Genetics and training response: why two people don't progress alike

Two people join the same gym, run the same programme, eat roughly the same and sleep about as much. Three months later one has added 15 kg to their squat and can see the change in the mirror; the other has added 5 kg and is wondering what they are getting wrong. The usual explanation is "genetics". That is partly right, and a lot less tidy than it sounds.

What follows separates three things that get blurred together whenever this comes up: what is firmly established, what is likely but still open, and what gets sold as science without being any.

What is firmly established

Differences in response to the same training are large and repeatable. When a group runs an identical, supervised programme, the results do not line up neatly around the average. Some gain twice the group mean, others barely register a change. The evidence here is consistent, and the pattern shows up whether you measure strength, muscle size or endurance.

Part of that difference is inherited. Comparisons within families and between twins show that starting points — muscle mass, strength, aerobic capacity — cluster clearly along family lines. Estimates of how much of the spread is inherited tend to land somewhere near half, but the figures move about from sample to sample and should not be treated as precise. Improvement itself, meaning how far someone shifts from their own starting point, also clusters within families.

Anatomy is fixed and it has consequences. Bone lengths, where a tendon attaches, hip and shoulder width, the number of muscle fibres you were born with — training does not change any of it. It sets your leverages, which lifts will feel natural, what a grown muscle looks like on you, and how much technical work a given movement will need before it feels comfortable.

Fibre type is partly inherited. The mix of fast and slow fibres varies between people and explains some of why one person naturally sprints better and another handles long distances better. Training shifts fibre subtypes and changes their size, but it does not rewrite the whole picture.

What is probable but not settled

There is no single muscle gene. The most plausible current picture is hundreds of variants, each contributing a tiny amount, interacting with sleep, diet, stress and your movement history. The individual variants that have been studied most explain a very small slice of the difference between people.

A true non-responder probably does not exist. When people who failed to progress on one dose of training are given more sets or more sessions per week, a large share of them start moving. The same person can also respond poorly on one measure, say strength, and perfectly normally on another, say endurance or size. This is persuasive, but the samples are small and the follow-up short — treat it as a working assumption, not a law.

The lasting trace of past training, often called muscle memory. The idea that a muscle which was once big comes back more easily has strong support in animal work and partial support in humans. That regaining is faster than building the first time is visible in practice and in measurements. Exactly why, and how long the trace lasts, is still poorly resolved.

How much of "genetics" is really hidden recovery. Sleep, chronic stress, protein intake and simple attendance vary between people as much as genes do, and they are far easier to change. How the spread in progress splits between those and inheritance has not been separated in a way that gives you a number.

What gets reported badly

Genetic tests that reveal whether you are a power or endurance type. They have been on sale for years, but the evidence that acting on their advice beats a plain three-month trial run is weak. The best-known variant in that story, the one tied to the alpha-actinin-3 protein, is indeed more common in elite sprinters, yet in any one individual it explains far too little to build a programme on.

Sorting people into ectomorphs, mesomorphs and endomorphs. As a rough description of build it is harmless conversation. As a basis for prescribing rep ranges, carbohydrate intake or training style it has no support.

"Bad genetics, so why bother." The variability being described is variability around an average that is positive. Almost everyone improves; the difference is in speed and in the eventual ceiling. For anyone in their first three years of lifting that ceiling is a theoretical question rather than a practical one — what is and is not known about it is laid out in the piece on the upper limit of muscle growth.

Measurement noise gets read as biology. Day-to-day swings in maximal strength of 5 per cent are ordinary, scale weight moves 1–2 kg on water and food alone, and body fat estimates carry more error than most people assume: calipers, bioimpedance scales and DEXA do not tell the same story. A few flat weeks are often a measurement problem rather than a physiological one.

Responding to a supplement is not the same as responding to training. With creatine, for instance, some people notice little because their muscle stores are already high from their diet. That has a clear mechanical explanation and says nothing about how well you respond to a barbell; the detail sits in the article on creatine dosing and the loading phase.

What this means for your training and diet

You do not choose your genetics, but you do choose the dose and the consistency. In practice:

• Give a programme 8–12 weeks before judging it. Anything shorter and you are reading noise. Log loads and reps, not how the session felt.
• If nothing moves, change the dose before you change the programme. The usual step is from 8–10 to 14–20 hard sets per muscle group per week, spread over two sessions rather than one.
• Track more than one outcome. Some people gain strength with little visible size change, others the reverse. Measure only one thing and you will award yourself non-responder status for no reason.
• Match exercise selection to your leverages. Long femurs change what a good squat looks like, and grip width in the deadlift is not a fashion choice. Pain that keeps coming back is not toughness to push through, it is a sign the variation does not suit you.
• Protein at 1.6–2.2 g per kg of bodyweight per day covers essentially everyone. Above that there is no extra growth on offer.
• Sleep 7–9 hours. It is the one variable that moves both recovery and the willingness to train, and it is the most underrated.
• Compare yourself with your own numbers from three months ago, not with someone else in the room.

The same picture from the point of view of two lifters on one programme is worked through in why two people on the same programme progress differently and in what is known about speed of response to training.

When to see a doctor

Slow progress on its own is not a medical problem. See a doctor, though, if it comes with unexplained fatigue lasting weeks, strength going backwards despite training regularly, unintended weight loss, breathlessness at efforts you used to handle easily, chest pain, or a family history of early heart trouble. Thyroid problems, anaemia, low iron and sleep disorders all produce a picture that passes easily for bad genetics.

In short

Differences in training response are real, large and partly inherited, and the evidence there is strong. Which genes and how much is unresolved, and no test you can buy will tell you today. What stays in your hands is the training dose, protein, sleep, and the patience to give it three months before drawing conclusions. For most people who believe they have bad genetics, changing the number of sets changes the picture.