UAB researchers review how senescent “zombie” cells contribute to skeletal muscle weakness with aging and disease, outlining emerging therapies such as senolytics and senomorphics that could help preserve muscle health and extend health span. go.uab.edu/42e78hN

Muscle mass peaks in your 30s, then declines 3–8% per decade. By age 80, you've lost roughly 30–50% of the muscle you had at your physiological peak. In this week's Beyond Healthspan podcast, we talk to Dr. Davis Englund (@DavisEnglund) about what drives that decline at the cellular level—and why senescent cells accumulating in muscle are a primary mechanism. Senescent cells don't just occupy space. They actively block muscle regeneration through inflammatory signaling that disrupts satellite cell function—the stem cells responsible for muscle repair. When Englund's group measured blood-based senescence markers in older adults, baseline senescence predicted training response. Higher senescent cell burden meant poorer adaptation to exercise. The implication: muscle decline during aging isn't just atrophy from disuse. It's an accumulation of damaged cells that sabotage the repair machinery. Englund explains: - Why senolytics help muscle repair in old mice but harm it in young ones - Which cell types in muscle become senescent (fibers vs. satellite cells) - How mTOR hyperactivity during aging drives sarcopenia instead of growth - Why exercise itself appears to have senolytic effects - The difference between clearing senescent cells and suppressing their inflammatory output - Why tissue-specific senolytics are the next therapeutic frontier

What did you miss at the November 2025 Nathan Shock Center Seminar? @DavisEnglund We hope to see you next time!

Myself and the rest of the @UABExerciseMed had a great time at the Tornado Alley Muscle Meeting last week. Outstanding talks from @ThalackerMercer @DavisEnglund and their trainees. Kudos to @KevinMurachPhD @DavisEnglund and the other organizers for putting on a great meeting.

Talented postdoc @KPapanikolaou93 showcasing his early work in the lab examining cellular senescence as a source of skeletal muscle dysfunction at UAB Postdoc Research Day. @UABHeersink @UABDeptMed @angadyadav2011

A 5+ year odyssey with @FerdinandvW “The 24-hour molecular landscape after exercise in humans reveals MYC is sufficient for muscle growth” in @emboreports embopress.org/doi/full/10.10… Congrats to 1st authors! @SebastianEdman @RonaldGJones3 Database: data.myoanalytics.com #myotwitter