"Exercise May Protect Cell Viability Under Oxidative Stress" by Emily A. Jones, Jose M. Moris et al.
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Abstract

Nasal breathing (NB) during exercise induces hypercapnic conditions, which may improve exercise performance. However, the impact of NB on cell viability (CV) remains unexplored. PURPOSE: This study investigated the effects of a single bout of exercise with NB on CV following lipopolysaccharide (LPS)-induced oxidative stress in peripheral blood mononuclear cells (PBMCs). METHODS: Twelve men (age=22.5±3.03 years) were randomly assigned to either the NB group (N=6) or the combined breathing (oral + nasal breathing, CB, N=6) group. Each group performed a graded maximal exercise test (GXT) on a recumbent bike. Plasma samples were collected before and immediately after the GXT to isolate PBMCs, followed by culturing for 12 hours, either with LPS (1µg/mL) or without LPS stimulation. RESULTS: There were no significant differences in CV between the NB and CB groups. CV did not differ between pre-exercise (92.78±1.52%) and immediately post-exercise (93.33±1.76%). However, after 12 hours of culture without LPS, CV was significantly lower in the immediately post-exercise condition (90.60±1.87%) than in the pre-exercise condition (93.45±1.49%, p=0.01). When stimulated with LPS and cultured for 12 hours, CV between the pre-exercise (90.16±2.04%) and immediately post-exercise conditions (91.70±1.50%) was not significantly different. However, both pre-exercise and immediately post-exercise CVs with LPS stimulation were significantly lower (p=0.029) than the pre-exercise CVs without LPS stimulation. CONCLUSION: Decreased CV following maximal exercise may be associated with exercise-induced physiological and biochemical stressors, such as reactive oxygen species, pro-inflammatory cytokines, and metabolic byproducts. Although CV decreased under oxidative stress conditions, a single bout of exercise showed a tendency to preserve viability, which may be attributed to exercise-induced reduction in susceptibility to LPS-induced viability loss by enhancing anti-inflammatory pathways and antioxidant defenses.

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