Applied Physiology #2 - Past 40, the muscle on your frame is doing metabolic, skeletal and structural work that has almost nothing to do with how it looks.
Second part of the applied physiology series. Where the first part treated recovery capacity as an account to be read, this one examines the demand on that account with the broadest return, ahead of a third part on the architecture of sleep rather than its duration.
Anyone holding down a serious job while training five to seven hours a week eventually has to rank those hours, and resistance work is usually the thing ranked last. It carries the reputation of a cosmetic pursuit, while the aerobic hours feel as though they are purchasing something a physician would sign off on. That ranking becomes difficult to defend once the tissue itself is examined, because muscle turns out to be the body's principal glucose store, an endocrine tissue in its own right, the only stimulus the skeleton reliably answers, and the buffer consumed by illness and immobility in later decades. What follows sets out the biology at the depth it deserves, then asks what each finding changes about an already crowded week.
This is an educational and strategic perspective, not personal medical advice.
The fibres that disappear first
Ageing does not thin muscle uniformly, and that detail changes what the training has to accomplish. Nilwik and colleagues set the leg muscle cross-sectional area of elderly men against that of young men and then read the biopsies, finding the shortfall sat almost entirely in the size of the type II fibres while fibre numbers were largely preserved (Nilwik et al., 2013). Sarcopenia, the age-related decline in muscle mass and function, is a targeted loss rather than a general one.
One compartment shrinks, and it happens to be the compartment reserved for force produced quickly. Type II fibres sit at the top of the recruitment order, which means they are engaged only when a task demands real force or real speed, and very little in a sedentary day or a steady aerobic hour issues that demand.
Tissue the body is never asked for is tissue it has no reason to fund. Expressed as behaviour rather than histology, what fades first is the ability to generate force in a hurry, which is the ability behind recovering a stumble, rising from a low seat unaided, or moving something heavy up a stairwell.
Fibres that lose their neuron
A parallel decline runs in the control system rather than the tissue. Each fibre answers to a motor neuron, and one neuron together with the fibres under its command constitutes a motor unit, the smallest thing the nervous system is able to activate. Neurons are lost with age, and their fibres are left without instruction.
Repair is attempted, in that adjacent neurons extend new branches and adopt the stranded fibres, so the remaining units grow larger and total mass is defended. Piasecki and colleagues applied intramuscular electromyography to the tibialis anterior and vastus lateralis in young men, older men without sarcopenia, pre-sarcopenic men and sarcopenic men, and located the point at which the repair gives out, since unit size had grown in the men who were not sarcopenic and had contracted in those who were (Piasecki et al., 2018).
The design was cross-sectional and the participants were male, and no claim can be made from it that training restores lost motor units, so it maps the failure without prescribing a remedy. Its useful residue is that strength depends both on the muscle a person possesses and on how completely they can summon it, and the summoning improves within weeks of loading heavy enough to require it.
The same protein, a smaller answer
Identical meals stop producing identical results, and the reason is traceable to specific signalling rather than to metabolism in the abstract. Cuthbertson and colleagues supplied graded amounts of essential amino acids to 44 healthy young and older men matched for build, and measured the synthetic response in the muscle itself.
Resting synthesis rates were the same in both groups, which disposes of the idea that older tissue is simply ticking over more slowly. The gap opened on the response side, where older muscle proved less sensitive and less responsive to an identical dose, and the sensing apparatus that translates amino acids into synthesis, mTOR, p70 S6 kinase, eIF4BP-1 and eIF2B, was both less abundant and less strongly activated after feeding, with NF-κB elevated alongside it (Cuthbertson et al., 2005).
The phenomenon is anabolic resistance, and its practical consequence is that the stimulus has to be raised before ageing tissue registers it. Mechanically that favours load heavy enough to be genuinely demanding, since a stimulus under the threshold is not a gentler version of training but a different activity altogether. A larger per-meal protein dose follows as a plausible corollary, though that extends past what the trial examined and is offered here with correspondingly less confidence.
An organ that speaks, and an organ that stores
Muscle has been reclassified over the past twenty years without much of the news reaching the people training it. Pedersen and Febbraio assembled the evidence that the tissue manufactures and releases several hundred peptides, collectively the myokines, which act on the muscle itself and also travel, exerting endocrine effects on fat, liver, pancreas, bone and brain (Pedersen and Febbraio, 2012).
Far from consuming the body's resources passively, muscle is in dialogue with most of the systems that deteriorate quietly.
The storage function is easier to quantify and lands closer to home for anyone watching their markers. When insulin is elevated, something in the region of 80 percent of the body's glucose disposal is handled by skeletal muscle, which is the reasoning behind DeFronzo and Tripathy's description of skeletal muscle insulin resistance as the opening move in type 2 diabetes, established years before glucose readings begin to look abnormal (DeFronzo and Tripathy, 2009).
Placed side by side, the two functions explain why resistance work registers in laboratory values with no obvious connection to lifting, because the muscle a person maintains is a substantial part of the capacity available to absorb what they eat.
What bone is listening for
General movement does not maintain the skeleton, which is why a good deal of sincere advice about bone density fails to deliver. Bone answers to mechanotransduction, the translation of mechanical strain into a cellular instruction, and the strain has to be both large in magnitude and rapid in application before the instruction is issued.
The LIFTMOR trial put that requirement to the test rather than presuming it. A hundred and one postmenopausal women with low bone mass were allocated either to supervised high-intensity resistance and impact training across eight months, two thirty-minute sessions weekly at five sets of five repetitions above 85 percent of a one repetition maximum, or to a low-intensity programme at home. Lumbar spine bone mineral density gained 2.9 percent under training and lost 1.2 percent under the control condition, femoral neck density and cortical thickness moved in favour of training, functional measures improved throughout, and the trial recorded one adverse event in the form of a minor back spasm (Watson et al., 2018).
Those participants are not the readers of this piece, and heavy loading in osteoporosis was for years regarded as reckless, so what carries across is the requirement rather than the percentages, namely that the skeleton responds to a narrow class of loading which essentially only resistance training supplies.
A predictor, not a lever
Hand grip looks like a trivial thing to measure until its predictive record is examined. Within the PURE study, grip strength ran inversely to all-cause mortality, with a hazard ratio of 1.16 attached to every five kilogram decrement, and it forecast all-cause and cardiovascular death more accurately than systolic blood pressure managed (Leong et al., 2015).
Precision matters with a result of this kind, because findings shaped like this are routinely inflated on their way to the reader. The relationship is associative, and no test was performed of whether improving grip strength improves anyone's outlook, which would require a trial that has not been run at comparable scale.
Weakness plausibly stands in for several things at once, among them nutritional state, a lifetime of accumulated activity, and disease already under way but not yet identified. Someone may be weak because they are falling ill, and an observational cohort cannot settle which way the causation runs. The defensible conclusion is procedural, in that strength deserves recording and tracking with the seriousness given to lipids or blood pressure, rather than being filed under personal preference about how to spend an afternoon.
The cost, stated plainly
Two genuinely heavy sessions occupy between ninety minutes and two hours weekly once warm-ups and inter-set rest are counted without optimism, and that time comes out of a schedule already committed to the aerobic training most people would rather protect.
Wilson and colleagues quantified the collision across 21 studies and 422 effect sizes. Hypertrophy registered at 1.23 under resistance training in isolation against 0.85 when endurance work ran alongside it, power separated similarly, and both the frequency and the duration of the aerobic component correlated inversely with gains in size, strength and power. Modality proved decisive in a way few people anticipate, since the decrements in hypertrophy and strength attached to running and not to cycling (Wilson et al., 2012).
A second cost rarely appears in the training literature at all. The first part of this series described a single autonomic account funded by training, work, disrupted sleep and emotional demand together, and heavy loading draws on that account rather than arriving free of charge, so two hard sessions cannot simply be appended to a punishing quarter and expected to produce the response they would in a calm one.
The timescale is the last of it. Adaptation accrues across months, no individual session announces itself, and a productive year yields a modestly heavier bar alongside a compositional shift visible only in widely spaced photographs, which is a thin dividend in motivational terms and the real explanation for most people stopping.
None of this displaces the rest of the work. Aerobic training develops the parasympathetic capacity the first part of this series was concerned with, in a manner resistance work does not replicate, and mobility training answers a narrower question examined in the second part of the Ironman series. Strength is simply the component most often absent, not the component that should crowd out the others.
The question to ask in twelve weeks
A single question distinguishes strength training from an activity that merely resembles it from outside. Do you know the load you handled on your principal lifts three months ago, and does today's load exceed it?
An inability to answer means the record on which progression depends was never kept, and unrecorded progression has a way of not occurring. An answer accompanied by an unchanged number means the practice has preserved a routine without supplying a stimulus, and the type II fibres, the motor units and the skeleton have been fielding an instruction they finished responding to some time ago.
A second assessment costs thirty seconds and requires nothing at all, in that you rise from a low chair five consecutive times without recruiting your hands, and observe whether the fifth repetition has degraded noticeably from the first. A disagreeable result describes your present reserve rather than your character, and reserves of that kind are responsive to attention.
Where Atlas Cove fits
An Atlas Cove week sets resistance work beside the recovery measurements rather than in a compartment of its own, so that the load someone accepts follows from the state they are actually in instead of from a template written in advance. The aim is that both habits, loading with intent and checking whether the loading is registering, outlast the journey home.
Muscle invites being read as an appearance and resists being read as an organ, which is precisely why it is surrendered first when a diary tightens. Read as an organ, it is the body's largest destination for glucose, a secretory tissue in dialogue with most of what declines slowly, the sole mechanical instruction the skeleton acts on, and the buffer that will decide how much an illness at seventy-five is able to remove. Defending it takes few hours and produces little drama, which is very likely the whole reason it goes.
This is an educational and strategic perspective, not personal medical advice.
Tom Wuerden · Co-Founder
Engineer turned Ironman