Effects of Calcium Channel Blockers on Resistance Training, Strength and Hypertrophy
Not sure if this is the best location for this question?
I have a high resting heart rate. I had been prescribed Cardizem LA, which is a Calcium Channel Blocker, for this condition. I figured that after losing so much weight and being so active that this condition would have corrected itself but it hasn't. My resting heart rate is about 68 or so when I'm on the medication. But, jumps to 85 or so when I'm off of it. This is a mild improvement, but not enough to warrant taking me off the drug.
I'm wondering what kind of impact this has on my training. I asked my doc, but he wasn't really able to give me much of an answer. He doesn't really understand weight training and can't seem to connect to what I'm doing.
Anyone have any ideas?
Also, I found this study (link below) but, I honestly can't make heads or tails of it. It's over my head.
From my own experience, I went down to a consistent 57-60 resting heart rate about 3 or 4 months after starting this kind of running (both track and gym equipment). It has been this way for about 4 years now.
I've went from 245lbs. to 175lbs. I don't do much aerobic work. I do one day a week of intervals, and one or two days of long slow walking. This has brought my resting heart rate down from 90-95 down to about 85 (sans medicine).
It might also be worth mentioning that I drink a lot of caffeine. I asked my doc about this and he said this its not likely the cause, but that it couldn't hurt to cut it out. With all the other changes that I've made over the past few years, cutting the caffeine hasn't been a priority. Though I'm thinking about taking that step soon.
From a strictly physiological and common sense point of view, I would think that it might effect your training. Calcium plays a huge part in muscle contraction, and if that's blocked, I would venture to guess that it could certainly hinder performance. I couldn't make much of that study either, though.
High caffeine consumption definitely affects heart rate (sympathetic stimulation). I was and still am to some degree a caffeine junkie. And by doing the training in the article and cutting caffeine my HR dropped dramatically. High resting HR can also be indicative of cardiac efficiency (again see article).
High Resting heart rate means less efficient. I'm not sure if that's what you meant.
And I thought a higher EF was better because it pumped blood more efficiently. That's what I have always heard and been told, even from doctors.
Yes.
EF is explained in the article. EF 55% or greater is normal. When EF gets very high it can be from a restrictive or tense/tight LV (means greater percentage of blood in LV being pumped out). My EF went down because stroke volume increased= more blood going out per beat, LV doesn't need to contract as hard to maintain same cardiac output (which is also why resting HR decreased), therefore EF decreased (but still normal value). So EF decreasing was good in this case (as I explain in the article).
Not sure if this is the best location for this question?
I have a high resting heart rate. I had been prescribed Cardizem LA, which is a Calcium Channel Blocker, for this condition. I figured that after losing so much weight and being so active that this condition would have corrected itself but it hasn't. My resting heart rate is about 68 or so when I'm on the medication. But, jumps to 85 or so when I'm off of it. This is a mild improvement, but not enough to warrant taking me off the drug.
I'm wondering what kind of impact this has on my training. I asked my doc, but he wasn't really able to give me much of an answer. He doesn't really understand weight training and can't seem to connect to what I'm doing.
Anyone have any ideas?
Also, I found this study (link below) but, I honestly can't make heads or tails of it. It's over my head.
Those results suggest the drug slows down muscle recovery from training, which I think is not a good thing.
The pharmacological action of the drug is actually dilation of some blood vessels (blood vessel contraction by smooth muscle is very calcium dependent) especially near the heart which reduces local blood pressure. Because the blood vessels are wider there is less resistance to pump blood through them so in this way the drug produces increased cardiac output.
This mechanism of action seems nice but I never liked amlodipine (most prescribed Ca channel blocker in my region) because of the less nice side effect profile. I don't know how your specific cardiovascular situation is, but there might be better drugs for you then calcium channel blockers, especially against high blood pressure but you did not mention that.
Personally I would not think of high resting heart rate in itself as a reason to prescribe drugs at all, so I guess there is more?
Otherwise it is always good try to improve your cardiac output by means of training, off course.
My EF went down because stroke volume increased= more blood going out per beat, LV doesn't need to contract as hard to maintain same cardiac output (which is also why resting HR decreased), therefore EF decreased (but still normal value). So EF decreasing was good in this case (as I explain in the article).
Quote:
"EF decreased slightly from 74% to 69% (the normal range is 55% or higher). This is actually good because it means that my heart doesn’t have to pump as hard (increased efficiency) since more blood is going out with each beat."
That doesn't make any sense. EF is a measure of the percentage of your blood in heart (well, usually just LV, as you said) pumped out with each beat. More is better in this case. I don't get why are you saying that it's good that it decreased?
A decreased EF means that your heart is now working less efficiently and will need a higher RHR to continue normal blood flow. EF can't go down if SV increases. EF = SV/EDV. Higher SV will always increase EF.
That doesn't make any sense. EF is a measure of the percentage of your blood in heart (well, usually just LV, as you said) pumped out with each beat. More is better in this case. I don't get why are you saying that it's good that it decreased?
A decreased EF means that your heart is now working less efficiently and will need a higher RHR to continue normal blood flow. EF can't go down if SV increases. EF = SV/EDV. Higher SV will always increase EF.
I have my master's in cardiopulmonary disease and I also spoke with 2 of the cardiologists I work with to make sure I had my facts straight before I submitted the article. It doesn't make sense because you don't understand the concept.
EF is the percentage of blood in the LV going out with each beat. If you look at the numbers in the article, EDV (end diastolic volume) increased from 135.9 ml to 168.54 ml. So the volume of the LV increased which lead to increased stroke volume. Since the amount of blood exiting with each beat is greater the heart doesn't have to contract as hard to maintain the same output (or in this case better output which is why my HR decreased). SV= EDV-ESV(end systolic volume).
I didn't include ESV in the article. But here it is:
Old values EDV-ESV= 135.9 ml- 35.6 ml = 100 ml (old stroke volume)
New EDV-ESV= 168.54 ml- 52.3 ml= 116 ml (new stroke volume)
Old EF 74% x 135.9 ml = 100 ml (old stroke volume)
New EF 69% x 168.54 ml = 116 ml (new stroke volume)
As you can see higher SV DOES NOT always increase EF (unless EF was already compromised below 55%). The LV is now more efficient because it has become more elastic. More volume exiting allows the heart rate to decrease to maintain the same cardiac output at rest. Cardiac output= stroke volume x heart rate.
I have my master's in cardiopulmonary disease and I also spoke with 2 of the cardiologists I work with to make sure I had my facts straight before I submitted the article. It doesn't make sense because you don't understand the concept.
EF is the percentage of blood in the LV going out with each beat. If you look at the numbers in the article, EDV (end diastolic volume) increased from 135.9 ml to 168.54 ml. So the volume of the LV increased which lead to increased stroke volume. Since the amount of blood exiting with each beat is greater the heart doesn't have to contract as hard to maintain the same output (or in this case better output which is why my HR decreased). SV= EDV-ESV(end systolic volume).
I didn't include ESV in the article. But here it is:
Old values EDV-ESV= 135.9 ml- 35.6 ml = 100 ml (old stroke volume)
New EDV-ESV= 168.54 ml- 52.3 ml= 116 ml (new stroke volume)
Old EF 74% x 135.9 ml = 100 ml (old stroke volume)
New EF 69% x 168.54 ml = 116 ml (new stroke volume)
As you can see higher SV DOES NOT always increase EF (unless EF was already compromised below 55%). The LV is now more efficient because it has become more elastic. More volume exiting allows the heart rate to decrease to maintain the same cardiac output at rest. Cardiac output= stroke volume x heart rate.
I do understand, and I also know what all of those terms mean. SV, by itself does always increase EF. That's a fact. I shouldn't have said that EF can't go down if SV increase. That was wrong. What I mean was, in this case, EDV just increased enough to make EF lower, but that doesn't take away from the fact that SV is directly proportional to EF.
I am, however, still missing something. I get that it became more elastic and therefore allowed for a greater EDV. The greater EDV naturally increases SV because there is more blood in the LV to pump. But you said "the amount of blood exiting is greater so the heart doesn't have to contract as hard". Doesn't the heart have to contract harder to cause the increased in blood exiting? That's what I'm not getting.
And why would an increased EF be good, because that's why my cardiologist and electrophysiologist told me in the past? I thought that lower heart rate and increased EF means the heart is not working as hard to get the blood circulating because it pumps less often and when it does, pumps out more blood. Please explain.
I don't know how your specific cardiovascular situation is, but there might be better drugs for you then calcium channel blockers, especially against high blood pressure but you did not mention that.
Personally I would not think of high resting heart rate in itself as a reason to prescribe drugs at all, so I guess there is more?
I did also have borderline high BP, but that is one thing that has corrected itself after the weight loss, improved diet, and increased activity.
I've gone off the medicine in the past to see what would happen. The BP stays low and within a normal range, but the heart rate goes back up.
I do understand, and I also know what all of those terms mean. SV, by itself does always increase EF. That's a fact. I shouldn't have said that EF can't go down if SV increase. That was wrong. What I mean was, in this case, EDV just increased enough to make EF lower, but that doesn't take away from the fact that SV is directly proportional to EF.
I am, however, still missing something. I get that it became more elastic and therefore allowed for a greater EDV. The greater EDV naturally increases SV because there is more blood in the LV to pump. But you said "the amount of blood exiting is greater so the heart doesn't have to contract as hard". Doesn't the heart have to contract harder to cause the increased in blood exiting? That's what I'm not getting.
And why would an increased EF be good, because that's why my cardiologist and electrophysiologist told me in the past? I thought that lower heart rate and increased EF means the heart is not working as hard to get the blood circulating because it pumps less often and when it does, pumps out more blood. Please explain.
SV DOESN'T always increase EF. Usually, but not always. The numbers I posted prove this.
Look at fractional shortening in the article (I hope you read the WHOLE article). Fractional shortening is EF expressed in different terms. Instead of looking at the percentage of total blood in the ventricle being ejected, fractional shortening (FS) is the percentage reduction in the LV chamber size during contraction. FS decreased from 43% to 39%. This shows the LV isn't contracting as hard. It doesn't have to because there is now a larger amount of blood in the ventricle so it doesn't have to pump as much of the total percentage to maintain output. It also doesn't have to do it as often which is why heart rate goes down.
Don't forget that most doctors look at things from a disease standpoint and not a performance one. Increased EF just means that a larger percentage of the blood in the ventricle is being ejected. Depending on the circumstances (disease or training adaptation) any increase or decrease in EF could be good or bad.
Like you stated EF = SV/ EDV
Baseline: 74%= 100 ml/ 135 ml
After: 69%= 116 ml/ 168 ml
SV doesn't always increase EF because there's one thing you aren't looking at.
EF= SV/EDV, but SV= EDV-ESV so technically EF=(EDV-ESV)/EDV
Looking at the numbers again.
Baseline: 74%= (135.9 ml- 35.6 ml)/ 135.9 ml
After: 69%= (168.54 ml- 52.3 ml)/ 168.54 ml
If ESV increases more (proportionally) than EDV, EF will go down even though EDV & SV might have gone up. This is why EF doesn't always go up if SV goes up.
Ca++ does have a pretty strong effect on the contraction process and it's "upstream" of a couple of powerful adaptation signals (calmodulin, calcineurin, and NFAT if anybody cares). As the study suggests, the calcium signal is pretty heavily involved in that.
That said, from memory Ca++ signaling is not quite as strong a mediator of fiber growth as it is a regulator of some other adaptive aspects (fiber type being a big one, atrophy signaling being another). There's some interaction with Akt-mTOR (IIRC, and that's where the hypertrophy effect will come in).
The question is whether or not you need that tissue breakdown and inflammation effect to really see adaptive growth, vs. "just" mechanical stretch/loading. I think in the long term yeah, but over the short term I don't know if it will affect very much.
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Look at fractional shortening in the article (I hope you read the WHOLE article). Fractional shortening is EF expressed in different terms. Instead of looking at the percentage of total blood in the ventricle being ejected, fractional shortening (FS) is the percentage reduction in the LV chamber size during contraction. FS decreased from 43% to 39%. This shows the LV isn't contracting as hard. It doesn't have to because there is now a larger amount of blood in the ventricle so it doesn't have to pump as much of the total percentage to maintain output. It also doesn't have to do it as often which is why heart rate goes down.
Gotcha. That makes sense now
Quote:
SV DOESN'T always increase EF. Usually, but not always. The numbers I posted prove this.
Don't forget that most doctors look at things from a disease standpoint and not a performance one. Increased EF just means that a larger percentage of the blood in the ventricle is being ejected. Depending on the circumstances (disease or training adaptation) any increase or decrease in EF could be good or bad.
Like you stated EF = SV/ EDV
Baseline: 74%= 100 ml/ 135 ml
After: 69%= 116 ml/ 168 ml
SV doesn't always increase EF because there's one thing you aren't looking at.
EF= SV/EDV, but SV= EDV-ESV so technically EF=(EDV-ESV)/EDV
Looking at the numbers again.
Baseline: 74%= (135.9 ml- 35.6 ml)/ 135.9 ml
After: 69%= (168.54 ml- 52.3 ml)/ 168.54 ml
If ESV increases more (proportionally) than EDV, EF will go down even though EDV & SV might have gone up. This is why EF doesn't always go up if SV goes up.
Are you reading anything I wrote? lol. I said ALL of that in my last post.
Quote:
Originally Posted by LiFeIsGoOd
I do understand, and I also know what all of those terms mean.SV, BY ITSELF does always increase EF.That's a fact. I shouldn't have said that EF can't go down if SV increase. That was wrong. What I mean was, in this case, EDV just increased enough to make EF lower, but that doesn't take away from the fact that SV is directly proportional to EF.
PMed because I feel bad continuing this in this thread.
The question is whether or not you need that tissue breakdown and inflammation effect to really see adaptive growth, vs. "just" mechanical stretch/loading. I think in the long term yeah, but over the short term I don't know if it will affect very much.
Trying to understand all of that in light of what I'm reading in your book.....
But, as for the last point, I'm having great results and I've been taking the Calcium Channel Blockers the whole time. So, at least for now its not effecting my gains. Perhaps its an issue of ideal v.s. sufficient.
I'll be talking with a new doctor soon as my old docs has left town. I'm hoping to find one who understand physical fitness a little better.
After some thought (regarding my post) I now realize that I stopped with the caffiene at about the same time as I started all of my track work. My sports med doc suggested that my adrenal system would probably appreciate a break from all the phony fight or flight sessions. I was up to 6 per day. Hmmmm. I wonder if that had anything to do with the big improvement with my resting heart rate.
Edit: I think I may be misunderstanding your thread. Are you concerned with how your meds are affecting your weight training or how to improve your resting heart rate and get off the meds?
Also, you should see a sports medicine doctor. In Canada we all have access to them as part of our health care system
Edit: I think I may be misunderstanding your thread. Are you concerned with how your meds are affecting your weight training or how to improve your resting heart rate and get off the meds?
You know this is sad, but I'd just sort of figured that I was stuck with a high resting heart rate. I know that I can effect it with lots of cardio, but lots of cardio is counter to my goals right now. But, it's interesting that you said that you did a lot of cardio for a period of time, and yet the results have stuck. I took this to mean that you later reduced the cardio but didn't see the heart rate return. I always assumed that you had to keep the cardio up to get the benefits.....and my knees can't take running for more than a day or two per week.
Recently I began wondering if I could do anything about it, and also what it might be doing to my strength training. Now, I'm wondering if quitting the caffeine and adding more cardio would reverse the situation.
You know this is sad, but I'd just sort of figured that I was stuck with a high resting heart rate. I know that I can effect it with lots of cardio, but lots of cardio is counter to my goals right now. But, it's interesting that you said that you did a lot of cardio for a period of time, and yet the results have stuck. I took this to mean that you later reduced the cardio but didn't see the heart rate return. I always assumed that you had to keep the cardio up to get the benefits.....and my knees can't take running for more than a day or two per week.
Recently I began wondering if I could do anything about it, and also what it might be doing to my strength training. Now, I'm wondering if quitting the caffeine and adding more cardio would reverse the situation.
I think you ought to try dropping the caffeine and adding some cardio. It certainly can't hurt.
You definitely have to keep your exercise up to maintain the effects of what you've done, but not always to the same degree. You can probably lessen the amount and still reap at least some of the benefits. If a high RHR is your case, then lowering that should be your goal, not whatever else you have in mind right now. That seems like the biggest issue to tackle, so make that the priority and take up the cardio if you think it will help. You don't have to run, so don't worry about the knees. Depending on what your issue is, the elliptical might alleviate that and the bike will probably take it away completely.
I don't think there's a lot of evidence that more cardio makes your resting heart rate lower. Some, I'm sure, is good. Cardio is a pretty general term. Vigorous weight training might count, as would sprinting, intervals, complexes, kettlebell swings, etc.
For a while, my resting HR was under 45 and all I did was play a lot of racquetball.
I don't think there's a lot of evidence that more cardio makes your resting heart rate lower. Some, I'm sure, is good. Cardio is a pretty general term. Vigorous weight training might count, as would sprinting, intervals, complexes, kettlebell swings, etc.
For a while, my resting HR was under 45 and all I did was play a lot of racquetball.
Racquetball can be cardio. Like you said, it doesn't really matter what form of cardio it is.
More probably does lower it. I think endurance athletes in general likely have lower RHR's than others.
I don't think there's a lot of evidence that more cardio makes your resting heart rate lower. Some, I'm sure, is good. Cardio is a pretty general term. Vigorous weight training might count, as would sprinting, intervals, complexes, kettlebell swings, etc.
For a while, my resting HR was under 45 and all I did was play a lot of racquetball.
Exactly. I think that conditioning is the point here. Vigorous weight training definitely counts as do the other methods you mentioned. You can give your cardiovascular system a going over everyday of the week without having to do track work. I would add swimming and rowing to your list above.
As for studies showing it's effect on lowering ones heart rate, I can only use myself as an example. I used to think that the high 70's to mid 80's was it for me. Since embarking on the conditioning thing, I've managed to keep it at between 57 and 60. I might also add that I use weight training to get/keep as much strength as I can while remaining at ~185.
There are many ways you can do cardio, but the heart rates you train at determine the adaptations that occur. Intense intervals and regular steady state cardio cause very different adaptations of the heart and muscles.
If you want to lower resting heart rate, you need to do less intense, but more volume work like stated in the article. You want to keep the volume of blood in the heart as high as possible to "stretch" the heart. This occurs at heart rates of 120-150. Do this at least 1-2 times a week for at least an hour each time if this is what you want. The type of activity doesn't matter, just the heart rate range. You can run, bike, use ciruits like kettlebells and bodyweight movements, etc.
If you stay in these lower heart rates (120-150), the cardio will not effect your strength or size at all and will actually help your recovery. After awhile you will notice that you recovery quicker between workouts and between sets during your workout.
Above a heart rate of 150, stroke volume no longer increases and above 160 actually goes down and then the strength of contraction will contribute more, but this will thicken the heart wall over time because it is now a "pressure" stimulus instead of a volume stimulus. Depending on you goals, this may be needed sometime, but to lower your resting heart rate you would need to work on the lower HR stuff for awhile first.
I appreciate everyone's input on this thread. I have a lot to consider.
One more question. I read that beta-blockers can have a substantial effect on lowering metabolism (as much as 15%). Does anyone know if Calcium Channel Blockers have the same effect? This could effect my caloric needs so it's important to know.
Betablockers are roughly the opposite of Clenbuterol, which is a beta agonist. If you know this stuff, it makes perfect sense that betablockers lower your metabolic rate. They are also no good for performance, they have a potential to make people faint when trying to catch the bus. For lower bloodpressure the ACE inhibitors are the better drugs imo.
But thats offtopic. As PowerManDL says, it is a totally different mechanism of action between betablockers and Ca channel blockers so the probability of having the same side effects is not exceptionally high. Calcium can influence metabolism, though. But that does not need need to mean the drug will do that.
If you wanna know if it does that, look in your drug information. If the side effects include weight gain, it could be because of that.
Quote:
Originally Posted by PowerManDL
Ca++ does have a pretty strong effect on the contraction process and it's "upstream" of a couple of powerful adaptation signals (calmodulin, calcineurin, and NFAT if anybody cares). As the study suggests, the calcium signal is pretty heavily involved in that.
That said, from memory Ca++ signaling is not quite as strong a mediator of fiber growth as it is a regulator of some other adaptive aspects (fiber type being a big one, atrophy signaling being another). There's some interaction with Akt-mTOR (IIRC, and that's where the hypertrophy effect will come in).
The question is whether or not you need that tissue breakdown and inflammation effect to really see adaptive growth, vs. "just" mechanical stretch/loading. I think in the long term yeah, but over the short term I don't know if it will affect very much.
This is also interesting, in fact at first glance I was not so sure to say it is a bad thing the drug does. I also see people using pro-inflammatory agents to get better gains. And it seems to be possible to make this work.
But the study measures biomarkers of damage, which are present for longer and for higher concentrations after the same stressor with the drug than without it, which I think means slower recovery.
Also the calcium channel blocker drugs must have some selectivity. If they worked on just every calcium channel they could only be used for biochemical assays to see if a process is calcium dependent, but men and mice would drop dead with it. So do you know if they have any affinity for any striated muscle calcium channels?
Trying to understand all of that in light of what I'm reading in your book.....
But, as for the last point, I'm having great results and I've been taking the Calcium Channel Blockers the whole time. So, at least for now its not effecting my gains. Perhaps its an issue of ideal v.s. sufficient.
I'll be talking with a new doctor soon as my old docs has left town. I'm hoping to find one who understand physical fitness a little better.
Yeah, if you go into it, is not so easy
Now it is also problematic to compare your results with the drug to...no results at all or something?
btw thank you for liking my picture,now those are all calcium channel blocker-free results you see
Most probably it is the issue of ideal vs sufficient.
Quote:
Recently I began wondering if I could do anything about it, and also what it might be doing to my strength training. Now, I'm wondering if quitting the caffeine and adding more cardio would reverse the situation.
In fact I don't really know what the current knowledge is about the caffeine, but I know we did a trial last year where BP and HR were measured and subjects receiving 400mg of caffein, or placebo. There was some difference in BP but not in HR.
Or the even less scientific story, "I also do loads of caffeine but have low resting HR".
I was also in the trial myself and they explained my low HR (which was an actual outlier) with the fact I am doing sports so much, but in fact I am not even doing so much cardio.Now this is already said in this topic, that other activities than what is normally called "cardio", can also have this effect.
Complicated topic, so will refrain from commenting in a scientific way, but just throwing out how a friend of mine spends nearly all of his leisure time in summer on the bicycle, cycling ginormous distances & then also spends a lot of his leisure time in winter on skates (marathon skating). Yet, his RHR is rather high (he is a caffeine junkie though).
Whereas I've always had a really low RHR even when I was doing zilch, nada nothing for exercise. It just dropped another 10 bpm when I was really into it.
Genetics are very powerful.
In short, I think you shouldn't worry too much about it.. maybe cut back a little on the caffeine.
Complicated topic, so will refrain from commenting in a scientific way, but just throwing out how a friend of mine spends nearly all of his leisure time in summer on the bicycle, cycling ginormous distances & then also spends a lot of his leisure time in winter on skates (marathon skating). Yet, his RHR is rather high (he is a caffeine junkie though).
Whereas I've always had a really low RHR even when I was doing zilch, nada nothing for exercise. It just dropped another 10 bpm when I was really into it.
Genetics are very powerful.
In short, I think you shouldn't worry too much about it.. maybe cut back a little on the caffeine.
Hope he got that checked?
Mine is very low from running/exercising a lot. I don't do it as much anymore and I probably overworked myself, but I rest at about mid 40s now.
Effects of Calcium Channel Blockers on Resistance Training, Strength and Hypertrophy
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