The Effect of a 10 day Cessation of Training in Older Endurance Athletes on Pathological Production of Nitric Oxide and Reactive Oxygen Species Levels in Circulating Angiogenic Cells
Corrigan, Kelsey J.
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Cardiovascular disease (CVD) is a serious disease, and is the leading cause of death in the United States. Aging and physical inactivity are two well-established risk factors for CVD. Previous research has identified circulating angiogenic cells (CACs) as a novel risk factor for CVD. CAC number and function are affected by aging and exercise. Nitric oxide (NO) and reactive oxygen species (ROS) are intracellular compounds which can affect the health of the vasculature and are also affected by exercise. Endothelial nitric oxide synthase (eNOS) is responsible for NO production within the endothelium, and eNOS "coupling" is a phenomenon that plays a role in the balance between production of ROS and NO. The literature also indicates that NO can be produced in either a pathological or physiological capacity depending on which isoform of NOS produces it. NO and ROS have been previously measured in CACs and have been shown to affect in vivo and in vitro outcomes related to vascular function. Although NO, ROS, and CACs have all been studied in relation to exercise, no previous studies have examined how the cessation of training in older endurance-trained athletes affects these intra-cellular compounds through the eNOS-coupling pathway. The purpose of this study was to examine the effect of a 10-day cessation of exercise training in older endurance-trained athletes on ROS, NO and the eNOS-coupling pathway in CD34+ cells. NO and ROS were measured in isolated fresh CD34+ cells using fluorescent dye assays. The mRNA expression of genes involved in the eNOS-coupling pathway (endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), dihydrofolate reductase (DHFR), and guanosine triphosphate cyclohydrolase 1 (GTPCH1)) were measured using semi-quantitative Polymerase Chain Reaction (Semi-qt PCR). Flow mediated dilation was measured to gain information about endothelial function. No significant differences were detected after the cessation of training in CD34+ intracellular NO or ROS levels. Flow mediated dilation (FMD) also did not change significantly following cessation of training. eNOS mRNA expression was significantly lower following cessation of training but iNOS, DHFR, and GTPCH1 did not change. Taking into consideration the current literature, we expected to see changes in all of the above variables with the cessation of exercise training. There were several limitations present in our study, which could have affected our outcomes. Research in this area, specifically the eNOS coupling pathway, is still very new and this study shows that additional research is still needed to elucidate the underlying mechanisms in CACs.