Prolonged skeletal muscle inactivity results in muscle fiber atrophy and weakness. Interestingly, endurance exercise training promotes a protective phenotype in skeletal muscle fibers that resists inactivity‐induced muscle wasting. The mechanism(s) responsible for this exercise‐induced preconditioning of muscle remain unknown and are explored in these experiments. In this regard, evidence reveals that activation of the classical arm of the renin‐angiotensin system (RAS) contributes to inactivity‐induced muscle wasting. Specifically, activation of the classical RAS pathway via the angiotensin II type I receptor (AT1R) is associated with activation of proteases and muscle fiber atrophy. Additionally, a non‐classical RAS axis exists that acts antagonistically to the classical RAS axis. Therefore, activation of the non‐classical RAS pathway via the Mas receptor (MasR) inhibits signaling through the classical RAS pathway. Indeed, pharmacological studies reveal that blockade of the AT1R and/or activation of the non‐classical RAS axis protects skeletal muscle against inactivity‐induced muscle atrophy. Studies also reveal that endurance exercise training decreases the abundance of AT1R and increases the quantity of MasR in blood vessels. If similar changes occur in skeletal muscles, these changes in receptor abundance could shift the RAS signaling to favor the non‐classical RAS axis and reduce activation of classical RAS signaling in muscle fibers during prolonged inactivity. These experiments test the hypothesis that endurance exercise training decreases the abundance of AT1R and increases the abundance of MasR in skeletal muscle fibers. To test this postulate, adult rats performed 10 days of endurance exercise training (60 min/day @ ~70% VO2Max). At the completion of the training protocol, the abundance of both AT1R and MasR were determined in isolated single muscle fibers. Moreover, a sensitive angiotensin II (Ang‐II) binding assay was employed to confirm exercise‐induced changes in AT1R abundance in muscle. The results reveal that endurance exercise training does not alter the protein abundance of either the AT1R or MasR in the soleus, plantaris, or diaphragm muscle fibers. Moreover, exercise training did not change the Ang II‐binding affinity within skeletal muscles. Collectively, these results do not support the hypothesis that endurance exercise training results in a decrease in the abundance of AT1R and an increase in MasR in skeletal muscle fibers. It follows that exercise‐induced changes in the abundance of RAS receptors does not appear to be the mechanism responsible for exercise‐induced protection of muscle fibers against inactivity‐induced muscle atrophy.Support or Funding InformationNIH AR064189 (SKP).