Mitochondrial ROS generation and function in skeletal muscle from older subjects (863.5)

Abstract

Oxidative damage is reported to be involved in loss of tissue function with aging and the potential role of mitochondria as a source of increased ROS generation has been attributed to the impaired mitochondrial function and oxidative damage to mitochondrial components that occurs with advancing age. Data have predominantly been obtained from rodent studies and there is limited information on the role of mitochondrial ROS generation in muscle from older humans. To determine the role of mitochondrial ROS in the muscle decline that occurs with aging, muscle biopsies from young (20‐30 years) middle‐aged (45‐55 years) and older(>60 years) healthy volunteers were taken from the vastus lateralis muscle. Analyses were performed in small bundles of permeabilized fibers including mitochondrial ROS changes in the presence of various ETC substrates and inhibitors, changes in mitochondrial respiration, membrane potential and changes in maximum calcium‐activated tetanic force. No differences in fiber cross‐sectional area or force generation in response to calcium stimulation were observed in fibers between age groups. Respiratory function, mitochondrial membrane potential and ROS generation, assessed via changes in superoxide and hydrogen peroxide were not significantly different between age groups. Our data challenge the concept that mitochondrial ROS generation plays a key role in human skeletal muscle aging.Grant Funding Source: Funded by the Medical Research Council, UK (Grant No: G1002120)