Affiliations: [a] Department of Pharmacology and Psychobiology, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
| [b] Physical Activity and Health Promotion Laboratory, University of the State of Rio de Janeiro, Rio de Janeiro, Brazil
| [c]
Salgado de Oliveira University Physical Activity Sciences Graduate Program, Rio de Janeiro, Brazil
Correspondence:
[*]
Corresponding author: Cristiane Matsuura, Av. 28 de setembro, 77, fundos,
5° andar, Vila Isabel, Rio de Janeiro, CEP: 20551-030, RJ, Brazil. Tel.: +55 21 2868 8652; Fax: +55 21 2868 8629; E-mail: cristiane.matsuura@pq.cnpq.br.
Abstract: Growing evidence has shown that acute exercise impairs erythrocyte membrane structure and function as a consequence of increased physical and chemical stress. Erythrocyte-synthesized nitric oxide (NO) is known to modulate membrane fluidity, and its bioavailability depends on the balance between its production and scavenging by reactive oxygen species. Here, we investigated whether a maximal exercise test could affect erythrocyte NO bioavailability and oxidative stress. Twelve men (26±4 years old, V̇O2peak 44.1±4.3 mL·kg–1·min–1) performed a treadmill maximal cardiopulmonary exercise test. Blood was collected at rest and immediately after exercise for erythrocytes isolation. Maximal exercise caused an increase in erythrocytes count, haemoglobin and haematocrit levels. There was no change in L-arginine influx into erythrocytes after exercise. Yet, nitric oxide synthase activity, and thus, NO production, was increased after maximal test, as well cyclic GMP levels. In relation to biomarkers of oxidative stress, maximal test resulted in increased levels of lipid peroxidation, and diminished superoxide dismutase activity. Neither glutathione peroxidase nor catalase activity was affected by maximal test. Our findings demonstrate that the increased erythrocyte membrane rigidity caused by an acute bout of exercise may be caused, in part, by an increased lipid oxidative damage caused by ROS produced exogenously.
