You might, at least if the intervention is preventative. (Sorry in advance if this is all review...) Muscle cells are not like most other cell types. A single muscle cell is more like a giant conglomerate of a bunch of cells, all merged within a single membrane. There's many nuclei in each muscle cell, many full sets of chromosomes, and the cell is big enough that most proteins will never diffuse from one end to the other before turning over. Unlike normal cells, the nucleii themselves can turn over independent of the cell - and muscle stem cells ("satellite cells", the first type of stem cell discovered IIRC) are primarily responsible for this turnover. Now, at this point we don't know for sure if satellite cell problems are the primary driver of age-related muscle loss, but they're definitely one of the top candidates (mitochondria are another). And if that is the main driver, then fixing stem cell aging would indeed fix muscle loss - not necessarily retroactively, but at least preventatively. The main takeaway here is that, while individual muscle cells are long-lived, their components still turn over. There's probably something upstream of muscle loss which drives it.

I guess this goes back to the issue of defining things and what you mean by hallmarks. If you define your hallmarks broadly enough they may include almost anything while being so vague that they are only useful for posters and ads. In the case of vague hallmarks you'd be right, if you fix them you're all good. But even in this extreme case I do expect the number of vague hallmarks to grow a little bit over time as we learn more. In fact, to me they feel incomplete and ill-defined already. Looking at the classic "The Hallmarks of Aging" paper (first published as López-Otín et al. 2013 I think) or Aubrey's seven causes of aging I do feel like they are way too vague. Let's take genomic instability as an example. Fix it and you make progress against aging. However, that is just an empty phrase like "repair the engine of the car"; that's usually the reason why it stops in the middle of the highway. Which genome, mitochondria, nuclear? Which pathway do you target? Hundreds of genes involved in repair, hundreds of genes involved in prevention of DNA damage via the intricate ROS- and stress-sensing pathways. Which type of lesion to prevent? Damaged bases or strand breaks? Which type of existing damage to repair and remedy post facto? Actual mutations (not just temporary damage), small indels, aneuploidies, large deletions, inversions, translocations or more complex chromosomal rearrangements and clonally expanded cell populations? Don't forget to fix chromatin organisation and epigenetic marks and all the inter-related extra-nuclear factors that promote genomic instability (could be inflammation, could be reduced autophagy, let's speculate). Want to use nanobots instead? Be my guest, then you are solving advanced physics, engineering and AI problems. Regarding incompleteness and definitions: Why did they choose to define telomere attrition as its own hallmark? First of all, this is an incredibily specific problem and secondly telomeres are part of the nuclear genome, i.e.