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Medicine - Year 1 > Soft tissue - Physiology > Flashcards

Soft tissue - Physiology Flashcards

1
Q

Muscle is a bundle of fibres that can contract to produce movement; this can be voluntary or involuntary. What are the 3 types of muscles and their roles?

A
  • Striated (skeletal) muscle - locomotion and posture
  • Smooth muscle - peristalsis
  • Cardiac muscle - heart contraction
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2
Q

Describe the structure of a skeletal muscle

A
  • Attaches to bone via tendon
  • Whole muscle contained within an eternal sheath extending from tendons called epimysium
  • Folds inwards to form perimysium
  • Single fibres within individual fascicles are surrounded by a sheath called endomysium
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3
Q

Fill out the structures of the skeletal muscle

A
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4
Q

Desribe the structure of a muscle fibre

A
  • Filled with myofibrils
  • Sarcolemma - plasma membrane
  • Sarcoplasm - cytoplasm
  • Sarcoplasmic reticulum (SR) - acts as a storage organelle for Ca2+
  • Transverse tubular system (TT) - invagination of sarcolemma
  • Triad - terminal cisternae of two SR and TT in close proximity
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5
Q

a) What is a sarcomere?
b) Describe the structure of a sarcomere

A

a) Unit of contraction of the myofibril

b)

  • Z-lines - either ends of sarcomere where thin filaments insert
  • M-line - origin of thick filaments and the middle of sarcomere
  • H-zone - zone of thick filaments only
  • A-line - overlap of thick and thin filaments
  • I-band - only thin filaments
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6
Q

Label the structure of the sarcomere

A
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7
Q

Describe the structure and function of the myosin (thick filament)

A
  • Myosin head - binds to actin
  • Tail is formed of 2 interwinded heavy chains
  • 2 regulatory light chains - required for ATPase activity
  • 2 alkali light chains - to help stabilise myosin head
  • Hinge region - allows moveemnt of myosin head
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8
Q

What is the role of the 2 regulatory light chains in myosin (thick filaments)?

A

Required for ATPase activity

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9
Q

What is the role of the 2 alkali light chains in myosin (thick filament)?

A

To help stabalise myosin head

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10
Q

What is the role of the hinge region in myosin (thick filament)?

A

Allows movement of myosin head

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11
Q

Describe the structure and function of the actin (thin filament)

A

Actin is the binding sit for myosin. It is composed of:

  • Tropomyosin - blocks myosin receptors
  • 3 Troponin molcecules that control tropomyosin position: C (binds to Ca2+), I (anchors complex to actin), T (binds to tropomyosin)
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12
Q

What is the role of troponin C?

A

Binds Ca2+ to itself causing a conformational change in the troponin complex

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13
Q

What is the role of troponin I?

A

Anchors complex to actin (by moving away from actin filament)

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14
Q

What is the role of tropinin T?

A

Binds to tropomyosin, pushes it away from myosin binding site, exposing it This allows myosin head to bind to actin

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15
Q

Describe the changes in the sarcomere when a contraction occurs

A
  • Z lines get closer together
  • I-band shortens
  • H-zone gets smaller
  • A band remains the same
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16
Q

Describe the sequences of events involved in muscle contraction

A

Excitation-contraction coupling

  • Action potential propagates along membrane and down T tubules
  • Opens voltage gated L-type Ca2+ channels on T tubules
  • This causes coupling between L-type Ca2+ channels (DHP receptor) and Ca2+ release channels (ryanodine receptor)
  • This opens Ca2+ channels from sarcoplasmic reticulum
  • Ca2+ is rleased into myofiibrils activivating troponing C and cross-bridge cycling

Initiation of cross-bridge cycling

  • Ca2+ binds to troponin C causing a conformational change to take place in the troponin complex
  • Troponin I anchors complex to actin by moving away from actin filament
  • Troponin T binds to tropomyosin to move it away from the myosin binding site and expose it
  • Myosin head binds to actin

The cross-bridge cycle in skeletalmuscle

  • ATP binds to myosin head causing dissociation of actin-myosin complex
  • ATP hydrolysis cause myosin head to return to resting conformation
  • Cross-bridge formation and then myosin head binds to another position on head
  • Release of Pi from myosin then myosin head changes conformation, causing a power stroke and filaments slide past eachother
  • ADP release

Termination contraction

  • Minor: Na-Ca exchanger (NCK) or Ca pump at plasma membrane
  • Major: Ca reuptake into sarcoplasmic reticulum by SERCA-type Ca pump
  • Calsequestrin (major Ca-binding protein in skeletal muscle) is located predominantly at triad juntion ready for next contraction
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17
Q

Describe the sequence of events involved in excitation-contraction coupling

A
  • Action potential propagates along membrane and down T tubules
  • Opens voltage gated L-type Ca2+ channels on T tubules
  • This causes coupling between L-type Ca2+ channels (DHP receptor) and Ca2+ release channels (ryanodine receptor)
  • This opens Ca2+ channels from sarcoplasmic reticulum
  • Ca2+ is rleased into myofiibrils activivating troponing C and cross-bridge cycling
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18
Q

Discuss how calcium and protein filaments in skeletal muscle interact during muscle contraction (initiation of cross-bridge cycling)

A
  • Ca2+ binds to troponin C causing a conformational change to take place in the troponin complex
  • Troponin I anchors complex to actin by moving away from actin filament
  • Troponin T binds to tropomyosin to move it away from the myosin binding site and expose it
  • Myosin head binds to actin
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19
Q

Describe the cross-bridge cycle in skeletal muscle

A
  1. ATP binds to myosin head causing dissociation of actin-myosin complex
  2. ATP hydrolysis cause myosin head to return to resting conformation
  3. Cross-bridge formation and then myosin head binds to another position on head
  4. Release of Pi from myosin then myosin head changes conformation, causing a power stroke and filaments slide past eachother
  5. ADP release
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20
Q

Describe the termination contraction in skeletal muscle

A
  1. Minor
  • Na-Ca exchanger (NCK)
  • Ca pump at plasma membrane
  1. Major
    * Ca reuptake into sarcoplasmic reticulum by SERCA-type Ca pump
  2. Calsequestrin (major Ca-binding protein in skeletal muscle) is located predominantly at triad juntion ready for next contraction
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21
Q

What does the amount of force generated by a muscle depend on?

A
  • Number of active muscle fibres
  • Cross-sectional area of muscle
  • Initial resting length of muscle
  • Rate at which muscle shortens
  • Frequency of stimulation
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22
Q

Describe the difference between isometric vs isotonic contraction

A

Isometric contraction - muscle length fixed; stimulation of muscle will cause increase in tension but no shortening

Isotonic contraction - muscle length not fixed; stimulation of muscle will cause muscle shortening provided tension generate is stronger than opposing load

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23
Q

Describe the two types of isotonic contractions

A
  • Concentric: in direction of contraction
  • Eccentric: opposite to direction of contraction
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24
Q

Describe the length-tension relationship in muscle contraction

A

Length-tension relationship is direct result of the anatomy of the thick and thin filaments overlapping within individual sarcomeres

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25
Q

Describe the role of titin in muscles

A
  • Muscles are elastic due to titin
  • Muscles are held at resting length by titin
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26
Q

When is maximal tension produced?

A

When thick and thin filaments overlap between 80-120%

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27
Q

a) What is the equation for power
b) Describe the relationship betweenforce and velocity

A

a) Power = force x velocity
b) As velocity increases, force decrease

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28
Q

There are 3 types of fibres: slow twitch (type 1), fast twitch (type 2a) and fast twitch (type 2b). Compare the different fibre types including their fatigue, colour, metablism, mitochondria and glycogen

A

Slow twitch (type 1)

  • Fatigue: resistant - prolonged endurance activity
  • Colour: red
  • Metabolism: oxidative
  • Mitchondria: high
  • Glycogen low

Fast twitch (type 2a)

  • Fatigue: resistance- either endurance or rapid force
  • Colour: Red (myoblobin)
  • Metabolism: mixed metabolism and has features of type 1
  • Mitochondira: higher
  • Glycogen: abundant

Fast twitch (type 2b)

  • Fatigue: quickly fatigue - Rapid force production
  • Colour: white (low myoblobin)
  • Metabolism: glycolytic
  • Mitchondria: fewer
  • Glycogen: high
29
Q

Fill out the table of the properties of fast and slow twitch muscle fibres

A
30
Q

What is the differnce in roles of long fibres compared to short fibres

A
  • Long fibres are good for rapid movemement
  • Short fibres are good for large forces
31
Q

Describe how the body beings to adapt to endurance excercise training

A
  • Increased mitochondrial function leading to increased oxygen
  • Increased hypoxia inducible factors (HIFs) - involved in gene control of red muscle cell production and glycolytic enzymes
  • Increased haemoglobulin
32
Q

Individuals vary in proportion of different fibre types. How does training affect the proportion of fibre types? and how does this affect athletes?

A

Training does not significantly change proportions of fibre types

Athletes find the sport that fits their abilities

33
Q

If you set off on a 1500m run. What changes in the body would occur?

A

Energy production x8 in first 3 minutes

Increase in:

  • Consumption of cellular fuel
  • Consumption of oxygen
  • Production of carbon dioxide
  • Heat
34
Q

Describe the role of creatinine phosphate in muscle contraction

A
  • Creatine combines with ATP
  • This forms creatine phosphate and ADP
  • Creatine kinase acts on creatine phosphate and ADP to regenerate creatine and ATP (used for muscle contraction)
35
Q

Name the three main stages of aerobic respiration and the products at the end of each stage

A
  1. Glycolysis - Glucose converted to 2 ATP + 2 Pyruvate
  2. Krebs cycle - acetyl coA onverted to 1ATP + 3 NADH + 1 FADH2
  3. Electron transport chain - main source of ATP production and requires oxyge
36
Q

Describe anaerobic respiration

A
  • Occurs when there is no oxyen
  • Pyruvate is converted to lactic acid (lactate)
  • Lactate is transported to liver and diverted to pyruvate (lactate dehydrogenase) to enter krebs cycleand produce ATP or gluconeogenesis occurs (liver and kidney)
37
Q

Describe what is used up and also produced in intense short-term excercise at:

a) 10-15s
b) Up to 2 mins
c) Several mins

A

a) Creatine phosphate and ATP produced
b) Glycogen to glucose-6-phosphate
c) Lactic acid build up and oxygen debt

38
Q

Describe what is used up or produced during longer less intense excercise

A
  • Glycogen from circulation
  • Glucose from plasma
  • Hepatic glucose production increases - short term glycogenesis and longer term gluconeogenesis
39
Q

What is V02 max?

A

Oxygen usage under maximal aerobic activity

40
Q

Describe the factors that affect VO2 max

A
  • Age - VO2 max decreases after 25
  • Sex - lower for females
  • Activity - improves with activityy, endurance training is better than intermittent training
41
Q

What does EPOC stand for?

A

Excess post excercise oxygen consumption

42
Q

Describe the fast and slow component of the recovery phase after excercise

A

Fast component

  • Resting levels of ATP and creatine phosphate stored

Slow component

  • Lactic acid converted to glucose in liver
  • Lactc acid converted to pyruvic acid
43
Q

Describe the bodys physiological response to increased oxygen demand

A
  • Increase in ventiltion rate
  • Increase in tidal volume (volume of air displaced during respiration, so more rapid and deeper breaths)
44
Q

What are the changes, if any, in blood gases during excercise?

A

Aterial O2 and venous CO2 do not change significantly during excercise beacuse the respiratory system can provide adequate aeration

45
Q

Describe how oxygen consumption changes during excercise

A
  • Oxygen consumption increases
  • Similar rate for first few seconds then it reaches steady state where lactate acid accumulation is minimal
46
Q

Describe the redistribution of blood flow as you excercise

A

As excercise continues, blood flow to the muscles increases substantially

47
Q

Describe the cardiac changes during excercise

A

Increase cardiac output therefore increased stroke volume (how much blood pumped out with each cycle) and increased heart rate

48
Q

Describe the autonomic control of cardiac output during excercise

A
  • Increase activity of sympathetic nerves to heart increases stroke volume
  • Decrease activity of parasympathetic nerves to heart increases heart rate
49
Q

a) What is stroke volume
b) Describe how this is increased during excercise

A

a) The amount of blood expelled by the heart in each beat

b)

  • CVS: central venous pressure changes diastolic filling pressure, more blood availabe to fill heart
  • TPR: Total peripheral resistance changes ability to expel blood into arterial system
  • Increase sympathetic activity or epinephrine causing increased contractability
50
Q

What does ‘Starlings law’ say?

A
  • The fuller the heart is, the harder it will contract inreasing the stroke volume (ventricular performance)
51
Q

Describe the autonomic control of heart rate during excercise and recovery

A
  • Excercise: change from parasympathetic (cPNA) to sympathetic (cSNA)
  • Recovery: shifts back to cPNA
52
Q

List the benefits of regular excercise

A
  1. Benefits of excercise and reducing CVD risk
  • Reduced blood pressure
  • Increased circulating HDL and reduced triglycerides
  • Changes in arterial wall homeostasis reducing atherosclerotic disease
  • Improved aortic valve function and reduction in calcification
  • Increased ventricular chamber wall thickness
  • Increased red cells (to a point)
  • Changes in cardiac vasculature to increase oxygen availability
  1. Inducing changes in body composition
  2. Decline in depression
53
Q

List the benefits of excercise on CVD risk

A
  • Reduced blood pressure
  • Increased circulating HDL and reduced triglycerides
  • Changes in arterial wall homeostasis reducing atherosclerotic disease
  • Improved aortic valve function and reduction in calcification
  • Increased ventricular chamber wall thickness
  • Increased red cells (to a point)
  • Changes in cardiac vasculature to increase oxygen availability
54
Q

Describe the components of the peripheral nervous system

A
  • Consists of all axons and ganglia outside CNS
  • Autonomic - parasympathetic and sympathetic
  • Somatic - efferent motor nerves (from CNS to periphery) and afferent motor nerves (from periphery to CNS)
  • Cranial nerves (except II)
55
Q

List the components of a motor unit

A
  • Anterior horn cell
  • Motor nerve axon
  • All the muscle fibre it innervates
56
Q

Large and small motor units are recruited depending on type of task and force. Explain this in further detail

A
  • Axons supply few muscle fibres for a precise task that requires a low level of force
  • Axons supply many muscle fibres for a less precise task that requires a high level of force
57
Q

Describe the structure and function of the cell membrane

A
  • Phospholipid bilayer
  • Largerly permeable to water soluble (hydrophilic) compounds and ionic species
  • Selectively permeable due to embedded proteins and water filled pored which function as: signal receptors, ion channels, tranporty mechanims, surveillance/recogition monitors, enzymes
58
Q

Describe the resting potential

A
  • BIG differences between the electrical potential inside the cell compared to the outside (-70to -90 mv)
  • Big differences between intracellular and extracellular ioninc concentration -Na is low inside and high outside and K is high inside and low outside
59
Q

Describe the origin of the generation of the membrane potential

A
  • The cell membrane is relatively permeable to K+
  • The cell membrane is relatively permeable to Na+
  • The resting membrane is predominantly a potassium diffusion potential
  • Equilibrium between conc gradient and voltage gradient
60
Q

This is NERNST equation. where

E = potential difference

R = universal gas constant

F = Faraday constant

T = absolute temp

Z = valency

What does that NERNST equation seek to find?

A

The equilibrium potential that promotes equal diffusion of potassium in both directions despite the different concentration OR the concentration ratio of an ion necessary to generate a particular potential difference

61
Q

What is the difference between Goldman’s equation and Hodgkin’s equation?

A

The Goldman equation - considers the effect of all charged species and their membrane permeabilities on the equilibrium potential

The hodgkin equation - considers only Na and K concentration and ionic permeabilitiy

62
Q

Explain how the resting membrane potential is maintained

A
  • Na-K ATPase pump - moves 2 K+ molecules into the cell for exchange for 3 Na+ moved out. This maintains a concentration gradient of Na and K
  • Na and K leaky channels - Higher concentration of K+ inside the cell in comparison to the outside of the cell so K+ will diffuse from the inside of the cell to outside of the cell via its leaky channels.
63
Q

What is an action potential?

A

Rapid depolarisation of the cell membrane potential which travels along the length of the cell without a decrease in amplitude

64
Q

Discuss the propagation of an action potential

A

Initiation

  • Initially the resting potential is raised slighty by a small ionic change,external potential change, mechanical force, excitatory post-synaptic potential (EPSP), or an AP generated upstream

Upstroke

  • The threshold voltage for the opening of the VgNa channel is reached so VgNa channels open
  • Na+ flows into the cell down its electrochemical gradient rapidly, depolarising the cell membrane potential, from -70mV to +30mV

Repolarization

  • The VgK channels open and so the VgNa channels close
  • K+ flows out of the cell down its electrochemical gradient through open VgK channels
  • The cells become repolarised back near the resting membrane potential
  • Once the action potential starts it has to complete due to the regenerative opening of VgNa channels

Refractory period

  • Following the action potential,the Vg channels become inactive and refractory
  • Refractory period - the duration before aother action potential can be generate, regardless of the stimuli
65
Q

Decsribe what is happening at each stage from 1-6

A
66
Q

Describe the characteristics of the propagation of the action potential

A
  • Unidirectional due to the refractory period of the VgNa channels
  • The propagated signal does not vary in amplitude (only frequency) and is a digital signal - this is a significant limitation and therefore required a large number of different nerves serving different specific functions
67
Q

The conduction velocity depends on the rate at which the membrane ahead can reach threshold. Discuss two main factors that will affect the conduction velocity

A
  1. Diameter - the larger the diameter the faster it takes for the action potential to reach threshold (hence the faster the conduction velcoity)
  2. Insulation - myelinated axon
  • Schwann cells produce myelin
  • Between the schwann cells are nodes of raniver
  • The action potential jumps from node to node and diffuses along the insulated parts of the axon - known as saltatory conduction
  • Reduces loss of conduction, speeds conduction and saves energy
68
Q

Describe the role of schwann cells on axons

A
  • Schwann cells act as an insuator
  • They produce myelin
  • Between the schwann cells are nodes of ranvier - Na channels are clustered at each node
  • The action potential jumps from node to node and diffuses along the insulated parts of the axon - known as saltatory conduction
  • Reduces loss of conduction, speeds conduction and saves energy
69
Q

Describe synaptic transmission in the somatic and autonomic nervous systems

A
  1. The arriving action potential (AP) triggers VgCa channels in the presynaptic membrane to open at the nerve terminal
  2. Ca enters the terminal and triggers a cascade of reactions causing the vesicles of acetylcholine (Ach) to intergate (fuse) with the presynaptic
  3. This releases the contained Ach neurotransmitter into the synaptic cleft
  4. Ach neurotransmitter diffuses across the synaptic cleft and binds to acetylcholine receptors (AchR) which is a ligand-gated ion channel on the post-synaptic muscle membrane
  5. Ions, mainly Na+, flow in and depolarize the muscle membrane in the same way as an axon
  6. A muscle AP is propagated over the muscle cell membrane (sarcolemma) and down the T tubules to the inner aspect of the muscle fibre

Medicine - Year 1 (61 decks)

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