Probably because of the small population of people that today’s world population descends from, and the fact that mutation possibilities that are lethal or highly disadvantageous to survival don’t persist and are by default ruled out (core/important regions stay conserved between people).

The idea that a lot of our DNA is inert stems from when the human genome was sequenced, and they found out only a small percent of it codes for genes that go on to get translated into proteins. But, over time, scientists are finding that these non-coding regions of DNA don’t do nothing; in fact, they play many biological roles in regulating the expression of protein-coding genes and can have significant physiological impacts and relevance.

Two important things for this question that are getting a little mixed up:

1. You’re describing the ‘hayflick limit’, which states that a human cell dividing by mitosis (replicating itself) can only do so ~40-60 times before the telomeres are too short and the cell has natural processes built in to stop it from replicating and just hang out (senescence) or kill itself (apoptosis). While this phenomenon does play some role in and correlate with cellular-level aging, most general education and schools teach this as the main reason behind aging itself in general, which isn’t completely true. Most humans demonstrate ageing and die before their cells actually reach those hayflick limits - I believe studies calculate humans to be able to reach ~120 years before 40-60 mitotic cell replications are reached. Thus, lifespan (length) and healthspan (quality) of life are clearly influenced by many more factors that JUST the hayflick limit. There are genetic and environmental factors that can damage DNA, cause chronic inflammation, there’s the free-radical hypothesis, other reasons for cell senescence, ways to clear senescent cells (or not), etc.

2. Differentiated cells like ‘muscle cells’ don’t only exist due to mitosis, which is what relates to the hayflick limit. Certain cells like resident stem cells or pluripotent cells don’t have limits to their replication. When damaged and weaker muscle cells are cleared out by activities like exercise, they are often replenished by their respective stem-like cell populations. Others mentioned mitochondrial biogenesis too. Exercise confers so many more benefits to quality of life and lifespan, that the small effects it may have on cells dividing by mitosis are far outweighed by the hayflick limit impacting your lifespan (again, see point 1). Studies show that people who regularly exercise or Olympic athletes in non-contact sports tend to actually live longer than those who don’t.