Jenkins: Impact of Exercise on Cardio Health

I know this is not exactly NEW news, and that's my fault. I've been holding on to this gem for a few weeks now. No good reason, except that I forgot I had it.

Nathan Jenkins is a third-year doctoral student in the Kinesiology Department who was awarded a $5,000 grant by American College of Sports Medicine to continue his research into the effects of exercise on cardiovascular health. Jenkins and his laboratory team, led by professor Jim Hagberg, have already published papers on the topic in three highly regarded health journals. (But most importantly is he claims to be a regular Healthy Turtle reader!)

Healthy Turtle: At this time last year, you told The Healthy Turtle you were in the process of researching whether or not physical activity promotes favorable conditions inside EPCs to perform the job. So ...what exactly does that mean?
Nathan Jenkins: We examine the activity of a number of molecules and genes involved in EPC function. As one example, nitric oxide is a molecule we are particularly interested in. In mature endothelial cells (lining inner walls of blood vessels), nitric oxide stimulates relaxation of the blood vessels. High nitric oxide levels are associated with low blood pressure and good cardiovascular health, whereas low levels are associated with chronically constricted, inflamed, unhealthy vessels. Therefore, EPCs nitric oxide levels are of interest because EPCs are programmed to replace or repair damaged endothelial cells.

HT: How has the research evolved since that point?
NJ: We have recently published a paper on our findings indicating large differences between active and inactive groups in EPC nitric oxide levels, and we were able to experimentally determine a molecular mechanism underlying this effect. We have also recently published two additional papers indicating that cessation of physical activity in previously active older men is associated with changes in the number of circulating EPCs and total antioxidant status, and that exercise may influence EPC function through the actions of a blood clotting factor known as thrombin.

HT: Is there anything in this research study so far that has surprised you?
NJ: The most surprising finding to me has been how, especially in sedentary individuals, a single bout of exercise dramatically alters the molecular features of these cells.

HT: Why is this research study important? What are the implications?
NJ: The two points of fact that we usually point to as underlying rationale for this work are:
(i) that conventional cardiovascular risk factors such as cholesterol and triglyceride levels explain only ~50% of actual cardiovascular disease cases, and
(ii) only ~60% of the physical activity-mediated reduction in cardiovascular disease risk can be explained by effects on conventional risk factors.

We believe it is important to improve our understanding of novel risk factors such as EPCs to determine whether they may explain the "risk-free" cases of cardiovascular disease and/or whether these cells explain the improvement in cardiovascular health through regular exercise. We also believe that our work could have many important clinical implications. For example, EPCs are currently being used in cell therapy trials in which heart attack patients have their own EPCs infused directly into their damaged coronary arteries. While some trials have reported favorable outcomes following therapy, the results have not been as promising as originally hoped. Our work might indicate that the results *might* be improved if exercise were used as an adjunct to cell therapy.