T Nation

Preferred BP Med?

[quote]Diana Bolann wrote:
bushidobadboy wrote:
Well beta blockers (as Pris mentioned) place an artificial upper limit on your HR. This limits performance…

Bushy

BBB,

Is this the mechanism of action or a side effect?[/quote]

Beta blockers work by blocking adrenergic receptor sites. These sites are stimulated by the sympathetic nervous system (fight or flight) - i.e. the adrenals Some of the causes are peripheral vasoconstriction and increase heart rate, amoung many more things. - For example your adrenergic system causes bronchial dilation via the beta 2 receptors, and we all know about clenbutoral on this site. - This is a prime reason why such drugs as metoprolol cannot be prescribed to asthmatics, or those with Chronic obstructed pulmonary disorders who are dependant on their salbutemol to keep their airways open. As Metoprolol can block this action!

Basically metoprolol retards your cardiovascular system from responding to adrenilin which in turn promotes both reduce cardiac work load, pre load and afterload. This is very benificial to those with heart disease who cannot ‘overstress’ their heart for fear of causing ischemia/ angina, which could lead no only to further infarction but other changes such as cardiomeggally. Anyway complicated topic with lots of to discuss, but the above is basically the mechanisms of action.

[quote]DrSkeptix wrote:
Diana Bolann wrote:
bushidobadboy wrote:
Well beta blockers (as Pris mentioned) place an artificial upper limit on your HR. This limits performance…

Bushy

BBB,

Is this the mechanism of action or a side effect?

Just some small quibbles.

  1. Prisoner is spot on, once again.

  2. OP: I hope you had a urinalysis and that there was no blood or protein in your urine.

  3. Calcium channel antagonists are not calcium antagonists. While it is true that there may be small aberrations of the neuromuscular action (detectable by electromyography), this is not likely at all to be noticed by an athlete in terms of change in skeletal muscle performance.

  4. Instead, what is important–with many agents including the beta-blockers–is the total circuit: reducing cardiovascular resistance and improving cardiac output, which will be experienced as an improvement in in athletic performance, even if there is a “ceiling” on heart rate responsiveness. (This does not apply in a lot of situations of ill health, but I don’t suppose Diana Bolann has any of those.)[/quote]

Yes but my thinking: in someone who per say has a healthy rhythm, (no atrial fibrilation for eg.) these drugs will not improve cardiac output, as they will work to slow conduction. That should have effects on atrial kick - reducing preloads due to too much vasodialation as well will effect in turn, the stroke volume and output. In an athlete this would effect performance at the cellular level as gas exchange would be slowed, and lactate levels would rise quicker during peak althetic performance. Not to mention also that peak cardiac rate would be reduced slowing recovery.

[quote]InTheZone wrote:
Diana Bolann wrote:
Holy crap. Two days of lexapro, ToprolXL, Ambien and Vitamic C and I am at 122/69.

Nuts.

Can someone explain why the beta/calcium blockers are bad for athletes?

     Forgot a question I had relating also. Does anyone know just how bad it is to go on cycle with moderate/light doses while taking these meds, and how bout HOT-ROX too? Just curious, I'm sure it depends on length and compounds and diet, but in general how safe/unsafe is it to play this game while on bp meds? Just watch the bp?

Mine didn’t go up very much when taking the ACE inhib and cycling a shorty.

                   TBN[/quote]

Unsure as to the exact compostion of this supplement (as it always seems to be changing), but from what I know it contains some kind of adrenergic stimulant, and some kind of thyroid simulating compound.

The stimulant may or may not be canceled out by the beta blockers, and the thyroid stimulation compound which can have eventual effects in cellular metabolism via the mitochondria may increase lactate in which the circulatory system may lag a little on removing, due to the effects of the betablocker on the cardiovascular system

this of course is simply conjecture on my part though.

[quote]Prisoner wrote:
DrSkeptix wrote:
Diana Bolann wrote:
bushidobadboy wrote:
Well beta blockers (as Pris mentioned) place an artificial upper limit on your HR. This limits performance…

Bushy

BBB,

Is this the mechanism of action or a side effect?

Just some small quibbles.

  1. Prisoner is spot on, once again.

Yes but my thinking: in someone who per say has a healthy rhythm, (no atrial fibrilation for eg.) these drugs will not improve cardiac output, as they will work to slow conduction. That should have effects on atrial kick - reducing preloads due to too much vasodialation as well will effect in turn, the stroke volume and output. In an athlete this would effect performance at the cellular level as gas exchange would be slowed, and lactate levels would rise quicker during peak althetic performance. Not to mention also that peak cardiac rate would be reduced slowing recovery.[/quote]

I am guessing that you are an ICU nurse, and if you are not, you are simply talented!

Beta blockers slow AV or junctional conduction, yes, and they separately slow heart rate. The Purkinje fiber slowing is not important in athletics. The point you make about heart rate and preload is respected; it makes a big difference in the ICU with weakened cardiac muscle.
But in the brutishly healthy–and the athletic hypertensive–I argue that it is peripheral vascular resistance that limits athletic performance. (High PVR reduces cardiac output and strains heart muscle.)

The limitation to aerobic performance is oxygen delivery to peripheral tissues; the hypertensive person has improved cardiac output and tissue O2 delivery when vascular resistance falls, whether by ACE or by beta-blocker. (“Negative chronotropy” is not the dominate issue here, as it is other situations.) After that, blunted heart rate response becomes important. (And that is why I agree strongly with you: Ramipril is a great choice for athletic young men, especially if there is proteinuria.)

In short, you are the man!

[quote]Prisoner wrote:
InTheZone wrote:
Diana Bolann wrote:
Holy crap. Two days of lexapro, ToprolXL, Ambien and Vitamic C and I am at 122/69.


Forgot a question I had relating also. Does anyone know just how bad it is to go on cycle with moderate/light doses while taking these meds, and how bout HOT-ROX too? …
Unsure as to the exact compostion of this supplement (as it always seems to be changing), but from what I know it contains some kind of adrenergic stimulant, and some kind of thyroid simulating compound.

The stimulant may or may not be canceled out by the beta blockers, and the thyroid stimulation compound which can have eventual effects in cellular metabolism via the mitochondria may increase lactate in which the circulatory system may lag a little on removing, due to the effects of the betablocker on the cardiovascular system

this of course is simply conjecture on my part though.[/quote]

All hail Cy Willson!

Without betrraying any secrets, HOT-ROX has yohimbine—gaaa!–and an adenylate cyclase stimulator. I would guess that neither is directly blocked by beta blockers. But in any organ bed, who knows what the balance of actions would be? Coronary dilation or coronary spasm? Renovascular changes?
Better not to mix these, not that I claim any authority, other than that conferred by abject fear!

[quote]DrSkeptix wrote:
Prisoner wrote:
DrSkeptix wrote:
Diana Bolann wrote:
bushidobadboy wrote:
Well beta blockers (as Pris mentioned) place an artificial upper limit on your HR. This limits performance…

Bushy

BBB,

Is this the mechanism of action or a side effect?

Just some small quibbles.

  1. Prisoner is spot on, once again.

Yes but my thinking: in someone who per say has a healthy rhythm, (no atrial fibrilation for eg.) these drugs will not improve cardiac output, as they will work to slow conduction. That should have effects on atrial kick - reducing preloads due to too much vasodialation as well will effect in turn, the stroke volume and output. In an athlete this would effect performance at the cellular level as gas exchange would be slowed, and lactate levels would rise quicker during peak althetic performance. Not to mention also that peak cardiac rate would be reduced slowing recovery.

I am guessing that you are an ICU nurse, and if you are not, you are simply talented!

Beta blockers slow AV or junctional conduction, yes, and they separately slow heart rate. The Purkinje fiber slowing is not important in athletics. The point you make about heart rate and preload is respected; it makes a big difference in the ICU with weakened cardiac muscle.
But in the brutishly healthy–and the athletic hypertensive–I argue that it is peripheral vascular resistance that limits athletic performance. (High PVR reduces cardiac output and strains heart muscle.)

The limitation to aerobic performance is oxygen delivery to peripheral tissues; the hypertensive person has improved cardiac output and tissue O2 delivery when vascular resistance falls, whether by ACE or by beta-blocker. (“Negative chronotropy” is not the dominate issue here, as it is other situations.) After that, blunted heart rate response becomes important. (And that is why I agree strongly with you: Ramipril is a great choice for athletic young men, especially if there is proteinuria.)

In short, you are the man!

[/quote]

lol! no I am not an ICU nurse - close though as I work ER and tend to send them a lot of business!

I get your point though regarding the vascular resistance.

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An anecdotal nugget for the topic…

A few days ago I felt like I could rip a cow’s head off and eat it in one sitting. My workouts consisted of deadlifting 450+ lbs for reps as well as benching 90lb dumbells and then chinning. Then I would go running immediately afterwards.

Mind you I am not on the juice and haven’t been for several months. I also had extremely bad bacne along with the high BP and nice strength.

Anyway, now three days later I fee peaceful, I have low BP, I couldn’t even run a goddam mile yesterday, and I could barely squat 200 lbs!! Not to mention my bacne is clearing up and I feel like a pussy overall.

I’m not sure what gives but I’m not liking this 100%.

Oh and I am on the metoprolol BTW.

[quote]bushidobadboy wrote:
DrSkeptix wrote:
3. Calcium channel antagonists are not calcium antagonists. While it is true that there may be small aberrations of the neuromuscular action (detectable by electromyography), this is not likely at all to be noticed by an athlete in terms of change in skeletal muscle performance.

.)

Hmmm. Did you get this information regarding ‘small aberrations of neuromuscular action’ from the texts, or from experience?

I ask, because although you are right about Ca channel blockers not being Ca ‘blockers’, you are not quite so accurate in your assessment of effects on skeletal muscle.

Years ago, when I did my training for exercise prescription for special populations, it was stated that in the experience of the lecturer, Ca channel blockers DO in fact affect quite a high proportion of patients, despite what the pharm companies would have us believe.

This was backed up in my subsequent dealings with cardiac rehab patients that were prescribed Ca channel blockers.

A high proportion of them reported excessive weakness in skeletal muscle - though of course some of them could have just been lazy, lol.

Bushy[/quote]

Good observations.
Cardiac rehab patients have oodles of reasons to be weak; chiefly, disuse atrophy. (3 days in a bed requires 3 weeks of rehabilitation!). But calcium channel blockers have not been reported to inhibit the force of contraction of skeletal muscle. (Smooth muscle is a different story.) I was able to find only a few human emg studies. (There is a no report of diaphragm muscle weakness, a good clinical marker of myotoxicity.)
Further, to my knowledge, the drugs act on the channels of the cell membrane, not on the internal sarcomere (I looked that one up, subject to revision).

It looks like the OP likes metoprolol.
Now here is the experiment for Bushy and Prisoner: weightlifters, on treadmills, randomized to ramipril vs metoprolol. Which has the higher aerobic exercise tolerance? VO2 max? Cardiac outputs?

(Another Nobel Prize gone wanting.)

[quote]Diana Bolann wrote:
Oh and I am on the metoprolol BTW.[/quote]

yeah, you are not the first guy on the boards to report those findings with that medication

[quote]DrSkeptix wrote:
It looks like the OP likes metoprolol.
Now here is the experiment for Bushy and Prisoner: weightlifters, on treadmills, randomized to ramipril vs metoprolol. Which has the higher aerobic exercise tolerance? VO2 max? Cardiac outputs?

(Another Nobel Prize gone wanting.)

[/quote]

off the cuff I would say ramipril, and I would be really hesitant to put anyone on a treadmill who needed to be on metoprolol.

[quote]bushidobadboy wrote:
DrSkeptix wrote:
3. Calcium channel antagonists are not calcium antagonists. While it is true that there may be small aberrations of the neuromuscular action (detectable by electromyography), this is not likely at all to be noticed by an athlete in terms of change in skeletal muscle performance.

.)

Hmmm. Did you get this information regarding ‘small aberrations of neuromuscular action’ from the texts, or from experience?

I ask, because although you are right about Ca channel blockers not being Ca ‘blockers’, you are not quite so accurate in your assessment of effects on skeletal muscle.

Years ago, when I did my training for exercise prescription for special populations, it was stated that in the experience of the lecturer, Ca channel blockers DO in fact affect quite a high proportion of patients, despite what the pharm companies would have us believe.

This was backed up in my subsequent dealings with cardiac rehab patients that were prescribed Ca channel blockers.

A high proportion of them reported excessive weakness in skeletal muscle - though of course some of them could have just been lazy, lol.

Bushy[/quote]

yeah bushy that is a hard one to determine by anecdotal evidence, as most people who have an MI need a good long while to recover - it effects their entire body. Activities are curbed such as work, driving, e.t.c. and their endurance and strength drops due to loss of cardiac output both caused by the Muscle damage and the drugs they are placed on to decrease workload of the heart.

obviously they don’t lose motor movements so the calcium channels in the skeletal muscles must still be working fine.

[quote]DrSkeptix wrote:

It looks like the OP likes metoprolol.

[/quote]

Although the metoprolol seems to be effectively lowering the BP, the funny thing is that I liked having high BP. I felt good and strong with high BP. I only took the meds because my doc suggested it after a routine check-up. The only benefit I am noticing from the drugs is a lack of tension headaches.

I just realized that my anecdote was unclear. I wrote “a few days ago I felt like ripping a cow’s head off etc…” That time referred to the time BEFORE I started the drugs. Sorry about that.

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This post was flagged by the community and is temporarily hidden.

[quote]bushidobadboy wrote:
Another point is that whilst Ca is certainly needed within skeletal muscle, it is at the motor endplate that I believe the ‘weakness’ occurs.

For anyone reading, not familiar with the neuromuscular junction, I will briefly say that it is the influx of Ca into the synaptic end bulb of the axon that causes release of the neurotransmitter ACH into the synaptic cleft, that triggers the action potential along the length of the myofibril.

Impede the influx of CA, and you reduce the amount of ACH released, reducing the innervating effect on the muscle fiber.

I suppose the effect could be seen as similar to myesthenia gravis. Obviously the cause is totally different, but the end result - less ACH being ‘seen’ by the motor endplate, would have the same conclusion - a percieved weakness in skeletal muscle.

Bushy[/quote]

really, I havn’t looked at my physiology text in a long time but I could swear it was the opposite - it is the calcium that is released stimulated by ACH.

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For steroid induced hypertension one might take a look at Catapres (clonidine). Often times a nightly dose can do the trick. The following summary may be helpful, although it is a cut and past from an Rx source. Bonus: potential GH release.

"Clonidine stimulates alpha-adrenoreceptors in the brain stem. This action results in reduced sympathetic outflow from the central nervous system and in decreases in peripheral resistance, renal vascular resistance, heart rate, and blood pressure. CATAPRES tablets act relatively rapidly. The patient’s blood pressure declines within 30 to 60 minutes after an oral dose, the maximum decrease occurring within 2 to 4 hours. Renal blood flow and glomerular filtration rate remain essentially unchanged. Normal postural reflexes are intact; therefore, orthostatic symptoms are mild and infrequent.

Acute studies with clonidine hydrochloride in humans have demonstrated a moderate reduction (15% to 20%) of cardiac output in the supine position with no change in the peripheral resistance: at a 45° tilt there is a smaller reduction in cardiac output and a decrease of peripheral resistance. During long term therapy, cardiac output tends to return to control values, while peripheral resistance remains decreased. Slowing of the pulse rate has been observed in most patients given clonidine, but the drug does not alter normal hemodynamic response to exercise.

Other studies in patients have provided evidence of a reduction in plasma renin activity and in the excretion of aldosterone and catecholamines. The exact relationship of these pharmacologic actions to the antihypertensive effect of clonidine has not been fully elucidated.

Clonidine acutely stimulates growth hormone release in both children and adults, but does not produce a chronic elevation of growth hormone with long-term use."-Rx List,The Internet Drug Index.(http://www.rxlist.com)