Study finds more about athletes' sudden death

Until recently, the sudden death of athletes had puzzled scientists. While they knew that the deaths could be linked to a mutation of the protein myosin -- a molecular motor that produces much of the body's muscle action -- they did not know about how the protein functioned. But in a study directed by H. Lee Sweeney, a physiology professor in the School of Medicine, scientists discovered a way to observe the movement of the protein, giving them a sense of how the death occurs. The study showed a rotating area within the myosin molecule, which is responsible for actions such as heartbeat and eye motion, according to Sweeney. "It's a protein that produces movement in the cell, and most importantly, it's the motor that runs the heart and skeletal system," Sweeney said. Sweeney will continue studying the protein and its mutations, which result in the disease called hypertrophic cardiomyopathy. This disease is the greatest single cause of sudden death among young people and has been linked to the deaths of several prominent athletes. The on-court collapse and death of Loyola Marymount University basketball player Hank Gathers in 1990 was attributed to the disease, and the November death of Olympic gold medal ice skater Sergei Grinkov has been speculatively linked to mutant myosin. And Boston Celtics basketball star Reggie Lewis's death was officially attributed to the disease, despite rumors that it was brought on by drug abuse. Lewis collapsed on-court during a game two years ago and later died while preparing to return to the team. Sweeney said the mutant myosin reduces the heart's pumping ability. In order to counteract the slower rate, the heart enlarges, ultimately blocking blood flow to the heart and causing death. "These mutations compromise the power output of this motion," he said. "Now you have a heart that essentially is underpowered for what it has to do. The heart just keeps getting bigger and bigger." Athletes are especially at risk of dying from the disease because of the excessive physical strain they exert. "Physical exertion will make it worse because during physical exertion, the heart is called upon to work harder," Sweeney said. "So anyone who has this disease is at risk of dying during exercise." And the situation is further exacerbated because the condition is so difficult to detect. "The average physical would never pick up this disease," Sweeney said. He explained that even if a physician noticed that an athlete had a large heart, it could very possibly be ignored because it is common for physical exertion to cause the heart to grow. Sweeney conducted the study with Ronald Milligan, an associate member of the Scripps Research Institute. And the findings were reported in the December 14 issue of the journal Nature. "Now we're going to focus in more detail on what these mutations do to the protein and how to counterattack these mutations," Sweeney said.

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