Genetics. I know it’s a touchy subject. Discussing genetics means addressing some of the most fundamental and emotion-laden questions we face.
How much of success comes from talent, and how much from hard work?
How much control do we really have over our outcomes?
Am I really in control of my life, or am I just a product of my DNA and my environment?
Hell, even most scientists (at least in America) aren’t particularly interested in studying genetics’ impact on athletic performance, and the government isn’t interested in funding such research. I think this is a topic that makes everyone a little uneasy.
I assume that we’re all coming to this discussion with our own prior beliefs and biases. As with most topics of discussion, it seems like the most extreme voices are also the loudest.
On one hand, we have the notion that’s deeply ingrained into the Western (and especially American) psyche that hard work is the only thing that separates the best from the rest; we start life on a level playing field, and the choices we make are the sole determinants of our outcomes. This was the cornerstone of John Locke’s tabula rasa (blank slate) philosophy that was at the cornerstone of the enlightenment, and it’s been bolstered in recent years by Malcolm Gladwell’s 10,000-hour rule (which, I’ll note, is mostly wrong. More practice tends to be better than less practice, but there’s nothing magical about 10,000 hours, and 10,000 hours of practice does not guarantee you’ll become a master of whatever you were practicing).
On the other extreme is genetic determinism: the idea that your fate is preprogrammed by your genes and the environment that you grow up in. You may feel like you’re in the driver’s seat, but really you’re just along for the ride, slave to genes and circumstance (this idea is also overly simplistic).
Most of us, I think, believe something in between those two extremes. In this article, I want to explore the degree to which factors that are largely outside of your control influence your success in the gym and discuss how I think we should respond to that information.
Just a quick note before we dive in: In this article, I’m using “genetics” as a catch-all term for all of the factors that have worked together to shape your responsiveness to training as an adult. Among these are truly genetic factors (discrete genes), genomic factors (higher level genome-wide interactions), and factors that were at work in utero and your environment in early childhood that have shaped your body and the way it responds/adapts to training (factors that aren’t purely genetic, but that have a very strong influence on the rest of your life). In effect, when I use the term “genetics,” it’s generally short-hand for “factors that shape how you respond to training that are mostly or entirely outside your control once you’re an adult.” Unless you’re someone researching genetics and heritability, the distinction between those factors and the super granular details really don’t matter very much.
But I thought our genes were 99.9% similar…
A lot of people automatically recoil at the idea that genetics significantly shape our responsiveness to training.
After all, humans share 99.9% of the same genes. Sure, there’s some variation, but it can’t be that large, can it?
As an aside, 99.9% is the commonly cited figure you’ll see in most textbooks. Actually, people of European ancestry got about 1.5-2% of their genes from Neanderthals, and some Aborigines and Pacific Islanders got up to 6% of their genes from Denisovans – another ancient group of hominids. However, those other groups were very similar to homo sapiens (the genes themselves are very, very similar), and with another 100,000+ years of evolution and interbreeding under our belts, these slightly different ancestries likely don’t make a huge difference. Just a fun fact to be aware of.
So, you’d expect us all to be almost exactly the same, right?
Well, actually, we are … at least at the level of what proteins we can make. Genetic similarities only tell you how many of the same proteins two animals can make, and most animals that function in similar ways (for example, mammals, all of whom are warm-blooded and give birth to live offspring) are necessarily going to share a whole bunch of the same proteins. Behind the huge physical differences we see, there are a ton of similarities on the cellular level. Those similarities deal with much more fundamental functions like metabolism, immune function, reproduction, digestion, and respiration, all of which are managed by a whole host of genes that we all share as humans and that we largely share with all other mammals.
Small differences make a huge impact on your phenotype (how you actually look and function), though. We share 97-99% of our genes with other primates like chimpanzees, gorillas, and baboons, 92% of our genes with mice, 44% of our genes with a fruit fly, and 26% of our genes with yeast.
Under the microscope, our DNA may only be 1% different from a chimp, or 8% different from a mouse, but at the level of the entire organism – how we look, how we think, and how we function – I think we’d all agree that the gap between humans and chimps is larger than 1%, and the gap between humans and mice is larger than 8%. Small differences (even the 0.1% difference between humans) in our DNA can mean big differences in appearance and function.
Furthermore, there are different versions of various genes that function a bit differently, while still being a part of that 99.9% similarity. For example, there are two versions of the ACTN3 gene (which we’ll discuss later) which plays a role in explosive performance. One version of the gene is beneficial for power performance, and the other version of the gene has a negative effect on power performance (and may have a positive effect on aerobic performance). So far, there are 22 genes like this that have been identified for strength/power performance, with one version of the gene being beneficial, and the other version of the gene having a neutral or negative effect.
On top of different versions of genes, you can also have varying numbers of the same gene. For example, the gene that codes for salivary amylase – an enzyme that starts the digestion of starches as you chew – is the same in almost everyone, but different people vary in how many copies of the gene they have. The more copies of the gene you have, the lower your obesity risk is. The people with the fewest copies (fewer than 4) have an 8x higher obesity risk than the people with the most copies (more than 9). People with more salivary amylase genes and higher salivary amylase are able to break down more starches as they chew, which may help them feel satisfied sooner when eating and allow for better blood sugar and insulin regulation.
Finally, even if you have the same number of the same versions of the same genes, gene expression also differs between individuals due to both lifestyle and epigenetic factors.
So, while we may be 99.9% genetically similar, there’s still a lot of room for those genes to behave very differently between individuals.
How much variability is there for getting jacked?
The short answer: A lot.
Before training, about 80% of the total lean mass differences between people can be explained by genetic differences. Of course, lean mass scales with height and weight (both of which are also strongly genetically influenced), but even after controlling for height and weight, genetics still explain about half of the variation in lean mass relative to body size. Other factors related to performance are strongly influenced genetically as well. Height and skeletal structure are, obviously, and about 45% of muscle fiber type distribution seems to be explained by genetic factors (and the non-genetic influences primarily occur during early childhood, which you also don’t have much control over).
Once you add training into the mix, things diverge even more.
In one study, 585 people trained their non-dominant arm for 12 weeks. The study involved 6 sets of curls and triceps extensions, building from 12rm loads to 6rm loads over the course of the study (linear periodization). It wasn’t explicitly stated, but I’m assuming the training sessions were only once per week. On average, the participants’ biceps got about 19% bigger and their 1rm biceps curl increased by about 54%.
However, the range of responses was huge. Several people’s biceps actually got slightly smaller (even though they were untrained at the start of the study), while one person’s got 59.3% larger. The variability in strength gains was even larger, from several people not gaining any strength at all, to one person increasing their 1rm biceps curl by 250%.
Another study looked at quad growth. This one also used untrained subjects, but it employed a more intense training program – 3 sets of 8-12 (to failure) for squats, leg press, and knee extensions, 3x per week, adding weight when possible for 16 weeks.
After training, they split the 66 subjects into three groups: “nonresponders,” “modest responders,” and “extreme responders.” The nonresponders and extreme responders were the quarter of participants who gained the least and most amount of muscle (17 per group), while the modest responders were in the middle one-half (32 people).
On average, the nonresponders’ muscle fibers didn’t get meaningfully bigger or smaller.
The modest responders’ muscle fibers got about 28% bigger on average. Not too shabby for 16 weeks of training.
The extreme responders’ muscle fibers grew 58% on average. They got roughly twice the results of the modest responders.
In fact, one person’s muscle fibers actually grew dramatically more than even the average extreme responders.’
Assuming that person’s average muscle fiber cross-sectional area was near the extreme responders’ group mean to begin with, that would mean his/her muscle fibers got 75-80% larger in only 16 weeks.
Interestingly, group differences for strength gains were much smaller. While the extreme responders’ muscle fibers grew twice as much as the modest responders’, and the nonresponders’ muscle fibers didn’t grow at all, total strength gains were fairly similar. The nonresponders’ and modest responders’ 1rm leg extensions increased by about 35-38% over the course of the study, while the extreme responders’ 1rm got about 45% stronger. The extreme responders still did the best, but the gap was much smaller.
What’s telling, though, is the pattern of strength gains. All the groups gained a pretty similar amount of strength in the first 8 weeks. However, the nonresponders made almost 80% of their total strength gains in the first 8 weeks of the study and didn’t get much stronger thereafter, while the modest responders and extreme responders only made about 2/3 of their total strength gains in the first 8 weeks and were still gaining strength at a solid pace after 16 weeks.
This makes sense: Most of the initial strength gains you make in response to training revolve around neural adaptations; you do gain muscle, but you also get much better at producing force with the muscle you already have. The nonresponders could gain strength at the same pace as the modest and extreme responders for the first 8 weeks because their lack of hypertrophy wasn’t much of hindrance yet. However, after another two months, only the two groups with robust muscle growth were able to keep adding strength quickly.
One thing worth noting in this study is that it included young men and young women (20-35 years old), as well as older men and older women (60-75 years old). The natural inclination might be to assume that the extreme responders were simply the average young men in the study, while the nonresponders were primarily the older subjects. However, that wasn’t the case. While the young men tended to be either modest or extreme responders, and 38% of the older subjects were non-responders, each age/sex group had at least one member in all three responder clusters, and about half of the members of each group wound up in the modest responders cluster.
It’s also worth noting that training volume, intensity, and adherence were reported in this study; none of those variables differed between groups. You can’t just assume the extreme responders got better results because they trained harder.
Another study by Davidsen follows this same trend. This study is noteworthy because it was the only one (that I’m aware of) specifically studying the range of hypertrophy/strength responses where nutrition was controlled and monitored.
Out of a group of 56 trainees, the researchers compared the top and bottom ~20% of responders. The high responders gained roughly 4x as much lean mass over the 12-week training program: 4.5kg (~10lbs) versus a bit over a kilo (2-2.5lbs) of lean mass for the low responders. The high responders’ type I muscle fibers grew 16% versus 6% for the low responders, and the high responders’ type II muscle fibers grew 26% versus 8% for the low responders.
Much like the previous study, though, differences in strength gains were much smaller. The high responders’ leg press and leg extension strength did increase slightly more than the low responders’ did, but the differences didn’t reach statistical significance (it was close for leg extension, though: 72% vs. 59%, p = 0.075).
Lest you think the variability in training response only applies to strength training, a major, multi-site aerobic training study found a huge degree of variation as well.
They trained 481 sedentary participants for 20 weeks. The average VO2max (the primary measure of maximal aerobic power) increase was around 300-450 mL of oxygen per minute. However, some people actually saw a small decrease in VO2max, while others had increases larger than 1,000mL of oxygen per minute – more than doubling the average increase.
Good training for you may not be good training for me
There’s at least one major weakness of the four studies I discussed in the last section: All the participants in each study used the same training program.
In other words, each study doesn’t necessarily tell you the range of how well people respond to training in a general sense; they tell you the range of responses to an individual training program. This also helps explain the non-responders. These studies don’t say that some people are simply unable to gain muscle, strength, or endurance. They say that the training programs used in the studies didn’t increase some people’s muscle mass, strength, or endurance.
If you spend enough time in the gym, it becomes obvious that different people respond better or worse to different styles of training. Some of this variability can be ascribed to factors that universally affect how people ought to train and how they respond to training – factors like training history, stress outside the gym, how much sleep they’re getting, whether they’re in a calorie surplus or deficit, whether they’re eating enough protein, etc. However, it’s foolish to assume that such factors explain all of the variability. At a very basic level, different stuff just works better or worse for different people.
Now, there are certainly things that tend to work better or worse for the majority of people. That’s the type of stuff that science typically tells you, and the type of stuff you learn as a coach if you have a predominant training system that you tweak over time based on how the majority of your athletes respond. That’s the type of stuff I typically write about on this site: the stuff that we know works the best (or at least better than the alternatives) for most people, most of the time. I’m not saying for a second that anecdote trumps evidence.
Not everyone is the “average” trainee, and not everyone responds well to the same type of training the “average” trainee does. Just pick any popular training program, and run a Google search for reviews of that program. Universally, you’ll find people who did astoundingly well and people who got terrible results. Some people do better training with higher reps, and some people do better training with lower reps. Some people thrive on more variety in their training, and some people do better sticking with a small number of exercises. Some people need higher training frequency, and others do best with lower training frequency.
There’s not just a ton of scientific evidence to back up this observation yet, but the studies are starting to accumulate.
- 3 sets of 5 reps at 85% 1RM with 3 minutes of rest between sets
- 4 sets of 10 reps at 70% 1RM with 2 minutes of rest between sets
- 5 sets of 15 reps at 55% of 1RM with 1 minute of rest between sets
- 4 sets of 5 reps at 40% of 1RM with 3 minutes of rest between sets
After each workout, they looked at the athletes’ acute testosterone and cortisol responses. They trained each athlete for 3 weeks with the protocol that elicited the highest testosterone:cortisol ratio, and for 3 weeks with the protocol that elicited the lowest T:C ratio. Each of the four protocols elicited the highest T:C ratio for some people, and the lowest for others. The athletes gained dramatically more strength on the protocol that gave them the highest T:C ratio. Each of the four protocols got some people great results, and other people middling-to-poor results. Unfortunately, however, this was a very short study, so it’s impossible to draw too solid of conclusions from it.
Another study found that people with a particular variant of the ACE gene gain strength just as well with single-set training programs as with multi-set training programs, whereas people with the other (more common) variant tend to do their best training with multiple sets.
Finally, a recent study actually used genetic information to prescribe different training programs.
The researchers selected 15 gene variants that have been previously associated with either power output or endurance. They examined those gene variants in two groups of athletes – one group from a variety of sports, and one group that was exclusively composed of soccer players – and identified the athletes who had more of a power-related genotype, and those who had more of an endurance-related genotype based on the different versions of those 15 genes they possessed.
They tested the athletes with the countermovement jump (to test power output) and a 3-minute cycling test (to test endurance) at the beginning and end of an 8-week strength training program.
The athletes trained with one of two training programs: one program used 30% of the athletes’ 1rms and employed higher reps, and one program used 70% of the athletes’ 1rms and employed lower reps.
Half of the people with each genotype trained with low reps, and half trained with high reps. The hypothesis was that using a training program that matched your genotype would produce better results, so the researchers expected the people with power genotypes to do better with heavier weights and lower reps, and for the people with endurance genotypes to do better with lighter weights and higher reps.
Sure enough, that’s what they found; the athletes who used the training plan matched to their genotype got almost 3x the results, on average, compared to the athletes who trained with the protocol mismatched to their genotype.
The researchers also looked at the high responders, modest responders, and low responders for each test. For both the countermovement jump and the 3-minute cycling test, 80%+ of the high responders were on the training program that matched their genotype, around half of the modest responders were on the training program that matched their genotype, and less than 20% of the low responders were on the training program that matched their genotype.
Now, I do have to give a word of caution about this particular study. One of its main aims was to validate a proprietary algorithm used by a private company (DNA fit), and the lead researcher is in that company’s sport performance department. There were clearly financial incentives behind getting “good” results like this. Furthermore, there were a lot of dropouts, which also makes me raise an eyebrow.
On the other hand, they did run the experiment twice and get similar results with two different cohorts of athletes, and I recognize one of the authors, John Kiely, as a very well-respected coach and academic; it would surprise me if he’d put his name on the study if there was any fishy business, but it’s impossible to know for sure. (Kiely’s work is excellent, by the way. Everyone should read this essay.)
The main takeaway here is that research is starting to validate the observation that athletes and coaches made long ago: people don’t just differ in terms of how well they respond to training in general; they also differ in what type of training they respond best to. Or, at the very least, that’s the direction the research is leaning, and I personally expect it to keep leaning further in that direction as more work is done.
Short-term vs. long-term
Keep in mind: All of these studies are short-term. Sure, some of them may run 16-20 weeks, but you’re going to be training for decades. These studies tell you about the variability in short-term training responses, but they don’t tell you very much about the results you can expect long-term.
Long-term results also seem to be strongly influenced by genetic/heritable factors. There are four major factors that will determine how much muscle (and therefore strength) you can ultimately build:
- The size of your frame. Assuming the other measures of skeletal size (breadth and depth) are as heritable as height, about 70-95% of the variation in frame size is explained by heritable factors.
- How many muscle fibers you’re born with. Muscle fiber number is set at birth due to both genetic factors and uterine environment and remains essentially unchanged throughout adulthood. Yes, there’s some evidence for muscle hyperplasia (increase in muscle fiber number, rather than hypertrophy – increased size of the individual muscle fibers – which is the primary route of muscle growth), but for all intents and purposes, you’re stuck with the same number of muscle fibers from the day you’re born until you start gradually losing muscle fibers in old age. If you’re born with fewer muscle fibers, that will cap how much muscle you can ultimately build.
- How well you respond to training. We’ve already covered this. While the studies to date really just show that some people respond better than others to individual training protocols, it’s also undeniable that some people really do just respond better to training in general.
- Whether you take steroids or not. It seems that how well you respond to exogenous hormones is genetically influenced as well. Obviously, steroids make a larger and larger impact with higher doses, but – in general – it seems that steroids help people gain roughly twice as much muscle over the course of a training career.
Now, to know for sure the degree to which genetic factors impact long-term muscle growth, we’d need a 20-year randomized control trial with great adherence and training/nutrition programs optimized for all of the individuals in the study. Unfortunately, that’s never going to happen.
However, there are a couple of ways to roughly estimate your long-term potential to gain muscle and strength based on the size of your frame. I wrote about them here and made some nifty on-page calculators you can play around with:
How can I know how good my genetics are?
At this point, you’re probably wondering if there’s an easy way to tell whether you have good genetics for getting jacked and strong.
There isn’t. Not an easy, accurate way at least.
Now, you can get genetically tested. However, most of the genes that have been identified so far that affect performance are known to affect either endurance or power performance, not necessarily strength and hypertrophy. While strength and hypertrophy affect power output, many of these genes (like the ACTN3 gene) affect structural proteins that impact power output independent of muscle size and capacity for force output. Most of these genes were identified by examining the genetic profiles of successful athletes in endurance sports like running and cycling, and power sports like sprinting, jumping, or throwing. There’s a bit less known about the genes that directly impact strength and hypertrophy.
Additionally, most of the genes that are currently known to affect strength, muscle mass, and performance contribute very little (less than 2-3% for most of them) to results individually. Add to that the fact that there are 22 genes thus far that are known to affect power or strength performance, and you’re almost guaranteed to get a mixed bag of results if you got gene tested. Based on the known frequencies of the “good” and “bad” versions of those 22 genes, almost everyone would have the “good” version of between 8 and 14 of those genes, which isn’t unambiguously good or bad news for anyone. (Just as a fun aside, the odds of an individual having the “good” version of all 22 genes is roughly 1 in 2,000 trillion; in other words, it’s a near certainty that no human being has ever existed who had perfect genetics for strength/power performance, and as more genes are discovered that affect strength/power performance, those odds will just keep getting smaller and smaller.)
Even the rare single genes that do independently make a large difference don’t guarantee you’ll be a great (or even good) athlete, and their absence doesn’t preclude you from still becoming an elite athlete.
For example, the ACTN3 gene codes for a protein that’s crucial for rapid muscle contraction in fast-twitch muscle fibers; many of the other genes known to affect performance alter some specific signaling pathway slightly in some way or another, but the ACTN3 gene makes a protein that directly impacts how powerfully a muscle can contract. Obviously, it’s an important gene for power performance – probably the most important individual gene yet identified – and unsurprisingly, most elite power athletes have two working copies of this gene. However, in one study, 8% of elite male sprinters (“elite” defined as having represented their country in international-level competition) had no working copies of the gene, and 39% only had one working copy of the ACTN3 gene. Now, all of the Olympic sprinters in the sample had at least one working copy of the gene, so two non-functional copies of the ACTN3 gene may very well guarantee you won’t be an Olympic-level sprinter, but a non-negligible proportion (about 1 in 12) of international-level sprinters were still able to compete with a “bad” genetic draw for a crucially important gene for power performance. Likewise, two working copies of the ACTN3 gene don’t guarantee you’ll be a particularly good sprinter; it just slightly increases your odds.
Check out this study comparing the genetic profiles of elite rowers to the genetic profiles of non-athletes, for instance. While the Master of Sport rowers in this study did have higher allele frequencies for “good” gene variants than the non-athletes, the differences weren’t particularly big – enough to let a scientist know those genes are helpful, but not enough to make them overly predictive unless perhaps you had the “good” or “bad” versions of all of them.
So, taken in totality, gene testing is an easy way to predict potential (provided you’re willing to drop a few hundred bucks on it), but likely not a particularly accurate way, unless someone just happened to be an outlier with an exceptionally, unambiguously good or bad genetic draw.
You could also get muscle biopsies taken before and after a workout to analyze changes in gene expression, satellite cell activation and proliferation, and microRNA levels. These have all been shown to be mildly-to-strongly predictive of muscle growth. Of course, most people aren’t going to go quite that far. Here’s a video of a muscle biopsy. If you want to go that route, though, then more power to you. And if you’re willing to take a few trips to and from a lab, getting your muscle protein synthesis rate measured for 48 hours after a workout and comparing it to average rates may give you a quite accurate idea of how much muscle you’ll keep gaining (as long as you’ve been training for at least three weeks), but most people wouldn’t want to sink the time and money into that process.
Data gleaned from biopsies and measured rates of protein synthesis seem to be accurate (more accurate than gene testing most of the time, at least), but getting this data for yourself isn’t nearly as easy.
Finally, there are the “methods” most commonly used to predict potential for getting big and strong: how jacked you were naturally before you started lifting, or how much strength you gained in your first few months of training.
Unfortunately, neither of these methods are particularly useful; their predictive value borders on zero.
In Davidsen’s study, the high and low responders for hypertrophy were physically indistinguishable to start with. They had, on average, the same BMI, the same amount of fat-free mass, the same size fast-twitch and slow-twitch muscle fibers, and the same 1rm leg press, and the same 1rm leg extension.
In Bamman’s study, the high and low responders also had the same size muscle fibers and the same levels of strength to start with.
In Hubal’s study, the amount of muscle gained didn’t correlate with initial muscle size.
In another study examining the effects of different molecular and gene networks on muscle growth, the authors split people out by quartiles based on their growth response. They noted that baseline lean mass, age, and physiological characteristics were the same between all four quartiles, and “the highest and lowest quartiles for lean mass gain had exactly the same proportion of males and females.”
Changes in strength tell a similar story. Remember, the high and low responders in Davidsen’s 12-week study gained similar amounts of strength. In Bamman’s study, the nonresponders, modest responders, and extreme responders all gained the same amount of strength for the first 8 weeks, and the modest responders and extreme responders gained the same amount of strength over all 16 weeks. In Hubal’s 12-week study, there was actually a negative correlation between initial strength and amount of strength gained (the people who were the weakest initially actually gained the most strength), while there was no meaningful correlation between initial muscle size and hypertrophy, seeming to indicate that propensity for growth likely wasn’t strongly associated with strength gains.
In general, it seems that trainability and initial size and strength are completely independent factors. The best of the best are likely people who have high baseline amounts of strength and muscle while also being highly trainable, but it doesn’t seem that your size and strength when you first hit the gym influences how well you’ll respond to training.
That means those inspiring stories of, “I was so skinny, and then I got JACKED in spite of the fact that I obviously have bad genetics” are, unfortunately, bullshit. Those people had the same odds of responding well to training as anyone else did.
Similarly, it seems that, on average, high responders and low responders gain similar amounts of strength for at least the first 8-12 weeks of lifting, then have divergent responses thereafter.
That means that even if your strength gains aren’t all that stellar for your first few months of lifting, you may still be gifted for putting on size, ultimately giving you a high ceiling for strength gains. In the story of the tortoise and the hare, this would be the tortoise. Of course, that means there are also hares who initially gained a lot of strength when they first start lifting, but who had issues putting on enough muscle to keep getting stronger.
Genetics vs. practice
In the nature/nurture debate (which is largely fizzling out because the answer is a clear “both” almost all the time), there’s also the trusty third option: “This is all fatalistic bullshit, and I’ll pull myself up by my own bootstraps with my hard work, dedication, and 10,000 hours of practice. Get out of my way, plebs.”
Unfortunately, that’s probably not going to happen.
A recent meta-analysis found that practice generally accounts for less than 1/4 of the variability in performance across broad domains. For sports, amount of practice seems to only account for about 18% of the variability in performance. Practice and hard work do certainly matter, but you can’t outwork a bad genetic hand.
The way I think of it, working really hard and really smart can move you up a “level.”
If you have the genetics to be poor (with a “normal” amount of work), you can work your way up to “average.”
If you have the genetics to be average, you can work your way up to “good.”
If you have the genetics to be good, you can work your way up to “great.”
If you have the genetics to be great, you can work your way up to be among the best of the best.
But the person at the top of the heap? They worked hard, but they also picked the best set of parents.
(It’s also worth noting that how consistently someone will practice – conscientiousness – is somewhat influenced by genetics as well.)
Does this apply to diet as well?
Yes. Obesity is highly heritable (due to genes, uterine environment, and early childhood influences), and a series of studies by Bouchard showed that in response to long- and short-term overfeeding, the rate of gain and loss for both weight and fat varied 3- to 10-fold, with twins tending to gain/lose similar amounts of both weight and fat.
In one particular example, after 84 days of being overfed by 1,000 calories per day, the most unlucky person gained every last ounce of weight they were “supposed to” given the caloric surplus and their baseline metabolic rate (almost 30lbs) and had massive increases in abdominal fat, while the luckiest person gained a shade less than 10lbs and virtually no abdominal fat. Of course, genetics can’t break the laws of thermodynamics; this variability was likely due to varying changes in Non-Exercise Activity Thermogenesis (NEAT). In another example, after 93 days of eating maintenance calories while adding cycling to cause a caloric deficit, the luckiest person lost 5x as much abdominal fat as the least lucky person.
What can I do about it?
How you can use this information for your own training and expectations
Here what we know: There’s a huge variability of responses to training, and the type of training people respond best to seems to vary as well.
However, there’s no easy and accurate way to know how well you’ll respond to training, or what type of training you’ll respond best to.
Also, as I discussed in a previous article, expectations can dramatically affect outcomes.
You never know how good of a hand you were dealt until you play it with the expectation that it’s a good hand. Furthermore, you need to train consistently for at minimum four months before you can have a reasonable idea of how well you respond to a particular training program if you’re just starting out (you’ll probably have a good idea sooner if you’re more experienced). If you don’t respond well initially, you should try out at least 2-3 more programs with different programming styles to see if you simply didn’t respond well to the first style of training, while you may still respond very well to another style of training. This piece of advice applies to people who respond well to training too: Don’t be afraid to experiment with your training until you find a style that best suits your unique psychology and physiology.
If you don’t put in at least a year of consistent, challenging training with a good attitude and high expectations about your prospects, you probably aren’t justified in confidently claiming that you have bad genetics for lifting. Yes, your genetics may be to blame for lackluster results, but you shouldn’t be quick to jump to that conclusion and use it as an excuse. If you do so, you may just be turning it into a self-fulfilling prophecy and wind up squandering your potential.
However, maybe you’ve been at this for several years and you’re pretty damn sure you just didn’t pick the right parents to get super big and strong. If that’s the case, my best advice for you is to simply work on finding ways to enjoy training more. Find a style of training that’s simply fun and helps you stay excited about training, and shift from worrying about outcomes to focusing on enjoying the process.
Strength training has too many benefits to list (but some biggies include improved cognitive health, improved self-esteem, and decreased mortality risk), and many of them don’t necessarily depend on the hypertrophy and strength gains you make; many of them come from the process itself. Perhaps the biggest benefit is that continued strength training will help you age more gracefully; muscle strength and functionality tends to drop off faster with age than muscle mass itself, due somewhat to neurological changes, but primarily due to disuse (which also precipitates some of those neurological changes). Continuing to lift may not help you build much more muscle and strength, but it will help you maintain muscle, strength, and functionality as you age.
It’s also worth noting that your “genetics” can improve over time. No, not the actual genes themselves, but epigenetic factors (things that influence which genes get turned on and off) tend to change for the better in response to exercise, and along with/in addition to epigenetic factors, gene expression patterns, systemic inflammatory state, and your body’s hormonal environment tend to change and improve in response to training as well. All of these things can help you respond better to training. I’m not going to blow smoke up your ass and say that these shifts will take you from zero to hero, but I know plenty of people whose results are barely noticeable over any short-to-moderate-length period of time, but who’ve still attained solid results over 5-10+ years by simply grinding away and making improvements little by little.
If you have good genetics for training … you probably don’t need a pep talk. Keep getting jacked.
How you can use this information to view others’ results
- Don’t be a dick to people who are having a hard time. Don’t automatically assume someone’s being lazy because they haven’t reached some arbitrary level of strength in some arbitrary period of time. Some people just don’t respond nearly as well as others. It’s not fair, but that’s just the way it is.
- Don’t automatically assume someone knows what they’re talking about because they’re big and strong, or that they don’t know what they’re talking about because they’re smaller and weaker. This is a point I raise to my own detriment, but it’s one I feel strongly about. (Here’s an old article I wrote on the topic; if I could re-write it, I’d use Science and Practice of Strength Training and Zatsiorsky and Kraemer as my examples instead of Supertraining, Siff, and Verkhoshansky, but on the whole it’s one of my few older articles I don’t cringe re-reading). On the whole, I’d assume that bigger and stronger people are more knowledgeable as a group, but that doesn’t necessarily apply to all individuals. Don’t write off someone smaller and weaker than you, because they may have just not been dealt a great genetic hand for training.
Wrapping it up
Genetics, along with other factors that are outside your control by adulthood (including uterine environment and circumstances in early childhood), strongly influence how well you respond to training. Genetic factors likely influence the style of training you’ll respond best to, as well.
However, there’s not an easy, accurate test to predict how well you’ll respond to training. In fact, high responders and low responders, on average, have nearly identical amounts of muscle and strength pre-training, and since early strength gains are primarily driven by neural factors rather than hypertrophy, differences in strength gains take more than 3 months to show up.
You need to put a lot of time and effort into training (with a good attitude and high expectations) before you can blame genetics for your lack of progress.
Since there is such a huge range of responsiveness to training, you shouldn’t automatically assume someone knows what they’re talking about because they’re jacked, or that they’re lazy or know less about training because they’re not an impressive physical specimen.
At the end of the day, all you can do is train hard for a long time, experiment with your training style, and play the hand you were dealt to the best of your abilities.
If you’d like to hear even more about genetics and their impact on training, check out the webinar I’ll be holding on June 9th on this topic (Note: that is not an affiliate link, and I’m not compensated based on the number of attendees).