Improved impedance to maladaptation and enhanced VCAM-1 upregulation with resistance-type training in the long-lived Snell dwarf (Pit1dwdw) mouse

Abstract

Snell dwarf mice with the Pit1dw/dw mutation are deficient in growth hormone, prolactin, and thyroid stimulating hormone and exhibit >40% lifespan extension. This longevity is accompanied by compromisedmuscular performance. However, research regarding young (3-month-old) Snell dwarf mice demonstrateexceptional responsivity to resistance-type training especially in terms of a shifted fiber type distribution andincreased 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 maladaptivedecreases in performance and muscle mass. This was accompanied by retainment of the remodeling capacity inmuscles of Snell dwarf mice to increase VCAM-1 protein levels and a shift in myosin heavy chain (MHC) isoformdistribution with training. Even decreasing training frequency for control mice, an alteration which protectedmuscles from maladaptation at 12 months of age, did not result in the overt remodeling observed for Snelldwarf mice. The results demonstrate a distinct remodeling response to resistance-type exercise operative in thecontext of the Pit1dw/dw mutation of long-lived Snell dwarf mice