One of the most interesting and important findings about how the skeleton responds to exercise came from a simple experiment done in the 1970s by a group in America. And what they did was they took x-rays of the humerus, the upper arm, of professional tennis players. And they x-rayed both sides, the serving arm and the non-serving, non-dominant arm, and they compared the bones. What they found was that in the serving arm, the bone was 30% thicker than the non-serving arm. That’s not really surprising because tennis is such an asymmetric exercise. Most of the exercise is done with that single dominant arm. And what it tells us is something extremely fundamental. That is that the response of the skeleton is site-specific.
It happens at the place that’s being loaded or unloaded. And that means it can’t be controlled by circulating hormones, which are going around your body and affecting all of your different parts of your body in the same way. They’re a constant throughout your blood system. It also means that it can’t be controlled by some general level of fitness, the sort of VO2 max, your ability to exchange oxygen which otherwise can be quite predictive of fitness. What we know is that it’s something that happens at the site where the bone is loaded. And if we’re going to understand that, we need to think about what does happen at the site where the bone’s load.
Now because I’m standing up, I’m putting pressure on my legs, and in fact, I’m shortening my bones by a very small amount. And if I jump and land like this with my knees straight, it’s very uncomfortable and unpleasant, but momentarily, I shorten my bones by a bit more as I land. And we can measure this by fixing strain gauges onto the surface of the bones in people and in animals. If you look at a range of different species, the wings of birds flying, the limbs of race horses charging across a track, and humans running in a lab with strain gauges on the bones, the maximum deformation of the bone is about the same regardless of size.
It’s a very small amount. It’s about 0.2%. And we transfer that by multiplying it by 10 to the 6th. We call it 2,000 microstrain. But it is a simple ratio of the deformation over the original length. And that number tells us how much the bone has deformed. Now the interesting thing about it is that as soon as you see the same number appearing in a range of different species and different sizes of animals, it starts to point towards there being some sort of feedback mechanism which is controlling how much that number should be. And what we think is that the maximum strain that your skeleton is exposed to is a thing that’s measured and compared with what would be optimal.
My habitual activity will generate these sorts of strains - of 2,500 microstrain, that sort of amount - by doing the most vigorous things I do. If I start exercising more, then my bones will be deformed more by the higher levels of exercise or less by a lower level of exercise. And we can construct a feedback mechanism where if that number, 2,000 microstrain is the target, then high levels of activity will cause new bone to form so that the bone gets thicker and stronger and stiffer. And that means that in response to the high level of activity, the bone deforms less back to its target strain of 2,500.
If instead of increasing exercise I reduce my levels of activity, then that low strain will cause bone resorption from this to make it thinner and more flexible. And therefore, the low levels of activity will generate those peak strains of about 2,500 microstrain. But there is rather more to it than that. There are several other variables which make a difference to how the skeleton responds. And probably the most important one of those is how rapidly you apply or remove the loads. When I did my little jump and landed on my heels, it was a very sharp impact, and momentarily, I deformed my bones by probably I should think about 1,500 microstrain.
For a very short period of time, the strain went up and then went down again. And the rate at which that happened is a very potent stimulus. If I was to load my bones very slowly over three or four seconds, that would have almost no effect as a single stimulus. If I do these jumps with very high rates of strain, that’s a very potent stimulus. So rate of strain matters as well as the magnitude of the strain. The time spent is relatively unimportant.
That means that if I exercise for a short period of time, I can switch on the maximum bone forming response with that brief period of exercise, and if I do it for much longer, it doesn’t really make much difference. Now in practical terms, that’s probably somewhere in the vicinity of 20 minutes for people. So if you go to the gym and you do some vigorous exercise for 20 minutes, you are probably switching your skeletal response on as much as it’s possible to do. Essentially, you can strength train your skeleton, but not endurance train it.
And this leads us to the concept which is a reasonably easy one of how we can actually tell whether the exercise that we’re doing is going to have an effect on the skeleton. And that is, does it build big muscles? And if you do exercises which give you big muscles, then you have bones which are correspondingly increased as a result of that. If you do some exercise which doesn’t build muscle mass - distance running, this sort of thing - then the chances are that your skeleton will be either unaffected or not affected very much.
So if you need to know what to do to make your skeleton stronger, it’s important to impose relatively high magnitudes of force during your exercise at rapid rates and for a relatively short period of time. And if you want to repeat that during the day, that’s fine. And if those exercises give you strong muscles, then you’ll get strong bones as well.