Applied physiology series, part two. Part one read recovery as a budget you can learn to spend; this one looks at the withdrawal from that budget that returns the most, before part three turns to sleep architecture rather than sleep hours.
Strength work was the first thing I cut. Every time.
Through the years I was building toward long-distance triathlon, the gym session was the one with no race consequence I could point at, so whenever a week got tight it went. The endurance numbers stayed fine. My VO2 max read 51.6 that October in Cascais, down on where it had sat in April, and the race still went the way I wanted it to. What I was quietly giving up across those years was the ability to produce force fast, and I never caught it, because an endurance training log has no column for that.
If you train six or seven hours in a week and work eats the rest, you have to decide what those hours are for. Strength usually loses that argument. It looks like the vanity option, the thing you do for how you look rather than for how long you last, while the endurance work feels like it’s buying something a doctor would recognise.
The physiology disagrees, and the margin isn’t small.
So, the narrow claim: strength training has the widest set of downstream effects per hour you put in. Endurance and mobility work aren’t wasted. They do things lifting can’t touch.
This is an educational and strategic perspective, not personal medical advice.
The fibres you stopped asking for
Ageing doesn’t thin muscle evenly. Everything else here follows from that.
Look at what the biopsies showed. Nilwik and colleagues compared leg muscle cross-sectional area in young and elderly men, and the difference tracked almost entirely to the size of the type II fibres, with the number of fibres largely intact (Nilwik et al., 2013). Sarcopenia, the age-related loss of muscle mass and function, is selective. One compartment deflates while the rest holds.
Type II fibres are the fast, high-force ones, and they sit at the top of the recruitment order, which means your nervous system reaches for them last and only when a movement demands real force or real speed. Sitting comes nowhere near that threshold. Neither does walking, and neither, and this is the part people resist hardest, does a steady aerobic hour. A compartment the body never gets asked for is a compartment it has no reason to keep.
What goes, then, is speed of force. You meet it when a kerb arrives sooner than you thought and you catch yourself, or when the low chair suddenly wants a hand on the armrest that it didn’t want three years ago. Nothing athletic about either. It’s the ordinary business of a day, and the reserve is there or it isn’t.
Underneath that sits the version of muscle that matters most and gets discussed least: the reserve your body draws down during illness, injury and the long immobilities that arrive later.
Some fibres lose their address
One level up from the tissue, in the wiring, a second loss runs at the same time.
Every muscle fibre answers to a motor neuron. One neuron plus all the fibres it commands makes a motor unit, the smallest thing your nervous system can switch on. Motor neurons die off with age, and when one goes, the fibres it owned are orphaned.
The body does have a repair strategy, in that surviving neighbours sprout and reinnervate the abandoned fibres, so the remaining motor units grow bigger and the muscle holds together with fewer controllers in charge. That strategy has a ceiling. Intramuscular electromyography on the tibialis anterior and vastus lateralis, run across young men, non-sarcopenic older men, pre-sarcopenic men and sarcopenic men, found the expansion happening as you would expect in the men who weren’t sarcopenic. In the sarcopenic men it hadn’t happened, and their motor units measured smaller than the ones carried by the older men without sarcopenia (Piasecki et al., 2018).
Handle that one carefully. It’s cross-sectional, every subject was male, and it locates the failure without showing that lifting reverses it.
What it does clarify is worth carrying. Strength is partly how much muscle you own and partly how much of it you can still reach, and heavy, deliberate, well-recovered efforts are what exercise the reaching. Which is why the first few weeks of sensible training change what you can lift long before they change what you weigh.
Why the same meal does less at fifty
Feed older muscle the same protein and you don’t get the same result, and the reason is more specific than a story about slowing metabolism.
Forty-four healthy young and older men of similar build were given varying doses of essential amino acids, and muscle protein synthesis was measured directly. Basal rates came out indistinguishable between the groups, which kills the intuitive idea that old muscle simply idles. The deficit sat in the response. Older muscle proved both less sensitive and less responsive to the same amino acid signal, and the machinery inside the fibre that senses amino acids and turns them into new protein, mTOR, p70 S6 kinase, eIF4BP-1 and eIF2B, showed lower expression and weaker activation after feeding, alongside a sharp rise in the inflammation-associated transcription factor NF-κB (Cuthbertson et al., 2005).
Call it anabolic resistance. The signal has to be louder before older muscle registers it at all.
The direct reading here is about protein. Sensitivity and responsiveness both fall, so the dose per meal has to be bigger to clear the same bar. Or rather, that’s the reading a dose-response trial is actually built to support, which is worth saying because the inference people usually draw from this paper is a different one.
That other inference travels further than Cuthbertson went. Anabolic resistance does argue for load that genuinely challenges the tissue over the token resistance a general fitness class hands you, because a stimulus below threshold buys you very little of what a stimulus above it buys. But this trial dosed amino acids, not barbells. Take it as a reasonable extension and not as a result.
The organ nobody counts as an organ
Muscle got reclassified over the past two decades and most people were never told.
Pedersen and Febbraio set out the case that skeletal muscle produces, expresses and releases several hundred peptides, the myokines, which act locally on the muscle and also travel in the blood to reach fat, liver, pancreas, bone and brain (Pedersen and Febbraio, 2012). Muscle sits in conversation with nearly every system that fails slowly, including the one between your ears.
On that last one I’ll go further than the evidence takes me, and I want to be visible about it rather than sly. I think strength and endurance work are the base for the mind as much as the body, and that we file as psychological a fair amount of what a badly conditioned body is producing. No paper behind that here. The literature I’d need is associative, the causal arrow runs in both directions, and I’d be doing precisely what I complain about if I dressed a belief up as a finding. So take it as a working position. It’s also the thing I’d most like someone to prove me wrong about, properly, with a trial.
The second function has a hard number on it, and past 40 it’s the one that should get your attention. Under insulin-stimulated conditions, roughly 80 percent of the glucose your body disposes of goes into skeletal muscle, which is why DeFronzo and Tripathy describe skeletal muscle insulin resistance as the initiating defect in type 2 diabetes, sitting there for decades before blood sugar rises far enough for anyone to notice (DeFronzo and Tripathy, 2009).
Put those together and the metabolic case turns concrete. The muscle you carry sets much of the storage capacity available for every meal you eat, which is the unglamorous reason strength work turns up in blood markers that look unrelated to lifting.
Unglamorous is the whole problem. A large, well-evidenced lever that moves at the speed of months will never compete for attention with the toxin of the quarter, and there is always a toxin of the quarter, because that is what the market pays for. Nobody ever built an audience on carry more muscle and go to bed earlier.
Bone listens for one specific message
Bone isn’t maintained by movement in general. That’s why so much well-meant advice about bone density disappoints.
It answers to mechanotransduction, where mechanical strain gets converted into a cellular signal, and the strain has to be high in magnitude and delivered at a high rate before the signal counts as worth building for. A narrow specification.
LIFTMOR tested that specification directly instead of assuming it. A hundred and one postmenopausal women with low bone mass were randomised either to eight months of supervised high-intensity resistance and impact training, twice weekly for thirty minutes, five sets of five reps above 85 percent of one repetition maximum, or to a low-intensity home programme. Lumbar spine bone mineral density rose 2.9 percent in the training group and fell 1.2 percent in the controls. Femoral neck density and cortical thickness both favoured training, every functional measure improved, and across the whole trial there was one adverse event: a minor back spasm (Watson et al., 2018).
Those women aren’t the typical reader here, and heavy loading in osteoporosis was held to be too dangerous to recommend for years. What transfers is the mechanism. Bone answers to load of a particular character, and outside of impact work the only reliable source of it is resistance training, which is why lifting speaks to the skeleton in a language it acts on.
The number that outperformed blood pressure
Grip strength is an odd thing to care about until you see what it predicts. In the PURE study, every five kilograms of grip lost came with a hazard ratio of 1.16 for all-cause mortality, and grip predicted all-cause and cardiovascular mortality more strongly than systolic blood pressure did (Leong et al., 2015).
Now the half that gets dropped every time this finding resurfaces. It’s an association. PURE never tested whether raising anyone’s grip lowers their risk, which would be a different study, and grip is almost certainly standing in for a lot at once: nutritional status, decades of accumulated activity, illness that has started without being diagnosed yet. Someone can be weak because they are becoming unwell. A cohort study can’t tell you which way the arrow points.
Fine. It still justifies a change of procedure. Treat strength as a vital sign, measure it next to blood pressure and lipids, track it across years, and take it seriously when it moves the wrong way.
What the work costs, and what it costs elsewhere
Two properly heavy sessions a week come to ninety minutes or two hours once you count the warm-up and the rest between sets honestly. Those hours come out of a week that already holds the endurance training you probably care about more.
Wilson and colleagues pooled 21 studies and 422 effect sizes to put a number on the interference. Hypertrophy showed an effect size of 1.23 for strength training alone against 0.85 when the same training ran concurrently with endurance work, power showed a comparable gap, and both the frequency and the duration of the endurance work correlated negatively with gains in size, strength and power. Modality mattered more than most people expect. Running produced significant decrements in hypertrophy and strength; cycling didn’t (Wilson et al., 2012).
The training literature tends to miss a second cost. Part one described the autonomic account that training, work, sleep debt and emotional load all draw on, and heavy lifting is a withdrawal from that same account. Stack two hard sessions onto an unchanged week during a brutal month at work, and the tissue will not answer the way it answers in a quiet one.
Then the pace of the thing. Strength adapts across months, a session that feels like a breakthrough is rare, and the reward for a good year is a slightly heavier bar plus a change in body composition you only really see in photographs taken far apart. I put on about 2 kg across a twelve-week build. Perfectly good result. Looks like nothing.
None of which argues the other work should go. Aerobic training builds the parasympathetic capacity part one was concerned with, in a way lifting doesn’t, and mobility work has its own narrower and frequently misunderstood job, covered separately in the Ironman series. Strength is usually the missing piece. Crowding out the rest would be its own mistake.
The twelve-week question
One question separates strength training from the thing that looks like it from outside. Can you name the load you used on your main lifts twelve weeks ago, and is today’s higher?
If the first half stumps you, the record that progress depends on was never kept, and progress nobody writes down tends not to happen. If you can answer it and the number hasn’t moved, you’ve maintained a habit and not delivered a stimulus. Your type II fibres, your motor units and your skeleton have all been getting a message they finished adapting to a while back.
Second check. Half a minute, no equipment. Stand up from a low chair five times without using your hands, and notice whether the fifth is clearly worse than the first. That tells you where your reserve sits today. It says nothing about your character, and it responds well to being acted on.
Where this leads
This is close to why an Atlas Cove week puts strength work next to the recovery data instead of in its own silo, so the load someone takes on gets decided from their actual state and never from a template. The thing I want surviving the flight home is small: load deliberately, then check whether the loading landed.
Muscle is easy to read as decoration and hard to read as an organ. That’s why it goes first when the calendar fills. Considered as an organ it’s your largest site of glucose disposal, a secretory tissue talking to most of the systems that go wrong slowly, and the only mechanical signal your skeleton reliably answers.
The work is modest in hours and dull in feel. Probably the whole reason it keeps getting skipped. Start anyway.
This is an educational and strategic perspective, not personal medical advice.
The views are the author's own and not statements by Atlas Cove Lda.
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Sources
Nilwik, R., Snijders, T., Leenders, M., Groen, B. B. L., van Kranenburg, J., Verdijk, L. B., & van Loon, L. J. C. (2013). The decline in skeletal muscle mass with aging is mainly attributed to a reduction in type II muscle fiber size. Experimental Gerontology, 48(5), 492–498. DOI: 10.1016/j.exger.2013.02.012
Piasecki, M., Ireland, A., Piasecki, J., Stashuk, D. W., Swiecicka, A., Rutter, M. K., Jones, D. A., & McPhee, J. S. (2018). Failure to expand the motor unit size to compensate for declining motor unit numbers distinguishes sarcopenic from non-sarcopenic older men. The Journal of Physiology, 596(9), 1627–1637. DOI: 10.1113/JP275520
Cuthbertson, D., Smith, K., Babraj, J., Leese, G., Waddell, T., Atherton, P., Wackerhage, H., Taylor, P. M., & Rennie, M. J. (2005). Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle. The FASEB Journal, 19(3), 422–424. DOI: 10.1096/fj.04-2640fje
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DeFronzo, R. A., & Tripathy, D. (2009). Skeletal muscle insulin resistance is the primary defect in type 2 diabetes. Diabetes Care, 32(Suppl. 2), S157–S163. DOI: 10.2337/dc09-S302
Watson, S. L., Weeks, B. K., Weis, L. J., Harding, A. T., Horan, S. A., & Beck, B. R. (2018). High-intensity resistance and impact training improves bone mineral density and physical function in postmenopausal women with osteopenia and osteoporosis: the LIFTMOR randomized controlled trial. Journal of Bone and Mineral Research, 33(2), 211–220. DOI: 10.1002/jbmr.3284
Leong, D. P., Teo, K. K., Rangarajan, S., Lopez-Jaramillo, P., Avezum, A., Orlandini, A., et al. (2015). Prognostic value of grip strength: findings from the Prospective Urban Rural Epidemiology (PURE) study. The Lancet, 386(9990), 266–273. DOI: 10.1016/S0140-6736(14)62000-6
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