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Old 12-03-2006, 11:22 AM   #1
Jason Arsenault
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I just got perscribed beta blockers last week and am very frustrated. I feel like my cardio conditioning has dropped. I also dont know how I should be training on these pills or if I should just train as usual. Anyone out there have any experience with this?
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Old 12-03-2006, 11:39 AM   #2
Andy Shirley
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First question: Why is a 28 year old on a beta-blocker? Which one?

A study: work fam safe link to study of BB use while training
http://heart.bmj.com/cgi/content/abstract/48/1/33

You heart rate will be lower in training when beta blocked.
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Old 12-03-2006, 12:27 PM   #3
Jason Arsenault
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Nadolol. The reason for it is the Dr. wants to lower my heart rate (blood pressure is text book) to see if it fixes a different problem. Kinda complicated. resting heart rate now is 50bpm

(Message edited by 2Survive on December 03, 2006)
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Old 12-03-2006, 08:32 PM   #4
Andy Shirley
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Migraine? Tremor?

Note also that Nadolol is not cardiac specific, it will also act a bronchconstrictor, which might be another angle on why you feel your "cardio" has gotten worse. It has. Your heart cannot respond the same as before, it is chemically limited in its response by the BB.

Overview of Side Effects of BB from UptoDate(work fam safe):unlinkable due to subscription service
"Major side effects of beta blockers

Philip J Podrid, MD


UpToDate performs a continuous review of over 350 journals and other resources. Updates are added as important new information is published. The literature review for version 14.3 is current through August 2006; this topic was last changed on March 16, 2006. The next version of UpToDate (15.1) will be released in February 2007.

INTRODUCTION — Most of the major adverse effects of beta blocking drugs result from beta-adrenoreceptor blockade. Many signs and symptoms can therefore be induced because the beta receptors affect multiple metabolic and physiologic functions. Other reactions apparently unrelated to beta blockade can occur, but they are uncommon.

The major side effects associated with the use of beta blockers will be reviewed here. The clinical use of these drugs for the treatment of arrhythmias, hypertension, myocardial infarction, and heart failure are discussed separately. (See "Indications for use of specific antihypertensive drugs" and see "Beta blockers in acute myocardial infarction" and see "Use of beta blockers in heart failure due to systolic dysfunction").

ADVERSE CARDIAC EFFECTS DUE TO BETA BLOCKADE — Major cardiac effects caused by beta blockade include the precipitation or worsening of congestive heart failure, and significant negative chronotropy.

Heart failure — Beta blockers may cause heart failure in patients with preexisting myocardial dysfunction since the maintenance of cardiac output in such patients depends in part upon sympathetic drive. Increased peripheral vascular resistance, induced by nonselective beta blockers, also may contribute to the decline in myocardial function in this setting. On the other hand, drugs with intrinsic sympathetic activity (ISA), such as pindolol, may be less likely to impair myocardial function [1].

Despite these concerns, only a minority of patients with stable heart failure deteriorate after the initiation of beta blocker therapy. As an example, worsening of heart failure was observed in only 6 percent of patients with chronic heart failure who were being treated with carvedilol [2]. Furthermore, beta blockers are often beneficial in such patients, improving survival in patients with systolic heart failure and improving diastolic function in patients with diastolic heart failure. (See "Use of beta blockers in heart failure due to systolic dysfunction" and see "Treatment and prognosis of diastolic heart failure").

Negative chronotropic effects — Slowing of the resting heart rate and the development of sinus bradycardia is a normal response to treatment with a beta blocker. This effect is less prominent with drugs with ISA. Nevertheless, all beta blockers are relatively contraindicated in patients with sick sinus syndrome, especially if there is a further reduction in rate, unless an artificial pacemaker is present.

Beta blockers also depress conduction through the atrioventricular node, potentially causing heart block. Use of a beta blocking drug can therefore lead to a serious bradyarrhythmia in patients with an underlying complete or partial AV conduction defect, especially if the patient is also receiving another agent that impairs AV nodal conduction such as digoxin or a calcium channel blocker. Compounds with ISA may cause less impairment of atrioventricular conduction [3].

Beta blocker withdrawal — Acute withdrawal of a beta blocker can lead to substantial morbidity and even mortality [4]. Patients with underlying coronary disease may develop accelerated angina, myocardial infarction, or sudden death [5-7]. This can occur even in patients who have no previous history of coronary symptoms [7].

These withdrawal symptoms are due to increased sympathetic activity, which is a probable reflection of adrenergic receptor upregulation during the period of sympathetic blockade [8]. The degree to which this will occur depends upon the relationship between the rate at which beta blockade wears off and the rate at which the receptors downregulate (the latter has a half-life of 24 to 36 hours) [9]. Thus, a hyperadrenergic state is most likely with short-acting drugs (such as propranolol), since receptor upregulation will persist after the antihypertensive effect has disappeared [4,9]. Gradual tapering of the propranolol dose will diminish the risk of withdrawal [6]. In comparison, withdrawal syndromes are relatively unusual with longer-acting agents (such as nadolol) [4,9].

ADVERSE NONCARDIAC EFFECTS DUE TO BETA BLOCKADE — The lungs, peripheral blood vessels, glucose metabolism, and central nervous system are all affected by beta blockade although the clinical magnitude of the last three effects seems less pronounced that originally thought.

Increased airways resistance — Beta blockade with nonselective agents prevents bronchodilation due to bronchial beta-2 receptors [10]. This can lead to increased airways resistance in patients with bronchospastic disease, a problem that is less likely to occur with compounds with ISA or beta-1 selectivity [11-13]. Beta-1 selectivity is not absolute, however, and may diminish at higher doses. It has also been suggested that combined beta and alpha blockade with labetalol or carvedilol may be better tolerated than nonselective agents in patients with chronic lung disease [14].

All beta blockers should be avoided in patients with severe disease; nonselective beta blockers should generally be avoided in susceptible patients with mild to moderate disease, while the selective beta blockers or possibly combined alpha and beta blockers should be used cautiously and at low doses. Furthermore, many patients with asthma are treated with beta agonists. This issue of beta blocker therapy in patients with chronic obstructive disease is discussed more fully elsewhere. (See "Management of the patient with severe COPD and coronary artery disease" section on Beta blockers).

Exacerbation of peripheral arterial disease — Initial studies with nonselective beta blockers (eg, propranolol) in patients with severe peripheral vascular disease described a variety of complications including worsening claudication, cold extremities, absent pulses, and, in some cases, cyanosis and impending gangrene [15]. Raynaud's phenomenon can also be a manifestation of nonselective beta blockade [16,17]. It was thought that both the reduction in cardiac output and blockade of beta-2-receptor-mediated skeletal muscle vasodilation contribute to the vascular insufficiency [18]. Beta blockers with beta-1 selectivity or ISA do affect the peripheral vessels to the same degree as the nonselective drugs.

A meta-analysis of published studies in patients with mild to moderate peripheral vascular disease found no exacerbation of symptoms with beta blockers [19]. Thus, the concern may be overstated, particularly in patients with mild to moderate disease treated with a beta-1 selective agent [20]. (See "Medical management of claudication").

Facilitation of hypoglycemia — Epinephrine, acting via the beta-adrenergic receptors, has important effects on glucose metabolism. It increases glucose production by stimulating both glycogenolysis and gluconeogenesis from amino acids, glycerol, and pyruvate. It also increases the delivery of these gluconeogenic substrates from the periphery, inhibits glucose utilization by several tissues, and, via the alpha-2-receptors, inhibits insulin secretion. (See "Physiologic response to hypoglycemia in normal subjects and patients with diabetes mellitus").

All of these actions help to protect against the development of hypoglycemia. In addition, epinephrine induces early warning symptoms of neuroglycopenia, such as sweating and anxiety.

Studies published in the 1960s showed that nonselective beta blockers can retard recovery from insulin-induced hypoglycemia [21] and that the reactions are more likely to be severe [22,23]. The latter effect is presumably due to diminished or absent early warning signs [24,25]. However, later studies showed that the effects on glucose metabolism may be less prominent with beta-1 selective drugs and those with ISA [26,27] and that an increased risk of serious hypoglycemia among patients with diabetes mellitus was hard to demonstrate [27]. Furthermore, carvedilol appears to promote glucose utilization and lower insulin levels in patients with type 2 diabetes [28]. (See "Treatment of hypertension in diabetes mellitus", section on Beta blockers).

Hyperkalemia — Catecholamines have potentially important clinical effects on potassium balance, primarily by influencing the distribution of potassium between the extracellular fluid and the cells. In particular, stimulation of the ß2-receptors by epinephrine promotes the movement of extracellular potassium into the cells, thereby lowering the plasma potassium concentration. (See "Sympathetic activity and potassium balance").

These effects on potassium balance can be reversed by ß-adrenergic blockers, which will tend to impair potassium entry into the cells, thereby raising the plasma potassium concentration after a potassium load. This is most likely to occur with the nonselective ß-blockers (such as propranolol or labetalol); in contrast, the ß1-selective agents such as atenolol have little effect, since the ß2 receptors remain intact [29].

In most cases, the administration of ß-blockers is associated with only a minor elevation in the plasma potassium concentration of less than 0.5 meq/L, as the potassium that cannot enter the cells is excreted in the urine. True hyperkalemia is rare unless associated with a superimposed problem such as a marked potassium load, severe exercise (which is associated with the release of potassium from the cells into the extracellular fluid), hypoaldosteronism, or end-stage renal disease [30-32]. Hyperkalemia has also been reported in renal transplant recipients treated with labetalol [33].

Depression, fatigue, sexual dysfunction — Depression, fatigue, and sexual dysfunction are commonly cited side effects of beta blockers, and may be one reason why use of beta blockers is lower than desired for some approved indications [34]. However, these associations are primarily based upon case series and randomized trials with methodologic flaws.

The best available data on this issue come from a systematic review of randomized trials, which found no increased risk of depression with beta blocker therapy, and only small increases in fatigue and sexual dysfunction [35]. The review included 15 randomized, placebo-controlled trials involving more than 35,000 patients who were followed for a minimum of six months. Both patient reported symptoms and withdrawal of therapy were investigated. The following findings were reported:

There was a small significant increase in risk of fatigue (18 per 1000 patients, 95% CI 5-30). This is equivalent to one additional report of fatigue for every 57 patients treated per year.
There was a small significant increase in risk of sexual dysfunction (5 per 1000 patients, 95% CI 2-8). This is equivalent to one additional report of sexual dysfunction for every 199 patients treated per year.
There was no significant annual increase in risk of reported depressive symptoms.
It has been hypothesized that lipophilic drugs (eg, propranolol, atenolol) are associated with a higher incidence of central nervous system effects such as fatigue and depression because of their ability to penetrate the central nervous system. However, lipid solubility of the beta blockers did not affect the risk of adverse effects in this review.
In trials testing early generation beta blockers (propranolol, timolol), the risk of fatigue, but not depression or sexual dysfunction, was higher (relative risk 1.78, 95% CI 1.08-2.93) when compared with later generation beta blockers. However, the number of trials was small and the confidence intervals were wide.
Thus, although beta blockers appear to cause small increases in the risk of fatigue and sexual dysfunction, the risk is much lower than previously thought, and beta blockers should not be withheld based upon concerns about developing these adverse effects."
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Old 12-03-2006, 08:43 PM   #5
Jason Arsenault
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well, that explains why I get somewhat winded climbing stairs... Thanks for your help. Might need to have a talk with my Dr. Not good for the ol' chasin bad guys thing...:bolt:
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Old 12-05-2006, 10:33 AM   #6
Tim Weaver
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My Romulan translator is on the fritz. No matter how hard I bang it on the table, it doesn't work....

Can someone translate that medical thing into a shorter, English-laden paragraph?

And...is metropolol (Lopressor) a beta-blocker?
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Old 12-05-2006, 01:48 PM   #7
Elliot Royce
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I've had to take them for short periods in the past. Huge impact on athletic performance. And on energy levels, etc. I had a policeman hockey player friend who had to take them permanently and it really made playing hockey tough for him. Of course, he had been a semi pro football player, weighed 280lbs at 6'4" (not really that obese, just big) and had been a beat cop for 20 years, so he had a number of health issues.
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Old 12-05-2006, 10:07 PM   #8
Andy Shirley
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Metoprolol is a very common beta-blocker. It is more beta-1(cardiac) specific.

Just about anything ending with -olol is a betablocker. Atenolol, labetalol, metprolol, carvidelol, bisoprolol, timolol, nadolol, propanolol.
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Old 12-08-2006, 02:10 AM   #9
Ben Nance
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Real brief oversimplified rundown for some:

Your body has 2 general beta receptors: Beta 1 and Beta 2.

Stimulation of the Beta 1 receptors primarily affect the heart by increasing heart rate and strength of contraction (epinephrine aka adrenaline is a good example)

Stimulation of the Beta 2 receptors primarily affect the lungs and cause dilation of the smooth muscles of the lower airway (example: Albuterol Inhalers or other asthma "rescue" inhalers)

Beta Blockers inhibit those receptors by a variety of means, depending on the specific drug. This, in turn, lowers the heart rate. These can SEVERELY hinder your ability to compensate for increasing workload from exercise.

Hope that helps clear it up a little bit for some.

I'm curious as to why they were prescribed.
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Old 12-08-2006, 02:48 AM   #10
Andy Shirley
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Ben,
Nice overview.

I am also curious.
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