BCAAs For Endurance

 Parece que se confirma e o uso de BCAA durante o treino é benéfico



It's got a bit snowed under by all the recent studies in which BCAAs inhibit muscle breakdown during intensive exertion, but originally supplements manufacturers brought BCAAs onto the market at an energy supplement for athletes. They were on the right track, according to an animal study by amino-acid producer Ajinomoto from 2006, which showed that rats given extra BCAAs, glutamine and arginine voluntarily clock up more metres on a treadmill.

Physical exertion causes muscle to convert amino acids into energy. To do this the muscle cells use BCAAs, branched-chain amino acids, where possible. For the enzymes involved in energy provision, the branched side chain is like a handle: it gives them a better grip.

Because of this, taking BCAAs before and during a training session reduces muscle breakdown. The muscle cells convert the additional BCAAs into energy, thus saving the BCAAs in the muscle proteins. Another ergogenic effect of BCAA supplementation is that it reduces fatigue. The mechanism here is a little more complicated.

When muscles are active they absorb BCAAs from the blood. They don't absorb the amino acid L-tryptophan, so tryptophan molecules remain in the blood. The brain also absorbs amino acids from the blood, but the amount of amino acids that reach the brain is limited. If physical exertion reduces the amount of BCAAs in the blood, then the amount of tryptophan molecules that reach the brain increases. Enzymes convert tryptophan there into the neurotransmitter serotonin. A peak in brain serotonin levels during training causes drowsiness and fatigue.

So the remedy for tiredness is obvious: make sure there are more BCAAs in the blood.

The researchers wanted to test this theory, so they gave a group of rats feed containing two percent BCAAs. A control group was given food containing extra glutamine. The rats had a treadmill in their cage. The Japanese recorded the number of metres the rats ran on the treadmill and they saw that the BCAA group became more active.



In another experiment the researchers gave the rats two bottles of drinking water in their cage. One bottle contained ordinary water and the other contained a solution of BCAAs, L-glutamine and L-arginine. The water contained per litre 15.2 mmoles L-leucine, 9.9 mmoles L-isoleucine, 11.1 mmoles L-valine, 16.6 mmoles L-glutamine and 13.9 mmoles L-arginine.

As the experiment progressed, the rats drank more of the water that contained amino acids and less of the ordinary water. At the same time they ran further on the treadmill.



In another experiment, water with amino acids added prevented the concentration of serotonin in the brain from increasing as a result of physical exertion. In that experiment the rats had to run for 55 minutes in a treadmill, after which they were given 8 ml water – with and without amino acids.



In the lateral hypothalamus [LH] of the rats that had been given extra amino acids, less serotonin was released than in the rats that drank ordinary water.

Why Diets Don't Work: Starved Brain Cells Eat Themselves, Study Finds

ScienceDaily (Aug. 3, 2011) — A report in the August issue of the Cell Press journal Cell Metabolism might help to explain why it's so frustratingly difficult to stick to a diet. When we don't eat, hunger-inducing neurons in the brain start eating bits of themselves. That act of self-cannibalism turns up a hunger signal to prompt eating.

"A pathway that is really important for every cell to turn over components in a kind of housekeeping process is also required to regulate appetite," said Rajat Singh of Albert Einstein College of Medicine.
The cellular process uncovered in neurons of the brain's hypothalamus is known as autophagy (literally self-eating.) Singh says the new findings in mice suggest that treatments aimed at blocking autophagy may prove useful as hunger-fighting weapons in the war against obesity.
The new evidence shows that lipids within the so-called agouti-related peptide (AgRP) neurons are mobilized following autophagy, generating free fatty acids. Those fatty acids in turn boost levels of AgRP, itself a hunger signal.
When autophagy is blocked in AgRP neurons, AgRP levels fail to rise in response to starvation, the researchers show. Meanwhile, levels of another hormone, called -melanocyte stimulating hormone, remain elevated. That change in body chemistry led mice to become lighter and leaner as they ate less after fasting, and burned more energy.
Autophagy is known to have an important role in other parts of the body as a way of providing energy in times of starvation. However, unlike other organs, earlier studies had shown the brain to be relatively resistant to starvation-induced autophagy.
"The present study demonstrates the unique nature of hypothalamic neurons in their ability to upregulate autophagy in response to starvation that is consistent with the roles of these neurons in feeding and energy homeostasis," the researchers wrote.
Singh said he suspects that fatty acids released into the circulation and taken up by the hypothalamus as fat stores break down between meals may induce autophagy in those AgRP neurons. Singh's research earlier showed a similar response in the liver.
On the other hand, he says, chronically high levels of fatty acids in the bloodstream, as happens in those on a high-fat diet, might alter hypothalamic lipid metabolism, "setting up a vicious cycle of overfeeding and altered energy balance." Treatments aimed at the pathway might "make you less hungry and burn more fat," a good way to maintain energy balance in a world where calories are cheap and plentiful.
The findings might also yield new insight into metabolic changes that come with age given that autophagy declines as we get older. "We already have some preliminary evidence there might be changes with age," Singh said. "We are excited about that."

A Possible Cure for Age-Related Muscle Loss?

Ever notice – as you grow older – that things just seem to get heavier? Ever watch a person of advanced age struggle to hoist a carry-on bag into the overhead compartment of an aircraft?

As we age, our muscles become weaker. It starts at around age 40 and progresses until 75, when muscle strength pretty much falls off a cliff.

Doctors recommend exercise to counter the loss, but it inevitably progresses. Some people have tried hormone supplements – testosterone, human growth hormone and insulin-like growth factor-1 to hold off Mother Nature. But the long-term safety of those therapies is in question.

Exciting new research released Tuesday by doctors at Columbia University Medical Center may have found a novel new way to prevent age-related muscle weakness. Dr. Andrew Marks has been targeting something called the “ryanodine receptor” in muscle cells.

Without getting too complicated, muscle cells use calcium to contract. Each cell has a little “gas tank” of calcium in it. When the brain sends a signal to the muscle to contract, the ryanodine receptor acts like a fuel pump and releases calcium into the cell, where it’s used to pull muscle fibers together. When the brain tells the muscle to relax, the receptor pumps calcium back into the tank, and the fibers separate.

As we age, the mechanism becomes damaged from stress and allows an unusual amount of calcium to leak out of the cell. Think of it in terms of a rusty old gas tank developing a small leak. Eventually enough calcium (gasoline) leaks out that the muscle (car) can’t function properly.

Basically, the muscle runs out of gas and over time, withers away.

Using a new drug (s107) developed by pharmaceutical startup ARMGO Pharma, Marks treated mice that were 24 months old – the equivalent of 70 in human years. The mice, which were becoming weak and sedentary could spend 50 percent more time on the exercise wheel than before. The drug had slowed the calcium leak in their muscles and improved muscle function.

So – how is this different from exercise or hormone treatments? Dr. Marks says they build muscle mass. But they don’t necessarily improve muscle function the way this drug does.

What if people didn’t wait until old age to begin treatment? What if the drug was used as a preventive beginning at say – age 50? Could age-related muscle loss be prevented altogether? 

Marks said that’s very possible.

There’s another aspect of Marks’ research that is very interesting. Age-related muscle weakness occurs by much the same mechanism as muscular dystrophy in children. As people grow old, they literally acquire a form of MD.

Which begs a question. If the drug reverses some of the effects of age-related muscle loss, could it be a possible treatment for Muscular Dystrophy? That’s something Dr. Marks told me he is looking into.

He’d also like to see his therapies used in developing countries where heart failure and other age-related muscle conditions go untreated.

The other big question: When could this be available for human use?

The drug is currently in Phase II trials for treatment of heart failure. Dr. Marks says he hopes to begin Phase II trials among people of advanced age for muscle-weakness/loss within a year.

It should also be pointed out that Dr. Marks is a founder of ARMGO Pharma and stands to become a very rich man if the FDA approves this new drug. That said, he is also a noted and well-respected researcher who has received numerous awards and citations for his ground-breaking research.

Read more: http://www.foxnews.com/health/2011/08/02/possible-cure-for-age-related-muscle-loss/#ixzz1UMR2NNzU

100-Year-Olds Just as Unhealthy as the Rest of Us

tenarians may have a great deal of wisdom to share, but this apparently does not include advice on how to live to age 100.

Researchers at the Albert Einstein College of Medicine of Yeshiva University have found that many very old people — age 95 and older — could be poster children for bad health behavior with their smoking, drinking, poor diet, obesity and lack of exercise.

The very old are, in fact, no more virtuous than the general population when it comes to shunning bad health habits, leaving researchers to conclude that their genes are mostly responsible for their remarkable longevity.

But before you fall off the wagon and start tossing down doughnuts for breakfast just because your Aunt Edna just turned 102, remember that genetics is a game of chance. What didn't kill Aunt Edna still could kill you prematurely, the researchers cautioned.

The chosen few

The study, appearing Aug. 3 in the online edition of the Journal of the American Geriatrics Society, followed the lives of 477 Ashkenazi Jews between the ages of 95 and 112. They were enrolled in Einstein College's Longevity Genes Project, an ongoing study that seeks to understand why centenarians live as long as they do. About 1 in 4,400 Americans lives to age 100, according to 2010 census data.

A research team led by Nir Barzilai compared these old folks with a group of people representing the general public, captured in a snapshot of health habits collected in the 1970s. The people in this control group were born around the same time as the 95-and-above study group, but they have since died.

The living, old people in the study were remarkably ordinary in their lifestyles, Barzilai said. By and large, they weren't vegetarians, vitamin-pill-poppers or health freaks. Their profiles nearly matched that of the control group in terms of the percentage who were overweight, exercised (or didn't exercise), or smoked. One woman, at age 107, smoked for over 90 years.

Whatever killed the control group — cardiovascular disease, cancer and other diseases clearly associated with lifestyle choices — somehow didn't kill them. "Their genes protected them," Barzilai said. [10 Easy Paths to Self Destruction]
Put down that doughnut
Barzilai said that it would be wrong to forego health advice with the assumption that your genes will determine how long you will live. For the general population, there is a preponderance of evidence that diet and exercise can postpone or ward off chronic disease and extend life. Many studies on Seventh Day Adventists — with their limited consumption of alcohol, tobacco and meat — attribute upward of 10 extra years of life as a result of lifestyle choices.
Note also that those people now age 100 lived in an era when obesity was nearly nonexistent and when daily exercise such as walking down streets or up a few flights of steps was more common. Barzilai said anyone can benefit from exercise at any age, even these indestructible old people pushing and exceeding triple digits.
The big picture for the Longevity Genes Project is to identify those genes keeping folks alive for so long and then use them as targets for drug development. For example, most people treated successfully for heart disease ultimately die well before their 90s from yet another age-related disease. This is because we "never change the aging process" with our treatments and cures, Barzilai said.
That is, we can't turn everyone into centenarians by curing one disease at a time.

"Aging is the major risk factor," Barzilai said. If researchers can figure out which genes work to slow aging and make ordinary people more resilient to chronic disease, we all will have a much better chance of reaching our 100th birthday — and have enough breath to blow out the candles.

Christopher Wanjek is the author of the books "Bad Medicine" and "Food At Work." His column, Bad Medicine, appears regularly on LiveScience. Follow LiveScience for the latest in science news and discoveries on Twitter @livescienceand on Facebook.

fonte: http://news.yahoo.com/100-olds-just-unhealthy-rest-us-111004075.html