Mechanism of Action
- Blocks beta-receptors of the sympathetic nervous system
- Some agents act primarily on beta receptors in the heart
- these are called cardioselective
- Beta- blockage results in decreased heart rate, blood pressure, and contractility of the heart
- thereby reducing the demand for oxygen by the heart
Treatment
- High blood pressure (hypertension)
- Chest pain (angina pectoris)
- Abnormal heart rhythms (arrhythmias)
- Migraine headaches
- Previous MI patients
- Reduce the risk of death after a heart attack
- Glaucoma, Ocular hypertension
- Eg: Carteolol, Timolol, Betaxolol
- Anxiety (off-label)
Non-selective Beta Blockers
- Carteolol (Cartrol, Ocupress, Teoptic, Arteolol, Arteoptic, Calte, Cartéabak, Carteol, Cartéol, Cartrol, Elebloc, Endak, Glauteolol, Mikelan, Poenglaucol, Singlauc)
- Used to treat glaucoma
- Also a serotonin 5-HT1A and 5-HT1B receptor antagonist
- Carvedilol (Coreg)
- Also decreases peripheral vascular resistance through alpha-1 blockade
- Labetalol (Normodyne, Trandate)
- Also decreases peripheral vascular resistance through alpha-1 blockade
- Nadolol (Norpramin)
- Oxprenolol (Trasacor, Trasicor, Coretal, Laracor, Slow-Pren, Captol, Corbeton, Slow-Trasicor, Tevacor, Trasitensin, Trasidex)
- Also exhibits intrinsic sympathomimetic activity
- Lipophilic beta blocker which more easily passes the blood–brain barrier associated with higher incidence of CNS-related side effects
- Penbutolol (Levatol, Levatolol, Lobeta, Paginol, Hostabloc, Betapressin)
- Also exhibits intrinsic sympathomimetic activity
- Pindolol (Visken)
- Also exhibits intrinsic sympathomimetic activity
- Propranolol (Inderal)
- Sotalol (Betapace, Sotalex, Sotacor, Sotylize)
- Prescribed only for serious arrhythmias
- Prolongs QT Interval
- Timolol (Betimol)
- Also used to treat glaucoma and ocular hypertension
β1-selective Beta Blockers
- Acebutolol (Sectral, Prent)
- Also exhibits intrinsic sympathomimetic activity
- Lipophilic beta blocker which more easily passes the blood–brain barrier
- No HDL decrease, unlike most beta blockers
- Atenolol (Tenormin, Norpramin)
- Higher risk of type 2 diabetes
- Betaxolol (Betoptic, Lokren, Kerlone)
- Also used to treat glaucoma
- Bisoprolol (Zebeta, Concor)
- Celiprolol (Cardem, Selectol, Celipres, Celipro, Celol, Cordiax, Dilanorm)
- Also exhibits intrinsic sympathomimetic activity
- Metoprolol Succinate (Lopressor, Metolar XR)
- Long-acting beta-blocker
- Nebivolol (Bystolic, Nebilet)
- Decrease peripheral vascular resistance through promoting nitric oxide (NO) release
- Significantly increases stroke volume while maintaining cardiac output
Effect on Weight
- Lowered resting metabolic rate (RMR) (Bélanger & Boulay 2005)
- Weight gain usually occurs in the first few months of treatment (Bélanger & Boulay 2005)
- Limits the increase in RMR normally observed following aerobic exercise (Bélanger & Boulay 2005)
- Beta blockers such as Carvedilol don't increase weight gain.
Effect During Rest
- Decreased resting heart rate (ACSM 2013, Gladson 2011, Niedfeldt 2002)
- 30-35% reduction (Tesch 1985)
- Less decrease by intrinsic sympathomimetic activity (ISA) and Beta Blocker (ACSM 2013)
- Decreased blood pressure (ACSM 2013)
- Decreased systolic blood pressure (Gladson 2011)
- Decreased rate pressure product (Gladson 2011)
- Decreased arrhythmias (ACSM 2013)
- Decreased ST depression (Gladson 2011)
- Increased diastolic function (Gladson 2011)
- Increased myocardial efficiency (Gladson 2011)
- Increased myocardial oxygen consumption (MVO2) (Gladson 2011)
- Decreased coronary blood flow (Gladson 2011)
- Increased diastolic filling time (Gladson 2011)
Effect on Exercise
- Decreased heart rate during exercise (ACSM 2013, Gladson 2011)
- Less decrease by cardioselective Beta Blocker (ACSM 2013)
- 20 to 30% decrease in maximum heart rate (Gladson 2011)
- Decreased blood pressure (ACSM 2013)
- Impairment of cardiac output
- Decrease in cardiac output (Niedfeldt 2002)
- Decrease or no change in cardiac output (ACSM 2013)
- 5 to 23% decrease in cardiac output (Gladson 2011)
- Possible increased stroke volume (Tesch 1985)
- No effect on stroke volume (Niedfeldt 2002)
- Increased stroke volume during moderate exercise (Gladson 2011)
- Impairment of maximum oxygen uptake (Niedfeldt 2002)
- Decreased acute (single dose) VO2max (ACSM 2013)
- Decrease of 5-15% (Tesch 1985)
- Increased chronic VO2max (ACSM 2013, Gladson 2011)
- Decreased acute (single dose) VO2max (ACSM 2013)
- Decreased exercise ischemia (ACSM 2013)
- Decreased ischemic threshold (Gladson 2011)
- Increase in vascular resistance (Niedfeldt 2002)
- No effect on plasma volume (Niedfeldt 2002)
- No effect on muscular strength and power
- No effect on psychomotor performance
- Potentially greater ability to perform athletic events requiring high levels of motor control under emotional stress (Tesch 1985)
- Exercise / Work Capacity
- Increased exercise capacity (Gladson 2011)
- Increased exercise capacity
- Patients with angina (Dreeben-Irimia 2008)
- Patients with cardiovascular disease (Gladson 2011)
- Selective β-blockers more than non-selective β-blockers
- Decreased exercise capacity
- Patients without angina (Dreeben-Irimia 2008)
- Patients with hypertension but no cardiovascular disease (Gladson 2011)
- Impaired work capacity as reflected by the ability to perform intense short term or more prolonged steady-state exercise. (Tesch 1985)
- Significant decrease in training (Niedfeldt 2002)
- Exercise performance ability is more greatly impair following a beta 1- and beta 2 receptors (non-selective than beta 1-selective) blockade as opposed to only a beta 1-receptors (beta 1-selective blockers) blockade at equal reductions in heart rate. (Tesch 1985)
- Increased total exercise time (Gladson 2011)
- Earlier fatigue and lactate threshold (Niedfeldt 2002)
- Increase in perceived exertion levels (Niedfeldt 2002)
- Increase acute (single dose) RPE during exercise.
- This effect partially subsides with long term treatment (Tesch 1985)
- Possible exacerbation of exercise-induced bronchospasm or asthma (Niedfeldt 2002)
Metabolic Effects
- Both selective and non-selective β-blockers disrupt the utilization of fat, glucose, and triglycerides during exercise
- However, non-selective β-blockers have greater disruptions
- However, benefits of selective β-blockers are lost at higher doses
- However, non-selective β-blockers have greater disruptions
- Greater metabolic disruptions and fatigue occurs at peak plasma concentrations
- Generally 90 minutes after administration
Nonselective β-blockers
- Some Nonselective β-blockers may cause adverse effects to the CNS (Gladson 2011)
- Fatigue
- Depression
- Nightmares
- Thermoregulatory effects during exercise (Gladson 2011)
- 10% accelerated sweating response
- Increased risk of dehydration
- Decreased skin blood flow
- Peripheral constriction
- Reduce cardiac output
- Fluid replacement is important to prevent drop in blood pressure
- 10% accelerated sweating response
- Metabolic effects during exercise (Gladson 2011)
- Increased fatigue
- Decreased adipose and intramuscular lipolysis
- Decreased glycogen breakdown
- Decreased blood glycogen levels
- Decreased hepatic glycogenolysis
- Decreased hepatic gluconeogenesis
- Possible decrease of glucose utilization by working muscles
Recommendations
- Exercise same time each day to avoid variations in plasma concentration of β-blockers
- Take appropriate actions when experiencing any adverse effects of exercise.
- Patients on Beta-blockers who achieved 65% age-predicted maximal heart rate had a similar adjusted mortality rate as those not on Beta-blockers who achieved 85% age-predicted maximal heart rate (p >0.05) (Hung 2016)
Recommended Populations
- Recommended to those with coronary artery disease
Populations Not Recommend
- Not recommended to those with asthma, endurance athletes, collegiate athletes
- Caution when prescribing some beta-blockers to patients with asthma or bronchospasm
Banned Status
- Banned in precision sports (ie: shooting, archery, diving, ice skating
References
American College of Sports Medicine (2013). Guidelines for Exercise Testing and Prescription, William & Wilkins, 9, 401
Bélanger M, Boulay P (2005). Effect of an aerobic exercise training program on resting metabolic rate in chronically beta-adrenergic blocked hypertensive patients. J Cardiopulm Rehabil. 25(6):354-60.
Dreeben-Irimia O (2008). Physical Therapy Clinical Handbook for PTAs. Jones and Bartlett Publishers, 373.
Gladson B (2011). Pharmacology for Rehabilitation Professionals, Elsevier Saunders (2) 486-490.
Hung RK, Al-Mallah MH, Whelton SP, Michos ED, Blumenthal RS, Ehrman JK, Brawner CA, Keteyian SJ, Blaha MJ (2016). Effect of Beta-Blocker Therapy, Maximal Heart Rate, and Exercise Capacity During Stress Testing on Long-Term Survival (from The Henry Ford Exercise Testing Project). Am J Cardiol. 2016 Dec 1;118(11):1751-1757.
Tesch PA (1985). Exercise performance and beta-blockade. Sports Med. 1985 Nov-Dec;2(6):389-412.
Niedfeldt MW (2002). Managing Hypertension in Athletes and Physically Active Patients. Am Fam Physician. 1;66(3):445-453.