Muscle tissue 2 Flashcards

1
Q

A. Neuromuscular junction (NMJ)

A

As mentioned previously, muscles contract due to a rapid release of CALCIUM (Ca+2) from the Sarcoplasmic reticulum (SR).

Recall how Ca+2 binds to the troponin/tropomyosin complex which allows sliding of the filaments (contraction).
This rapid influx of Ca+2 into the muscle fiber is due to an electrical impulse called an action potential (AP) (more on APs next module).
For now, just understand that it’s an electrical signal that causes changes to the membrane which causes different ion channels to open/close which in turn causes Ca+2 to be released.

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2
Q

Somatic motor neurons

A

– nerves that extend from the brain & spinal cord (both part of the central nervous system) that are responsible for somatic movements. These terminate at the sarcolemma of a muscle fiber (the plasma membrane of the muscle fiber). Thus the junction between the neuron and the muscle fiber is called the neuromuscular junction.

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3
Q

Synaptic cleft

A

– the space between the end of the somatic neuron (axon terminal) and the muscle. The synapse is how different nerves communicate with one another (this includes the cleft).
Neurotransmitter (NTs). APs CANNOT jump across this gap. Instead, chemicals called neurotransmitters are used to propagate the signal across the cleft. There are hundreds of naturally occurring NTs in the body. Some may have an excitatory effect, while others will be inhibitory (depending on the specific synapse). NB: NTs are discussed extensively in chapters 12-17.

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4
Q

Acetylcholine (ACh)

A

– the neurotransmitter that is released at the NMJ (stored in vesicles in the pre-synaptic terminal).

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5
Q

Motor endplate

A

– the side of the synapse which consists of the muscle sarcolemma containing ACh receptors (ligand-gated receptors). This is also known as the post-synaptic membrane/terminal.

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6
Q

B. Generation of the action potential at the NMJ:

A
  1. Release of ACh – nervous impulse arrives at the axon terminal causing the stored ACh inside vesicles to be exocytosed into the cleft and migrate to the motor endplate.
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7
Q
  1. Activation of ACh receptors
A

– ACh binds to their corresponding receptors on the motor endplate, which in turn opens sodium (Na+) channels, causing Na+ to flow into the sarcolemma (membrane) of the muscle.

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8
Q
  1. Production of the AP
A

– the rapid influx of Na+ into the muscle fiber causes an increase in positive charge within the cell. This generates a further action potential which is propagated along the sarcolemma into the T-tubule system, causing a secondary release of Ca+2 that ultimately causes the muscle to contract.

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9
Q
  1. Termination of ACh
A

– ACh is broken down by an enzyme acetylcholinesterase (AChE), and the end products are recycled back into the axon terminal to make new ACh molecules for the next time it’s needed.

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10
Q

Steps involved in initiating muscle contraction

A

AP arrives at the pre-synaptic terminal
ACh (neurotransmitter) is released
3. ACh travels across the NMJ via fast diffusion
4. ACh binds to & stimulates receptors on the post-synaptic membrane
5. Na+ channels open up and Na+ rapidly enters the muscle cell
6. An action potential is generated at the post-synaptic membrane (post-synaptic action potential)
7. AP travels along the sarcolemma (all directions) and down the T-tubules
8. This triggers the release of Ca+2 from the sarcoplasmic reticulum
7. Ca+2 binds to troponin in the sarcoplasm causing tropomyosin to change position (revealing the myosin-binding sites on actin)
8. Myosin can now bind with actin
9. ATP attached to myosin heads is hydrolyzed to ADP + phosphate
10.Muscle contraction occurs

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11
Q

Note

A

: NMJs tend to be located at the middle of muscle fibers. This allows the APs to reach both ends of the muscle cells more quickly (travelling in both directions). In other words, the APs travel towards the origin and insertion of a muscle and thus allow the most forceful contraction.

REMEMBER! Muscle fibers contract evenly throughout the entire length of the muscle!!!

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12
Q

Botox

A

is the clinical use of botulinum toxin – the poison derived from clostridium botulism (anaerobic bacteria).

This substance has the effect of blocking the release of ACh from axon terminals in the NMJ.
When ACh isn’t released, corresponding ACh receptors aren’t stimulated and no muscle AP is generated (thus no muscle contraction!).

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13
Q

C. Cardiac muscle tissue:

A

Recall that cardiac muscle tissue is striated and involuntary.
Ca+2 ions are found in the SR and the interstitial fluid. High levels of Ca+2 in cardiac muscle tissue allows prolonged contraction (up to 10-15 times longer than skeletal muscle). More on this in AP200.
Cardiac muscle tissue has auto-rhythmicity (it contracts in response to its own self-generated action potentials).

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14
Q

In the heart there are 2 nodes:

A

Sinoatrial (SA) node
Atrioventricular (AV) node
These nodes are responsible for the automatic rhythmic contractions of the upper and lower portions of the heart, which results in the characteristic “lubb dubb” we hear as heart sounds.
The average heart contracts about 75 times/minute during rest.
Recall that between heart cells are intercalated discs (increased/thickened areas of the sarcolemma made up of gap junctions & desmosomes). What was the purpose of these?

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15
Q

D. Smooth Muscle Tissue:

A

Recall: smooth muscle tissue is non-striated and involuntary
Like cardiac muscle tissue, it also has auto-rhythmicity; an AP sent to one smooth muscle fiber will in turn be transmitted to neighbouring fibers (allowing them to contract in unison).
E.g. When the digestive control centers in the brain send nerve signals to the stomach and small intestines to begin contraction, only one or a few action potentials are needed to stimulate the entire organ to contract.

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16
Q

There are 2 types of smooth muscles:

A

Visceral (single unit) – more common – more like cardiac fibers
Multi unit – less common

Very similar to physiology of skeletal except:
Much slower contractions (onset and duration) It takes much longer for a contraction to initiate and the duration may be for hours.
Has the ability to stretch and distend to much greater lengths.

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17
Q

E. Muscle metabolism:
There are 3 ways in which muscles can generate ATP for
contraction.

A
  1. Creatine phosphate (CP)
    High-energy molecule found only in muscles
    Creatine is produced in the liver, kidneys & pancreas, then transferred to muscles.
Creatine kinase (CK), an enzyme, transfers a phosphate (PO4) group from ATP to creatine making creatine phosphate (this is a reversible reaction).                          ATP + creatine  creatine phosphate + ADP  ATP + creatine
This readily accessible form of energy provides maximum muscle contraction for up to 15 secs of activity.
The breakdown product of creatine is creatinine, a metabolite excreted in the urine.
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18
Q
  1. Anaerobic glycolysis
A

Occurs in the absence of oxygen
Takes place in the sarcoplasm
This is the BREAKDOWN of glucose (glycolysis) in a series of steps to form ATP
This process results in 2 molecules of ATP & 2 molecules of pyruvic acid (which go on to aerobic respiration to form lots more ATP)
During heavy exercise when not enough oxygen is available, the pyruvic acid is converted into LACTIC ACID, which travels to the liver and is converted back to glucose (however in high doses this contributes to the temporary rise in the blood acidity and is thought to cause muscle soreness).
Produces enough ATP for maximum muscle contraction for 30-40 secs of activity (i.e. 400 meter dash).

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19
Q
  1. Aerobic respiration
A

Occurs in the presence of oxygen
Takes place in the mitochondria of cells
Uses the pyruvic acid* (aka pyruvate) from anaerobic glycolysis and processes it further using Krebs cycle & the electron transport chain to produce large amounts of ATP (more in AP200!).
* This process may also use fatty acids & amino acids.
Involved in exercise that lasts longer than several minutes (E.g. marathon runners)
Generates the highest amount of ATP (about 30-32 for each glucose molecule), plus heat, water, and CO2.
The oxygen that drives aerobic respiration comes from hemoglobin (blood) & myoglobin (muscle fibers).

20
Q

Muscle fatigue

A
– the inability to maintain forceful contraction after prolonged periods (possible reasons include lack of O2, Ca+2, lack of ATP or buildup of metabolic waste products).
Oxygen debt (AKA recovery oxygen uptake) – the period following strenuous exercise where the body continues to attempt to replenish the normal resting values of oxygen in tissues
21
Q

Motor unit

A

– includes the somatic motor neuron & all the muscle fibers it innervates (it may be 1 neuron per muscle fiber or >3000 fibers/neuron) [fig. 10.13 pg 321] – more on this in Chp 13.
On average, in skeletal muscles, it’s 1 neuron/150 muscle fibers.
Basically muscles which are responsible for precise movements will have smaller motor units (less muscle fibers per motor neuron).

22
Q

Twitch contraction

A

– brief contraction of all the muscle fibers in a motor unit in response to a single AP. Muscle twitches last about 20-200 msec which is very long compared to the muscle AP (1-2 msec).

23
Q

Fasciculation

A

– involuntary contraction of a motor unit which is visible under the skin. May be harmless or the result of a number of different pathologies (M.S., ALS etc.)

24
Q

Contraction:

A

(a) latent period – action potential sweeps the sarcolemma and Ca+2 is released
(b) contraction period – Ca+2 binds to troponin, tropomyosin changes shape, crossbridges form, contraction occurs
(c) relaxation period – cross bridges break, Ca+2 is taken up and restored.
(d) refractory period – period in which a subsequent AP will not be able to generate a muscle contraction

25
Q

Frequency of stimulation:

A

stimulation of muscles by APs may not occur consecutively – it could even occur before the muscle fiber has a chance to relax.

Wave summation – muscle stimuli arriving at different times which tend to cause larger than normal contractions.

Un-fused (incomplete) tetanus – sustained but wavering contraction due to stimuli arriving @ 20-30 times/sec

Fused (complete) tetanus – completely sustained contraction due to stimuli arriving @ 80-100 times/sec so the fiber has NO time to relax.

26
Q

Electromyography (EMG)

A

– electrodes are used to determine muscle activity (muscle action potentials) and to diagnose certain muscle conditions such as muscular dystrophy. The print out of this is called a myogram.

27
Q

Motor unit recruitment

A

– the process by which the number of active motor units increases.
This allows for smooth movement and delays muscle fatigue (smaller fibers generally are recruited first, followed by larger fibers when the duration and amount of force required increases).

28
Q

Muscle tone

A

– the amount of tension or tautness of a muscle at rest d/t weak, involuntary contractions of its motor units
This explains the constant muscle tone we can measure in blood vessels, GI organs, postural muscles

Flaccid paralysis – loss of muscle tone and reflexes, atrophy, and degeneration of muscles
Usually associated with lower motor neuron injuries

Spastic paralysis – excess muscle tone and reflexes
Usually associated with upper motor neuron injuries

Rigidity – increase in muscle tone with no affect on reflexes. I.e. What occurs in tetanus (disease caused by the bacterium clostridium tetani).

29
Q

Muscle tone

A

– the amount of tension or tautness of a muscle at rest d/t weak, involuntary contractions of its motor units
This explains the constant muscle tone we can measure in blood vessels, GI organs, postural muscles

Flaccid paralysis – loss of muscle tone and reflexes, atrophy, and degeneration of muscles
Usually associated with lower motor neuron injuries

Spastic paralysis – excess muscle tone and reflexes
Usually associated with upper motor neuron injuries

Rigidity – increase in muscle tone with no affect on reflexes. I.e. What occurs in tetanus (disease caused by the bacterium clostridium tetani).

30
Q

Types of Skeletal Muscle Fibers:

A

There are several types of skeletal muscle fibers based on the amount of myoglobin and mitochondria they contain as well as the speed at which they contract.

31
Q

Red muscle fibers

A

have lots of myoglobin and mitochondria, a large blood supply, and therefore appear dark (dark meat of chicken, steaks etc.).

32
Q

White muscle fibers

A

have less myoglobin and mitochondria, less blood supply, and therefore appear white (chicken breast etc.).

33
Q

Slow oxidative (SO) fibers

A

a.
Smallest in diameter (least amount of myofibrils).
Weakest (generates the least amount of force).
Dark red color since it contains many mitochondria & blood capillaries and therefore uses mainly aerobic respiration (which is why they are called oxidative fibers).
Muscle contractions are very slow, but can sustain longer durations (tends to be more resistant to fatigue).
Marathon runners & postural muscles.

34
Q

Fast Oxidative-Glycolitic (FOG)

A

Typically the largest fibers
Red color d/t them containing many mitochondria & blood capillaries (it uses aerobic metabolism). However, they also have high levels of glycogen (uses anaerobic glycolysis, too).
Muscle contractions are faster than SO
Sprinters, runners

35
Q

Fast Glycolitic Fibers (FG)

A

Appears white because it has the least amount of myoglobin, capillaries, and mitochondria.
Can generate the strongest contractions for the shortest amount of time.
Weight lifters, body builders, & baseball pitchers.

36
Q

Note:

A

All skeletal muscles have a mixture of these 3 types of fibers (i.e. biceps has FG, SO, & FOG).
Postural type muscles tend to have more SO fibers, whereas quads and hamstrings tend to have both SO & FOG fibers.
The ratio of these fibers in our muscles is genetically determined however you MAY be able to change this slightly with different forms of exercise (I.e. running, lifting weights, etc.).

37
Q

Principles of movement:

A

all skeletal muscles have an:
Origin (O)
The place where the muscle ‘begins’ (originates)
Tends to be the more stable of the 2 attachments

Insertion (I)
Where the muscle ‘ends’ (inserts)
Tends to be the less stable of the 2 attachments

Action (A)
What the muscle does (its movements)

38
Q

Some muscles have multiple origins, insertions and actions.

A

Generally, in skeletal muscle, the insertion moves towards the origin. For example, with the biceps the elbow moves to the shoulder when the muscle contracts.Origin and insertions generally do not switch, however, there are some exceptions. E.g. The rectus abdominus (abs) during the conventional “sit-up” or reverse crunch.
All muscles will receive stimulation from at least 1 nerve (some have more than 1).
All muscles will have multiple sources of blood supply – both arterial (oxygenated blood) and venous (deoxygentated blood). Usually they have 1 main artery and vein

39
Q

Agonist –

A

primary muscle involved in a specific movement. E.g. Brachialis in elbow flexion

40
Q

Antagonist –

A

primary opposer to the agonist’s action. E.g. Triceps in elbow flexion

41
Q

Fixator/stabilizer

A

– muscle that helps stabilize a joint or bone so that the agonist can perform its actions. E.g. Deltoids in elbow flexion

42
Q

Synergist

A

– muscle that aids in the movement of the agonist. E.g. Biceps in elbow flexion

43
Q

Isotonic concentric contraction

A

– forceful contraction of a muscle as it shortens. E.g. Biceps in elbow flexion

44
Q

Isotonic eccentric contraction

A

– forceful contraction of a muscle as it lengthens. E.g. Biceps in elbow extension

45
Q

Isometric contraction

A

– forceful contraction of a muscle without a change in its length. E.g. Holding a beer at the pub!