On a Whim

by Mat in Vadnais Heights

For the last six weeks, I’ve been training for a half-marathon. This is something I’ve been doing every spring for a number of years. It’s an effective way to get myself back in shape after a winter’s worth of sitting around the house. I’ve noticed, however, that this year’s training has entailed a lot more day-after muscle fatigue than previously. I guess this is to be expected. I’m edging into my late fifties, after all. But while contemplating my discomfort (read “gripping my calf and grimacing in pain”), I did also take time out to wonder a few things. The muscles in my legs, the lower legs especially, are noticeably more defined than they were a couple of months ago. And a couple of months after the race, they’ll return to normal. So how does that work, exactly? How do your muscles know it’s time to grow and, even more strangely, that it’s time to shrink?

Biologically, it makes perfect sense that you’d want to do this. It’s costly to grow and maintain muscle tissue. There’s no point in keeping big muscles around if you’re not going to use them. Better to spend your hard-won resources of protein and energy elsewhere. But you do need to hang onto enough muscle tissue to keep your day-to-day exertions covered. What to do? Well, there are multiple processes going on here, but for brevity’s sake, I’ll highlight just a couple. The others have dovetailing effects, and you can read up on them if you’re into it.

The process of building new muscle is called muscle protein synthesis (MPS). I could get all fancy and throw around terms like “mTOR pathway activation” and “insulinlike growth factor,” but let’s stick to plain language. The most often cited (but maybe not most important) mechanism operates via the small amount of muscle damage incurred by exercise, called microtears. The idea is that these tears cause nearby stem cells to fuse to the damaged fibers. The stem cells then use amino acids drawn from dietary proteins to grow into full-fledged muscle cells. The muscle is thus repaired and also enlarged at the same time.

For a long time, microtears were assumed to be the primary driver of muscle synthesis, but there are other pathways to increasing muscle mass that likely play a larger role. The key thing to remember is that all of them are ultimately biochemical responses to exertion of, tension in, or changes to the muscle fibers. A symphony of causes rather than a solo act, but nothing too mysterious.

The above explains why muscles get larger with exercise, but how do they shrink with a lack of exercise? How does your body know when to reverse the process? Here’s where things get fun.

Like so many questions of the form “how does this non-thinking thing X know to do Y,” the answer is that your body does not know when it’s time to put on the brakes. It doesn’t have to because there’s a parallel process called muscle protein breakdown (MPB) that is going on all the time. Tossing out more of the polysyllabic biology terms, this time we have the “ubiquitin-proteasome pathway” and the “autophagy-lysosome system.” Using the former as our example, ubiquitin is a relatively small molecule that latches onto the proteins within existing muscle fibers. Then the much large proteasome seeks out the muscle proteins that have ubiquitin attached, chews them up, and recycles the components.

So, there’s a baseline rate at which muscles are always going to pieces (breakdown) and an ever-shifting rate at which muscles are being built (synthesis). The combination of these two processes is called the muscle protein turnover. Your muscles live at the point of equilibrium between them. If your exercise level remains more or less the same over an extended period, it may look like nothing is changing, but in fact, your muscles are being continuously broken down and rebuilt to the same level, maintaining the status quo. If your exercise level drops because of, say, an illness or a prolonged attack of laziness, the equilibrium point changes. Synthesis drops off, and so breakdown takes over, causing muscles to shrink … but the process doesn’t go on forever. Smaller muscles must work harder to do the same job, meaning they are under more tension, incur additional microtears, etc. This reactivates synthesis. Before long, a new balance point is reached, and the shrinking halts.

Conversely, if you train for a sporting event, then synthesis temporarily gains the upper hand. It outstrips breakdown, and the muscle grows. But this also cannot go on forever. Larger muscles don’t have to work as hard to accomplish the same job, so overall tension and exertion are less, fewer microtears appear, and the rate of synthesis drops off accordingly. And again, a new equilibrium point is struck.

I am oversimplifying this enormously. The several processes going on in both synthesis and breakdown cover different specific cases, but in the broad strokes, this is what it looks like. When you drill down into biological systems, you see this kind of thing all the time. Stuff that appears to require reasoning or awareness or at least evaluation turns out to be nothing but subtle, blind chemical processes going about their business. I’m not any kind of biologist, but if I had to guess, I’d say that 99%+ of all the processes that go on in a typical human body are unthinking and autonomous. You might make the conscious decision to eat an apple because you’re hungry, but you don’t consciously direct the steps of its digestion. Or your respiration, or heartbeat, or the activities of your immune system. You’re happy to let those operate on their own.

Yeah, I’d say 99% unthinking and autonomous is a reasonable estimate. On my less charitable days, I think that for a small percentage of the people I meet, it’s actually 100%. But most likely that’s just my bad mood talking.