Intensive exercise induces changes of endothelial nitric oxide synthase pattern in human erythrocytes.

Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society

PubMedID: 18977310

Suhr F, Porten S, Hertrich T, Brixius K, Schmidt A, Platen P, Bloch W. Intensive exercise induces changes of endothelial nitric oxide synthase pattern in human erythrocytes. Nitric Oxide. 2009;20(2):95-103.
The synthesis of nitric oxide (NO) in the circulation has been attributed exclusively to the vascular endothelium, especially to endothelial cells. Recently, it has been demonstrated that red blood cells (RBCs) express the endothelial NOS isoform (eNOS). In addition, RBCs have been assumed to metabolize large quantities of NO due to their high content of hemoglobin. In addition to its known action on endothelial cells, NO seems to possess cardiovascular effects via regulation of RBC deformability. To get a better understanding of the question whether RBCs endothelial NOS (eNOS) is affected by intensive exercise undertaken by elite athletes, the present study aimed to investigate eNOS content, activated eNOS, phosphorylation states of eNOS (eNOSSer(116), eNOSSer(1177), eNOSThr(495)) and nitrotyrosine in erythrocytes of international-class field hockey players following a two-day long intensive training camp. Blood samples were taken before and immediately after the training camp. The athletes were required to complete at least two training sessions per day. The results showed that eNOS content, activated eNOS, eNOSSer(1177), and nitrotyrosine were significantly (p<0.05) down-regulated after the training camp. In contrast, eNOSSer(116), and eNOSThr(495) did not show significant changes, although eNOSThr(495) (p=0.081) tended to decrease. Hemoglobin and hematocrit were significantly decreased after training camp. In conclusion, this study gains new insights into a possible down-regulation of eNOS and NO production in human RBCs following high intensity exercises. It can be speculated that the reduction of eNOS and the combined reduction of eNOS activity influence erythrocyte deformability and lead subsequently to a rheological impairment.