Frontiers in bioscience (Landmark edition) · 2026
Aerobic Running Training Attenuates Lipid and Protein Oxidation and Modulates Membrane Dynamics in Metabolically Active Tissues.
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Piedrafita Eduardo, Bascuas Pablo Jesús, Bataller-Cervero Ana Vanessa, Berzosa César
Аннотация
BACKGROUND: Chronic aerobic exercise is known to modulate oxidative stress, yet comparative analyses across multiple tissues remain limited. This study aimed to evaluate the effects of different training durations on oxidative damage and membrane fluidity in metabolically active tissues, including skeletal muscle, heart, and brain.
METHODS: Forty male Sprague-Dawley rats were randomly assigned to four groups (n = 10/group): control (CON), and aerobic treadmill training for 1 week (1W), 4 weeks (4W), and 12 weeks (12W). Training consisted of four 60-minute sessions per week, alternating intensities at 35% and 80% of maximal velocity. Quadriceps skeletal muscle, heart, and brain were collected. Oxidative damage was assessed via malondialdehyde and 4-hydroxyalkenals (MDA + 4-HDA) and protein carbonyl content. Membrane fluidity was evaluated in plasma and mitochondrial membranes using fluorescence spectroscopy. Statistical analyses were performed using one-way analysis of variance followed by Tukey post-hoc tests.
RESULTS: Aerobic training significantly reduced MDA + 4-HDA levels in skeletal muscle and heart compared with control values, with a downward trend in brain tissue that did not reach statistical significance. Protein carbonyls decreased significantly in skeletal muscle at 4W and 12W, but remained unchanged in heart and brain (despite lower mean values observed in all training groups compared with the control). Plasma membrane fluidity declined significantly in all tissues, especially at 4W and 12W, indicating structural remodeling. Mitochondrial membrane fluidity values were lower in heart and skeletal muscle across the different training groups, with statistically significant differences observed only and remarkably in skeletal muscle compared with control values; meanwhile, values remained stable in brain tissue. These findings reveal tissue-specific biochemical and biophysical adaptations to aerobic training.
CONCLUSIONS: Chronic aerobic treadmill training induces protective adaptations against oxidative stress in skeletal muscle, heart, and brain. The reduction in lipid peroxidation and protein oxidation, along with changes in membrane fluidity, reflects enhanced cellular resilience and structural integrity. These results support the role of sustained aerobic exercise as a non-pharmacological strategy to mitigate oxidative damage and promote tissue health. The rat model used provides translational relevance for understanding exercise-induced protection mechanisms.
METHODS: Forty male Sprague-Dawley rats were randomly assigned to four groups (n = 10/group): control (CON), and aerobic treadmill training for 1 week (1W), 4 weeks (4W), and 12 weeks (12W). Training consisted of four 60-minute sessions per week, alternating intensities at 35% and 80% of maximal velocity. Quadriceps skeletal muscle, heart, and brain were collected. Oxidative damage was assessed via malondialdehyde and 4-hydroxyalkenals (MDA + 4-HDA) and protein carbonyl content. Membrane fluidity was evaluated in plasma and mitochondrial membranes using fluorescence spectroscopy. Statistical analyses were performed using one-way analysis of variance followed by Tukey post-hoc tests.
RESULTS: Aerobic training significantly reduced MDA + 4-HDA levels in skeletal muscle and heart compared with control values, with a downward trend in brain tissue that did not reach statistical significance. Protein carbonyls decreased significantly in skeletal muscle at 4W and 12W, but remained unchanged in heart and brain (despite lower mean values observed in all training groups compared with the control). Plasma membrane fluidity declined significantly in all tissues, especially at 4W and 12W, indicating structural remodeling. Mitochondrial membrane fluidity values were lower in heart and skeletal muscle across the different training groups, with statistically significant differences observed only and remarkably in skeletal muscle compared with control values; meanwhile, values remained stable in brain tissue. These findings reveal tissue-specific biochemical and biophysical adaptations to aerobic training.
CONCLUSIONS: Chronic aerobic treadmill training induces protective adaptations against oxidative stress in skeletal muscle, heart, and brain. The reduction in lipid peroxidation and protein oxidation, along with changes in membrane fluidity, reflects enhanced cellular resilience and structural integrity. These results support the role of sustained aerobic exercise as a non-pharmacological strategy to mitigate oxidative damage and promote tissue health. The rat model used provides translational relevance for understanding exercise-induced protection mechanisms.