Lecture 7 Flashcards
Epimysium
connective tissue that surrounds the entire muscle tissue
Perimysium
connective tissue surrounding a bundle of muscle fibers
Endomysium
a network of connective tissue, which surrounds individual muscle fibres
Fascicle
a group of muscle fibers is “bundled” as a unit within a muscle
Sarcolemma
the plasma membrane of the muscle cell
- surface membrane of 1 muscle fibre
Sarcomere
the basic contractile unit of muscle fibre
What activates muscle contraction?
I.e. leads to Ca2+ release
At the neuromuscular junction:
(1) a nerve impulse from the axon comes into the nerve ending and releases Ach into the synaptic cleft
- Ach diffuses across the synaptic cleft and attaches to Ach receptors on the sarcolemma
(2) muscle action potential depolarizes transverse tubules at the sarcomere’s A-I junction
(3) T-tubule system depolarization causes Ca2+ release from the sarcoplasmic reticulum lateral sacs
(4) Ca2+ binds to troponin in actin filaments and tropomyosin (“rope”) moves away from the binding sites on actin
- allowing for myosin to bind
What is the Cross Bridge Cycle
a series of molecular events that triggers muscle contraction
- Sarcomere shortens when myosin heads in thick myofilaments form cross-bridges with actin molecules and thin myofilaments
What has to happen before the Cross Bridge Cycle can begin?
Myosin head must be activated
- this occurs when ATP binds to the myosin head and is hydrolyzed to ADP and inorganic phosphate the energy liberated from the hydrolysis of ATP activated myosin head – forcing it into the cocked position
What happens to initiate the Cross Bridge Cycle
Formation of a cross bridge is initiated when calcium ions released from the sarcoplasmic reticulum bind to troponin
- binding causes troponin to change shape
Tropomyosin moves away from the myosin binding sites on actin, allowing the myosin head to bind actin and form a cross bridge
What are the 4 steps of the Cross Bridge Cycle?
- Cross-bridge formation
- Power Stroke
- Cross-bridge detachment
- Reactivation of the Myosin head
Cross Bridge Cycle:
Step 1 - Cross-bridge formation
Activated myosin head binds to actin forming a cross bridge
Inorganic phosphate is released and the bond between myosin and actin becomes stronger
Cross Bridge Cycle:
Step 2 - Power Stroke
ADP is released and the activated myosin head pivots
Sliding the thin myofilament toward the center of the sarcomere
Cross Bridge Cycle:
Step 3 - Cross-bridge detachment
When another ATP binds to the myosin head the link between the myosin head and actin weakens and the myosin head detaches
Cross Bridge Cycle:
Step 4 - Reactivation of the Myosin head
ATP is hydrolyzed to ADP and inorganic phosphate
The energy release during hydrolysis reactivates the myosin head, returning it to the cocked position
Key points of the Cross Bridge Cycle
As long as the binding sites on actin remain exposed, the cross-bridge cycle will repeat
As the cycle repeats the thin myofilaments are pulled toward each other and the sarcomere shortens
- This shortening causes the whole muscle to contract
Cross-bridging ends when calcium ions are actively transported back into the sarcoplasmic reticulum
Troponin returns to its original shape allowing tropomyosin to glide over and cover the myosin binding site on actin
What is muscle relaxation?
When the second ATP binds to the myosin head, weakening the link between myosin and actin
- when 1 myosin head detaches
What is the definition of neuromuscular fatigue?
A failure to maintain the required force during a given task;
- An exercise-induced decline in maximal muscle force or power production capacity
- Central fatigue
- Peripheral fatigue
Central NS
Brain
Spinal Cord
Peripheral NS
Spinal nerves (autonomic and somatic)
Muscle units
- note: e-c coupling = excitation contraction coupling
What is voluntary activation (VA)
the amount of recruitment of muscles during a voluntary contraction effort
What is the Twitch Interpolation technique (ITT)?
A test that determines central vs. peripheral fatigue
- necessary to discriminate between central and peripheral fatigue mechanisms
Consists of stimulating a representative sample of the muscle belly through an electric shock both during a voluntary contraction and at rest
- Stimulation to the femoral nerve
Explanation of ITT
MVC force output is the maximal voluntary force that your central nervous system + your muscles (i.e., peripheral system) can produce
- (MVC - maximum voluntary contraction)
Reduction in MVC does NOT inform us whether the deficit is from the brain or the muscle
Larger SIT after fatigue means a reduction of CNS to drive muscle voluntarily
Smaller resting twitch after fatigue = a reduction of the exercised muscle’s ability to produce force.
- This is peripheral fatigue (this is not voluntary)
Decreased voluntary activation means central fatigue
*To measure voluntary activation, you need BOTH SIT and RT
Superimposed Twitch (SIT)
The size of SIT indicates central fatigue
During ITT, SIT is measured by stimulating the femoral nerve after (during) voluntary contraction
Potential or Resting Twitch (RT)
Size of RT indicates peripheral fatigue
- measured by looking at RT before and after exercise
How do you calculate Voluntary activation?
Voluntary activation = 1–SIT/RT*100
ex. Voluntary activation = [1– (2/300)]*100 = 99.3%
* this means there is a 0.7% deficit
Central Fatigue
When the brain region related to fatigue and pain sensations is activated and the brain sends fewer voluntary motor signals to the skeletal muscles
- The sensation of fatigue and pain reduces muscle contraction and thus maximal voluntary force or power production capacity decreases
Why do we have central fatigue?
Afferent feedback theory:
- High-intensity exercise results in the accumulation of metabolic by-products such as lactate and hydrogen ions in your muscles
- These metabolites activate sensory afferent neurones, called group III/IV afferent, which in return convey pain- and fatigue-related sensory signals to the brain
Central fatigue in simple terms
Metabolites activate afferent receptors in your muscles and send signals to the brain that generate pain and fatigue
- Brain “panics” and reduces signals to muscles (central motor output)
What happens when fentanyl is injected into the spinal cord?
It blocks the group III/IV afferents and maintains the voluntary motor drive to the exercising muscles
- same as an epidural injection during labour
What is shown in this graph?
That power output was significantly higher in participants with fentanyl
- but only in the 1st half
- 2nd half: fentanyl participants had significantly less power output (why? peripheral fatigue)
Control & placebo participants had steady power output and steady central & peripheral fatigue
What are the Mechanisms of peripheral fatigue?
Neuromuscular junction
Calcium availability
Metabolic alterations
Slowing of relaxation
Mechanisms of peripheral fatigue: Neuromuscular junction
Inhibition of pre- and post-synaptic areas
Inadequate Ach release
Mechanisms of peripheral fatigue:
Calcium availability
decreased release of Ca+
Mechanisms of peripheral fatigue: Metabolic alterations
decreased the level of ATP and PCr
Mechanisms of peripheral fatigue: Slowing of relaxation
slowed down Ca+ reuptake
slowed down actomyosin detachment
What activates muscle contraction?
I.e. leads to Ca2+ release
At the neuromuscular junction:
(1) a nerve impulse from the axon comes into the nerve ending and releases Ach into the synaptic cleft
- Ach diffuses across the synaptic cleft and attaches to Ach receptors on the sarcolemma
(2) muscle action potential depolarizes transverse tubules at the sarcomere’s A-I junction
(3) T-tubule system depolarization causes Ca2+ release from the sarcoplasmic reticulum lateral sacs
(4) Ca2+ binds to troponin in actin filaments and tropomyosin (“rope”) moves away from the binding sites on actin
- allowing for myosin to bind
What activates muscle contraction?
I.e. leads to Ca2+ release
At the neuromuscular junction:
(1) a nerve impulse from the axon comes into the nerve ending and releases Ach into the synaptic cleft
- Ach diffuses across the synaptic cleft and attaches to Ach receptors on the sarcolemma
(2) muscle action potential depolarizes transverse tubules at the sarcomere’s A-I junction
(3) T-tubule system depolarization causes Ca2+ release from the sarcoplasmic reticulum lateral sacs
(4) Ca2+ binds to troponin in actin filaments and tropomyosin (“rope”) moves away from the binding sites on actin
- allowing for myosin to bind
