Muscle fiber size, myonuclear domain, and fat mass phenotypes in pre-migratory snow buntings

• Main Authors: Vézina, François, O'Connor, Ryan, Le Pogam, Audrey, De Jesus, Aliyah, Love, Oliver, Jimenez, Ana
• Format: Other/Unknown Material
• Language: unknown
• Published: Zenodo 2021
• Subjects: Plectrophenax nivalis
• Online Access: https://doi.org/10.5061/dryad.gxd2547kx

In long-distance migrants, preparation for migration is typically associated with increases in fat and body mass, and with an enlargement of pectoralis muscle mass that likely improves flight performance. Although changes in muscle mass or size have been well described in migratory birds, potential changes in muscle ultrastructure during this transition still deserves scrutiny. Using outdoor captive snow buntings ( Plectrophenax nivalis n = 15) measured during their transition into a spring migratory phenotype as a model system, we studied changes in pectoralis muscle ultrastructure and predicted that muscle fiber diameter could increase in parallel with the gain in body mass. We also expected that larger fibers could either recruit satellite cells to support cellular maintenance and protein turnover, increase myonuclear domain (cytoplasm per nuclei) with the potential increase for protein turnover load per myonucleus, or existing myonuclei could undergo endoreduplication. Buntings increased body mass by 46% within a month, largely due to a > 6-fold increase in body fat. However, this increase in body mass was also associated with a 36% increase in muscle fiber diameter. Both pectoralis muscle mass (r 2 = 0.57-0.77) and fiber diameter (r 2 = 0.32) correlated with total body mass, without any change in the number of nuclei per fiber. Consequently, variation in myonuclear domain (i.e. the amount of cytoplasm per nucleus), was also positively associated with body mass (r 2 = 0.51). Therefore, buntings preparing for migration may experience an increase in muscle contraction force due to larger muscle fibers, but this is also coupled with increases in myonuclear domain, which may force these cells to increase protein production to safeguard satellite cells.