Flashcards in Muscle III Deck (15):
stem cells. Source of myoblasts to repair injured muscle.
They respond to many signals (FGF, IGF, NO...). Damaged muscle cell produces factors like LIF that trigger satellite prolif.
CT fibroblasts interact with satellite cells to regulate proliferation of each cell type. They prevent premature differentiation of satellite cells.
Satellite cells and Duchenne
The cells are weakened and damaged by the absence of dystrophin.
So satellite cells are constantly fusing to repair the muscle... and satellites get depleted/ lose ability to keep up.
More myofilaments added and muscle fibers get larger.
Part of this response is that satellite cells divide and fuse to provide the nuclei and protein synthesis machinery to support extra volume of muscle cell.
Types of repair in cardiac muscle?
NO satellite cells.
Little or no repair after heart attack. Damaged area has scar tissue made by fibroblasts.
Maybe repair from circulating stem cells from bone marrow, unclear.
Some research is trying to get cardiac fibroblasts to turn into myocytes.
Smooth muscle repair?
Cells dedifferentiate, enter mitosis, regenerate new muscle cells.
This may help contribute to smooth muscle tumors...
Hypertrophy or hyperplasia?
NO ADDITION OF NEW FIBERS.
You just increase the cross-sectional area of each cell by adding new myofibrils.
Can you change fiber types?
Nope. Under normal conditions you might get fast to fast intermediate... but not fast to slow.
Sprinters are born not made...
Both a decrease in force production and speed of contraction.
Can be due to impairment at any point from motor neurons to events at SR.
Major steps don't include motor neuron, neuromuscular synapse, AP potential initiation or propagation along surface...
Major steps affected in fatigue
Propagation of AP into t-tubule
Release of Ca from SR
Effect of Ca on the myofilament interaction
Force generation by the myofilaments
High frequency stimulation
1.) K builds up and Na is reduced in restricted space of t-tubular network
2.) Get AP of reduced amplitude or AP failure in inner part of t-system
3.) Outer part but not inner part of fiber contracts.
This fatigue recovers in seconds (exchange time for diffusion of t-system is just a few seconds).
More typical kind of fatigue
Due to metabolic changes, primarily an increase in Pi and a decrease in pH.
Skeletal muscle burns ATP to contract, one for each myosin/actin cycle and one for each Ca pumped back into SR.
HOwever phosphocreatine replenishes ATP, so levels of ATP don't change much in strenuous contraction. Result is decreased phosphocreatinine and increase in creatinine and Pi.
Why does increased Pi and H ions lead to decreased Ca release? not clear.
Troponin and fatigue
The effect of Ca on troponin is reduced in fatigue (maybe H ions competing with
Elevated pi and H+ in muscles
This reduces force generated by myosin pulling on actin... but which part of conformational change is unclear.
Smooth muscle is complex
Hard to categorize. Sometimes needs SR sometimes does not.
Endothelial cells and neurons produce NO ==> it increases cGMP levels --> smooth m. RELAXATION
this is how viagra and cialis work (prevent cGMP breakdown, enhancing NO action, relaxing smooth m).