Improved impedance to maladaptation and enhanced VCAM-1 upregulation with resistance-type training in the long-lived Snell dwarf ( Pit1 dw/dw ) mouse

• Published in: Aging (Albany, NY.) Vol. 14; no. 3; pp. 1157 - 1185
• Main Authors: Rader, Erik P, Naimo, Marshall A, Ensey, James, Baker, Brent A
• Format: Journal Article
• Language: English
• Published: United States Impact Journals 03.02.2022
• Subjects: Animals; Dwarfism, Pituitary - genetics; Electric Impedance; Longevity - genetics; Mice; Mice, Mutant Strains; Research Paper; Up-Regulation; Vascular Cell Adhesion Molecule-1 - genetics; Vascular Cell Adhesion Molecule-1 - metabolism; plantarflexor muscles; skeletal muscle; stretch-shortening contractions
• ISSN: 1945-4589; 1945-4589
• DOI: 10.18632/aging.203875

Snell dwarf mice with the mutation are deficient in growth hormone, prolactin, and thyroid stimulating hormone and exhibit >40% lifespan extension. This longevity is accompanied by compromised muscular performance. However, research regarding young (3-month-old) Snell dwarf mice demonstrate exceptional responsivity to resistance-type training especially in terms of a shifted fiber type distribution and increased protein levels of vascular cell adhesion molecule-1 (VCAM-1), a possible mediator of such remodeling. In the present study, we investigated whether this responsiveness persists at 12 months of age. Unlike 12-month-old control mice, age-matched Snell dwarf mice remained resistant to training-induced maladaptive decreases in performance and muscle mass. This was accompanied by retainment of the remodeling capacity in muscles of Snell dwarf mice to increase VCAM-1 protein levels and a shift in myosin heavy chain (MHC) isoform distribution with training. Even decreasing training frequency for control mice, an alteration which protected muscles from maladaptation at 12 months of age, did not result in the overt remodeling observed for Snell dwarf mice. The results demonstrate a distinct remodeling response to resistance-type exercise operative in the context of the mutation of long-lived Snell dwarf mice.