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How to Keep Your Muscles Strong with a Pill
« on: June 29, 2007, 03:32:26 PM »
howtokeepthebigmuscleswhz7 - How to Keep Your Muscles Strong with a Pill - Science and Research


How to Keep Your Muscles Strong with a Pill - Scientists try to stop muscle wasting
By: Stefan Anitei, Science Editor - Softpedia


You go to the gym, train hard for some months, but – holly s**t – you must pump iron for life to keep looking like that. A drug stopping the dismantling of the muscles would be your dream product to get rid of the gym for a while.

As soon as we stop exercising, muscle proteins start melting; idle muscles just keep a high metabolism without any use. When food and exercising are constant, while muscle growth and breakdown are in a subtle equilibrium. Lack of exercise and starvation do not necessarily induce muscle atrophy (wasting), but also microgravity in the case of astronauts, and many conditions like kidney failure, cancer and AIDS. Once the muscle is lost, exercising turns more difficult, and a vicious cycle is created.

Anabolic steroids could stop the atrophy, but they have undesirable side effects (impotence for example) and still require exercising.

Researchers found that muscle atrophy is an active process induced by a complex of genes, so that they focus on shutting it off to stop muscle wasting. The process uses the ubiquitin-proteasome pathway (UPP), employed to break down unwanted proteins in the cell. Tagged proteins are chopped by proteasomes into their component amino acids, which are reused.

Muscle proteic filaments within cells are melted,
but the number of muscle cells stays the same, they just get thinner and weaker. At least 90 genes, called atrogenes, are linked to atrophy. Atrogin1 and muRF1, were found in 2001 and are the only two atrogenes active just during muscle atrophy. They encode ubiquitin ligases, the enzymes that tag the proteins to break down.

Their activity is almost zero in normal muscles, but booms in sick animals; when shut off, the atrophy stops, after both disuse and disease.

A group from Purdue University in West Lafayette, Indiana, discovered increased activity of the gene erg1 in mice experiencing muscle atrophy. This gene encodes a potassium channel protein encountered in both skeletal and cardiac muscle. In heart muscle, the channel presents two varieties, erg1a and erg1b, which help the heart maintain its rhythm by letting the muscle repolarize after each beat.

A mutated erg1 induces "long QT" syndrome, when the heart muscle cannot repolarize fast enough, situation in which sudden heart failure can occur, erg1a was found responsible for the appearance of atrophy. An existing antihistamine drug, astemizole, inactivates erg1a channels and has anti-atrophy effects in mice, and in healthy animals, muscles even grew bigger. Erg1a could be involved in the ubiquitin-proteasome pathway, but it is not known precisely how.

Still, the astemizole not only shut off erg1 channels in skeletal muscle, but also in the heart, inducing long QT syndrome, and it was withdrawn in 1999.

In 2004, a team led by Alfred Goldberg, a cell biologist at Harvard University, focused on gene controllers, like Foxo that drive the activity of many atrogenes. When Foxo is turned off, atrophy stops.

Another issue: insulin and insulin-like growth factor 1 (IGF-1), involved in muscle synthesis, can also impede muscle breakdown by inhibiting Foxo and the atrogin1 gene. Rising levels of IGF1 significantly increased the mice’s strength, even when they did not exercise. That's why both IGF-1 and insulin are banned, being considered doping drugs in sports. "You don't see active Foxo in normal muscle because insulin and IGF-1 suppress it, but exactly how inactivity or disease activates Foxo we're still trying to find out." said Goldberg.

Foxo could be connected to the erg1a-mediated atrophy. Several companies are developing researches for drugs that stop the atrogin1 protein, and proteasome inhibitors like Velcade, employed in cancer, that could speed down muscle atrophy.

A drug against muscle atrophy would be beneficial for patients who have to stay in bed for days, easing their recovery. Weaning patients off respirators would become easier as the diaphragm would not be weakened. Disease or broken bone would not necessarily cause weakness, and long physiotherapy treatments. Aging people too would benefit from these drugs which could prolong their independent life.

NASA funds many of these researches: on a trip to Mars, astronauts would lose about 25 % of their muscle mass and would be too weak to perform any operation there.

Of course these drugs will be extremely tempting for athletes for doping, but for couch potatoes, too.
Of course, the effects are different from those that come after training, which has also other physiological effects like better blood supply to muscles, more mitochondria – that "fuels" all the burnings in the body, inside the muscle cells – stronger bones, and better brain circulation.

Still, skipping gym for a few weeks would rather encourage people to go to the gym, as restarting a training schedule would be less painful.

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"All that is needed for evil to succeed is, that decent human beings doing nothing". (Edmund Burke)



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