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Physiology > Muscles > Flashcards

Muscles Flashcards

1
Q

Organisation of muscles

A

Muscle -> fibre cells -> myofibrils -> 12-18m thick and 5-8mm thin filaments -> myosin and actin

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2
Q

Functions of a contracting tissue allow

A

Movement of whole/part of body/to manipulate objects
Propel contents through various hollow tubes
Empty contents of certain organs into external environment

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3
Q

Organisation of skeletal muscle

A

Fibres lie parallel - connect tissue
Single skeletal muscle cell = fibre - multinucleate, large, elongated, cylindrically shapes, extend entire muscle length
Myofibrils are contractile elements of fibre - regular thick (myosin) and thin (acton) filaments, striations
SKM CM striated, SM unstriated
SKM voluntary, CM SM involuntary

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4
Q

Sarcomere

A

Functional unit of skeletal muscle - 2 Z lines

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5
Q

A band

A

Dark, thick filaments (and overlapping thin)

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6
Q

H zone

A

Middle of H band without thin filaments

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7
Q

M line

A

Vertically down A band - mid H zone

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8
Q

I band

A

Light, thin filaments not n A band

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9
Q

Titin

A

Large, elastic protein extending from M line along thick filament to Z lines. Helps to stabilise site of thick filaments in relation to thin filaments. Increases muscles elasticity like a spring

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10
Q

Myosin

A

Contractile protein forming this filaments
2 identical tail ends wrapped around each other towards centre
2 identical globular heads project at one end and point outwards, forming cross bridges between thick and thin filaments
Cross-bridge has actin-binding site and myosin ATPase site

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11
Q

Actin

A

Contractile protein forming thin filaments
Spherical molecules with specific binding sites for myosin heads
Regulatory proteins also involved

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12
Q

Tropomyosin

A

Regulatory proteins - thread-like molecule lying end to end alongside groove of actin spiral covering actin sites

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13
Q

Troponin

A

Regulatory protein - 3 pp units Troponin C, I and T
Stabilises tropomyosin in blocking myosin binding sites. When Ca2+ bound, tropomyosin moves away -> cross-bridges and contraction

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14
Q

Muscle contraction

A

Sliding filament mechanism
Ca2+ released into sarcoplasm from SR
Myosin heads bind to actin and swivel and bend towards centre of sarcomere by a power stroke
ATP ends to myosin head and detaches from actin
Hydrolysis of ATP transfers energy to myosin head to reorient it
Contraction continues if Ca2+ high and ATP available
Causes thin filaments to slide inwards over stationary thick filaments towards middle if A band and pull Z lines closer
Sarcomeres shorten

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15
Q

Neuromuscular junction

A

Presynaptic motor neutrons and post synaptic muscle fibre
Release of Ach stimulus for contraction
SR and transverse tubules link excitation to contraction
SR fine network interconnected compartments surrounding and segments wrapped around A and I bands - terminal cisternae
T tubules are membranous perpendicular extensions of surface membrane from surface of muscle cell to central portions of muscle fibre. AP on surface membrane spreads into T-tubule - release of Ca2+ from SR into cytosol -> dihydropyridine receptors

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16
Q

Skeletal muscles

A

Groups of fibres bundled together and attached to bones
Connective tissue divided into bundles - extends beyond ends -> tendons
Contraction strength depends on number of muscle fibres and tension by each contacting fibre and motor units

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17
Q

Skeletall motor units

A

Number of muscle fibres varies per unit
Precise, delicate movements = fewer fibres per unit
Asynchronous recruitment of motor units helps delay/prevent fatigue
Tension development: frequency of stimulation, length of fibre, fatigue and fibre thickness

18
Q

Skeletal muscle tension

A

Produced inside sarcomeres and transmitted to bone via connective tissue and tendons before it can be moves. Muscle attached to at least 2 different bones across a join - origin and insertion

19
Q

Skeletal contraction types

A

Isotonic - tension remains constant as muscle changes length - concentric or eccentric
Isometric - “constant length” - levers

20
Q

Skeletal muscle energy

A

ATP is prime source
Creating synthesis mainly in liver from aa
Phosphorylated -> phosphorylcreatine -> energy “store” in muscle
Exercise = ADP -> ATP
Glycolysis anaerobic high intensity exercise

21
Q

Muscle fatigue

A

Defence mechanism to protect muscle from reaching a point without ATP
Central fatigue happened when CNS cant adequately activate motor neurones - working muscles. Psychological?

22
Q

Types of skeletal muscle fibre

A

Slow oxidative, fast oxidative, fast-glycolytic

23
Q

Muscle spindles

A

Control motor movement from 3 levels of input
Groups specialised muscle fibres -> intrafusal fibres
Each spindle own private efferent and affrarent nerve supply
Stretch reflex

24
Q

Smooth muscle

A 
Visceral and multi-unit
Lack visible cross-striations
Spindle-shaped cells with single nucleus
Arranged into sheets within muscle
No Z lines - dense bodies
No troponin, myosin doesn't block cross-bridge binding sites
25
Q

Organisation of smooth muscle

A

3 types of filament: thick myosin, thin actin and in between
Thick/thin at slight diagonal - diamond shaped attic
Myosin in thick filaments - cross-bridges along entire length = thin filaments slide for longer

26
Q

Invitation of contraction of smooth muscle

A

Ca2+ dependent phosphorylation of myosin
Ca2+ drom SR -> membrane channels, no T tubule
Ca2+ binds to calmodulin, activating kinase enzyme, phosphorylating myosin, activating myosin ATPas -> m+a
Ca2+ slow removal - longer contraction and graded response

27
Q

Multi-unit smooth muscle

A

Neurogenic (stimulate day nerves)
Made from multiple, discrete units functioning independently - no gap junctions
Units must be separately stimulated by nerves to contract e.g. large artier, large airways to lungs

28
Q

Single-unit smooth muscles

A

Myogenic - stimulus originates in muscle and doesn’t need nervous stimulation
Fibres exited and contact as a single unit due to gap junctions - functional syncytium
Contraction is slow and energy-effieicet
May be phasic (neurogenic) - contracts in bursts - triggered by AP - increase in Ca2+
Or tonic - partially contracted always - “tone” - low resting point - no bursts of activity but varies above/below tonic state

29
Q

Factors influencing smooth muscle contractile ability

A

Spontaneous depolarisation of cells
Signalling molecules -> NTs from autonomic neurones (Ach) and hormones
Local changes in extracellular fluid - pH, O2, osmolarity, ions
Stretch - contract even when toned - more stretched e.g. bladder (relax)
Respond to stretch by contracting - stress relaxation response

30
Q

Cardiac muscle

A

In heart walls
Similar striations to skeletal muscle (fibres in branching network, 2 lines)
Cells joined at intercalated discs
Gap junctions and desmosomes between cells (syncytium)
T-tubules
Autonomic NS
Well developed SR
Many mitochondria and myoglobin (O2)
Ca2+ from SR and cytosol
Resting memo potential ~-90mV
AP generated intrinsically by pacemaker cells
One unit - syncytium and gap junctions
Each AP = full contraction and relaxation - no grade for cont like SKM

31
Q

Cardiac muscle APs

A

Spontaneous, rapid depolarisation of cells - pacemaker potential, threshold Na+
Plateau phase Ca2+
Slow depolarisation
Rhythmic firing
SA and AV nodes
Firing rate controlled by sympathetic and parasympathetic NS

32
Q

Firing of pacemaker cells

A

Movement Na+, K+ Ca2+ via ion channels
At -60mV, Na+ channels open with slow inward current
Slow depolarisation -> Ca2+ channels open = depolarisation
K+ channels open - depolarisation then slow depolarisation
2 APs together (summation) cannot happen in CM

33
Q

Pacemaker activity

A 
Intrinsic automaticity of SAN = 100 ppm
SAN controls heart rate
Nervous and hormonal SAN/AVN control 
AVN independent activity 
Latent pacemakers in conduction system - e.g. Purkinje fibres can take over if AVN/SAN fail
34
Q

Cardiac output =

A

Heart rate x stroke volume

35
Q

Tetanus of cardiac muscle

A

2nd AP cant trigger until excitable membrane recovered from first
No summation due to slow depolarisation

36
Q

Exercise on cardiac muscle

A

“Trained” heart larger muscle cells and bigger ventricles

Pathological hypertrophy - change in heart size due to physiological problem e.g. value insufficiency, hypertension

37
Q

Myasethenia gravis

A

Autoimmune damage of NMJ

38
Q

Muscular dystrophy

A

Inherited degeneration of SKM fibres

39
Q

Natural wear and tear

A

Injury, age (strength decreases with age due to fat infiltration)

40
Q

Stretch reflex

A

Patellar tendon - knee jerk reflex, monosynaptic myotatic spinal reflex
Receptor -> sensory neuron -> integration centre -> motor neuron -> effector

41
Q

Enhancing nature

A

Training = muscle
Over-training = muscle damage
Dangers of steroids

Physiology (9 decks)

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