How To Prevent Age Related Muscle Mass

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.

As most are aware, with aging comes a general decline in many hormones, in particular, anabolic hormones such as Growth Hormone (GH), 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 GH declines dramatically with age. In old age, GH levels are only one-third of that in our teenage years. In addition, aging adults have a blunted GH 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 GH, 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.

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.

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.

To summarize, 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.

I’m going to conclude this article the way most people would start it, with the good news and the bad news. The bad news is, millions of people will suffer from a mostly avoidable loss of functionality and will become weak and frail as they age from a severe loss of muscle mass. The good news is that you don’t have to be one of those people. One thing is very clear: it’s far easier, cheaper, and more effective to prevent sarcopenia – or at least greatly slow its progression – than it is to treat it later in life. Studies have found, however, that it’s never too late to start – so don’t be discouraged if you are starting your sarcopenia fighting program later in life. People following my programs for either weight loss or weight gain (in the form of muscle…) will be following the proper guidelines for avoiding sarcopenia.

Immune system molecules may promote weight loss

The calorie-burning triggered by cold temperatures can be achieved biochemically -- without the chill -- raising hopes for a weight-loss strategy focused on the immune system rather than the brain, according to a new study by UC San Francisco researchers.The team determined that two signaling molecules secreted by cells of the immune system trigger the conversion of fat-storing white fat cells to fat-burning beige fat cells. Ajay Chawla, MD, PhD, an associate professor of medicine at the UCSF Cardiovascular Research Institute, led the study.

Working with mice, Chawla's team discovered that the signaling molecules, called interleukin 4 and interleukin 13, activate cells known as macrophages, which in turn drive the fat conversion. In one experiment the researchers gave interleukin 4 to fat mice, which increased beige fat mass, leading to weight loss.

The finding builds on previous work by Chawla's team, which reported in 2011 in Nature that cold activates part of the immune system, and specifically activates interleukin 4 in fat. In the new study, Chawla's team determined that both interleukin 4 and interleukin 13 recruit macrophages to fat and that the production of molecules called catecholamines by the macrophages causes the browning of white fat.

When the researchers inhibited interleukin 4 signaling in white fat, they found that the mice made less beige fat, burned less energy, and could no longer maintain normal body temperature in the cold.

The study results are likely to further fuel the quest to identify new ways to pharmaceutically tame obesity by targeting how much energy we burn, not just how many calories we ingest, according to Chawla."If you could increase energy expenditure by even a few percent, over a period of a year or two year you would make a big difference," he said.

The new discovery is surprising, Chawla said, because it makes it clear that this control mechanism for fat burning bypasses components of the autonomic nervous system that govern many physiological adaptations. "Nutrient and energy metabolism has largely been thought to be under the control of the brain and endocrine system," he said.
In comparison to the nervous system, the immune pathway might be more easily manipulated to increase energy expenditure, Chawla said. In fact, another study published simultaneously in Cell by researchers from the Dana-Farber Cancer Institute and Harvard Medical School reports the identification of a hormone, produced in fat tissue after cold exposure, that activates interleukin 4 and interleukin 13 to drive fat burning.

Humans and other mammals shiver to keep warm, but cold also triggers the growth of fat cells that burn fuel, instead of the fat cells that store it. Keep humans indoors at 61 degrees to 63 degrees Fahrenheit without allowing them to bundle up, and they lose weight, research shows. That's because they adapt by generating more fat-burning cells to help them keep warm.

In contrast to the power-converting mechanisms in white fat cells, the gears in the power plants within fat-burning fat cells spin inefficiently. This causes them to burn more energy and generate heat. The trigger for this accelerated fat burning is the activation within the cell's power plants -- called mitochondria -- of a protein called uncoupling protein 1 (UCP1). Cells with UCP1 are capable of heat generation and fat burning, and are known as brown fat or beige fat, depending on the tissue from which they originate. They have more mitochondria than white cells and therefore have a darker tinge.

In comparison to other mammals, ranging in size from mice to bears, until a few years ago it was widely thought that humans had little brown or beige fat and little potential to generate it.

Although Chawla and many other researchers now believe that the potential to exploit brown fat for weight loss is significant, the amount of individual variation when it comes to brown fat reserves and the potential to generate more brown fat is unclear. "We don't know what the dynamic range is," Chawla said. "It appears that women have more, that we have less as we age, and that obesity is associated with having less brown fat."

Additional UCSF study authors include postdoctoral fellows Yifu Qiu, PhD, Khoa Nguyen, PhD, and Justin Odegaard, MD, PhD; and Richard Locksley, MD, a professor of medicine and Howard Hughes Medical Institute investigator. Richard Palmiter, PhD, professor of biochemistry and Howard Hughes Medical Institute investigator at the University of Washington, also is a co-author of the study. The research was funded by the National Institutes of Health and the American Heart Association.

Sleeping longer makes athletes faster

If athletes force themselves to sleep two hours longer every day, their reaction speed increases and they get faster. Sleep researchers at Stanford University in the US discovered this when they performed experiments with basketball players.

Too little sleep leads to increased body fat, reduced testosterone levels, and decreased oxygen uptake, and animal studies have shown that it leads to muscle decay as well. On top of this, your immune system works better if you get enough sleep, and there are indications that good-quality sleep can extend your life expectancy.

So it’s logical that athletes perform better if they make sure they don’t miss out on sleep. But can athletes improve their performance by going a step further? By making sure they get lots of extra sleep? In 2011 Cheri Mah of Stanford University showed results of a human study that showed this could be the case.

Mah used 11 students from the basketball team for her experiment. She got them to increase the amount of sleep they got to 10 hours a day over a period of 5-7 weeks. Before they started on the ‘sleep extension’ the subjects all slept just under eight hours a day. They thought that this was enough sleep.

Although the textbooks say that eight hours’ sleep is enough, Mah observed that increasing the amount of sleep had a positive effect on the players. She used the Psychomotor Vigilance Task test to measure the players’ reaction times, and discovered that these became faster as a result of more sleep. In the Psychomotor Vigilance Task the subjects look at a black screen. When a point of light appears they have to press a button as fast as possible.

Before starting to sleep longer the athletes had an average of 16.2 seconds for an 86-m sprint. Extending their sleep reduced this to 15.5 seconds.

The subjects also found that they felt better for more sleep: less angry, depressed, stressed, tired and confused, and they had more energy. In addition their aim became better and more accurate.

“This study reveals an athlete’s inability to accurately assess how much sleep one actually obtains each night, thus leading to a misperception regarding the duration of sleep that constitutes adequate nightly sleep time”, the researchers conclude.