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Finally, an imbalance in GSSG:GSH ratio induced ER stress and dependency on the ER-associated degradation pathway, driven by a shift in protein disulfide isomerases towards their oxidized forms

Mischley LK, Standish LJ, Weiss NS, Padowski JM, Kavanagh TJ, White CC, Rosenfeld ME

Production of these reactive oxygen species is known to occur as a result of a few different mechanisms: 1) mitochondrial origin in which free radicals either escape scavenging enzymes or develop due to an error in oxidative processes, 2) inside the capillary endothelium where a hypoxic and reoxygenation process is created during intense exercise as well as during various types of cardiovascular disease, and 3) an oxidative burst from inflammatory cells which are commonly mobilized as a result of the muscle or tissue damage which is well-documented with extended or eccentric-based exercise[1]