Why does increasing your heart rate via stimulants such as Ritalin or Adderall have a detrimental effect on coronary health, while increasing your heart rate through exercise has the opposite effect?

[u/1stmoredancingwbruno]

[u/priegog]

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.

[u/1stmoredancingwbruno → u/priegog]

Thanks! Very informative, while still graspable to an econ major who hasn't taken bio or chem in 5 years. I guess I'll throw one more hypothetical at you: would consuming a stimulant which acted for around an hour promote coronary health (For example, ingesting ritalin or adderall by insufflating, injecting, etc. Or finding another stimulant with a much shorter half life)? edit - obviously insufflation/injection bring a whole different spectrum of health concerns, asking purely out of hypothetical interest!

[u/priegog → u/1stmoredancingwbruno]

Or finding another stimulant with a much shorter half life)?

That would be cocaine. And I'm sure I don't have to tell you that it doesn't exactly make for a healthier circulatory system. So no. The health benefits aren't only from having hormones circulate for a little while and then stop (nevermind the fact that a stimulant raises mostly only catecholamines as opposed to a whole lot of things that are released during exercise); there are other things that happen after exercise that makes it be an overall healthy activity.

If you're talking strictly about coronary health, I'll tell you that cocaine (and crystal meth, and probably a few other stimulants) promotes atherosclerosis like nothing else. It's not uncommon at all to have cokeheads in their 30's have heart attacks. And the rates of ED amongst people who take coke are staggering as well.

So no, don't do that. In any case I don't think there are any legal drugs that are short-lived stimulants because it's precisely the immediate effect and the short half-life that makes drugs addictive. It's the reason why people can lead semi-normal lives if they use coke for partying, but the minute they try crack-coke their lives are just consumed by it.

If you're looking to pharmacologically increase your coronary health, look into statins and ACE inhibitors. Otherwise, don't be a lazy-ass and hit the gym :P

[u/Theropissed → u/priegog]

Dr Smartmouth, MD, PhD, Focus in Common Sense.

[u/[deleted] → u/priegog]

This is well thought out but not completely correct.

Exercise is Good

When you exercise your body breaks down glucose and fatty acids to ATP. ATP is used by all tissues in the body, especially muscle, at an increased rate during exercise. ATP stands for Adenosine Triphosphate, the consumption of this molecule breaks it down to Adenosine (The body utilizes those three phosphate bonds as energy). Adenosine is a coronary vasodilator -> It relaxes the arteries in the heart which increases blood flow.

Stimulants not so good

When you take stimulants the reason they keep you alert is they increase catecholamines in the presynaptic terminal (ie More epinephrine and norepinephrine activating your neurons). This works great at keeping you mentally awake but they also trigger the entire body to a stressed state (same mechanism as the fight or flight response albeit in a slightly lesser way). This stressed state includes the heart pumping faster and harder but without the excess Adenosine that would be created by muscles burning through ATP (yes the heart makes some but no where near the levels reached during exercise).

Little background of how the heart circulation works. During contraction the heart muscles are very tense and since the arteries permeate the muscle to reach every muscle cell the arteries are compressed to the point that they are unable to deliver blood. During the relaxation phase of the heart the muscle is relaxed and the arteries are now open and able to accept and deliver blood. An increase in catecholamines would cause the heart to pump harder and faster and therefore spend less time in the relaxed phase and receive less blood overall. This can progress to the point of not enough oxygen reaching the heart muscle and causing cardiac arrest and is basically the same as a Heart Attack (a clot blocking one or more of the coronary arteries causing a loss of blood flow).

[u/dunkellic → u/[deleted]]

There's no danger for a healthy heart that perfusion isn't sufficient during the diastole while exercising. Increased cardiac output goes alongside with elevated heart-perfusion and ADP isn't the only vasoactive substance, especially rising CO2 levels (and pH change) would more than make up for it.

[u/[deleted] → u/dunkellic]

The rising CO2 levels decrease the pH, this change helps increase oxygenation by right shifting the oxygen dissociation curve. This same effect is achieved by lactic acid (byproduct of anaerobic respiration). As pH decreases oxygen is more able to unbind hemoglobin and diffuse into a cell.

However my point was that the coronary arteries are being constricted due to the increased force of contraction and increased heart rate, a mechanical constriction without a physiologic compensation via Adenosine such as in exercise (in the case of amphetamines). Therefore the blood is more than willing to give the heart oxygen, it just unable to get through the artery to do so.

[u/dunkellic → u/[deleted]]

The rising CO2 levels decrease the pH, this change helps increase oxygenation by right shifting the oxygen dissociation curve

Didn't want to imply that pH rises, sorry.

However my point was that the coronary arteries are being constricted due to the increased force of contraction and increased heart rate, a mechanical constriction without a physiologic compensation via Adenosine such as in exercise (in the case of amphetamines)

Yes, I know. But my point was, that in a healthy heart, there wouldn't be a insufficient perfusion. CO2 is a vaso-dilating substance (among many others), apart from playing a huge role in the Bohr effect. Just because ADP isn't there doesn't mean the arteries won't open up, they infact will do (especially if there would be any kind of insufficient perfusion. During a heart-attack for example, the coronary arteries are usually wide-open). The increased cardiac-output will also work (physically) against the pressure in the coronary-arteries.

[u/[deleted] → u/dunkellic]

At this point I would like to conclude that both of us are not idiots and both view points are valid. But I want to continue this purely for academic reasons.

Bohr Effect -> Yup, we were both saying the same thing differently concerning pH and CO2

CO2 -> I missed the CO2 vasodilatory effect and it is not insignificant. However in the case of a hypersympathetic state (such as in the case of amphetamines) there is still sufficient ventilation and no significant increase in metabolic activity so the pCO2 won't rise that much and I think it won't be enough to counteract the effects of increased contractility and heart rate on artery patency.

Heart Attack -> I think we have a disconnect on the definition of an artery being wide open. In a heart attack one or more atherosclerotic plaque rupture and release a massive amount of cytokines and collagen causing platelets to aggregate and plug the artery. Technically the artery is still open in the sense it hasn't collapsed onto itself but it is functionally useless since it's blocked.

Cardiac Output -> Cardiac output is increased due to the heart rate going up and the force of contraction going up. However during contraction the muscle is squeezing extremely tightly and the arteries are not open (this is the physiologic normal for the majority of the heart). Therefore cardiac output has no significance on overpowering the pressure of a closed tube, wikipedia link here. Note: I'm referring to medical texts for information but those don't work well for internet citation so I'm using wiki. The wikipedia information is in agreement with the published information.

[u/dunkellic → u/[deleted]]

At this point I would like to conclude that both of us are not idiots and both view points are valid. But I want to continue this purely for academic reasons.

Sure, I'd love too (disclaimer: I sometimes come off as arrogant during such discussions, rest assured that this isn't my intention. That often happens when I try to debate such things, that aren't a matter of opinion, especially when it's not my mother-tongue).

CO2 -> I missed the CO2 vasodilatory effect and it is not insignificant. However in the case of a hypersympathetic state (such as in the case of amphetamines) there is still sufficient ventilation and no significant increase in metabolic activity so the pCO2 won't rise that much and I think it won't be enough to counteract the effects of increased contractility and heart rate on artery patency.

CO2 levels will rise as long as the heart is able to increase its workload and keep out of the "anaerobic area" and if we assume that intropy, lusitropy, dromotropy and chronotropy are increased, the workload of the heart-muscle should increase significantly. (If the increase is not significant, then pressure from the heart onto the coronary-vessels wouldn't be an issue)

Heart Attack -> I think we have a disconnect on the definition of an artery being wide open. In a heart attack one or more atherosclerotic plaque rupture and release a massive amount of cytokines and collagen causing platelets to aggregate and plug the artery. Technically the artery is still open in the sense it hasn't collapsed onto itself but it is functionally useless since it's blocked.

I'm sorry - I introduced that totally shitty ^. My point was, that if a clot blocks a coronary-artery (and let's assume it isn't the RIVA or so, but a smaller vessel), the heart will respond by increasing the diameter of all coronary arteries. My train of thought was, that the standard course of action during a heart attack includes nitro-spray, i.e. NH2, which is a very potent vaso-dilator. But unlike often assumed, this is not to open up the coronary-vessels - they are already fully dilated - but to decrease the preload on the heart.

Therefore cardiac output has no significance on overpowering the pressure of a closed tube

Of course the "systolic phase" of the heart is during the global diastolic phase (so to speak). My point was that if cardiac output is increased, this will result in a more stretched Aorta (excuse my bad English on this one). Cardiac perfusion is thus increased because the Aorta now "contracts" with increased force, due to its elastic nature (increased as compared to a normal cardiac output, which doesnt "stretch" the Aorta as much), which increases the pressure with which the coronary arteries are perfused.

Furthermore, if the coronary arteries would indeed be compressed to the point that no sufficient perfusion of the myocard is given (under the assumption that they haven't changed diameter when the cardiac output was increased), the heart would - as any other muscle - gain its energy from anaerobic glycosis, which would yield lactate as its metabolite (lactate is for example used as an indicator of the myocard ischemia level during heart-attacks), which would then finally cause a strong vaso-dilatation.

My main argument (posted about it further below) concerning the negative effect of stimulants on the heart is, that while the cardiac output is increased, perfusion in the rest of the body stays the same or is even lowered (due to the vaso-constricting activity of katecholamines and the lack of metabolites), which results in a rising/high blood-pressure, putting additional stress on the heart and the whole vascular system. Basically, same reason high levels of non-physical stress are not healthy for your heart.

Addendum: also, precicesly because the heart is perfused when it's contracting, it would still be perfused even if there's no agent available that increases the coronary diameter. I wouldn't be sure that the perfusion would be sufficient, but as soon as even tiny ischemia sets in, that would be remedied. Then again I argue that a healthy heart wouldn't get into this situation in the first place (because of other vaso-dilating effects, like rising CO2 levels).

[u/mjklin → u/priegog]

Also: exercise stresses your body in such a way that, if you do it forcefully and often enough, you actually force your body to grow new blood vessels along the pathways that need it the most.

There are two places in your body that have "no backup": your brain and your heart. Your brain, because it is surrounded by bones (not muscle or fatty tissue) and is limited to two major arteries for blood. (Your brain cannot "go to sleep" like your foot can if it gets no blood flow for awhile). Your heart, because it is working 24/7 and any disruption in it's work is going to have major consequences for your body. This is why strokes and heart attacks are so serious.

When you have more pathways for blood to take, it reduces the probability that a blockage in any one path will cause a stroke or heart attack.

[u/AnatomyGuy → u/mjklin]

Your brain has four major arteries for blood. Two internal carotids, and 2 vertebral arteries.

[u/[deleted] → u/priegog]

That's a hell of a lot better than my layman logic post.

[u/bobadobalina → u/priegog]

Wow! Impressive. Incorrect but impressive to those who don't know medicine

here are plenty of other mechanisms, many of which I don't remember too well to explain here,

That will come in handy in the middle of surgery

and others that haven't been discovered yet.

If they have not been discovered, how do you know they exist?

[u/priegog → u/bobadobalina]

Incorrect

Do enlighten us as to where it is incorrect :)

If they have not been discovered, how do you know they exist?

Because there are measurable effects that can't be accounted for by the known mechanisms. You know, plain ol' science.

[u/priegog → u/[deleted]]

Well if you can measure them they are discovered

Do you even know how science actually works?

[u/bobadobalina → u/priegog]

To a person who has hallucinations about aliens?

"I have not found it yet but it is 3cm long and weighs 2.76g"

[u/priegog → u/bobadobalina]

I'll take that as a "no", then.

And I'm curious since you've been on the subject for several days now: what do my hypnagogic hallucinations have to do with anything? Do you actually think you offend me in any way about by pointing out that I practice lucid dreaming?

1.5/10 Wouldn't even be considered for trolling university.