The senescent rat diaphragm does not exhibit age-related changes in caspase activities, DNA fragmentation, or myonuclear domain.

The diaphragm muscle is essential for normal ventilation and it is chronically active throughout the lifespan. In most skeletal muscles, aging is associated with increased oxidative stress and myofiber atrophy. Since the diaphragm maintains a unique chronic contractile activity, we hypothesized that these alterations would not occur in senescent diaphragms compared to young diaphragms. In addition, we investigated whether senescence leads to altered diaphragmatic caspase activity and myonuclear domain. We harvested diaphragm muscles from 6 and 24-26 month old male Fisher 344 rats (n = 10 per group). Measurements of protein carbonyls, caspase 2, 3, 9, and 12 activities, DNA fragmentation, myofiber cross-sectional area, and myonuclear domain of diaphragm muscles were performed. No age-related changes (p > 0.05) in diaphragmatic protein oxidation or activities of caspase 2, 3, 9, and 12 were observed between groups. In addition, DNA fragmentation, as detected by the ligation-mediated polymerase chain reaction ladder assay, was not different (p > 0.05) between young and senescent diaphragms. Importantly, the cross-sectional area and myonuclear domain of diaphragm myofibers from senescent animals were also not different (p > 0.05) from young diaphragms. In conclusion, our data show that the senescent diaphragm does not atrophy or exhibit changes in select markers of the apoptotic pathway and this may be a result of the diaphragm's unique continuous contractile activity.