Aging Is Not Related to Increased Cardiac Mitochondrial ROS Production in a Rat Model of Genetically Determined High or Low Exercise Capacity

Background: High exercise capacity is associated with lower risk for cardiovascular diseases and better outcome in disease and surgical interventions. Aging is associated with decreasing exercise capacity and increasing oxidative stress, originating to a great part from mitochondrial ROS production. In the model of rats with inherited high (HCR) or low (LCR) intrinsic exercise capacity, LCR present with one-third lower life expectancy and we aimed to assess if this is related to increased oxidative stress.

Method: Female adult (15 weeks) and old (100 weeks) HCR and LCR were tested for exercise capacity and cardiac function. ROS production from cardiac and skeletal muscle mitochondria was assessed and oxidative stress determined.

Results: Cardiac contractile function decreased with age and was higher in old LCR compared with old HCR (fractional shortening [%]: HCR old 31.2 ± 3.5 vs. LCR old 43.7 ± 2.9). Exercise capacity decreased with age in HCR only, but remained at a higher level than in LCR. Both cardiac and skeletal muscle showed a decrease of mitochondrial ROS production with age. In parallel, antioxidative capacity of catalase was increased with age which was more pronounced in LCR in the heart and in HCR in skeletal muscle (heart [U/mg]: HCR adult 2.86 ± 0.55 vs. HCR old 4.50 ± 0.45, LCR adult 2.91 ± 0.51 vs. LCR old 6.72 ± 0.66). However, oxidative protein damage increased to the same extent in old HCR and LCR (skeletal muscle carbonyl content [AU]: HCR adult 0.73 ± 0.10 vs. HCR old 1.46 ± 0.10, LCR adult 0.84 ± 0.07 vs. LCR old 1.85 ± 0.14).

Conclusion: The increase in oxidative stress with aging was found independent of genetically determined exercise capacity and seems to be associated with non-mitochondrial ROS production.

Publication History

Article published online:
03 February 2022