vitamin D in the elderly will stimulate an innovative approach to the problem of falls and fractures which constitutes a significant burden to public health budgets worldwide.”

Whey protein

As previously mentioned, many older adults fail to get enough high quality protein in their diets. Whey has an exceptionally high biological value (BV), with anti-cancer and immune enhancing properties among its many uses. As a rule, higher biological value proteins are superior for maintaining muscle mass compared to lower quality proteins, which may be of particular importance to older individuals. Finally, data suggests “fast” digesting proteins such as whey may be superior to other proteins for preserving lean body mass in older individuals.

Additional Nutrients of interest

There are several additional nutrients worth considering when developing a comprehensive supplement regimen designed to prevent and or treat sarcopenia. In no particular order, they are: fish oils (EPA/DHA), acetyl-l-carnitine, glutamine, and buffering agents such as potassium bicarbonate. There is good scientific reason to believe they would be beneficial for combating sarcopenia, but data specific to sarcopenia is lacking. For example, EPA/DHA has been found to preserve muscle mass (e.g. is anti-catabolic) under a wide range of physiological conditions. The anti-inflammatory effects of fish oils would also lead one to believe they should be of value in the prevention or treatment of sarcopenia. In general, fish oils have so many health benefits, it makes sense to recommend them here.

Acetyl-l-carnitine also offers many health benefits to aging people, and data suggests it should be useful in combating this condition. More research specific to sarcopenia is needed however.

Glutamine is another nutrient that should be useful in an overall plan to combat sarcopenia. Finally, data does suggest strongly that bicarbonate and citrate buffering agents containing minerals such as potassium, magnesium, and calcium can reverse the metabolic acidosis caused by unbalanced western diets. However, I hesitate to recommend this particular strategy as it does not address the root cause, which is the diet itself. Much greater health benefits will result from improving the diet over simply adding in this supplement. In addition, there are potential problems that could result from excessive intake of buffer salts, such as hyperkalemia and formation of kidney stones.

Exercise Considerations

Exercise is the lynchpin to the previous sections. Without it, none of the above will be an effective method of preventing/treating sarcopenia. Exercise is the essential stimulus for systemwide release of various hormones such as GH, as well as local growth factors in tissue, such as MGF. Exercise is the stimulus that increases protein and bone synthesis, and exerts other effects that combat the loss of essential muscle and bone as we age. Exercise optimizes the effects of HRT, diet and supplements, so if you think you can sit on the couch and follow the above recommendations…think again.

Although any exercise is generally better then no exercise, all forms of exercise are not created equal. You will note, for example, many of the studies listed at the end of this article have titles like: “GH and resistance exercise” or “creatine effects combined with resistance exercise” and so on. Aerobic exercise is great for the cardiovascular system and helps keep body fat low, but when scientists or athletes want to increase lean mass, resistance training is always the method. Aerobics does not build muscle and is only mildly effective at preserving the lean body mass you already have. Thus, some form of resistance training (via weights, machines, bands, etc.) is essential for preserving or increasing muscle mass. The CDC report on resistance exercise for older adults summarizes it as: “In addition to building muscles, strength training can promote mobility, improve health-related fitness, and strengthen bones.”

Combined with HRT (if indicated), dietary modifications, and the supplements listed above, dramatic improvements in lean body mass can be achieved at virtually any age, with improvements in strength, functionality into advanced age, and improvements in overall health and general well being.

Hopefully, the reader will appreciate that I have attempted to cover a huge amount of territory with this topic. Each sub-section (nutrition, hormones, etc.) could easily be its own article if not its own book. This means each section is a general overview vs. anything close to an exhaustive discussion. Below is guide to web sites that offer additional information regarding the topics covered in this article and should (hopefully!) help fill in any gaps.

To prevent or treat sarcopenia:

• Get adequate high quality proteins from a variety of sources as well as adequate calories. Avoid excessive animal protein and cereal grain intakes while increasing the intake of fruits and vegetables.
• Get regular blood work on all major hormones after the age of 40 and discuss with a medical professional if HRT is indicated.
• Add supplements such as: creatine, vitamin D, whey protein, acetyl-l-carnitine, glutamine, and buffering agents such as potassium bicarbonate.
• Exercise regularly – with an emphasis on resistance training – a minimum of 3 times per week.

Clomid (Clomiphine citrate) - best steroid for PCT

Clomid was one of the original drugs used in post-cycle-therapy to stave off gynocomastia and raise the body’s natural testosterone levels. There are some side effects involved with heavy prolonged use, such as vision problems, and there are more effective substances on the market that do the same thing, but Clomid is still an effective and inexpensive compound for any athlete’s post-cycle-therapy.

Clomid is the commonly referenced brand name for the drug clomiphene citrate. It is not an anabolic steroid, but a prescription drug generally prescribed to women as a fertility aid. This is due to the fact that Clomiphene citrate shows a pronounced ability to stimulate ovulation. This is accomplished by blocking/minimizing the effects of estrogen in the body. To be more specific Clomid is chemically a synthetic estrogen with both agonist/antagonist properties, and is very similar in structure and action to Nolvadex. In certain target tissues Clomid can block the ability of estrogen to bind with its corresponding receptor. Its clinical use is therefore to oppose the negative feedback of estrogens on the hypothalamic-pituitary-ovarian axis, which enhances the release of LH and FSH. This of course can help to induce ovulation.

For athletic purposes, Clomid does not offer a tremendous benefit to women. In men however, the elevation in both follicle stimulating hormone and (primarily) luteinizing hormone will cause natural testosterone production to increase. This effect is especially beneficial to the athlete at the conclusion of a steroid cycle when endogenous testosterone levels are depressed. If endogenous testosterone levels are not brought beck to normal, a dramatic loss in size and strength is likely to occur once the anabolics have been removed. This is due to the fact that without testosterone (or other androgens), the catabolic hormone cortisol becomes the dominant force affecting muscle protein synthesis (quickly bringing about a catabolic metabolism). Often referred to as the post-steroid crash, it can quickly eat up much of your newly acquired muscle. Clomid can play a crucial role in preventing this crash in athletic performance. As for women, the only real use for Clomid is the possible management of endogenous estrogen levels near contest time. This can increase fat loss and muscularity, particularly in female trouble areas such as this hips and thighs. Clomid however often produces troubling side effects in women (discussed below), and is likewise not in very high demand among this group of athletes.

Male users generally find that a daily intake of 50-100 mg (1-2 tablets) over a four to six week period will bring testosterone production back to an acceptable level. A very common regime of dosing is; 300 md/day 1, 100 mg/day for days 2-11, and 50 mg/day for days 12-21. This raise in testosterone should occur slowly but evenly throughout the period of intake. Since an immediate boost in testosterone is often desirable, many prefer to combine Clomid with HCG (Human Chorionic Gonadotropin) for the first week or two after the steroids have been removed. The kick-start from HCG also helps to restore the normal ability for the testes to respond to endogenous LH, which may be hindered for some time after the cycle is ended due to a prolonged state of inactivity. Once the HCG is stopped, the user continues treatment with Clomid alone. HCG should not be used for longer than two or three weeks though, as the resulting increased testosterone and estrogen levels may again initiate negative feedback inhibition at the hypothalamus. When planning your ancillary drug program, it is also important to remember that injectable steroids can stay active for a long duration. Using ancillary drugs the first week after a long acting injectable like Sustanon has been stopped may prove to be wholly ineffective. Instead, the athlete should wait for two to three weeks, to a point where androgen levels will be diminishing. Here the body will be primed and ready to restore testosterone production.

Clomid and HCG are also occasionally used periodically during a steroid cycle, in an effort to prevent natural testosterone levels from diminishing. In many instances this practice can prove difficult however, especially when using strong androgens for longer periods of time. There is also no exact method for using the two drugs in this manner. Some have experimented by periodically administering small doses of HCG along with one or two tablets of Clomid, perhaps for a few days at a stretch followed by a longer break. An on/off schedule would be implemented; for fear that this combination may lose some effectiveness if used continuously for this purpose. This method of intake may prove to be effective, although it is really much more feasible to stimulate testosterone production after the cycle than to try and maintain it for the long duration during.

In addition to helping with the post-cycle testosterone crash, this drug can also help with elevated estrogen levels during a steroid cycle. A high estrogen bevel puts an athlete in serious risk of developing gynecomastia, which is an obvious unwanted side effect. With the intake of Clomid, the athlete can hopefully reduce his risk for developing gynecomastia. The estrogen “blocking” properties of Clomid appear to be slightly weaker than Nolvadex in comparison however, which is why it is not usually thought of as an equal substitute for estrogen maintenance. Of course both drugs have similar actions in the body and are relatively interchangeable for this purpose. Clomid can likewise also be used as a maintenance anti-estrogen throughout the duration of steroid cycle with good confidence, just as is done with Nolvadex. In most instances this will prove equally sufficient, the drug effectively minimizing the activity of estrogen in the body and warding off gyno and excess water/fat retention. Unfortunately just as with Nolvadex this is not always the case however, and many find it necessary to addition another anti-estrogenic drug. The most common adjunct is Proviron, an oral DHT used to competitively lower aromatase activity and raise the androgen to estrogen ratio. The Clomid/Nolvadex and Proviron combination is extremely effective, although we could alternately replace them both with a more specific aromatase inhibitor such as Arimidex,Femara, or Aromasin. While stronger at combating estrogen in most cases, these drugs are also typically much more costly.

As for toxicity and side effects, Clomid is considered a very safe drug. Bodybuilders seldom report any problems, but listed possible side effects do include hot flashes, nausea, dizziness, headaches and temporarily blurred vision. Such side effects usually only appear in females however, as they feel the effects of estrogen manipulation much more readily than men. While female athletes can clearly gain some benefit from this substance, estrogen manipulation is probably not the most comfortable way to go about cutting up. Should it still be used for such purposed and side effects do become pronounced, the drug of course is to be discontinued and (at least) a break taken from it.

Clomiphene citrate is widely available on the black market in a variety of brand names as well as generic tabs and liquid versions.

Trenbolone Enanthate – top choice for mucle gains.

If you are looking for a safe, affordable, and highly effective anabolic steroid on the Internet, Trenbolone Enanthate is one name that could not be resisted for long. This is not just because this steroid is used and recommended by successful sportsmen and sport coaches, but also because it helps users attain a sense of “invincibility” without coming in proximity to steroid side effects.

Trenbolone Enanthate is considered to be one of the most popular and successful derivative of Trenbolone. This long-acting version of Trenbolone is highly effective for professional sportsmen striving to leave a mark for themselves in the cutthroat competitive world of today where performance is measured only by results and there is no scope for a single failure.

The chemical name of Trenbolone enanthate is 17beta-Hydroxyestra-4,9,11-trien-3-one and its molecular weight is 270.3706 g/mol at base. Trenbolone enanthate does not lead to Tren cough, which is a common complication experienced by steroid users experimenting with Tren derivatives. It has an exceptional anabolic/androgenic ratio of 500:500, which means that it is five times potent as testosterone.

One of the best things about Trenbolone enanthate is that the entire process of muscle building can be undertaken in a smooth and safe mode in as short as 2-4 weeks. When used in doses of 300-600 mg/week by men for 6-8 weeks, Trenbolone enanthate demonstrates its real power. This drug is not indicated (recommended) to girls and women, especially pregnant and breastfeeding women, and those having an existing allergy to the drug or any of its ingredients.

A Basic guide to Human Growth Hormone (HGH)

Human Growth Hormone (somatotropin – also referred to as rHGH, HGH, or GH) is created by the pituitary gland, the primary form consisting of a 191 amino acid chain. When we are young, HGH is in big part responsible for the proper growth of bones, muscle, and other tissues. Too little of this hormone and we remain dwarfs too much and we become giants and/or suffer from abnormal growth deformities. As we become adults, HGH is responsible for keeping muscles from wasting away, supports healthy immune system response, regulates aspects of our metabolic function dealing with increased fat metabolism and healthy body composition in later life, and maintains and repairs our skin and other tissues.

Our levels of HGH peak while we are adolescents and then begin to drop off sharply beginning in our 30’s. By our 60’s, our daily HGH secretion can be as little as 10% of what it was during our youth. Many of the markers of aging are affected by this decrease in HGH. Some of the results of this are:

• Increase in fat.
• Decrease in muscle and lean body structures.
• Decreased skin texture resulting in a less youthful appearance.
• Decreased bone density, onset of osteoporosis.
• Decreased brain function, loss of intellect with aging.
• Decreased sex drive.
• Decrease in overall physical and mental well being.
• Increase in sleep disorders, lower quality of sleep.
• Depression and fatigue.

The addition of supplemental HGH beginning in the latter 30’s can reverse or improve these symptoms in the majority of people attempting therapy. This is why you will often hear references with respect to HGH as “the fountain of youth” and other similar terms. It can present a better quality of life for those aging.

HGH is secreted from the pituitary in a pulsatile fashion, generally following a circadian rhythm. A number of stimuli can initiate an HGH secretion, the most powerful being short duration, high intensity exercise and sleep. During the first few hours of sleep (deep sleep stages – about 2 hours after you fall asleep), Somatostatin is turned off and GHRH is turned on, resulting in HGH pulses.

Growth Hormone Releasing Hormone (GHRH) produced by the hypothalamus stimulates HGH secretion. HGH, and IGF-1 create a negative feedback loop, meaning when their levels are high; it blunts release of GHRH, which in turn blunts the release of more HGH.

Somatostatin (SS), secreted by the hypothalamus as well as other tissues inhibits the secretion of HGH Somatostatin in response to GHRH and to other stimulatory factors such as low blood glucose concentration. High levels of IGF-1 also stimulate Somatostatin secretion.

Ghrelin is a peptide hormone secreted from the stomach. Ghrelin binds to receptors on somatotrophs and potently stimulates secretion of growth hormone. Ghrelin, as the stimulator for the growth hormone secretagogue receptor, potently stimulates secretion of growth hormone. The ghrelin signal is integrated with that of growth hormone releasing hormone and somatostatin to control the timing and magnitude of growth hormone secretion.

Once HGH is released, it is very short lived. It is generally metabolized and gone within a half-hour. During this half-hour, it travels to the liver and other tissues and induces them to secrete a polypeptide hormone called Insulin-like Growth Factor One (IGF-1).

As mentioned above, HGH is short lived, but during its short half-hour or so activity per burst from the pituitary, it exerts itself through direct and indirect effects.

Its direct effects are the result of the HGH binding its receptor on target cells. Fat cells (adipocytes) as well as myocytes (muscle cells) have HGH receptors. On fat cells, HGH stimulates them to break down triglyceride and suppresses the fat cells ability to uptake circulating lipids.

Its indirect effects are in the process we described in the section above. When HGH travels to the liver, one of the results of its pass through the liver is the livers secretion of IGF-1. When this IGF-1 is secreted, it stimulates proliferation of chondrocytes (cartilage cells), which result in bone growth. It also plays a part in stimulating both the proliferation and differentiation of myoblasts (the precursor to skeletal muscle fibers). IGF-1 also stimulates amino acid uptake and protein synthesis in muscle and other tissues. Other tissues (muscle, etc.) are acted on by the presence of HGH, also inducing their release of IGF-1.

HGH stimulates protein anabolism in many tissues. This reflects increased protein synthesis, decreased oxidation of proteins, and increased amino acid uptake. As mentioned above, HGH enhances fat utilization by stimulating triglyceride breakdown and oxidation in fat cells (adipocytes).

HGH can affect the function of other hormones. HGH can suppress the abilities of insulin to stimulate the uptake of glucose in tissues and enhance glucose synthesis in the liver, though administering HGH actually stimulates insulin secretion and can create a state of hyperinsulinemia. This combination can lead to decreased insulin sensitivity, which in turn can lead to hyperglycemia. HGH can in the right circumstances also have a slight inhibitory effect on the function of our thyroid hormones (and actually vice versa as well), though this varies greatly from individual to individual. The vast majority of users have no need to worry about this at all. Others wishing to increase their metabolism or enhance certain of HGH’s functions may wish to consider low dose thyroid to their HGH cycle. We’ll offer some strategies later in this guide.

So, we are looking at a hormone that can assist with maintenance and healing of most of the body’s systems, can create new cartilage, bone, and muscle cells, can assist with protein uptake, decrease the oxidation of proteins, and can accelerate the rate at which fat is utilized. This paints the picture of the excitement that follows HGH. How then do we utilize this to our advantage? Let’s take a look at some strategies.

There are a few strategies for increasing your own endogenous production of HGH. For the most part these aren’t going to give us a significant enough increase that would be necessary to promote all of the benefits mentioned above in their full measure, but for some (those still young) they will prove to be sufficient.

By adding several grams of Arginine and Glutamine to our daily supplement program, we can increase our levels of HGH. If we are very young or we are only in need of a modest jump in production, this may well do the trick. Short duration, high-intensity exercise (think heavy leg day – puking and all), will trigger our bodies to secrete a significant amount of HGH

Another possibility is to inject various related hormones or peptides. There are many available, such as GHRH, GHRP (and all of its analogs), and the like. These peptides are available from research companies and when injected at doses of 100mcgs per day, sub-q it does seem to show promise in increasing levels of HGH. At this stage the game, there isn’t a significant cost advantage to this over rHGH, but if we are trying to promote some of the other forms of HGH in addition to the primary form, or have no hope of securing a prescription for HGH (or other means of access) there may be an advantage to this course of action. Aside from these strategies, what are we left with? To state it simply, we need to inject exogenous rHGH.

True HGH only comes in the form of a lyophilized powder. Any other form that you see advertised or run across is NOT the real deal. The only way to administer true HGH is by sub-q or intramuscular injection. You will see studies that use IV as their method of administration, but that is certainly NOT recommended (in fact it is just outright crazy), nor necessary in any way for getting all of the benefits HGH has to offer.

HGH is somewhat fragile by nature, and it needs to be protected from light and heat. HGH should be stored between 36 and 46 degrees Fahrenheit at all times both before and after its reconstitution.

There are a couple of American brands of HGH that can survive in normal room temperature for a reasonable amount of time BEFORE reconstitution  but for the most part it is better to err on the side of safe rather than sorry. All brands of HGH should be refrigerated after being reconstituted, and all brands should be protected from light at all times.

How Is Testosterone Deficiency “low T” Diagnosed?

Testosterone deficiency, popularly known as “low Testosterone”, has entered the center stage in both the lay and medical communities. However, how is Testosterone deficiency (a.k.a. hypogonadism) diagnosed? What is the testosterone level threshold below which you can say you have low Testosterone? What are the references ranges for healthy men?

The Endocrine Society clinical practice guideline recommends making a diagnosis of Testosterone deficiency only in men with consistent symptoms and signs, who also have unequivocally low blood Testosterone levels. They recommend Testosterone therapy for men with symptomatic androgen deficiency, with the goal to improve their sexual function, sense of well-being, muscle mass and strength, and bone mineral density.

The Endocrine Society clinical practice guideline is against starting testosterone therapy in patients with:

• Prostate cancer or prostate-specific antigen (PSA) greater than 4 ng/ml or greater than 3 ng/ml in men at high risk for prostate cancer (such as African-Americans or men with first-degree relatives with prostate cancer without further urological evaluation).
• Hematocrit greater than 50%.
• Severe lower urinary tract symptoms with International Prostate Symptom Score (IPSS) above 19.
• Uncontrolled heart failure.

When Testosterone therapy is instituted, we suggest aiming at achieving Testosterone levels during treatment in the mid-normal range with any of the approved formulations, chosen on the basis of the patient’s preference, consideration of pharmacokinetics, treatment burden, and cost. Men receiving Testosterone therapy should be monitored.

The normative reference ranges for total and free Testosterone levels in healthy young men vary among assays and laboratories. While variation between laboratories for the same Testosterone assay (analytical method) is negligible, it should be noted that reference intervals for Testosterone (as well as LH and FSH) differ widely and significantly between assays.

In some laboratories, the lower limit of the normal range for total Testosterone level in healthy young men is 280–300 ng/dl (9.8–10.4 nmol/liter), and the lower limit of the normal range for free Testosterone level (measured by the equilibrium dialysis method) is 5–9 pg/ml (0.17–0.31 nmol/liter).

According to the medical guidelines, clinicians should use the lower limit of the normal range for healthy young men established in the specific assay that is used.

However, it should be noticed that many assays have established Testosterone reference ranges that were compiled from small convenience samples of subjects, and frequently used unreliable laboratory analytics based on the immunoassay technique, whose accuracy, particularly in the low range, has been questioned. Importantly, the immunoassay technique, which is the most widely used method for measuring total Testosterone levels, overestimates true levels and has very limited accuracy at levels below 300 ng/dl. Another study found that over 60% of the samples tested (with Testosterone levels within the adult male range) measured by most commercial assays had a spread of up to +/- 20% of those reported by LC-MS (liquid chromatography mass spectrometry), which is the gold standard Testosterone analytical method.

Table 1 shows reference ranges for total and free Testosterone levels, established in a large population of healthy young men aged 19-40 years and older men aged 70-89 years, using the gold standard LC-MS analytical method.

The first thing to note when comparing the reference ranges between young and older men is the dramatic decline Testosterone levels. Total Testosterone levels in older men are about 40-50% lower than that of younger men. Free Testosterone levels drop even more with age. This data confirms findings from previous studies which have shown that as men get older, levels of free (or bio-available) Testosterone decline at a faster rate than total Testosterone levels.

According to the approach used for defining reference limits for biological parameters, total and free Testosterone values below the 2.5th percentile (approximately 2 SD [standard deviations] below the mean) are deemed low. For total and free Testosterone in young men, this corresponds to 348 ng/dL and 70 pg/mL, respectively. The same applies to defining the high end of the reference limit (approximately 2 SD above the mean). For total and free Testosterone, this corresponds to 1197 ng/dL and 230 pg/mL, respectively.

As table 1 shows, the normal range for both total and free Testosterone is large, going all the way up to 1322 ng/dL in young men. This means that there is a lot of room for expression of different health outcomes when contrasting the low end with the high end of the normal range. In other words, it is very likely that being in the low end will have very different health consequences vs. being in the high end.

Symptoms

As stated by the US Endocrine Society, and also by European medical organizations, the diagnosis of Testosterone deficiency requires the presence of symptoms and signs suggestive of Testosterone. Table 2 lists symptoms and signs suggestive of androgen deficiency in men, according to the Endocrine Society.

TABLE 2. Symptoms and signs suggestive of androgen deficiency in men.

More specific symptoms and signs of low-Testosterone

• Reduced sexual desire (libido) and activity
• Decreased spontaneous erections
• Loss of body (axillary and pubic) hair, reduced shaving
• Very small or shrinking testes
• Inability to father children, low or zero sperm count
• Low bone mineral density
• Hot flushes, sweats

Other less specific symptoms and signs of low-Testosterone

• Decreased energy, motivation, initiative, and self-confidence
• Feeling sad or blue, depressed mood, dysthymia
• Poor concentration and memory
• Sleep disturbance, increased sleepiness
• Mild anemia (normochromic, normocytic, in the female range)
• Reduced muscle bulk and strength
• Increased body fat, body mass index
• Diminished physical or work performance

Questionnaires

Several questionnaires are available to help doctors make a diagnosis of Testosterone deficiency according to the current medical clinical guidelines. The Androgen Deficiency in Aging Men (ADAM) and the Aging Male Survey (AMS) questionnaires are two examples. Table 3 shows what you will get asked in the ADAM questionnaire.

Table 3: The Androgen Deficiency in Aging Males (ADAM) questionnaire.

1. Do you have a decrease in libido (sex drive)?
2. Do you have a lack of energy?
3. Do you have a decrease in strength and ⁄ or endurance?
4. Have you lost height?
5. Have you noticed a decreased enjoyment of life?
6. Are you sad and ⁄ or grumpy?
7. Are your erections less strong?
8. Have you noticed a recent deterioration in your ability to play sports?
9. Are you falling asleep after dinner?
10. Has there been a recent deterioration in your work performance?

If the answer is ‘yes’ to question 1 or 7, or at least 3 of the other questions, you might have a low Testosterone level.

While the ADAM and AMS questionnaires may be useful rough screening tools to screen for hypogonadism across the adult male lifespan, it should be noted that they (like all other questionnaires) are non-specific, i.e. lack diagnostic accuracy. In other words, a man who doesn’t fulfill the criteria can still have low Testosterone levels, and vice versa, a man who does fulfill the criteria can have Testosterone levels in the normal range. Therefore, the symptoms and signs related to lowTestosterone levels are only suggestive, not diagnostic of hypogonadism.

Stretch and anabolic steroid combination produces muscle growth

Imagine: an injury means you can’t train for a while, but you can use anabolic steroids. In this hypothetical situation you can maintain more muscle mass by doing stretch exercises. You may even be able to build up a little bit of muscle mass, according to an new animal study.

The researchers, who work at Kagoshima University in Japan, gave rats Methenolone  in a dose of 20 mg/kg bodyweight. The human equivalent of this dose is about 200-300 mg. The researchers injected the steroid directly into the small intestine. A control group was given no methenolone.

The rats were sedated, which meant that the researchers could stretch the animals’ right-hand gastrocnemius muscle. They did this 15 times a minute for 15 consecutive minutes. The researchers did nothing with the left-hand gastrocnemius.

Twenty-four hours later the Japanese observed that the combination of stretches and the anabolic steroid had boosted the synthesis of Mechano Growth Factor.  Mechano Growth Factor is a stripped down version of IGF-1. Fundamental research has shown that the anabolic effect of MGF is so strong that the researchers are convinced that the combination brings about muscle growth.

The researchers also looked at the synthesis of the anabolic signal proteins Myo-D and myogenin, but found no effect.

“Mechanical stimulation of skeletal muscle in conjunction with the administration of an anabolic steroid induced mRNA expression of Mechano Growth Factor.”, the researchers conclude. “This finding suggests that the combination of anabolic steroids with muscle stretching exercise could promote muscle strengthening in patients with muscle weakness.”

The reason that the researchers don’t attach so much importance to the absence of an effect of the stretch-methenolone combination on Myo-D and myogenin is probably to be found in an animal study. In that study the researchers used no steroids. In one group of experimental animals the researchers kept the right gastrocnemius muscle stretched for 15 minutes and did nothing with the left gastrocnemius.

In another group of rats the researchers stretched the right gastrocnemius 15 times a minute for a period of 15 minutes and did nothing with the left gastrocnemius. This is also the protocol that the researchers used in the experiments when they gave the rats methenolone.

At the end of the week the researchers observed an increased synthesis of Myo-Dand myogenin in the  group. Apparently muscle cells subjected to stretching need longer than a day to boost the production of Myo-D and myogenin.

“In conclusion, passive stretching for a short duration once daily at several days within a 1-week period is effective in the growth of the skeletal muscle”, the researchers conclude in the older study. “Repetitive stretching is suggested to have greater effects than continuous stretching. These findings suggest that passive stretching is useful in the prevention and maintenance of skeletal muscle tone in patients who are unconscious or paralyzed.”