Gingergrrl
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http://www.nytimes.com/2008/02/12/health/research/12musc.html?_r=1
The bolded parts are mine. I learned of this article from another group that I belong to and got permission to post it here. Am curious how this relates to ME/CFS especially in light of having a calcium channel auto-antibody. In the athletes, the cells are leaking calcium, and in someone like me, calcium is being blocked from entering the cell by an auto-antibody but maybe the mechanism (or consequence?) of shortness of breath, muscle weakness, pain, etc, is the same? Whether due to leaking or being blocked, the outcome is less calcium inside the cell if I am understanding this correctly? Would love to hear any thoughts on this and I think this med is experimental and not something available to try.
ETA: Click link to read the full article
The bolded parts are mine. I learned of this article from another group that I belong to and got permission to post it here. Am curious how this relates to ME/CFS especially in light of having a calcium channel auto-antibody. In the athletes, the cells are leaking calcium, and in someone like me, calcium is being blocked from entering the cell by an auto-antibody but maybe the mechanism (or consequence?) of shortness of breath, muscle weakness, pain, etc, is the same? Whether due to leaking or being blocked, the outcome is less calcium inside the cell if I am understanding this correctly? Would love to hear any thoughts on this and I think this med is experimental and not something available to try.
For decades, muscle fatigue had been largely ignored or misunderstood... In a report published Monday... Dr. Marks says the problem is calcium flow inside muscle cells. Ordinarily, ebbs and flows of calcium in cells control muscle contractions. But when muscles grow tired, the investigators report, tiny channels in them start leaking calcium, and that weakens contractions. At the same time, the leaked calcium stimulates an enzyme that eats into muscle fibers, contributing to the muscle exhaustion.
The new work in mice, Dr. Brooks said, “is exciting and provocative.” It is a finding that came unexpectedly from a very different line of research. Dr. Marks, a cardiologist, wanted to discover better ways to treat people with congestive heart failure... In his efforts to understand why the heart muscle weakened, Dr. Marks focused on the molecular events in the heart...
The intensified contractions, Dr. Marks and his colleagues discovered, occurred because the hormones caused calcium to be released into the heart muscle cells’ channels. But eventually the epinephrine and norepinephrine cannot stimulate the heart enough to meet the demands for blood. The brain responds by releasing more and more of those fight or flight hormones until it is releasing them all the time. At that point, the calcium channels in heart muscle are overstimulated and start to leak.
When they understood the mechanisms, the researchers developed a class of experimental drugs that block the leaks in calcium channels in the heart muscle. The drugs were originally created to block cells’ calcium channels, a way of lowering blood pressure. Dr. Marks and his colleagues altered the drugs to make them less toxic and to rid them of their ability to block calcium channels. They were left with drugs that stopped calcium leaks. The investigators called the drugs rycals... The investigators tested rycals in mice and found that they could prevent heart failure and arrhythmias in the animals...
ETA: Click link to read the full article
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