October 18, 2023 Flashcards
Do practice questions at beginning of lecture
explain the process of glycogen metabolism starting with epinephrine binding to Beta-2 adrenergic receptor
Epinephrine Binding to Beta-2 Adrenergic Receptor:
Epinephrine, also known as adrenaline, is released in response to various stimuli, such as stress or exercise.
Epinephrine binds to the Beta-2 adrenergic receptor on the surface of target cells, including liver and muscle cells.
Activation of Adenylate Cyclase:
Binding of epinephrine to the Beta-2 adrenergic receptor activates an associated enzyme called adenylate cyclase.
Adenylate cyclase catalyzes the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP).
cAMP as a Second Messenger:
cAMP acts as a second messenger, relaying the signal from the cell surface to the intracellular components.
Increased cAMP levels activate protein kinase A (PKA), an enzyme involved in signal transduction.
Activation of PKA:
Activated PKA phosphorylates various target proteins, including those involved in glycogen metabolism.
In the context of glycogen metabolism, one key target of PKA is glycogen phosphorylase kinase (GPK).
Activation of Glycogen Phosphorylase Kinase (GPK):
Phosphorylation by PKA activates GPK.
Active GPK, then phosphorylates glycogen phosphorylase
Activation of Glycogen Phosphorylase:
Phosphorylation of glycogen phosphorylase by GPK (or PBK as referred to in lecture) converts it from the inactive “b” form to the active “a” form.
Active glycogen phosphorylase (OR PBK) catalyzes the breakdown of glycogen into glucose-1-phosphate (G-1-P).
Conversion of G-1-P to Glucose-6-Phosphate:
Glucose-1-phosphate (G-1-P) is further converted to glucose-6-phosphate (G-6-P) by the enzyme phosphoglucomutase.
what is calmodulin (CaM)
a calcium-binding protein
what does calmodulin (CaM) do in Glycogen metabolism
Activation of Phosphorylase Kinase:
When the intracellular calcium levels rise, as is the case during certain cellular signaling events, calmodulin binds to calcium ions, which causes conformational changes in calmodulin.
Calcium-bound calmodulin then activates phosphorylase kinase. Phosphorylase kinase is an enzyme that is crucial for the regulation of glycogen phosphorylase.
Phosphorylation of Glycogen Phosphorylase:
Active phosphorylase kinase, stimulated by calmodulin, phosphorylates glycogen phosphorylase.
This phosphorylation converts the inactive “b” form of glycogen phosphorylase into the active “a” form.
Activation of Glycogen Phosphorylase:
The conversion of glycogen phosphorylase from its “b” to “a” form allows it to catalyze the breakdown of glycogen into glucose-1-phosphate.
Active glycogen phosphorylase (OR PBK) catalyzes the breakdown of glycogen into glucose-1-phosphate (G-1-P).
Conversion of G-1-P to Glucose-6-Phosphate:
Glucose-1-phosphate (G-1-P) is further converted to glucose-6-phosphate (G-6-P) by the enzyme phosphoglucomutase.
What does the “slow” activation of Glycogen metabolism consist of
happens via epinephrine binding
What does the “fast” activation of Glycogen metabolism consist of
happens via calcium binding to calmodulin which activates GBK/PBK
what are beta blockers
Beta blockers, also known as beta-adrenergic blocking agents, are a class of medications that primarily target and block the effects of adrenaline (epinephrine) and related hormones on beta receptors in the body.
These medications are commonly prescribed to manage various medical conditions, primarily those related to the cardiovascular system
can people who are taking beta blockers still use glycogen as a energy source during exercise?
yes because we have another mechanism in place that is not dependent on Beta receptors via calcium binding to calmodulin
what is most likely a limiting factor during long-term exercise of two, three, 4 hours in length @30%-60% Vo2 Max
liver glycogen and blood glucose hypoglycemia
NOT MUSCLE GLUCOSE
Hypoglycemia is a medical condition characterized by abnormally low levels of blood sugar (glucose).
what is most likely a limiting factor during long-term exercise of two, three, 4 hours in length @70%-80% Vo2 Max
Muscle glycogen hypoglycemia
What exercise intensity is the most optimal for muscle to glycogen at a fast rate/great degree during long periods of time
70%-80%
at 70%-80% exercise intensity glycogen is a limiting factor
under conditions of 90%-120% Vo2 max is glycogen a limiting factor? Is your performance limited by glycogen
no, rather ACIDOSIS is the issue because you are exercising at intensities way above the lactate threshold, producing much more lactic acid
you’re going to be fatigued as a result of acidosis
How does training affect glycogen usage during long duration exercises
training enhances mitochondrial content
more mitochondrial content = more beta-oxidation enzymes
more beta-oxidation enzymes = greater reliance on fat metabolism and you’re going to spare/save carbohydrate usage
this is important because we have gram quantities of carbohydrates and kilogram quantities of fat
what is the difference between a trained and untrained person during long duration exercises
trained person is not using glycogen at the same rate because they are able to use fat more than carbohydrate
thus “sparing”/preserving limited stored glycogen and reducing glycogen usage
what is glycogen “sparing”
an adaptation that occurs in endurance trained individuals, due to greater use of lipid substrates –> delays glycogen depletion and fatigue during exercise