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Cellular senescence is thought to play a major role in age-related diseases,which cause nearly 67% of all human deaths worldwide. Recent research in miceshowed that exercising mice had higher levels of telomerase, an enzyme thathelps maintain telomere length, than non-exercising mice. A commonly used modelfor biological aging was proposed by Penna. I propose two modifications of thePenna model that incorporate senescence and find analytical steady statesolutions following Coe, Mao and Cates. I find that models corresponding todelayed senescence have younger populations that live longer.

Live Young, Die Later: Senescence in the Penna Model of Aging