The Effect of Damaging Electric Muscle Contraction on Mitochondrial Health and Function

Abstract

High intensity and prolonged exercise have been known to cause at least a temporary reduction in mitochondrial function. However, it is unclear how long mitochondrial function may remain impaired. Electrically stimulated eccentric muscle contractions (EEMC) may offer insights into the mechanisms by which mitochondrial function is restored following damaging muscle contractions like what is seen following high intensity exercise. The effects of EEMC on mitochondrial function have not been investigated. The aim of this study was to determine the impact that EEMC has on mitochondrial function one week following a single bout of the electrical stimulation. Muscle biopsies were taken from the vastus lateralis of female subjects one week prior and one week after EEMC. Muscle fibers were then prepared for High Resolution Respirometry and Fluorometry analysis on an Oroboros O2K Fluo‐Respirometer. This approach allowed for real‐time evaluation of mitochondrial function and production of reactive oxygen species (ROS). We measured mitochondrial function using two different substrate‐uncoupler‐inhibitor‐titrations (SUITs) designed to evaluate carbohydrate‐supported respiration (SUIT‐1) and fatty‐acid supported respiration (SUIT‐2). Under SUIT‐1 conditions, maximum coupled respiration (OXPHOS) was not significantly different between the pre and post EEMC biopsies. Under SUIT‐2 fatty‐acid supported and phosphorylating conditions (with ADP), there was a significant increase in respiratory function in the post EEMC biopsy (p=0.045). Mitochondrial ROS production was not significantly different following recovery than the baseline measures under SUIT‐1 conditions. These data represent the first evaluation of mitochondrial function one week following EEMC. We also show that the previously demonstrated negative effect of high‐intensity exercise on mitochondrial function may be fully recovered one week after damaging contractions and that fatty‐acid supported respiration is improved at the same time point.