Sickle cell trait carriers who exercised regularly demonstrated improvements in oxidative biomarkers in response to exercise compared with carriers who did not exercise, according to study results.
Researchers from two sites in France assessed the following plasma levels of oxidative stress and antioxidant markers at baseline, immediately after a maximal exercise test and during recovery:
- Advanced oxidation protein products.
- Protein carbonyl.
- Glutathione peroxidase.
- Superoxide dismutase.
Nitrite and nitrate levels also were assessed at those time points. The three recovery time points were 1, 2 and 24 hours.
Participants were determined to be trained if they exercised for a minimum of 8 hours per week and untrained if they had no regular physical activity.
There were 10 trained sickle cell trait carriers, eight untrained sickle cell trait carriers, 11 trained controls and 11 untrained controls. The median age of participants was 23.5 years.
Trained participants had higher superoxide dismutase activities than untrained participants in response to exercise (P=.016) and had lower levels of advanced oxidation protein products (P=.028) and protein carbonyl (P=.01) in response to exercise.
Exercise was linked to a higher level of advanced oxidation protein products (P=.012), nitrotyrosine (P=.003) and protein carbonyl (P=.006) in untrained participants with sickle cell trait vs. trained participants with sickle cell trait.
Participants in the trained sickle cell group demonstrated higher superoxide dismutase activity (P=.002) and nitrite levels (P=.003) in response to exercise than those in the untrained sickle cell group.
“Our data indicate that the overall oxidative stress and nitric oxide response is improved in exercise-trained [sickle cell trait] carriers compared with their untrained counterparts,” the researchers wrote. “These results suggest that physical activity could be a viable method of controlling the oxidative stress. This could have a beneficial impact because of its involvement in endothelial dysfunction and subsequent vascular impairment in hemoglobin S carriers.”