Physical conditioning and nitric oxide production during exercise

• Main Author: Maroun, Martin J.
• Other Authors: Turcotte, Rene (advisor)
• Format: Others
• Language: en
• Published: McGill University 1995
• Subjects: Physical fitness; Nitric oxide; Exercise > Physiological aspects
• Online Access: http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35219

Nitric Oxide (NO) has been detected in the expiratory air of normal animals and human subjects. Recent experiments revealed that expiratory NO production rises during exercise and correlates well with O$ sb2$ consumption and heart rate. Whether or not physical conditioning influences expiratory NO output production remains unclear. In this study, NO concentration in expired gas was measured in 18 healthy male volunteers subdivided into 3 groups (sedentary, intermediate, athletes) based on their state of physical conditioning. Measurements were taken at rest and during two steady-state exercise bouts on a bicycle ergometer designed to elicit VO$ sb2$ of 1 and 2 1/min with the athletes performing an additional bout at VO$ sb2$ of 4 1/min. In the sedentary and intermediate groups, expired NO concentrations declined significantly with increasing VO$ sb2.$ In contrast, expired NO levels declined only slightly with increasing VO$ sb2$ in athletes. At a VO$ sb2$ of 2 1/min, expired NO concentrations were significantly higher in athletes compared with the other groups. When correlated with V$ rm sb{E},$ expired NO concentrations declined linearly with the increase in $ rm V sb{E}$ in sedentary and intermediate groups but not in the athletes. Only the athletes had a significant linear increase in NO output (expired NO x V$ rm sb{E})$ with increasing VO$ sb2$ (p $<$ 0.001). These results support the notion that physical conditioning increases expiratory NO output during exercise. We speculate that the rise in expiratory NO output in athletes might be due to increased vascular and/or epithelial production of NO. Enhanced vascular NO production may be the result of increased shear stress and/or upregulation of endothelial NO synthase gene expression.