Arginase Activity in Red Blood Cells Is Not Altered with Sub-maximal Exercise.

Abstract

Nitric oxide (NO) is an important mediator of exercise remodeling. Its role has been highlighted in the promotion of vascular growth as well as in mitochondrial function. While the endothelium has long been thought to be the dominant physiological source of NO, recent work has suggested that red blood cells (RBCs) express the enzyme endothelial nitric oxide synthase (eNOS) and may contribute to total NO production. Within RBCs, the NO production can be decreased by the activity of the enzyme arginase, which competes with eNOS for the substrate L-arginine. PURPOSE: The aim of the study was to test the hypothesis that RBC arginase activity is modulated by exercise. METHODS: Nine subjects (4 male and 5 females, age; 26±5 years, VO2peak; 54,8±8,1 mL/min/kg) performed a 60-min sub-maximal exercise bout corresponding to 65% of VO2peak. Blood samples were taken at rest (T0), 30 min in to the exercise (T1), directly after exercise (T2), 30 min post-exercise (T3) and 60 min post-exercise (T4). Arginase activity in RBCs was measured by colorimetric determination of urea formed from L-arginine substrate with α-isonitrosopropiophenone as a marker of urea content. RESULTS: Contradictory to our initial hypothesis, arginase activity was unaffected by exercise. No changes in urea production (T0; 0.52±0.08, T1; 0.50±0.08, T2; 0.51±0.09, T3; 0.51±0.09 and T4; 0.52±0.08 mM/g Hb, p>0.05) was seen between the resting blood sample and the ones taken during or after exercise. CONCLUSION: Arginase activity in RBCs is not modulated by sub-maximal exercise in young healthy subjects. Hence, the increase in eNOS activity and NO production from RBCs with exercise is most likely not explained by a reduced activity of arginase.