Is it bad to have lower strength per unit mass from myostatin inhibitors if it misleads AND if the extra growth gets in the way of high quality growth?

#1

##Recent Bryan Johnson Tweet##

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gpt5Pro:

Muscle: when “more” becomes dead weight

  • Strength per unit muscle (a.k.a. muscle quality) matters. With age, strength and power fall 2–5× faster than muscle size, mostly because nerves, motor units, and excitation–contraction coupling degrade. So if you inflate mass without fixing the wiring, performance lags and functional capacity drops. Frontiers+1
  • Drug-driven hypertrophy can be lopsided. Myostatin/ActRII blockade often increases lean mass dramatically, yet specific force (strength per CSA) may improve less or even fall. Reviews explicitly note “bigger muscle, lower quality” as a recurring pattern, especially outside neuro-muscular disease contexts. Translation: great DEXA, underwhelming torque. PMC
  • “Sarcoplasmic” vs “contractile” growth. If growth is mostly fluid, glycogen, enzymes and not myofibrils, strength per unit mass lags. This isn’t a fairy tale; there’s evidence this happens under some protocols. The muscle looks fuller; the barbell remains unimpressed. Frontiers+1
  • Tendon mismatch risk. Rapid muscle-up with slower tendon adaptation can raise local strain and nudge injury risk. Tendons do adapt, just on a different clock, which is why power work and isometrics at longer muscle lengths are often programmed to “teach” the tendon. PMC+1

Bottom line for muscle: Lower strength per unit mass is usually a liability unless absolute performance improves enough to offset the extra load. Otherwise you’ve added weight without adding useful force.

Bone: density isn’t destiny

  • Bone strength ≠ BMD. Strength depends on quantity and quality: geometry, microarchitecture, collagen cross-links, mineralization, microdamage, turnover. So higher “mass” can still mean brittle bone if the tissue quality is poor. PMC
  • When “more bone” backfires. Long-term oversuppression of turnover (e.g., with some antiresorptives) can accumulate microdamage and raise the risk of atypical femur fractures despite decent BMD. That’s a classic case of more material, worse material. Oxford Academic+1
  • How to track actual bone quality. Tools like trabecular bone score (TBS) and hip structural analysis give microarchitecture and geometry signals that predict fractures partly independent of BMD. If TBS or geometry stagnates while BMD climbs, that’s a red flag that the “growth” isn’t high quality. PMC+1

Bottom line for bone: If added mass doesn’t come with better architecture and material properties, you may increase fragility, not strength.

Can extra growth block “high‑quality” growth?

Unfortunately, yes. Three ways that happens:

  1. Resource crowding: Rapid hypertrophy with poor neural adaptation and tendon tuning hogs recovery resources and can blunt myofibrillar accrual or power adaptations. That’s the sarcoplasmic-tilt problem. Frontiers
  2. Misleading feedback loops: You see the scale and DEXA move and conclude training or a drug is “working,” so you stop chasing the hard stuff that actually raises quality: rate of force development, coordination, tendon stiffness, and skill. Strength plateaus while mass keeps creeping. Evidence: bigger muscles don’t automatically fix age‑related dynapenia. Frontiers
  3. Bone remodeling choke: If bone turnover is chronically suppressed, microarchitecture and toughness can worsen even as density rises. That “growth” can literally compete with, or mask, the right kind of remodeling you wanted. Oxford Academic

Guardrails so growth is actually useful

  • Score by function, not just size. Track relative strength (e.g., 1RM/body mass), peak power (CMJ or med‑ball throw), and grip strength. If these stagnate or fall while lean mass rises, quality is slipping.
  • For bone, add quality metrics. Ask for TBS on your next DXA, and if available, hip structural analysis. Improvements in TBS/geometry alongside BMD = higher quality growth. PMC+1
  • Program for quality: keep 1–2 days/week of heavy strength work and 1–2 days of high‑velocity power work; include long‑length isometrics and carefully dosed impact to bias tendon and bone adaptation, not just muscle swelling. Frontiers
  • If you’re using body‑comp‑shifting drugs: remember the pattern from ActRII blockade and GLP‑1 combos: body comp can improve without proportional performance. Treat the drug as a body‑composition tool; treat training as the quality tool. PubMed

Net answer: Lower strength per unit mass is usually a bug, not a feature. If the mass you’re adding doesn’t raise force, power, and tissue resilience, it’s misleading at best and counterproductive at worst. Fix the wiring, teach the tendons, improve the architecture. The mirror can lie; the force plate doesn’t.

1 Like
#2

We may argue that muscle tissue still constitutes a glucose sink, so at least one theoretical benefit is conserved. IF confirmed by evidence of course.

#3

I agree with @mccoy the skeletal muscle also contributes to glucose disposal, but it probably also carries some cost of adding cardiovascular stress simply from the extra mass. Not sure where the net benefit is. However, is anybody here jacked and shredded enough that this matters? :stuck_out_tongue: The way I see it, we’ll all be fighting a (losing) battle against sarcopenia as we age, so it makes sense to stock up while we can, and to try and slow the decline. If that is done naturally (i.e. no steroids or other PEDs) I can’t see any downside.

When it comes to longevity itself, function (VO2max, strength, mobility) does seem to be more important than body composition.

#4

…and probably, to the late bodybuilder in the video, it didn’t help that he had to ingest 16500 kcals per day to maintain that extra mass.

#5

Yeah, for sure. Once you’re using exogenous substances, you’ve already gone way outside of normal physiology, so all bets are off. I did (stupidly) use steroids in the past when I was in my late teens and early 20s, but thankfully never to massive excess. But the cardiac stress is definitely real - haemoglobin, HCT etc go up, plus all the extra body weight to push around.

#6

It seems like the literature on this is somewhat sparse and outdated. There is some support of myostatin blockers increasing strength when combined with weight lifting. We certainly will find out as these drugs will soon hit the market.