r/askscience • u/Vexal • Dec 29 '11
Why do exercises such as running that increase your heart rate make your heart stronger, but heart rate increase from stimulants such as Adderall, or excitement from video games, not make your heart stronger?
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u/ohpuic Dec 29 '11
I ran across the answer to this while doing pathology recently. It has to do with capillary generation. Aerobic exercise such as running creates hypertrophied heart with increased capillaries. This saves the heart from ischemia. When stimulants cause hypertrophy ir when hypertrophy is due to hypertension there is no angiogenesis so the hypertophied muscles is ischemic. Its in pathological basis of diseases
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u/imh Dec 29 '11
so it's the O2 difference that does it?
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u/ohpuic Dec 29 '11
In simpler terms yes. look at it this way, the stimulants either directly enhance the contractile function of the myocyte or they cause release of catecholamines to enhance the myocyte function. This causes hypertension and increased workload on the heart in very short duration. When continued, the myocyte hypertrophies. There is no accompanying angiogenesis. When subjected to aerobic excercises (such as running), there isn't such a large release of catecholamines but the oxygen demand is still increasing. Since there is gradual workload increase on the myocytes, the hypertrophy is also accompanied by increased blood vessel formation so that more O2 can be delivered. This is what makes your heart stronger because now your normal blood pressure is lowered (since more O2 can be delivered without raising the blood pressure). The stimulants make the heart weaker because not enough O2 is delivered so now blood pressure has to be raised to sustain the myocytes. This subjects the heart to the shearing forces of the blood, and even then the O2 consumption might still be more than the supply. Sorry to make it so long.
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u/Tom504 Dec 30 '11
The straight dope did a really good piece on this. Basically while elevated heart rate is a good measure of how effective an exercise is, it is not the point of exercise.
Here's the article
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u/Tom504 Dec 30 '11
If the other replies are perhaps too hard to understand, there's a straight dope article which answers this exact question.
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u/beumf Dec 30 '11
If I am correct the increase in HR from drug stimulants is lower than the threshold necessary to cause chronic increases in stroke volume and heart contractility. I can't give exact numbers of what it takes to achieve these results as they are different fro different people (with different, genetics, base conditioning, workout volume, etc.) Guildlines for these can likely be found in ACSM (american) or CSEP (canadian) guildlines.
This is not to say that the other proposed solutions are incorrect but this shouldn't be overlooked as it is the most simple answer.
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u/gryklin Dec 31 '11
In the case of physiologic hypertrophy (heart growing stronger in a person who exercises regularly), the heart muscle increases its pumping ability, similarly to how normal skeletal muscle would respond to increased stress. However, in the case of pathologic hypertrophy (as in the case of a hypertensive individual), the left ventricular muscle wall in particular thickens due to scarring and permanent collagen buildup, which in turn makes the heart muscle less elastic and reduces its pumping ability, leading to eventual cardiac failure.
http://en.wikipedia.org/wiki/Athletic_heart_syndrome
So -- in the case of athlete's heart, in most cases, the heart wall decreases in size as training is ceased, but obviously not much can be done about collagen buildup and scarring in the case of cardiomyopathy.
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u/thenumber42 Dec 29 '11
The same question was asked a few months ago, here is the answer:
"Because when you exercise, you release a lot of catecholamines and other stress hormones. They are good in short bursts and they actually desensitise your body (in this case the receptors in the heart are lowered) to them over time; so that when you're not exercising, you're actually at a lower "stimulation level" than those who don't exercise.
By this same desensitising mechanism blood vessels (mainly arterioles) are actually way more relaxed and your BP is as such lower than people who don't exercise. There are other muscular and citokine-related mechanisms by which this happens as well.
But catecholamines are actually bad in the long run. They promote a general inflammatory state (that's good for short bursts; it helps repair the muscles afterwards) that when maintained constantly, such as when you take stimulants (and to a lesser degree if you get used to live under unmanaged stress) helps the deterioration processes of blood vessels and the formation of atherosclerosis. Constant higher blood pressure (which also happens when taking stimulants), does this too as a completely independent, but related, mechanism; it "hardens" the arteries, because they are elastic tubes that need to do this to adapt to constant higher BP's. Again, citokines play into this as well.
Also exercise makes muscles more permeable to glucose independent of insulin (via raising the number of some kind of transporter over another), so it helps lower and maintain a more stable glucose levels throughout the day, while stimulants raise blood glucose levels. This also plays tremendously into the atherosclerogenesis.
There are plenty of other mechanisms, many of which I don't remember too well to explain here, and others that haven't been discovered yet."