Reent's
Reents Notes
Ch.1
Effects of Beta-Blockers on Metabolism
• Muscle triglyceride utilization in mediated by beta-2-stimulation
• Adipose tissue lipolysis is mediated by beta-1-stimulation
• It is important to consider (1) exercise intensity (2) duration of drug therapy when evaluating the effects of beta-blockers on exercise metabolism
Blood Glucose and Muscle Glycogen
• Glycogenolysis in skeletal muscle is mediated by epinephrine via stimulation of beta-2-receptors
• Beta-2-blockade impairs mobilization of glycogen stores during exercise, producing, in turn, lower serum glucose values
• Muscle glycogenolysis is unaffected by beta-blockade at submaximal exercise, but that max glyogenolytic rate at high exercise intensities can be impaired
Generalities
1. Cardioselective beta-blockers suppress maximum HR less than noncardioselective agents
2. Acutely, beta-blockers of all types reduce VO2 max (mean reduction of 6-14% in both healthy subjects and pt’s with cardiovascular disease. Although the training effect of regular exercise is suppressed most by nonselective agents it is still possible for subjects taking beta-blockers chronically to improve their fitness level as a result of an exercise program
3. Cardioselective beta-blockers interfere with utilization of energy substrates less than noncardioselective agents during exercise
Normotensive Subjects
• Beta-blockers generally exert negative effects on aerobic exercise performance; noncardioselective types exert more detrimental effects than do the cardioselective types o The difference may be due to a combination of metabaolic actions – impaired muscle triglyceride utilization, impaired glycogenolysis, impaired adipose lipolysis, disruption of potassium homeostasis
Hypertensive Subjects
• Beta-blockers exert more detrimental effects on exercise performance than do other types of antihypertensives such as alpha blockers, ACE inhibitors or calcium channel blockers
•
Ch.1
Effects of Beta-Blockers on Metabolism
• Muscle triglyceride utilization in mediated by beta-2-stimulation
• Adipose tissue lipolysis is mediated by beta-1-stimulation
• It is important to consider (1) exercise intensity (2) duration of drug therapy when evaluating the effects of beta-blockers on exercise metabolism
Blood Glucose and Muscle Glycogen
• Glycogenolysis in skeletal muscle is mediated by epinephrine via stimulation of beta-2-receptors
• Beta-2-blockade impairs mobilization of glycogen stores during exercise, producing, in turn, lower serum glucose values
• Muscle glycogenolysis is unaffected by beta-blockade at submaximal exercise, but that max glyogenolytic rate at high exercise intensities can be impaired
Generalities
1. Cardioselective beta-blockers suppress maximum HR less than noncardioselective agents
2. Acutely, beta-blockers of all types reduce VO2 max (mean reduction of 6-14% in both healthy subjects and pt’s with cardiovascular disease. Although the training effect of regular exercise is suppressed most by nonselective agents it is still possible for subjects taking beta-blockers chronically to improve their fitness level as a result of an exercise program
3. Cardioselective beta-blockers interfere with utilization of energy substrates less than noncardioselective agents during exercise
Normotensive Subjects
• Beta-blockers generally exert negative effects on aerobic exercise performance; noncardioselective types exert more detrimental effects than do the cardioselective types o The difference may be due to a combination of metabaolic actions – impaired muscle triglyceride utilization, impaired glycogenolysis, impaired adipose lipolysis, disruption of potassium homeostasis
Hypertensive Subjects
• Beta-blockers exert more detrimental effects on exercise performance than do other types of antihypertensives such as alpha blockers, ACE inhibitors or calcium channel blockers
•