T Nation

A new biotest supp??

Discovery could put exercise gurus out of business

WASHINGTON (AP) - It’s a couch potato’s dream: Instead of sweating and straining, people someday may simply pop a pill to get in shape, say researchers who have identified how muscle cells get stronger from regular exercise.

Researchers at Duke University and the University of Texas Southwestern Medical Center have found the chemical pathway that muscle cells use to build up their strength and endurance.

With that basic knowledge, it may now be possible to develop a pill that pumps up muscle cells without all that exercise, said Dr. R. Sanders Williams, dean of the Duke University of School of Medicine.

But the main target of the research is to help people with heart disease or other conditions that keep them from doing enough exercise to remain healthy, Williams said. “This could lead to drugs that will let people get the health benefits of regular exercise, even if they cannot exercise.”

That could improve the health of patients with heart or lung disease, or could lower the risk of Type II diabetes, for instance.

In the study, Williams and his colleagues created a group of mice with genes that over-expressed a signaling protein called calmodulin-dependent protein kinase, or CaMK. When this signaling protein is activated, it and another protein, calcineurin, trigger the physical changes that muscle cells undergo after intense exercise.

Williams said mice with a high level of CaMK expression developed more mitochondria in muscle cells and saw an increase of a type of cell called the “slow twitch” muscle. Those muscle cells power sustained activity, such as required by marathon runners.

The researchers found that mice with high levels of CaMK developed the same healthy muscle cells as mice that did exercise.

“The effect increases more of the slow twitch muscles, but it also increases the number of mitochondia in the fast twitch muscle cells,” he said. “That is very similar to what happens in very intense training.”

Mitochondria are structures inside a cell that provide energy by metabolizing oxygen and nutrition. Cells with many mitochondria can produce more work over a longer time. Physical training increases the number of mitochondria in muscle cells.

Here’s a link to the article on CNN if anyone cares to look at it. Today’s news.

www.cnn.com/2002/HEALTH/diet. fitness/04/11/couch.potato.pill.ap/index.html

i seriously hope that a product like that will never make it to the market. if they do make a product like that and it works, then you will have every non t-man and woman in existence tossing in their electric ab belts and buying that shit and thinking that they are in great shape while they still eat their potatoe chips and snickers bars. plus it will discourage all of the non-dedicated people in the gym to quit and just take some pill that they think will work just as good. also, from that article, it doesn’t seem like there would be an visual impacts a product like that would have on someones body. seems like it would just improve endurance a little bit. i can allready see it now on the paid for advertisements on the TV, “are you tired of working out. spending meaningless hours in the gym and actually having to sweat. well stop! yes thats right. for only 2 easy payments on 19.99 we will send you a 30 day supply of the revolutionary workout pill. you get the same benefits of working out without having to go to the gym. the cost of a gym membership alone can range anywhere up to $99 a month. but wait, theres more. call now and we will send you another 30 day supply for FREE. thats a 60 day supply for only 2 payments of 19.99…” then they will have some “fitness expert” claiming how they hav never seem a product work this great before and how they wish they had the product 10 years ago.

Fuck that headline. Laziness will be the end of our civilization. I do hope, though, that myostatin medication can be used to help those suffering from legitimate diseases.

It sounds like Duke University must have bought a bottle of Myostat. Biotest gurus, how does this work differently than Myostat? Does Myostat have the same potential benefit to the heart and lungs that Duke’s new discovery may have?

Do you really want to change all of your muscles to a slow twitch phenotype? I haven’t read the study yet, since I won’t get this copy of Science until next week, but for a bodybuilder or power athlete, this is the last thing you would want to do. You are tricking the muscle into thinking that you have been doing ultraendurance work. So, the ability to hypertrophy will be compromised. What they don’t talk about in the press clipping is the myosin ATPase change that you will likely see, as well as ultrastructural characteristics of the sarcomere that will be different with the slow twitch phenotype. None of these things would be desirable for someone trying to achieve maximal hypertrophy or strength. Further, you won’t get the central adaptations of increased cardiac output and stroke volume that are beneficial to cardiovascular health as well as making the muscle look more vascular and full. So, I don’t see much upside for the couch potato, or the power athlete. Where it would be of benefit would be to endurance athletes who could achieve muscular adaptations equivalent to training 30 or more hours per week, while conceivably only training 10-15. Just postulating, but this would certainly be of great value to endurance athletes. I imagine it might also be an effective fat loss agent for the obese as the increased mitochondria density would increase caloric expenditure and fat oxidation capacity. We’ll see.

There goes the world. Laziness will be what brings down the greatest country in the history of man.

I read a different version of this story, and
apparently the researchers did find some
mitochondrial adaptation in Type I fibers,
but there was much more adaptation in the Type II. But agreed, nothing to write home about for the strength athlete.

If you have an increase in the number of mitochondria in a type II fiber, it is likely being converted from a type IIb to a type IIx or IIa. Which is again a slower phenotype. It may be more complicated because mice exhibit the extra type II fiber compared to humans (e.g. humans type IIx and IIa vs. mice IIb, IIx, and IIa). I look forward to reading the study, but CaMK therapy still ain’t gonna replace working out. Although look at all the people on type II diabetes drugs right now, when all they have to do is walk around the block and cut out some sugar. So, what do I know.

Too me this is like nothing any of us will ever use or want to. I mean even if you could cause muscle damage with a pill that mimics exercise induced damage your still not getting any CNS adaption. Plus all the hormone release during exercise. Stupid stupid stupid. Maybe for ill patients it might hold some promise. :slight_smile: