EHS 385 Lecture Notes - Lecture 17: Adipose Tissue, Endoplasmic Reticulum, Glycogenolysis

• School: UMass Boston
• Department: Exercise and Health Science
• Course: EHS 385
• Professor: Rachel Drew

Document Summary

Strenuous activity: demands carbs (fat cannot substitute) Moderate, prolonged: fat metabolism increases as carb depleted. Systems work maintain normal blood glucose levels during exercise: liver 80 grams glucose before exercise, oxidation rates of glucose reach 1g/min in heavy/prolonged activity. Glycogenolysis related to exercise intensity: high intensity exercise results in greater/more rapid glycogen depletion. Plasma epinephrine powerful stimulator of glycogenolysis: high intensity exercise results greater increase plasma epinephrine. Breakdown muscle glycogen under dual control epinephrine-cyclic amp (camp) (via b adrenergic receptors) and ca++- calmodulin( enhanced during exercise due to ca++ release from sarcoplasmic reticulum) Breakdown of glycogen/delivery of fuel (glucose) parallels activation of contraction. Evidence role of ca++-calmodulin in glycogenolysis: propranolol (b receptor blocker) has no effect on muscle glycogen utilization. Controlled by hormones: permissive or slow-acting (thyroxine, cortisol, gh, fast-acting (epinephrine, norepinephrine, insulin, glucagon) Act in permissive manner to allow other hormones exert full effect: t3 enhances effect of epinephrine to mobilized ffa from adipose tissue.