block 4- bioenergenetics and muscle metabolism Flashcards
(35 cards)
ATP-IDC
-hydrolyses ADP and phosphate to make ATP=-31kJ mol-1
-not a long-term energy store
-body must constantly synthesize new ATP
-Three ATP synthesis pathways
1. ATP-phosphocreatine system (anaerobic
metabolism)
2. Glycolytic system (anaerobic metabolism)
3. Oxidative system (aerobic metabolism)
phosphocreatine system
Phosphocreatine (PCr): ATP recycling
* PCr energy cannot be used for cellular work
* PCr energy can be used to reassemble ATP
Replenishes ATP stores during rest
Recycles ATP during exercise until used up
- phosphcreatione has a high energy bond= breaks an phosphate group moves onto to ADP to reform ATP
-found in skeletal muscle but is a small supply
glycolysis preparation phase
.. Preparation phase:
* Traps glucose in cell
* Forms a compound that is
readily converted into 3C
molecules
* 2 molecules of ATP consumed
see imagine on slide if needed
glycolysis pay off phase
Harvesting of some of the free
energy of the intermediates
* 4 ATP produced therefore net gain of 2 ATP molecules
* 2 NADH produced
- so can make ATP directly and also indirectly via NADH
substrate-level phosphorulation
-direct transfer of a phosphate group from a donor molecule where the free energy of hydrolysis is higher than that for ATP
-no oxygen is required to make ATp
-e.g. phosphocreatine, glycolysis
lactate dehydrogenase
Used when: the supply of oxygen is inadequate
Allows formation of ATP by glycolysis by
regenerating NAD via lactate dehydrogenase.
-pyrua=vate gets convert to lactate . NADH allows this reduction to occur and then the lactate can be reused
-lactate gets transported through the blood and to the liver which can be civerted back to glucose = cori cycle
-not much energy cn be made
aerobic metabolism
-where we can get the most ATP from
Glycolysis
* Citric acid cycle
* Oxidative phosphorylation
-oxidative phosphorylation= don’t need to know the full details
-happens in the mitochondria
sources of energy
-stores of glucose and glycogen, (trained athletes will have higher glycogen stores and would be able to rely on theses alone)
-Triacylglycerols and mobilisable proteins see slide for proportions if needed. in the cases where glycogen stores arent enough and takes a lot of time.
-therefore carbohydrates are the first used store and then fats lastly . proteins can be used but there isn’t a store except our muscles so this would be an abnormal mechanism
glycogen metabolism
-Glycogen synthesis:
- glycogenesis
- key enzyme = glycogen synthase
Glycogen breakdown:
- glycogenolysis
- key enzyme = glycogen phosphorylase
fats (triacylglycerol) metabolism
-Hormonal signals control
mobilisation/.storage of
TAGs in adipose
Insulin
- promotes TAG storage
Glucagon/adrenaline
- promotes lipolysis
-fatty acid oxidation releases the energy store in TAG for anerobic metabolism
this occurs in the mitochondrial matrix
interaction of different energy systems
- 100m spint mainily produces ATP anareobically via phosphcreatine as its shorter so there’s enough ATP to rely on this
-moderate exercise e.g. 1000m. will start to use other metabolism such as anaerobic but also PCR carbohydrates
-long distance runs= aerobic metabolism =ox phos, carbohydrates and lipids
-see slide to explain the table
changes in fuels use
-not just turn pone system off they all overlapping
-e.g. as phosphocreatine starts to deplete the anerobic respiration system kicks in and then when the decreases aerobic respiration kicks in
-see graph on slide
oxidative capacity in the muscle
A measure of a muscle’s maximum ability to use oxygen
Expressed as μL O₂ consumed per gram of muscle per hour
Varies between muscles (e.g., postural vs. explosive muscles)
Determined largely by the activity of oxidative enzymes in mitochondria
muscle fibres types oxidative capacity
-Type 1= high oxidative capacity=more vasculiser and more mitrochondria and myoglobin
-type 2= would be the opposite. e.g. fewer mitrochondria
hormonal regulation of metabolism during excersize
- Adrenal galnd= adrenaline/noradrenaline
regulation of glucagon release
Low [glucose]
* Voltage-gated sodium and calcium channels are open
to fire action potentials
* Influx of Ca2+ stimulates glucagon secretion
High [glucose]
* Na channel inactivation prevents calcium influx and
glucagon secretion
* Linked to Katp inactivation
sources of glucose during moderate exercise
- Glycogenolysis in muscle (glycogen glucose 6-phosphate)
- Glycogenolysis in liver (glycogen glucose 6-phosphate)
- Gluconeogenesis in the liver (lactate, glycerol, amino acids glucose)
These effects are mediated by changes in hormones:
Increase in: glucagon
adrenaline
Decrease in: insulin
why can only adrenaline stimulate the breakdown of glycogen in skeltal muscle
-they only have areanlaine receptor
study alongside quilet for imgaes
What happens in skeletal muscle at rest
Energy demands are low
- Different fuels used depending on availability in the serum
- glucose
- amino acids
- fatty acids
- Excess glucose in serum stored as glycogen (the “fed state”)
- Insulin is the predominant hormone
How is insulin released at rest?-COME BACK PROBS CHEAT SHEET
- glucose levels increases receptors
-glucose entry through GLUT2 of pancreatic B -cells - intracellular ATP rises due to process like glycolysis etc…
-leads to an inhibition of Katp which depolarises the membrane
-influx of ca2+ = release of insulin vesicles
-increase in cytosolic Ca2+ triggers insulin secretion
how is insulin released in the skeletal muscle for more insulin?-CHEAT SHEET
- when insulin binds to the insulin receptor it activates pka
-then phosphatlyates proteins in the GLUT4 containing vesicles
- increases surface expression of GLUT4 therefore influx of glucose into the cell, = increase glucose for use of muscle cells.
-insulin pathway involved PIP2 described in proteins
How does insulin promote glycogenesis?
- Activation of glycogen synthase promotes
production of glycogen
- Inhibition of glycogen phosphorylase
slows glycogen breakdown
- High [ATP] inhibits glycolysis
