Muscles Flashcards
1
Q
True or false, skeletal muscle is always connected to at least 2 bones?
A
True
2
Q
What is the main function of skeletal muscle?
A
Maintains posture
Movement
3
Q
Cardiac and smooth muscle are both activated by which nervous system and are termed….?
A
Autonomic nervous system (parasympathetic/sympathetic)
Involuntary
4
Q
Which nervous system is skeletal muscle activated by? Is it voluntary or involuntary?
A
Somatic.
Voluntary.
5
Q
What is the function of skeletal muscle?
A
Voluntary movement and posture.
Purposeful locomotion.
Manipulation of external objects.
6
Q
What is the function of smooth muscle?
A
Involuntary movement of items along lumens.
Food in GIT, urine in ureters (peristalsis).
Blood vessels, glands.
7
Q
What is the function of cardiac muscle?
A
Pump blood, maintain blood pressure.
8
Q
What are some functions of muscle in general?
A
Heat production - metabolic by-product.
Protein source, mobilised as energy when other CHOs fail or are used up.
9
Q
What is muscle?
A
A group of fascicles.
10
Q
True or false, muscle fibres extend the length of the muscle, from tendon to tendon.
A
True.
11
Q
From smallest to largest, what are the components of muscle?
A
Myofilaments (Actin, myosin), Sarcomere, myofibril, muscle fibre, whole muscle.
12
Q
What is the name for the coat which encases a muscle fibre?
A
Fascicle.
13
Q
What is a muscle cell?
A
Muscle fibre. Also known as myocyte.
14
Q
Does skeletal muscle have a high concentration of mitochondria?
A
Yes. They are high energy muscles.
15
Q
What are the 4 major components of a neuro-muscular junction?
A
Axon, synapse, muscle fibre, myofibrils
16
Q
Within a myocyte, what are the cytoplasm and smooth endoplasmic reticulum referred to?
A
Sarcoplasm, sarcoplasmic reticulum.
17
Q
Within a myocyte, what is a mitochondria referred to? And the cell membrane?
A
Sarcosome is mitochondria.
Sarcolemma is membrane.
18
Q
Each muscle fibre is innervated by how many neurons?
A
One
19
Q
How many fibres can one neuron innervate?
A
Multiple.
20
Q
What are the contractile elements within myocytes?
A
Myofibrils.
21
Q
What gives skeletal and cardiac muscle its striated appearance?
A
Myofibrils.
Due to orderly arrangement of thick and thin filaments which run parallel to long axis.
22
Q
Describe the structure of a Sarcomere?
A
Z lines are boundaries, M line is mid line of Sarcomere.
H zone is area between overlap of actin and myosin filaments, A band is length of myosin filaments, I band is area between end of myosin and the Z line.
23
Q
What is the muscular protein present that holds myosin in place?
A
Titin
24
Q
On a Sarcomere, which band/zone is the contractile area?
A
I band.
25
What do contractions within muscle result from?
The sliding of interdigitating actin and myosin filaments.
26
Describe the components of a thin filament in skeletal muscle?
Composed of globular, contractile protein actin and the fibre tropomyosin.
Individual G actin molecules each have a myosin binding site, these molecules join together to form double helical strands that form the thin filament. Tropomyosin overlaps the binding sites for myosin on actin.
27
What is tropomyosin?
Regulatory protein.
28
What is actin?
Contractile protein.
29
What is troponin?
Regulatory protein.
30
What regulates skeletal muscle contraction?
Binding of calcium to troponin, causes removal of tropomyosin, exposing myosin binding sites.
31
What are the functions of the thee proteins of the troponin complex?
One attaches to actin, another to tropomyosin, third binds to calcium reversibly.
32
What are the different components of a myosin molecule?
Tail, head, actin binding site(tip of head), ATPase site(side of head).
A whole myosin filament has a portion of bare zone and and area with cross bridges.
33
What are the two binding sites in a myosin head?
Actin binding site, nucleotide binding site for ATP and ATPase.
34
Which component within the Sarcomere allows for muscle stretch?
Titin.
35
At any stage, do thick or thin filaments shorten?
No, they slide past each other.
36
Which to areas within a Sarcomere shorten upon contraction?
I band, H zone
37
The sliding within a Sarcomere is due to....
Cyclical formation and breaking of cross bridges (cross bridge cycle).
38
Where does the myosin head gain its energy from?
ATP hydrolysis
39
What is the high energy form of Myosin binding?
ADP and Pi bind to myosin.
| High affinity.
40
What is the low energy form of myosin head binding?
ATP.
| Low affinity.
41
Describe the power stroke stage of a cross bridge cycle.
Myosin head moves, pulling thin filament towards centre of muscle, thick and thin filaments detach and then return to reset for another power stroke.
Myosin head returns to initial position with ATP energy input.
42
Describe the 5 stages of the cross bridge cycle.
1. Binding of myosin to actin, Pi released, ADP remains on myosin head.
2. Power stroke, actin pulled towards middle of Sarcomere, ADP released.
3. Rigor (myosin in low energy form), new ATP binds to myosin head.
4. Unbinding of myosin and actin, ATP remains attached to myosin.
5. Cocking of myosin head (high energy form), ATP has been lost, ADP and Pi now bound.
43
What is the form of cycling that the cross bridge cycles demonstrate?
Asynchronous. Never break complete contact between all thick and thin filaments during contraction phase.
44
What is excitation-contraction coupling?
Sequence of events describing how an action potential in the sarcolemma causes contraction.
45
If no Ca is present during contraction what occurs?
Troponin holds tropomyosin over binding sites on actin, blocks myosin binding.
Muscle remains relaxed.
46
What is the role of Ca in contraction?
Ca binds to troponin, causes movement of troponin, causes movement of tropomyosin, exposes binding sites for myosin on actin, cross bridge forms, muscle contracts.
47
What is muscular contraction initiated by?
Signal from motor neuron.
48
What are the components of a motor unit?
Motor neuron and muscle fibres.
49
What are the steps of excitation-contraction coupling?
1. Acetylcholine is released for the axon terminal of motor neuron and binds to receptors in motor end plate. This binding triggers and action potential in the muscle cell.
2. Action potential propagates along sarcolemma and runs down T-tubule.
3. DHP receptors of T-tubule opens Ca channels in sarcoplasmic reticulum.
4. Ca increases in cytosol, binds troponin, shifting tropomyosin, exposing myosin binding sites.
5. Cross bridge cycle occurs.
6. Ca is actively transported back into lumen of SR following action potential.
7. Tropomyosin blocks myosin binding sites (muscle fibre relaxes).
50
How is Ca transported back to the sarcoplasmic reticulum?
ATPase in SR actively transports Ca from cytosol back into SR.
51
What happens if there is no ATP available for muscle cells?
Rigor Mortis. No breaking of cross bridge cycle.
52
What are the three sources of ATP within muscle?
Creatine phosphate
Oxidative phosphorylation
Anaerobic glycolysis
53
Discuss the role of creating phosphate in ATP production.
Creatine phosphate + ADP --> creatine + ATP
Enzyme is creatine kinase.
First source of ATP for muscles, can provide 4-5 x amount of ATP than is present in cell at rest.
One step phosphorylation reaction, very rapid.
Very small amount of creatine phosphate available in cell-used up within seconds/minutes. (Emergency escape response)
54
Discuss oxidative phosphorylation and its role in ATP production.
Primary energy source during light to moderate exercise. Requires oxygen, therefore animal must be able to increase ventilation rate and depth, increase heart rate and contraction, and dilate blood vessels supplying oxygen to muscle to support this.
Muscle stores glycogen that is converted to glucose by oxidative phosphorylation, lasts up to 30mins. After this time, fatty acids delivered to muscle by blood are dominant energy source.
55
Discuss anaerobic glycolysis's role in ATP production for muscle.
Occurs when oxygen supply is limited, during intense exercise.
Rapid production, less efficient than aerobic production as only 2 ATP produced per glucose. Limited glucose availability. Builds up lactic acid.
Limited duration of high intensity exercise, 30-45seconds (fight or flight response).
56
Describe how skeletal muscle contraction is controlled, from the brain to the Sarcomere.
Brain sends action potentials along the CNS, down spinal cord, via peripheral nerves to the motor neuron.
This motor neuron innervates several muscle fibres at motor end plates, the action potential crosses synapse and reaches muscle fibre.
57
Voluntary skeletal muscle contraction is controlled by what?
Central nervous system.
58
How is end plate potential produced?
ACh receptor channels open.
| Initiates action potential if the local spread of current is enough to open voltage-gated sodium channels.
59
What process terminates action potentials at motor end plates?
Acetylcholinesterase
60
What is grass tetany?
Due to Ca and Mg deficiency. Often aggravated by high K.
| Common in lush Spring pastures.
61
What is milk fever?
Flaccid paralysis due to no transmission of action potential. Inadequate Ca to stimulate release of ACh at synapse.
Affects skeletal and smooth muscle.
62
What is tetanus?
Bacterial toxin inhibits enzyme that degrades ACh so it stays bound to receptors. Muscle stays contracted.
63
Contraction in a muscle fibre occurs due to...
Response to single action potential.
64
True or false, a twitch is an all or nothing event for a given muscle fibre at rest.
True
65
True or false, a twitch can occur for one muscle fibre, one motor unit, or the whole muscle.
True.
66
What are the phases of a muscle twitch?
Latent period - time for action potential in muscle cell to onset of contractions.
Contraction phase - time during which tension is increasing, cross bridge cycling is occurring.
Relaxation phase - time during which the tension is decreasing back to zero. Ca is undergoing re-uptake by SR. Longest phase.
Diagram - tension v time (msec)
67
What are the two ways that frequency of stimulation can increase tension?
Treppe-stair case effect, each twitch relaxes completely before next, stronger twitch.
Summation-contractions can overlap and add because duration of contraction and latent period is longer than action potential. 4 phases to diagram, twitch, summation, incomplete tetanus, complete tetanus.
68
Increased fibre diameter means ........ Strength.
Increased.
69
Why does increased fibre diameter allow stronger contractions?
More filaments so more cross bridges can be made in each Sarcomere.
70
Does the length of fibre at onset of contraction affect the force generated?
Yes.
71
What factors affect whole muscle contraction tension?
Number of muscle fibres contracting.
Recruitment-number of muscle fibres contracting at the same time), occurs at level of motor unit and is one of the first reasons for an increase in strength with training.
72
What is an increase in tension a result of?
Recruiting of more and larger motor units.
73
Small motor units are important for what?
Small, weaker, delicate movements.
74
True or false, size of motor unit and fibre diameter are often related. Eg. Small motor unit innervates small fibres.
True.
75
In what order are motor units recruited?
Small (slow oxidative) --> mid (fast oxidative) --> large (glycolytic)
76
Why are small motor units recruited first?
Because they require less action potential stimulation as they are lower voltage.
77
The larger the motor unit, the more tension it generates. True of false?
True
78
What is muscular speed based on?
Rate of cross bridging.
79
What is the rate limiting step of cross bridge cycling/muscular speed?
ATP hydrolysis.
| The faster hydrolysis is, the faster the cycle.
80
Fast fibres have fast.....
ATPase enzyme.
| Vice versa for slow.
81
What are some characteristics of fast fibres?
Relax more rapidly, contract 2-3x faster than slow, recruited for more forceful contraction.
82
Describe the characteristics of oxidative fibres.
Primary energy from aerobic, oxidative phosphorylation.
More mitochondria, smaller diameter, many capillaries, higher myoglobin (darker red meat), resistant to fatigue as no lactic acid produced.
83
Describe some characteristics of anaerobic glycolytic fibres.
Primary energy from anaerobic glycolysis.
Use little oxygen, fewer mitochondria, larger diameter, fewer capillaries, low in myoglobin (paler meat), high glycogen stores and quick to fatigue (lactic acid decreases pH of cell).
84
Why is there no slow anaerobic glycolytic muscle?
Would be slow and fast to fatigue.
85
Describe the properties of slow oxidative fibres.
Slow myosin ATPase, high oxidative capacity (aerobic), lots of mitochondria (site of oxidative phosphorylation), rich blood supply, myoglobin (red meat), smaller diameter, little tension, fatigue slowly.
86
What are the properties of fast oxidative fibres?
Intermediate in many properties between slow oxidative and fast glycolytic. Intermediate diameter, high myosin ATPase activity, high oxidative capacity, myoglobin (oxygen storage), slow to fatigue but faster than slow oxidative.
87
What are the properties of fast glycolytic fibres?
High myosin ATPase activity, high glycolytic capacity, high glycogen stores, many glycolytic enzymes, no myoglobin (pale), large diameter, greater tension, fatigue rapidly due to lactic acid.
88
One muscle can have a mixture of fibre types, true or false?
True
89
True or false, within a single motor unit, all muscle fibres are the same type.
True, type depends on innervation.
90
Can fast oxidative fibres be converted to fast glycolytic?
Yes, metabolic patterns can change, speed however cannot.
91
What are some reasons for muscle fatigue?
High intensity exercise-accumulation of lactic acid, compassion of blood vessels, depletion of acetylcholine (NMJ fatigue).
Low intensity exercise-depletion of energy reserves.
Central fatigue-physiological fatigue.
92
What causes muscle tone?
Nerve impulses from brain stimulate groups of muscle fibres to contract and keep muscle toned. This is involuntary, normal muscles are always partially contracted.
93
What is a flaccid muscle?
A muscle whose nerve supply is destroyed, muscle fibres can no longer be stimulated to contract, muscle looses tone and becomes flaccid, eventually leads to atrophy.
94
Is cell division within muscle cells possible?
No - no new cells, change in muscle size is due to change in size of individual cells.
95
What is hyper trophy?
Increase in muscle size (increased size of myofibrils), increased production of actin and myosin.
Caused by near maximal force development (training, weight lifting).
96
What is atrophy?
Occurs due to lack of use, muscle decreases in size (loose myofibrils). Can be due to denervation, tenotomy, sedentary lifestyle, plaster cast, space flight.
Forms include disuse atrophy, or can get de-innervation atrophy, motor neuron destroyed.
Fibre loss occurs after 1-2 years, very difficult to replace these lost fibres.
Muscle performance affected as degeneration of contractile proteins, decreased max force of contraction and velocity of contraction.
97
What is hyperplasia?
Rare,formation of new muscle fibres, may be caused by endurance training?
98
What is normal growth within a muscle referred to?
Lengthening, no change in force development but muscle has increased shortening capacity and increased contraction velocity.
99
What are some forms of muscle remodelling?
Hyper trophy, hyperplasia, lengthening, atrophy.
100
What is coactivation?
When antagonist muscle maintains some tone.
| Increases precision of movement.
101
What are the two sensors responsible for muscle coordination and feedback control?
Muscle spindle fibres-detect muscle length.
Golgi tendon organ-detects tension.
Send afferent messages to spinal cord and brain on length and tension of muscle, allows cerebellum to determine positioning of body and adjustments required.
102
What factors of muscle physiology affect meat quality?
Fat, bruising (stress), fibre size, glycogen, fibre type, proteolytic enzymes, age of animal.
103
What is the name of the connective tissue layers within muscle?
Epimysium-outer layer (surrounds whole muscle), perimysium (connective tissue surrounding fascicles), endomysium (encase individual muscle fibres within fascicles).
104
Describe the anatomy of smooth muscle.
Not striated, small, spindle shaped cells, one nucleus per cell, small amount of sarcoplasmic reticulum. Functional unit runs between two 'dense bodies' rather than Z line.
Tropomyosin is present but not troponin. Slow myosin ATPase.
Actin and myosin arranged diagonally and is much longer, no sarcomeres, higher actin:myosin ratio, myosin has heads over entire length.
105
Describe the special features of smooth muscle.
Can operate over long lengths (60-75% shortening possible), can maintain force for long periods (hours, days, weeks), bell shaped length v tension curve, can be myogenic, very energy efficient (minimal O2 consumption required), has Ca action potentials (voltage gated Ca channels in caveolae), poorly developed SR,
106
Describe neuromuscular junctions in smooth muscle.
Autonomic nerve fibres branch and form diffuse junctions with underlying smooth muscle fibres.
Varcosities (nodule) in terminal axons contain neurotransmitter (equivalent to motor end plate in skeletal muscle).
Neurotransmitter is secreted into matrix coating and diffuses to muscle cells.
Excitation is transmitted by Ca action potential or simple diffusion of Ca into fibre.
107
What are the steps of excitation contraction coupling in smooth muscle?
1. Opening of Ca channels in plasma membrane (receptors in caveolae, voltage gated channels open allowing Ca to pass from ECF to ICF).
2. Ca triggers release of more Ca from sarcoplasmic reticulum (positive feedback).
3. Ca binds to calmodulin.
4. Ca-calmodulin complex activates myosin light chain kinase.
5. MLCK phosphorylates myosin light chain (head).
6. Cross bridge cycle occurs.
108
What are the major differences between excitation-contraction coupling in smooth and skeletal muscle?
Smooth muscle-Ca triggers cross bridge cycle by targeting myosin filaments. Myosin ATPase is 10-100 x slower, making smooth muscle contractions much slower.
Skeletal muscle-Ca targets actin filaments (removal of tropomyosin).
109
How does smooth muscle relax?
Phosphatase removes phosphate from myosin.
| Ca is actively removed from cytoplasm by Ca-ATPase and counter transported across cell membrane with Na.
110
Smooth muscle is innervated by....
The autonomic nervous system (parasympathetic and sympathetic).
111
Neural regulation of smooth muscle cells can be excitatory and inhibitory, true or false? Compare this to skeletal muscle.
True.
Skeletal muscle is only excitatory.
Eg. Parasympathetic stimulation causes contraction in GIT, sympathetic causes relaxation.
112
Where is the neurotransmitter in smooth muscle released from?
Varicosities.
113
Does smooth muscle have a specific neuromuscular junction?
No-diffuse binding of neurotransmitters to receptors.
114
What are action potentials in smooth muscle mediated by?
Calcium.
| Slower and longer than sodium mediated skeletal muscle.
115
What mediates action potentials in skeletal muscle?
Sodium.
116
Action potentials within smooth muscle may......
Inhibit contraction
Induce contraction
Cause changes in level of contraction.
117
True or false, within smooth muscle, action potential are no it necessary for low level contraction sometimes. Explain why.
True, resting ICF Ca levels are often high enough to allow low level of cross bridge cycling. Enough to maintain tone.
Can also be affected by hormones, chemicals or stretch.
118
What are the two types of smooth muscle?
Multi unit - autonomic neuron varicosities branch throughout muscle cells.
Single unit - single line of autonomic neuron varicosities above cells.
119
Describe some characteristics of smooth, single unit muscle.
Sheets of electrically coupled cells which act in unison, muscle fibres activated synchronously.
Often spontaneously active eg. Blood vessels, GIT.
Most common type.
Fibres connected by gap junctions, contract as syncytium (single unit).
120
Describe some characteristics of multi unit smooth muscle.
Tissue made of discrete bundles of cells which are densely innervated and contract in response to it innervation.
Eg. Ductus deferens, piloerectors. Often located in large airways, arteries, eye.
Few, if any, gap junctions. Each fibre acts individually, recieves own innervation (rich supply of neurons) and individual recruitment. No tone.
Occur where fine control required, contractions can be regulated by neurotransmitters and other chemicals.
121
Where do slow waves of the GIT originate?
Interstitial cells of Cajal.
Conducted into circular and longitudinal layers of smooth muscle.
Regulates orderly contraction in GIT.
122
In which type of smooth muscle can pace maker activity occur? Describe.
Single unit.
| Can happen by spontaneous depolarisations to threshold without requiring external nerve stimulus.
123
When does cardiac muscle get to rest?
During the refractive period in contraction cycle.
124
Cardiac muscle has properties of both skeletal and smooth muscle. True or false?
True.
125
Which similarities do cardiac and skeletal muscle share?
Striated sarcomeres, contractions regulated by troponin and tropomyosin.
T tubules convey action potential.
SR present but not as well developed in cardiac.
Similar to slow oxidative fibres of skeletal muscle-lots of myoglobin and mitochondria, slow to fatigue.
126
What similarities do cardiac and smooth muscle share?
Pacemaker cells, form functional syncytium, influenced by hormones and paracrines, Ca comes from extra cellular fluid and SR.
Innervated by ANS.
Gap junctions present.
