Muscle Physiology Flashcards
Functions of muscle
Support
Mechanical response to stimuli
Posture and movement
Store of glycogen and glucose
Store of protein
Thermoregulation (shivering)
Types of muscle
Skeletal
Cardiac
Smooth
Macroscopic layers of skeletal muscle
Surrounding epimysium around belly of muscle
Fascicles made up of bundles of muscle fibres surrounded by perimysium
Individual fibres made of myofibrils surrounded by endomysium
What is the generic pattern of nerve supply to most muscles
Single nerve ending at centre of muscle belly.
What is the surroundings of an individual muscle cell called
What does it consist of?
Special feature with function
Sarcolemma
Lipid bilayer membrane and polysaccharide/collagen outer layer
Deep penetrating invaginations called t tubules allow surface depolarisation to reach deep myofibrils
What’s the general structure of the inside of a muscle cell?
Sarcoplasm (specialised cytoplasm)
Myofibrils
What is special about contents sarcoplasm
Many mitochondria
Sarcoplasmic reticulum - intracellular store of calcium wound around myofibrils
Structure of a skeletal muscle myofibril
Bands/lines (name and parts)
Adjacent actin and myosin termed sarcomeres
Terminal z line separating blocks
I band (just actin)
A band (actin and myosin overlapping)
H band (just myosin in middle of adjacent A bands)
M line in middle of H band
Then reflected on other side
Where in the banding of a sarcomere are t tubules found
2 per sarcomere found at ends of h bands
What holds actin and myosin together in their side by side arrangement
Large protein call titin,
What makes up skeletal muscle thin myofilaments
Layout
Two molecules actin
Helical wrap of tropomyosin
Every half turn of tropomyosin is bound troponin
What subgroups make up skeletal muscle troponin
I, T, C
What makes up the thick myofilaments of skeletal muscle
Structure
Relationship to sarcomere bands
Myosin molecules (each with long tail and 2 short heads) packed together in helical bundle
Each head sticking out between actin chains
Tail region is h line
Overview of sequential steps of skeletal muscle contraction
Nerve action potential - depolarising of end plate and release of acetylcholine
Acetylcholine binds with receptor on muscle causing sarcolemma depolarisation
Depolarisation spreads over muscle and down t tubules
Depolarisation releases calcium from sarcoplasmic reticulum
Calcium binds to troponin C, tropomyosin releases from the actin exposing binding site
Myosin binds to actin repeatedly causing sliding of the fibres and shortening of muscle
Calcium pumped back into sarcoplasmic reticulum, tropomyosin re binds and contraction stops
What is the term for the linkage between nerve cell depolarisation and muscle cell contraction
Excitation contraction coupling
Anatomy of a neuromuscular junction
Flattened unmylinated nerve terminal
Junctions gap
Thickened convoluted folded sarcolemma
Physiological process when action potential reaches nerve end terminal at NMJ until receptor binding.
ACh containing vesicles fuse with cell membrane releasing ACh into junctional gap
ACh diffuses across gap and binds to nicotinic ACh receptors on sarcolemma
Ratio of ACh released from neurone vs number of receptors that need activating on muscle
Consequence
10:1
Reliable neurotransmission
Structure of nicotinic ACh receptor
5 membrane spanning sub units
2 alpha, 1 beta, 1 delta, 1 gamma
Activation and consequence of nicotinic ACh receptor
ACh binds to alpha subunit
Conformational change opens pore
Na enters cell rapidly down concentration gradient
Muscle membrane depolarisation
Physiology of myofibril depolarisation and action potential
Resting potential, duration, speed
Similar to neurone however:
Resting potential -90mV
AP lasts 2-4ms
Travels around 5m/s
What is the collective term for sarcolemma, t tubules and sarcoplasmic reticulum
Sarcotubular triad,
How does a myocyte AP result in calcium release
Activation of dihydropyridine receptor in sarcolemma - voltage sensitive calcium channel
Sensing of this by direct contact with ryanodine receptor on sarcoplasmic reticulum membrane - again calcium channel when open
Calcium moves into cell and out of SR down concentration gradient into sarcoplasm
Clinical correlation of ryanodine receptor in anaesthesia
Mutations responsible for malignant hyperthermia
Dantrolene is a ryanodine receptor inhibitor
How is positive feedback involved in myosin binding to actin
Calcium binds to troponin C causing conformational change of I and T
Troponin dissociates and tropomyosin moves exposing myosin binding site.
Binding of myosin then causes further displacement of tropomyosin and more binding sites exposed encouraging further cross bridging.
How do the myosin fibres move over the actin fibres once bound?
How is atp involved
Binding to actin causes conformational change in myosin causing head to move backwards resulting in movement of fibres
ATP binds to actin myosin complex causing disconnection of actin and calcium release
ATP hydrolysed on myosin leaving attached ADP and pi with potential energy
Calcium binds - myosin reattaches to actin
Power stroke occurs and adp and pi released
Then back to top
How do muscles produce a sustained contraction
Calcium pumps always pumping back into sarcoplasmic reticulum, however, repeated depolarisations cause it to increase faster than it can be cleared resulting in maximum power.
What is a skeletal muscle motor unit
The muscle cells Innervated by a single motor unit
How do muscles differ between fine control and course strength
Small motor units for fine control
How are multiple motor units in a muscle recruited in a contraction
Henneman’s Size Principle
Small motor units first followed by large units, allowing a graduated response and preserving fine control at beginning of response.
What limits duration of continuous whole muscle contraction?
Glycogen store in muscle
Decreased firing rate of nerve cells
Reduction of blood supply through contracted muscle with diminishing oxygen supply
How is muscle tone maintained
Low frequency discharge from motor nerve fibres using feedback from spindle fibres maintaining part state of contraction
How does rigour mortis occur
What stops it
Sarcoplasmic reticulum calcium pumps stop working and so ca levels continue to dissociate tropomyosin from actin
There is no atp available to release myosin head from actin
Stopped as autolysis breaks down muscle proteins
Types of skeletal muscle fibre and characteristics
Type 1a - red, slow twitch, high blood supply, myoglobin and mitochondria, low glycogen, slow to fatigue
Type IIa - red, moderate twitch, high blood supply, myoglobin and mitochondria, medium glycogen, slow to fatigue
Type IIb - white, fast twitch, low blood supply myoglobin and mitochondira, high glycogen, fast to fatigue
Which sort of muscle fibres atrophy with age most
Red fibres
What is the function of the muscle spindle system?
What are they
Provides background tone and modulation for accurate movements
Fusiform sensory structures located within each muscle belly
What signals do muscle spindle fibres relay?
Static - muscle length
Dynamic - stretch, rate of contraction
What happens on muscle spindle stretch
with nerve type
Stretch sensitive ion channels open,
Depolarisation
AP in Ia and IIa sensory nerves
1a sensory fibres monosynaptically synapse with alpha motor neurones triggering the muscle to contract opposing the stretch, also trigger inhibitory neurones to antagonistic muscle.
IIa nerves are used in proprioception
CNS trigger gamma efferent system to the spindle effecting their tension and thus tone of the muscle
What are golgi tendon organs
Mechanism including nerves
Function
Encapsulated nerve endings wrapped around tendon just distal to muscle insertion
Sense tension in the muscle resulting in a polysynaptic inhibitory discharge via 1b nerve fibre, interneurone then alpha motor neurone back to muscle in question.
Function is to protect muscle from too much tension/equalisation of tension between muscles
How is atp created
Phosphorylation of adp by creatine phosphate
Glycolytic phosphorylation
Oxidative phosphorylation in mitochondria
What are the features of adp creation by creatine phosphate
Immediate supply of energy but depletes in a few seconds
Used in explosive movement
Produces creatinine waste
Regenerated during relative rest
Features of glycolytic phosphorylation creating atp
Occurs in cytoplasm
Glycolysis creates pyruvate
Anaerobic and inefficient
Lactic acid waste product
May sustain contraction for a few minutes
How long do intracellular stores of glycogen last to provide for muscle contraction
10 minutes
What provides energy to muscles after glycogen exhausted
Blood glucose and fatty acids for first 40 mins then just fatty acids
What is the energy efficiency of muscles? Where does the rest go?
25%
Heat
What is smooth muscle
Locations
Involuntary muscle under control of autonomic nervous system
Found in viscera and blood vessel walls
Types of smooth muscle
Single unit - all contracts as one (most)
Multi unit - individual cells may contract alone (eg iris of eye, large arteries)
Differences between smooth and skeletal muscle
Smooth is:
Non striated
Smaller cells
Cluster rather than in parallel bundles
Different activation mechanism
How is the contraction mechanism of smooth muscle different to skeletal
Implications
Contractile fibres anchored to dense bodies on the membrane or in cytoplasm rather than z discs
Myosin in bundles with heads in different direction
More actin less myosin
Can contract to much shorter lengths (up to 80% reduction resting length)
How does the muscle action potential differ in smooth vs skeletal muscle
In smooth muscle depolarisation directly opens voltage gated calcium channels in cell membrane and depolarisation largely as a result of this rather than sodium .
How does calcium mediated activation of contraction occur in smooth muscle
Ca binds to calmodulin in cytoplasm
Calmodulin activates myosin light chain kinase causing cross bridging and cycling
NO troponin in smooth muscle cells and tropomyosin is present but function unknown.
What are the implications of the poor ATPase function of smooth muscle myosin vs skeletal muscle?
Stronger contraction per cell but slower
How do smooth muscle cells go to cause waves of depolarisation such as peristalsis
All smooth muscle cells have unstable resting membrane potential
In isolated cells causes irregular contractions but in large bodies of cells results in waves of depolarisation through adherens junctions
Can be triggered by physical stretch - an important factor of auto regulation in blood vessels
What happens if smooth muscles are tensioned and held at longer length
Tension in muscle gradually decreases - plasticity
What can modify smooth muscle contractions
Autonomic nervous system
Hormones (eg progesterone causing relaxation)
Local humoral factors (e.g. calcium concentration in ECF)
