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AUGUSTA, Ga. (AP) — Gary White, 43, has a condition that should make exercise more difficult, but you would never know it from watching him pump furiously on an exercise bike in the Laboratory of Integrative Vascular & Exercise Physiology at the Georgia Prevention Institute at Georgia Regents University. Cystic fibrosis has not slowed down the man who runs and polishes off 70 to 100 pushups before work every day.
"I've always been exercising, even when I was a kid," White said. "I just try to be active and not think much about my condition."
But exercise intolerance is a side effect of cystic fibrosis and GRU researchers are looking to see whether some interventions, from a generic form of Viagra to antioxidants, could help those patients do more.
Cystic fibrosis is a disease caused by a defect in the CFTR gene that helps control the movement of salt and water in and out of cells. Patients are prone to have sticky mucus that builds up in their lungs, traps bacteria and leads to damage. It also affects other organs, including the pancreas, which can lead to nutrition problems.
The GRU team has shown it also affects blood vessels and can lead to less elasticity, even if the lung function is normal, said Dr. Ryan Harris, the director of the lab and an assistant professor of pediatrics.
"These were kids, 13 years old (and) they had arteries that were similar to a 45-year-old adult," he said.
Now the GRU team is trying to identify whether that is the source of exercise intolerance and what intervention might work. Sildenafil citrate, the generic form of Viagra, is known to help dilate blood vessels. So the question becomes "once it dilates the vessels, will that improve exercise capacity?" said Dr. Caralee Forseen, a co-director of the GRU Cystic Fibrosis Center.
The idea would be to do it once and see whether it improves function and also administer it over time and see whether it improves blood vessel function and then exercise capacity, Harris said.
But the connection between blood vessel dysfunction and impaired exercise capacity is complicated by the fact that these patients also have impaired mitochondria, the powerhouse of cells, in the muscles themselves, he said.
"So now, what is contributing to the muscle's inability to use oxygen is what we are trying to understand," Harris said. "It's not the lungs because the lung function is normal. It could be the blood vessels; it could be the muscle itself."
Another angle is looking at oxidative stress, which the patients also have and can also affect blood vessel function, he said.
"We've seen that our patients have elevated oxidative stress and we're able to knock that down with an antioxidant cocktail and observe improvements in blood vessel function, suggesting that indeed oxidative stress is a contributing factor" to blood vessel dysfunction, Harris said.
That approach also appeals to him because it is "nontraditional."
"Incorporating blood vessels and exercise into (cystic fibrosis) therapies would, in my mind, be groundbreaking," Harris said.
That is particularly compelling in light of the fact that exercise intolerance is an important predictor of mortality in these patients independent of lung function, he said.
Predicting long-term survival is difficult for these patients but is probably improving because it is now a mandatory part of newborn screening, Forseen said.
"The thought is obviously if you can catch people earlier in the disease process, you can have a greater impact on survival," she said.
White said his parents were always given a grim outlook.
"My parents were told I wouldn't live past 6, then it was 18, 21," he said. And while his mother made sure he got his treatments, "they also let me go out and do what I want to do," White said.
His wife, Toni, now makes sure he gets his treatments and takes his medicine, and they exercise together.
"All my life I've been told I wouldn't live past" the next stage, White said. But he is still proving them wrong.
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Information from: The Augusta Chronicle , http://www.augustachronicle.com
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