The Big ol’ Muscle Training Primer, Part 2
Welcome to part 2 of The Big ol’ Muscle Training Primer. Let’s get going!
How Training Muscles Works
Your muscles are maintained and developed by training, or the intentional participation in activities which are designed to stress the muscles in a healthy manner. Running, swimming, lifting weights, doing push-ups, and every other exercise you’ve ever seen or done is a form of training. Training can be smart or dumb, effective or ineffective, sport-specific or generic, strength-focused or endurance-focused. The kind of training you should undergo is very much dependent on your goals and current state of fitness. No matter your specific needs, training your muscles follows the same basic principles.
This is the process by which muscles grow in response to a stimulus. The stimulus for the growth can be hormone changes, an increase in caloric intake (and protein intake specifically), or specific training geared towards muscle growth. Usually it’s a combination of these factors. The opposite of this process is atrophy, which is a loss of muscle mass from underuse, injury, sickness, malnutrition, negative stressors, or heavy drug/alcohol use.
Here’s the basic overview of how it works: you lift heavy weights, your muscle fibers get bigger, and over time you start to see it happen in the mirror.
Now to complicate it a little more…
Muscle fibers can be different lengths, anywhere from a small percentage of the whole muscle up to the whole length of the muscle. For instance, your bicep might have a fiber that runs the whole length, and another fiber that only goes about half-way through. Your muscles are made up of a bunch of fibers.
The muscle fibers themselves are made up of myofibrils in bundles. These are so small that 100 myofibrils bundled together are about the thickness of a human hair.
Going even smaller, myofibrils are made up of even smaller filaments called actin and myosin. For a point of reference, myosin filaments are the bigger ones, and they’re about 1/10,000 the thickness of a human hair. For every myosin filament you will also have six actin filaments, and muscle contraction is caused by these filaments pulling against one another in response to a nerve impulse.
Training doesn’t create more muscle fibers, but it does cause your body to create more myofibrils in the muscle fiber, as well as increase the number of myosin and actin filaments in each myofibril.
Newbie Gains Explained
When you first start training, you tend to get stronger much faster in the beginning than you do later in your progress. This creates an exponential progress curve at the start, followed by a linear progress curve later down the line. The initial exponential strength improvement is often called “newbie gains” by lifters, and they stem from neuromuscular adaptation. Here’s how it works…
During the first few days of a strength program your muscles respond to training by remaining in a heightened state of readiness. Your muscles will feel tighter than usual, like a rope stretched taut. You may notice your posture straightening a bit or feel a little stiff.
During the first few weeks, you’ll start to notice dramatic strength gains from week to week, and sometimes even from workout to workout. Your body learns to perform a movement by systematically recruiting motor units that can be applied to the exercise. Each motor unit is a grouping of muscle fibers and nerve cells that cause the muscles to contract in the right sequence to make a given movement occur. In the first weeks you become stronger because your body dedicates more and more motor units to the moves you’re practicing, until your body has the maximum number of units dedicated to it as it can. This is called neural adaptation; it’s a precursor to muscular adaptation. Speaking of which…
Unfortunately, now your exponential strength gain ends and your linear strength gains begin.
Once your body has all the motor units dedicated to a movement that it can use, your strength gain stops being from (relatively) fast neural adaptation, and starts stemming from the thickening of the muscle fibers themselves. This thickening occurs from the addition of new protein filaments to individual muscle fibers, as well as the thickening of the extant protein filaments you already have. It generally takes 4-6 weeks to start seeing muscle changes from training.
Building muscle is a slow process, requiring a high amount of consistently progressing stimulus and maintenance. The human body isn’t predisposed to staying at a high level of muscular development, because it takes a lot of resources to keep you that way, and not a lot of our everyday activity requires big muscles. Ironically this process is almost a Catch-22: it takes a high metabolism and lots of bodily resources to maintain the muscle, but if you let it slip your metabolism down-shifts to storing unhealthy levels of fat.
Last time, we talked about how the number of muscle fibers you have is influenced first by genetics and second by usage. The number of muscle fibers you start with is determined by birth lottery: if your parents are predisposed to looking like Greek deities with impressive musculatures that don’t take much work, chances are you will be too (not guaranteed, of course, but possible). For years it’s been thought that the only way you can change the number of muscle fibers in your body is on the downside: muscle fibers can atrophy and die, reducing the overall number of fibers you have available for movement. Mainstream science hasn’t quite shown us that hyperplasia – the splitting of muscle fibers due to training, thus increasing the number of total fibers in the body – is possible in humans.
Most of the evidence that science has given us for hyperplasia even being a thing is from animal studies. In one study, researchers added small weight to one wing of a bird, increasing the constant load on that wing for an extended period of time. At the end of the research period, the bird was euthanized and biopsies were done of both wings. Generally you would expect to see similar fiber size and density in both wings, but what they found was more interesting. Not only were the muscle fibers in the weighted wing bigger – which is typical of muscles undergoing regular stimulus – but the weighted wing also had a significantly higher muscle fiber density compared to the unweighted wing. At some point, the muscle fibers began to split, creating new fibers that subsequently hypertrophied to become larger.
These results have been seen in other animals, like rats, where muscles trained to a significant degree by regular stimulus were dissected. In these cases, pockets of smaller muscle fibers were seen inside the otherwise large and healthy muscle tissue. This evidence suggests that the fibers split during training in response to the animals’ needs for stronger muscles. The other explanation is that somehow select muscle fibers atrophied while all the others got stronger, and that seems very unlikely.
So what about humans?
Well the big issue here is that you can’t train a human and then autopsy them right afterwards to count their muscle fibers. That kind of thing is hard to justify and get funding for. The second issue is that humans have many, many more muscles and muscle fibers per muscle than smaller animals. For instance your bicep can have more than 500,000 muscle fibers and that isn’t even the biggest muscle group you’ve got. This makes it incredibly hard to find small differences in muscle fiber density, even if those differences would be considered statistically significant.
One promising study looked at the cadavers of otherwise healthy young men between the ages of 18-32, specifically taking cross-sections of their left and right Tibialis anterior muscles (see picture). Using fancy scientific analysis (specifically, myofibrillar adenosine triphosphate characteristics) they determined that the left leg muscle had a higher total number of muscle fibers than the right leg muscle. All of the young men were right-handed, and the brain tends to compensate for handedness by favoring one side over the other (left side in this case). The findings show that daily, low level stimulus of a muscle group can seemingly cause muscles to undergo hyperplasia, providing more opportunity for growth and development.
Another animal study more directly tested muscle training (e.g. weight training) to determine if hyperplasia was possible in cats from the stimulus. Dr. William Gonyea of UT Southwestern Medical Center in Dallas, Texas found that when the cats used one paw exclusively to “train” (i.e. press a lever to receive food reward), the working arm showed between 9-20% increase in muscle fiber count. The cats that pressed the lever slowly and deliberately also saw greater muscle growth than the cats which pressed the lever quickly/ballistically.
Whew! I think that’s enough science for today. Next time we’ll talk about what training can be used to induce hypertrophy and, maybe, hyperplasia too.