Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 2 > muscle tissue A&P > Flashcards

muscle tissue A&P Flashcards

1
Q

muscle tissue percentage body weight

A

40-50%

depending on body fat, gender, muscle mass etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

4 functions of muscle tissue

A

motion

stabilize/posture

store/move substance
(blood, food, urine,)
–> peristalsis

heat via shivering (thermogenesis)

5th function? store glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

circular muscles that act as gate-keepers…

A

sphincter muscles

regulating movement from one part of body to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

smooth muscles move

A

food (GI tract)

blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

_____ is an involuntary response using voluntary muscles

A

shivering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 types of muscle tissue

A

cardiac

skeletal

smooth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

smooth muscle function in BV

A

e.g. regulates diameter of arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

skeletal muscle fibres

A

elongated,

cylindrical

multinucleated

striated (VIA ARRANGEMENT OF contractile proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

skeletal muscle fibres – note these functions

A

protect internal organs

protects entrance/exit to digestive, respiratory, urinary tracts (I.e. sphincter muscles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cardiocytes

A

short, branched, USUALLY SINGLE NUCLEUS

interconnected via intercalated discs

striated, involuntary

MOVES BLOOD, MAINTAINS BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

intercalated discs

A

transverse thick portion of membrane

VIA DESMOSOMES & GAP JUNCTIONS

desmosomes stronger (INTERMEDIATE FILAMENTS VIA KERATIN)

gap junctions for electrical signal (ion movement)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

desmosomes also via glycoprotein ____

A

cadherin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

smooth muscle cells

A

short, spindle-shaped, nonstriated,

SINGLE nucleus, INVOLUNTARY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

smooth muscle cells functions

A

Move food (PERISTALSIS), urine, reproductive secretions

diameter of respiratory pathway (bronchi**)

DIAMETER OF BLOOD VESSELS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

sphincter pupillae and dilator pupillae

A

dilate and constrict pupils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

muscle cell types by speed of contraction

A

skeletal = FAST
cardiac = INTERMEDIATE
smooth = SLOW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

muscle cell types by Nervous system type

A

skeletal = SOMATIC
cardiac = AUTONOMIC
smooth = AUTONOMIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

muscle cell types by shape

A

skeletal = CYLINDER
cardiac = BRANCHED/CYL
smooth = FUSIFORM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

muscle cell types by # of nuclei

A

skeletal = MANY (PERIPHERAL)

cardiac = (GENERALLY ONE – CENTRE)

smooth = (ONE – CENTRE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

muscle cell types via connection

A

Cardiac = INTERCALATED DISCS (GAP + DESM)

smooth muscle cells = GAP JUNCTIONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

4 properties of muscle tissue

A

1) CONTRACTILITY
2) EXCITABILITY
3) EXTENSIBILITY
4) ELASTICITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

2) excitability

A

ability to receive and respond to stimulus from NERVOUS SYSTEM, or ENDOCRINE SYSTEM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

3) Extensibility

A

Same as plasticity (?)

ability to stretch/lengthen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4) Elasticity

A

ability to return to original length

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

epimysium

A

covers outer later of skeletal muscle

CONTINUOUS with tendon

CONTINUOUS with PERIOSTEUM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

epimysium composition

A

DENSE IRREGULAR CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

epimysium function

A

separates skeletal muscle from other muscles, or organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

epimysium vs tendons

A

continuous with tendons

HOWEVER, tendons DENSE REGULAR CT (?)

epimysium DENSE IRREGULAR CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Epimysium VS deep fascia

A

epimysium connected to DEEP FASCIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

PERIMYSEUM

A

covers muscle fascicles

ALSO DENSE IRREGULAR CT

collaged + elastic fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

muscle fascicles

A

GROUP OF MUSCLE FIBRES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ENDOMYSIUM

A

surrounds individual muscle fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

FASCIA

A

DENSE IRREGULAR CT

“Deep” fascia covers EPIMYSIUM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

fascia other functions

A

lines body walls, limbs

SUPPORTS/surrounds muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

two types of fascia

A

1) SUPERFICIAL fascia

2) DEEP fascia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Superficial fascia

A

below dermis (?)

AKA SUBCUTANEOUS layer

AKA HYPODERMIS

blends w/ deepest part of skin

SEPARATE muscle from skin (DERMIS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Deep fascia

A

BELOW superficial fascia (?)

OVER muscle (over epimysium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Superficial fascia densely packed with

A

nerves, blood vessels, adipose tissue (and other CT), & LYMPH vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Deep fascia …

A

DENSE (IRREGULAR?) CT

fills space between individual skeletal muscles –
FACILITATES MOVEMENTS BETWEEN SKELETAL MUSCLES (reduce friction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Deep fascia can surround individual muscles or GROUPS of muscles

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

When around groups of muscles, deep fascia forms _____

A

fascial compartments with groups of muscles (perhaps with similar function/actions?)

E.G. (lower leg)
ANTERIOR compartment

DEEP POSTERIOR compartment

SUPERFICIAL POSTERIOR compartment

LATERAL compartment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Tendon

A

DENSE REGULAR CT

extend via muscle fibres to bone

TENDON CAN BE continuous w/
a) Epimysium
b) Perimysium
c) Endomysium

I.e. INVOLVES STRUCTURES OF EACH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Aponeurosis

A

similar structure to TENDON

Broad and flat instead of cylindrical

MUSCLE TO BONE or MUSCLE TO MUSCLE

E.g.
Epicranial APONEUROSIS (GALEA Aponeurotica

THORACOLUMBAR fascia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

SYNOVIAL TENDON SHEATHS

A

skin for tendons

CERTAIN PARTS – tendons experience more wear/stress

E.G.
HAND, WRIST, FOOT, ANKLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

synovial tendon sheaths parts

A

Synovial lining / synovial cover of tendon

SYNOVIAL SHEATH

mesotendon, and SYNOVIAL CAVITY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Tenosynovitis

A

inflammation of tendons + Synovial sheaths

(E.G. In hands/feet)

E.g.
DeQuervain’s Tenosynovitis (Gamer’s thumb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

muscle fibres via ____blasts

A

myoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

note myocyte, cardiocyte, and cardiomyocyte

note muscle fibre, myocyte, myofibre

A

note myofibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

number of skeletal muscle fibres

A

predetermined at birth

(GENERALLY?) does NOT CHANGE via MITOSIS

can grow/heal but not increase in #

HYPERTROPHY but NOT HYPERPLASIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

mechanism of Hypertrophy

A

stress causing microtears –> Stimulates repairs, causing cell size increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

anabolic steroids and muscle fibre hyperplasia

A

.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

embryonic development and muscle fibre hyperplasia

A

during embryonic development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

When do muscle cells exit cell cycle?

A

@ G0 Phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

G0 PHASE?

A

“If cells don’t pass the G1 checkpoint, they may ‘loop out’ of the cell cycle and into a resting state called G0, from which they may subsequently re-enter G1 under the appropriate conditions. At the G1 checkpoint, cells decide whether or not to proceed with division based on factors such as: Cell size. Nutrients.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

ATROPHY

A

loss of MYOFIBRILS (and therefore, size)

Via lack of USE
E.g.
FRACTURE

Via innervation LOSS (Neurodegenerative Disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Satellite Cells (AKA myosatellite cells)

A

embryonic cells

remain in skeletal muscles throughout adulthood

Can REPLACE damaged muscle fibres (“to some degree”)

MUSCLE TISSUE REGENERATION AFTER INJURY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

myofibre diameter and length

A

100microMETERS in DIAMETER

can span entire muscle length (“up to 30cm”)

(?) Longest fibres in sartorius, up to 600mm (60cm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Muscle fibres

A

myofibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

cell membrane of muscle fibre

A

SARCOLEMMA

(underneath endomysium)

SURROUNDS myoFIBRILS and SARCOPLASM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Sarcolemma

A

selective permeability

DETERMINED RMP (resting membrane potential)

NOTE REVERSAL OF CHARGE (faciliates muscle contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

change in charge of muscle fibre via…

A

Via Neuron signal

SPREADS ACROSS ENTIRE SARCOLEMMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

MYOFIBRILS

A

contractile organelles

VIA MYOFILAMENTS (contractile proteins)

Myofilaments give muscles STRIATIONS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Myofibril diameter

A

1 MICROMETER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How many myofibrils per myocyte?

A

approximately 2000 myofibrils per MYOCYTE

I.e. MUSCLES OF UNTRAINED INDIVIDUAL

Hypertrophied muscles could have 4000 (?) or more (?) MYOFIBRILS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Myofilaments

A

within myofibrils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

2 types of myofilaments

A

1) THICK FILAMENTS (myosin filaments)

2) THIN FILAMENTS (actin filaments)

thick filaments 15nm diameter
thin filaments 7nm diameter

Thick via MYOSIN protein
Thin via ACTIN protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Myoglobin (within sarcoplasm)

A

binds O2 for ATP production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Sarcoplasmic reticulum

A

membranous sacs – SURROUND myofibrils

SPECIALIZED smooth ER

Sarcoplasmic reticulum stores Ca2+ – necessary ion for muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

T tubules (Transverse tubules)

A

invagination/holes of SARCOLEMMA

facilitate SARCOPLASMIC reticulum via nerve impulses

T-TUBULES surrounded by terminal cisternae of SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Terminal cisternae of SR

A

dilated terminal regions of SR

FORMED on both sides of Transverse Tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Triads of myofibrils

A

trio consisting of TRANSVERSE tubule

+

two terminal cisternae

Triad
= 1 T-tubule from outside (via sarcolemma)
+ 2 terminal cisternae from within muscle fibre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

3 categories of muscle proteins

A

1) contractile proteins

2) regulatory proteins

3) structural proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

1) contractile proteins

A

found inside myofibrils

types:
i) MYOSIN
= THICK FILAMENTS
= GOLF CLUBS TWISTED TOGETHER
= has ACTIN binding sites

ii) ACTIN
= THIN FILAMENTS
= shaped like golf balls
= has MYOSIN binding sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Sarcomere

A

functional unit of striated muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Z-disc

A

on ends of 1 sarcomere unit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

M-line

A

mid-line of 1 sarcomere unit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Myosin molecule

A

2 golf clubs twisted together

MYOSIN TAIL
MYOSIN HEADS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

thick filament

A

composed of molecules of Myosin aligned
SIDE TO SIDE
and
END TO END
– with heads facing away

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

2) REGULATORY PROTEINS

A

1) Troponin

2) Tropomyosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Thin Filaments

A

composed not JUST of ACTIN

TROPOMYOSIN is part of thin filament COMPLEX

troponin is also part of complex
TROPONIN IS BINDING SITE FOR CALCIUM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

function of tropomyosin

A

BLOCKS myosin binding site during muscle RELAXATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Z-disc structure

A

THIN (Actin) filaments extend from Z-discs

THICK (Myosin) filaments aligned on M-line, in BETWEEN the thin filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

4 structural proteins

A

1) Titin

2) Myomesin

3) Nebulin

4) Dystrophin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

2) Myomesin

A

forms M-line

stabilizes THICK filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

1) Titin

A

indirectly attached Thick filaments to Z-discs on either side

LIKE A COIL

helps to return filaments to original position after stretch or contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

3) Nebulin

A

connects thin filaments to Z-discs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

4) Dystrophin

A

links thin filaments to SARCOLEMMA (stability)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

muscular dystrophy

A

protein dystrophin is lacking in this pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

sarcomere

A

(from z disc to z disc)

THE UNIT THAT CONTRACTS

myofibril is repeating sarcomeres

WHEN SARCOMERES CONTRACT, MYOFIBRILS CONTRACT, MUSCLE FIBRE CONTRACTS, MUSCLE CONTRACTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

WHY STRIATED?

A

arrangement/contrast of thin/thick filaments (NOTE A BAND – region signifying entire length of thick filament in sarcomere unit) – darker band of striations)

“darker regions have more overlap” (???)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

lines and bands

A

Z lines

I band

A band

M line

H band

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Z lines (Z discs)

A

protein structures on edges of sarcomere unit

stabilize filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

A band

A

entire length of thick filaments (including where overlapping with thin filaments)

CREATES DARKER striation

A in “dArk”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

I band

A

signifies region of thin filaments with NO OVERLAP

I in “lIght”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

M line

A

middle of sarcomere

PASSES THROUGH MIDDLE OF THICK FILAMENTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

H band (H zone)

A

signifies region of thick filaments with NO OVERLAP with thin filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Zones/lines/bands during contraction

A

Z-lines come closer together

H BAND becomes smaller and disappears

I BAND becomes SMALLER

and A BAND REMAINS SAME

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

SLIDING FILAMENT THEORY OF MUSCLE CONTRACTION

A

MYOSIN HEADS of thick filaments attach to myosin binding sites of ACTIN proteins

— They then PULL actin (thus Z-discs) towards each other

— SHORTENS SARCOMERES, leading to muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

4 steps of the CONTRACTION CYCLE (sliding filament theory)

A

1) ATP hydrolysis (@ MYOSIN heads)

— 2) formation of “Cross bridges” – Myosin heads attaching to binding site on ACTIN

— 3) Power stroke = fast motion of myosin heads pulling thin filaments

— 4) breaking of cross bridge (ADP molecule detaches and New ATP molecule attaches)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

1) ATP hydrolysis

A

ATPase in myosin heads breaks down ATP to ADP

— Causes myosin head to become energized

— positions myosin heads appropriately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

2) formation of “Cross bridges”

A

Ca2+ from Sarcoplasmic reticulum is released

— Ca2+ attaches to TROPONIN

— Causes Tropomyosin to shift and REVEAL the MYOSIN BINDING SITES of the ACTIN proteins

— MYOSIN heads bind to MBS of ACTIN proteins, thus forming CROSS BRIDGES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

3) Power stroke

A

ADP falls off myosin heads

— Myosin heads perform power stroke in direction of centre of sarcomere (towards M-line

— Sarcomere shortens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

4) Breaking of cross bridges

A

another molecule of ATP binds to cross bridge

— Causes myosin head to release from ACTIN proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

under what conditions do steps in SLIDING FILAMENT theory continue

A

as long as there is ATP and Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Ca2+ depends on

A

Nerve impulses stimulating Ca2+ release from sarcoplasmic reticulum

— If there is a nerve impulse, Ca2+ is present, and contraction takes placec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

ATP availability and myosin heads

A

ATP is needed for Myosin head to release from Actin

— If no ATP, muscle stays contracted

— RIGOR MORTIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Length-tension relationship

A

amount of overlap between thick and thin filaments determines the amount of force generated (% maximal)

— IDEAL OVERLAP = maximal possible force

— too little overlap = less possible

— too much overlap = less possible

— SARCOMERE TOO SHORT OR TOO LONG = LESS POTENTIAL FOR MAXIMAL FORCE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Excitation-contraction coupling

A

generation of AP in SARCOLEMMA –> Start of muscle contraction

— Signal from motor neuron reaches muscle fibre (sarcolemma)

— Ca2+ is released from sarcoplasmic reticulum via signal

— Ca2+ binds to troponin, which causes tropomyosin to shift and expose the MBS of ACTIN proteins

— Excitation-contraction coupling is the process of Ca2+ release & fibre contraction via NEURON signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Steps of excitation-contraction coupling

A

1) neural control

2) Excitation

3) Ca2+ release

4) Contraction cycle begins

5) Sarcomeres shorten

6) muscle tension is produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Steps of excitation-contraction coupling (outlined)

A

1) neural control
— AP @ NMJ begins process —

2) Excitation
— AP causes ACETYLCHOLINE (ACh) release via motor neurons
— leads to EXCITATION (AP) @ SARCOLEMMA —

3) Ca2+ release
— muscle fibre AP travels via T-tubules (transverse tubules)
— Via Terminal Cisternae (Sarcoplasmic reticulum)
— leads to release of Ca2+ in Sarcoplasmic reticulum) —

4) Contraction cycle begins
— Ca2+ binds to troponin
— Tropomyosin shifts off of MBS of Actin
— Cross bridges form

5) Sarcomeres shorten

6) muscle tension is produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

importance of neuron signalling

A

As long as motor neuron signals are present, Ca2+ will be present via Sarcoplasmic reticulum (Via T-tubules and T-Cisternae)

— Muscle will thus continue to contract (ATP must be present as well)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

when neuron stimulus ends

A

SR calcium channel closes

— Ca2+ pumps return remaining Ca2+ into Terminal Cisternae

— CALSEQUESTRIN (protein) binds to Ca2+ in Sarcoplasmic reticulum

— Stores Ca2+ in SR for next contraction

— Tropomyosin resumes original position after Ca2+ leaves Troponin, thus preventing cross bridge formation

— MUSCLE RELAXES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

misc fact about Ca2+ in SR vs cytosol @ rest

A

10,000x higher Ca2+ levels in SR than cytosol of muscle fibre, when muscle at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Muscle injuries, exercise, and other random facts

A

DOMS

— via microscopic tears after strenuous exercise

— pain, tenderness, stiffness, edema

— repair is done via SATELLITE CELLS

— SATELLITE CELLS use amino acids to build new proteins

— pre-workout & post-workout protein intake facilitates this process

113
Q

muscle strains

A

muscle and tendon injuries

— excessive force on muscle fibres

— pain, dysfunction, fibrosis (scar tissue)

— note that muscles strain while ligaments sprain

114
Q

muscle cramps

A

muscle spasms/pain

— extended usage

— lack of blood flow

— dehydration

— buildup of lactic acid & other wastes

115
Q

skeletal muscle fibre types

A

1) Fast glycolitic (fast fibres)

2) fast oxidative (intermediate fibres)

3) slow oxidative (slow fibres)

116
Q

how do skeletal muscle fibres differ. What variables?

A

differ in SIZE, in INTERNAL STRUCTURE, in METABOLISM (type), in RESISTANCE TO FATIGUE

117
Q

Slow oxidative fibres (slow fibres) – how much longer do they take to contract?

A

3x longer to contract compared to fast fibres (Fast glycolitic fibres)

118
Q

slow oxidative fibres (slow fibres) – how much is diameter compared to fast fibres

A

1/2 diameter of fast fibres (Fast glycolitic fibres)

119
Q

slow oxidative fibres (slow fibres) – resistance to fatigue compared to fast fibres

A

longer sustained contractions = fatigue resistance

120
Q

how is ATP produced i slow oxidative fibres?

A

via aerobic ATP production

121
Q

how does structure of slow oxidative fibres facilitate aerobic ATP production?

A

MANY MITOCHONDRIA

—Extensive capillary network (for oxygen exchange)

MYOGLOBIN –> (protein pigment) –> binds/stores O2 in muscle fibres (similar in function to Hemoglobin)

122
Q

how do slow oxidative fibres appear in colour?

A

they appear red due to Myoglobin pigment protein, and DUE TO EXTENSIVE CAPILLARY NETWORK

123
Q

fast Glycolitic fibres PEAK tension time

A

in <0.01 second

124
Q

fast glycolitic fibres diameter and why large diameter? – storage of glycogen (where?)

A

large diameter

DENSELY PACKED WITH MYOFIBRILS = POWERFUL CONTRACTIONS

large glycogen reserve (in SARCOPLASM)

125
Q

fast glycolitic fibres fatigue rate?

A

fatigue rapidly

126
Q

fast glycolitic fibres ATP production (?)

A

ATP produced anaerobically

127
Q

how do fast glycolitic fibres appear in colour?

A

appear white due to LACK OF MYOGLOBIN

128
Q

Fast oxidative muscle fibres (intermediate muscle fibres) – how do they produce energy? contraction speed?

A

combination of aerobic and anaerobic metabolism

muscle contractions faster than SLOW OXIDATIVE but slower than FAST GLYCOLITIC

129
Q

fast oxidative muscle fibres appearance in colour and structure

A

many mitochondria and Blood Capillaries

—- LOW MYOGLOBIN

—- light red colour

—- GLYCOGEN ALSO PRESENT = anaerobic glycolysis

130
Q

the terms RED and WHITE muscle

A

Red muscle = lot’s of blood flow, MYOGLOBIN, Mitochondria

—- = high fatigue resistance
—- = slow
—- = small diameter muscle fibres
—- E.g. Postural muscles

131
Q

White muscle

A

= Little blood flow, less MYOGLOBIN, less Mitochondria

—- low fatigue resistance
—- fast
—- large diameter muscle fibres
—- E.g. Eye muscles

132
Q

Muscles have MIXTURE of fibre types

A

Mix reflects function

—- E.g. Back/calf = Slow
—- E.g. Eye/hand = fast

133
Q

what determines ratio of fast to slow muscle fibres in different muscles?

A

there are some typical patterns of fast/slow ratio (such as push muscles usually having more fast twitch muscle fibres in untrained adults)

—- RATIO can be genetically determined

—- RATIO can be modified with training (Via Specific adaptation to imposed demands)

134
Q

ORIGIN of a muscle tends to be more…

A

more stable, less mobile

Insertion tends to be less stable, more mobile

135
Q

blood and nerve supply to muscles

A

all muscles are innervated by at least 1 nerve (often more)

—- All muscles will have multiple sources of blood supply (ARTERIAL/VENOUS) —- Usually 1 main artery/vein is present

136
Q

AGONIST (AKA PRIME MOVER)

A

muscle which contributes the most in a specific movement

E.g.
BRACHIALIS IS THE PRIME MOVER IN ELBOW FLEXION

137
Q

ANTAGONIST

A

primary opposition to prime mover (AGONIST)

E.g.
Triceps Vs flexion of forearm @ elbow

138
Q

SYNERGIST

A

muscle that aids the PRIME MOVER (agonist)

E.g.
biceps brachii and brachioradialis are synergists of Brachialis during flexion of the forearm @ the elbow joint

139
Q

Fixator/stabilizer

A

muscle that stabilizes a joint so AGONIST can perform its action

140
Q

isotonic movements/contractions

A

skeletal muscle length changes

—- Concentric and eccentric

141
Q

Isometric contractions/movements

A

muscle length does not change, but there is tension in the muscle

142
Q

more about concentric contraction

A

muscle tension exceeds load

— muscle shortens and tension is constant (ISO-tonic)

— SPEED of contraction inversely related to weight of load

143
Q

eccentric

A

muscle tension is less than the load

— muscle lengthens against load (elongates)

— rate of elongation depends on how much the load exceeds the muscle tension

144
Q

what happens if muscle contraction ends, but load is not removed?

A

muscle stretches until

2) Tendon breaks
—
3) “ELASTIC RECOIL OPPOSES LOAD”

145
Q

isometric

A

muscle length does not change

tension does not exceed load, load does not exceed tension

E.g.
Postural muscles

146
Q

do muscles bulge during isometric contractions?

A

yes, but not as much as during ISOTONIC contractions

147
Q

Lever and fulcrum

A

Lever = rigid beam + FULCRUM

—– EFFORT & LOAD are applied to each end of the beam

148
Q

what is the fulcrum?

A

fulcrum is point on which beam pivots

149
Q

3 types of levers

A

1st class lever, 2nd class lever, 3rd class lever

150
Q

1st class lever (EFL)

A

Effort –> fulcrum –> load

E.g.
Posterior neck muscles holding head up

151
Q

2nd class lever (FLE)

A

Fulcrum –> load –> Effort

— Load is between Effort and Fulcrum

— I.e. WHEELBARROW LEVER

— BIOMECHANICALLY THE STRONGEST IN BODY

E.g.
CALVES when doing calf raises on stairs

152
Q

3rd class lever (FEL)

A

Fulcrum –> effort –> load

— effort is between load/fulcrum

— TWEEZER LEVER

E.g.
Hip Flexors raising leg

— NOTE: THIS is MOST COMMON LEVER IN BODY

153
Q

proprioception and proprioceptors

A

proprioception = perceiving sense of position/movement in space (INDEPENDENT OF VISUAL SENSORY FEEDBACK) & perception of equilibrium and balance

154
Q

proprioceptors

A

proprioceptors are responsible for proprioception

— proprioceptors read the muscle LENGTH, MOTION/POSITION, TENSION, etc

155
Q

Examples of proprioceptors

A

1) Muscle spindles, AND 2) Golgi Tendon Organs

156
Q

1) muscle spindles

A

proprioceptors in muscle belly

— Adjust via changes in muscle length (stretch)

— muscle spindle reflex contracts muscle to prevent tearing of muscle tissue during overstretch

157
Q

1) muscle spindles structure

A

composed of INTRAFUSAL MUSCLE FIBRES

— = 3-10 specialized muscle fibres, embedded within muscle belly

— ITRAFUSAL MUSCLES FIBRES are specialized skeletal muscle fibres that served as sensory receptors (PROPRIOCEPTORS)

— Normal contractile muscle tissue is called EXTRAFUSAL MUSCLE FIBRES

158
Q

note difference between INTRAFUSAL and EXTRAFUSAL muscle fibres

A

.

159
Q

innervation of Muscle spindles

A

1) sensory nerve endings – deliver sensory information from INTRAFUSAL FIBRES of muscle spindle to the nervous system

2) motor nerve endings

160
Q

MOTOR NERVE ENDINGS of INTRAFUSAL MUSCLE FIBRES of Muscle Spindles

A

GAMMA MOTOR NEURONS innervate intrafusal muscle fibres

— GAMMA MOTOR NEURONS regulate sensitivity of muscle spindle to stretch stimulation
(Perhaps depending on external factors that determine muscle receptiveness to a given stretch)

— NOTE that extrafusal muscle fibres are innervated via ALPHA MOTOR NEURONS (Skeletal muscle contractions)

161
Q

Gamma motor neurons and what impact their firing rate has with how sensitive a muscle spindle (w/ intrafusal fibres) becomes to stretch

A

increased firing rate of Gamma motor neurons results in increased sensitivity to stretch in the Muscle Spindle

—- more firing = more sensitive muscle spindle

162
Q

Muscle spindle and the stretch reflex

A

contractile reflex in response to rapid stretching of muscle

— protects muscle from tearing, and in the event of injury results in less severe damage, such as strain

163
Q

GOLGI TENDON ORGAN

A

at musculo-tendinous junction

— monitors tension/force at tendon

164
Q

GTO reflex

A

inhibits muscle to protect the muscle & TENDON from damage/strain

165
Q

A few muscle pathologies

A

1) muscular dystrophy

2) Myasthenia Gravis

3) Fibromyalgia

166
Q

1) muscular dystrophy

A

inherited

— destroys muscle tissue leading to degeneration of skeletal muscle fibres

— COMMON type is DUCHENNE MUSCULAR DYSTROPHY (DMD) – effects almost exclusively males

167
Q

common type of muscular dystrophy and mechanism

A

DUCHENNE muscular dystrophy

— DYSTROPHIN protein is not produced, or barely produced

— leads to tears in SARCOLEMMA during muscle contraction

168
Q

signs and symptoms of Muscular dystrophy including prognosis

A

signs/symptoms clear by age 2-5 = lack of coordination, falling, stumbling, etc.

— most pass away by 20 years old, due to cardiac/respiratory failure

— currently, there is no cure, and stem cell & genetic research is on-going

169
Q

2) Myasthenia Gravis

A

autoimmune disorder

— antibodies that bind to ACh receptors, at the NMJ —-> Block them from binding ACh (Acetylcholine)

170
Q

myasthenia gravis signs, symptoms, prognosis

A

chronic, progressive weakening and fatigue of muscles

— could lead to eventual death due to paralysis of RESPIRATORY/CARDIAC muscles

— first affects muscles of face/neck/jaw – arms/legs affected later

— Drug therapy done, but no cure
—> immunosuppressants
—> cholinesterase inhibitors (CHOLINESTERASE breaks done ACh (Acetylcholine))

171
Q

why does MG worsen with activity and improve with rest?

A

because immune system activity increases with activity

172
Q

3) Fibromyalgia

A

IDIOPATHIC

— Pain/tenderness around the body, including muscles and related connective tissues such as ligaments, tendons, Sheaths/fascia

— diagnosed in past 20 years

— affects women more than men

— pain during rest and activity, as well as when pressure is applied

173
Q

other symptoms of FM

A

headaches, insomnia, fatigue, depression

174
Q

treatments for FM

A

antidepressants, NSAID, massage, physiotherapy, chiropractic heat, exercise

175
Q

“abnormal pain perception processing” and FM

A

more sensitive to pain than people without FM

176
Q

NMJ

A

TERMINAL END of Somatic Motor Neuron

MEETS WITH…

Skeletal muscle (@ Motor end plate)

SYNAPTIC CLEFT in b/w

177
Q

“Synapse”

A

they “synapse” (connect) together

I.E. axon terminal synapses w/ Motor end plate

SITE for transmission of AP from nerve to muscle

178
Q

“Somatic”

A

pertaining to body

179
Q

somatic neurons

A

nerves/neurons that extend from brain/Spinal cord (CNS)

RESPONSIBLE for somatic movements

SOMATIC MOTOR NEURONS terminate @ SARCOLEMMA OF MUSCLE FIBRE

180
Q

NMJ 2

A

junction b/w neuron and muscle fibre

181
Q

Synaptic cleft

A

space b/w axon terminal and motor end plate

DIFFERENT nerves communicate via SYNAPSE

181
Q

Neurotransmitters

A

chemicals that propagate AP signal across SYNAPTIC CLEFT

182
Q

how many types of Neurotransmitters

A

hundreds of NTs

some excitatory, some inhibitory

183
Q

Acetylcholine (ACh)

A

NT released @ NMJ

184
Q

Presynaptic terminal

A

Axon terminal before synapse

185
Q

ACh stored in…

A

pre-synaptic terminal in VESICLES

186
Q

motor end plate

A

post-synaptic membrane @ NMJ (on muscle fibre)

187
Q

motor end plate consists of…

A

muscle fibre Sarcolemma containing ACh receptors (ligand-gated receptors / ION CHANNELS)

188
Q

the (receptors) LIGAND-GATED ION CHANNELS of motor end plate

A

ligand-gated

which ligand?
ACh is the ligand

SODIUM ION CHANNELS

189
Q

PRESYNAPTIC TERMINAL (2)

A

AKA presynaptic Membrane

MOTOR NEURON, axon terminal

190
Q

POSTSYNAPTIC MEMBRANE / TERMINAL

A

Motor end plate of muscle fibre

191
Q

the process @ NMJ of AP –> Ca2+ release from Sarcoplasmic reticulum

A

nerve impulse arrives at AXON TERMINAL

cause VOLTAGE GATED Ca2+ Channels to open

Ca2+ causes ACh VESICLES to undergo EXOCYTOSIS

ACh goes across synaptic cleft to ligand gated Na+ Ion channels

Na+ FLOWS INTO MUSCLE FIBRE (SARCOPLASM)

192
Q

INCREASE OF POSITIVE CHARGE IN CELL (DEPOLARIZATION*****)

A

influx of Na+ increases charge of muscle fibre

193
Q

Na+ ion channels @ synaptic cleft vs. adjacent to synaptic cleft

A

@ synaptic cleft = LIGAND gated

Elsewhere = VOLTAGE GATED

I.e.
CHANGE in voltage in cell (DEPOLARIZATION) LEADS TO Voltage gated Na+ ION CHANNELS opening

194
Q

after Na+ ligand gated and voltage gated ION CHANNELS open

A

AP propagated along sarcolemma into T-TUBULES (Transverse tubules)

—–> TO TRIADS –> @ Terminal Cisternae of Sarcoplasmic reticulum —> Ca2+ released from SR

195
Q

Depolarization & Repolarization

A

depolarization = away from RMP –> less negative / more positive

repolarization = towards RMP –> less positive / more negative

196
Q

Terminating AP (3 methods)

A

1) ACh moves out of synaptic cleft via DIFFUSION

2) ACh broken down by enzyme Acetylcholinesterase (AChE)

3) (NOT APPLICABLE TO ACh) –> Other small NTs removed from Syn Cleft via REUPTAKE

197
Q

REUPTAKE

A

“the absorption by a presynaptic nerve ending of a neurotransmitter that it has secreted.”

198
Q

Note Sodium Potassium pump

A

brings cell environment back to RMP

198
Q

Acetylcholinesterase @ ACh – End products are…

A

“the end products are recycled back into the axon terminal to make new ACh molecules for the next time they’re needed”

199
Q

after Ca2+ is released from SR (review)

A

“Ca+2 binds to troponin in the sarcoplasm causing tropomyosin to change position (revealing the myosin-binding sites on actin)

“ATP attached to myosin heads is hydrolyzed to ADP plus phosphate (energizing myosin heads and allowing crossbridges to occur)

“Muscle contraction occurs”

200
Q

Botox

A

clinical use of botulinum toxin

“poison derived from clostridium botulism (anaerobic bacterium)”

blocks the ACh release from presynaptic motor neurons

no muscle contraction – muscle paralyzed

201
Q

Botulinum toxin

A

one of themost lethal substances known

1 nanogram (10-9) per kilogram can kill a human

intravenous dose of just 10-7g would be fatal to a 70kg person
I.e.
0.000001g (one millionth of a gram)

202
Q

heart is

A

hardest working muscle in body

203
Q

how many beats per day

A

over 100,000 times

204
Q

how many beats per minute

A

average 75

205
Q

cardiac muscle tissue is ____ and ____

A

striated

involuntary

206
Q

heart uses which ion

A

Ca2+ from SR and Interstitial fluid

207
Q

why heart prolonged contraction

A

high levels of Ca2+

208
Q

how much longer contraction?

A

10-15 times longer for cardiac muscle tissue

209
Q

cardiac muscle tissue has auto-_____

A

autorhymicity / auto-excitability

NO NERVE SUPPLY NEEDED

self-generated APs

210
Q

pace-maker cells

A

Self-excitable

RHYTHMIC waves of contraction to adjacent cells throughout heart

211
Q

Where are pacemaker cells

A

@ 2 nodes:

1) SINOATRIAL NODE
2) ATRIOVENTRICULAR NODE

= Automatic rhythmic contractions of upper/lower portions of heart

212
Q

SMOOTH MUSCLE IS ____ and ____

A

Non-striated & Involuntary

213
Q

is smooth muscle autorhythmic

A

can be autorhythmic – but is also influenced by NERVOUS system

214
Q

how does AP travel b/w smooth muscle cells

A

AP in one smooth muscle fibre transmitted to neighbouring fibres —-> CONTRACTION IN UNISON

215
Q

how nervous system influence smooth muscle

A

digestive control centre in brain send nerve signal to stomach / small intestine

ONLY ONE/FEW ACTION POTENTIALS ARE NEEDED TO STIMULATE ENTIRE ORGAN TO CONTRACT

216
Q

Structure of smooth muscle

A

THICK FILAMENTS ATTACHED TO DENSE BODIES (similar functionally to Z-disc)

INTERMEDIATE FILAMENTS interconnect Dense Bodies —> Receive tension from contraction

217
Q

Caveolae of Smooth Muscle tissue (AND NOTE about Ca2+ & SR)

A

pouchlike invagination containing Ca2+

LESS SR in smooth muscle cells – NO TRANSVERSE TUBULES

I.e.
MORE RELIANCE ON EXTRACELLULAR Ca2+ than intracellular (from SR)

218
Q

Calmodulin and Smooth muscle tissue

A

protein in smooth muscle that binds to Ca2+

REGULATORY protein –> similar to TROPONIN in skeletal muscle

CALMODULIN eventually activates MYOSIN heads –> contraction occurs

219
Q

what happens mechanically when smooth muscle contracts?

A

MYOSIN/ACTIN complex pulls on DENSE BODIES, which pulls on INTERMEDIATE FILAMENTS —> cell contracts

220
Q

3 energy systems

A

Creatine phosphate (CP) aka Phosphagen System

Anaerobic glycolysis

Aerobic respiration aka Oxidative System

“All 3 Systems active at any given time, but magnitude and contribution of each depends on INTENSITY and DURATION of activity”

221
Q

Creatine phosphate (CP) system

A

high energy bond in creatine phosphate (CP) aka phosphocreatine (PCr) to create ATP

ATP + creatine –> creatine phosphate + ADP –> ATP + creatine

222
Q

where is creatine produced

A

liver, kidneys & pancreas, then transferred to muscles.

223
Q

creatinine

A

breakdown product of creatine is creatinine, a metabolite excreted in the urine

224
Q

creatine phosphate system duration

A

Provides ATP for short-term (15 secs), high intensity exercises

225
Q

CREATINE KINASE

A

ENZYME

transfers a phosphate (PO4) group from ATP to creatine making creatine phosphate (reversible reaction)

226
Q

elevated Creatine kinase

A

Elevated CK-MM = skeletal muscle damage

Elevated CK-MB (myoglobin?) = cardiac muscle damage

227
Q

ANAEROBIC GLYCOLYSIS

A

Takes place in the sarcoplasm

breakdown of glucose to yield 2 x pyruvate molecules

2 molecules of ATP & 2 molecules of pyruvic acid (pyruvate?)

228
Q

pyruvate can…

A

can go to aerobic respiration to form more ATP if oxygen is present (aerobic)

can get converted into lactic acid if no oxygen is present (anaerobic)

229
Q

pyruvate duration

A

ATP for moderate to high intensity, short term exercise
2 minutes (30-40 seconds of maximum contraction)

230
Q

pyruvate –> lactic acid (anaerobic process) —> CORI CYCLE

A

ATP synthesis occurs faster – is limited in duration

inefficient:
6 ATP used, 2 ATP gained

231
Q

Cori cycle

A

@ MUSCLE:
glucose –> 2 ATP + 2 Pyruvate (GLYCOLYSIS)

2 Pyruvate –> 2 Lactate

@ LIVER:
2 lactate –> 2 pyruvate + 6ATP –> GLUCOSE (Via Gluconeogenesis)

Back to muscle:
Glucose goes to muscle

232
Q

Lactic acid buildup misunderstood

A

Not entirely responsible for muscle burn during exercise

(Protons created during breakdown of ATP created at a faster rate then can be cleared –> H+ ions)

233
Q

Lactic acid 3 myths

A

Myth 1:
“Burn” from lactic acid
—> Not from lactic acid –> from H+ ions during ATP breakdown = increased acidity

Myth 2:
Lactic acid is waste
–> NOT waste –> 75% is recycled –> lactate to glucose

Myth 3:
lactic acid causes DOMS
–> lactic acid flushed in 30-60mins –> DOMS is via microtrauma

234
Q

aerobic respiration

A

mitochondria

oxygen

235
Q

aerobic respiration and pyruvate

A

Uses pyruvic acid

LARGE AMOUNT OF ATP via KREB’S CYCLE and ELECTRON TRANSPORT CHAIN

236
Q

aerobic respiration can also use

A

FATTY ACIDS

AMINO ACIDS

237
Q

Duration of aerobic respiration

A

several minutes to hours

238
Q

ATP generated

A

30-32 ATP
+ Heat, CO2, & H2O

239
Q

oxygen for aerobic respiration

A

HEMOGLOBIN (blood) & MYOGLOBIN

240
Q

3 systems – durations

A

0-6s = Phosphagen = very intense

6-30s = phosphagen & Fast glycolysis = intense

30s-2m = fast glycolysis = heavy

2-3m = fast glycolysis & oxidative = moderate

3+ mins = oxidative = light

241
Q

Muscle fatigue – possible reasons

A

1) O2 lack
2) CO2 buildup
3) ATP lack (no glycogen)
(Or depleted Phosphagen system)

4) metabolic waste buildup

242
Q

phosphagen depletion / repletion

A

rapidly depleted (15 secs)

fatigue partially from phosphagen depletion

repletion = within 8 minutes (Via aerobic metabolism and glycolysis)

243
Q

phosphagen pre-exercise concentrations increased via

A

1) supplementation

2) Aerobic and anaerobic training / conditioning

244
Q

glycogen depletion / repletion (HOW MUCH GLYCOGEN?

A

300-400g in muscle tissue
70-100g in liver

245
Q

how glycogen pre-exercise concentration increase?

A

1) aerobic / anaerobic conditioning

2) carb-loading

246
Q

how long till glycogen levels depleted

A

90+ minutes exercise

247
Q

instead of carb-loading

A

replace lost glycogen during mid-exercise carbs

drinks, gels, bars etc

248
Q

oxygen replenishment, oxygen debt, EPOC

A

Oxygen debt

recovery oxygen

EPOC (excess post-exercise oxygen consumption)

249
Q

what is excess oxygen during EPOC used for

A

Resynthesis of ATP and creatine phosphate

Resynthesis of glycogen from lactate

tissue oxygen resaturation

venous blood oxygen resaturation

skeletal muscle oxygen resaturation

myoglobin oxygen resaturation

250
Q

motor unit

A

somatic motor neuron and all muscle fibres it innervates

251
Q

motor unit size varies

A

1 muscle fibre per neuron

> 3000 muscle fibres per neuron

252
Q

motor unit average size

A

1 neuron for 150 muscle fibres

253
Q

motor unit size vs precision

A

more precise movements = smaller motor unit (less muscle fibres per neuron)

254
Q

muscle twitch length vs AP length

A

1-2 msec = AP
20-200 msec = muscle twitch

255
Q

muscle twitch define

A

brief contraction of muscle fibres in motor unit via AP of neuron

256
Q

muscle twitch duration varies

A

E.g.
eye muscle = quick
gastrocnemius = less quick
soleus = even less quick

Also note –> more precise & more delicate muscle (like eye muscle = smaller motor unit)

257
Q

fasciculation

A

involuntary contraction of motor unit –> visible under skin

can occur under normal conditions or under pathological conditions of nervous system

258
Q

motor unit contraction stages

A

1) latent period

2) contraction period

3) relaxation period

4) refractory period

259
Q

latent period =

A

AP via sarcolemma –> Ca2+ released via SR – BUT NO TENSION YET***

260
Q

contraction period

A

Ca2+ to troponin, tropomyosin change shape, crossbridge form, contraction occur

261
Q

relaxation period

A

cross bridge break

Ca2+ taken up and restored

262
Q

relative and absolute refractory period

A

absolute = no

relative = requires higher than usual stimulus (stronger AP?) to contract

263
Q

Frequency of stimulus (AP?) as a variable

A

determines PEAK TENSION

264
Q

how is tension determined in skeletal muscle?

A

1) amount of tension produced by each muscle fibre (VIA FREQUENCY OF STIMULATION?)

2) number of muscle fibres stimulated

265
Q

Frequency of stimulation and Myogram

A

1) wave summation

2) Unfused tetanus

3) fused/complete tetanus

266
Q

wave summation

A

second stimulus before muscle fully relaxes

SECOND CONTRACTION IS STRONGER THAN FIRST

I.e.
Wave summation

267
Q

wave summation = stronger contractions —> up to ___x greater than single twitch

A

up to 5x stronger contraction

268
Q

unfused tetanus

A

sustained contraction, but muscle fibre partially relaxing between summation (I.e. Wavering)

stimuli arriving @ 20-30 times/sec

Unfused tetanus = jagged curve on myogram

269
Q

fused/complete tetanus

A

completely sustained –> muscle fibre has no time to relax partially

stimuli/AP arriving @ 80-100 times/sec

270
Q

why fused?

A

sustain long/powerful contraction

271
Q

motor unit recruitment

A

INCREASE OF ACTIVE MOTOR UNITS

–> “recruited”

Neuromuscular system efficiency –> greater efficiency of nervous system –> higher rate of stumuli/AP –> higher peak tension of single muscle fibre & muscle fibres within motor unit

–> AND HIGHER NUMBER OF MUSCLE FIBRES / Motor units activated —> = higher amount of tension produced

272
Q

motor unit recruitment & movement/fatigue

A

smooth movement

delays muscle fatigue

273
Q

motor unit recruitment – which fibres first?

A

smaller fibres recruited first

–> larger fibres recruited when duration/amount of force increase

274
Q

flaccid paralysis

A

loss of muscle tone

hyporeflexia

muscle atrophy

275
Q

why flaccid paralysis

A

Lower Motor Neuron injury/damage

Trauma
Nervous system disorders (e.g. ALS)
Guillain-Barre Syndrome
Polio
Nerve compression
Myasthenia Gravis

276
Q

spastic paralysis

A

increased muscle tone

hyperreflexia

Upper motor neuron injuries/damage:
stroke
Multiple sclerosis
traumatic brain injury
spinal cord injury
cerebral palsy

277
Q

Rigidity (“RIGOR”)

A

increase in muscle tone

no effect on reflexes

muscle cannot relax

can occur w/ tetanus (disease caused by bacterium Clostridium tetani)

tetanus can also cause tetany

278
Q

tetany

A

“a condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium.”

279
Q

muscle tone

A

amount of tightness/tension of muscle at rest

via small amount of subconscious contraction of motor units

280
Q

muscle tone, blood vessels, GI organs, postural muscles

A

for maintaining adequate BP

for facilitating digestion/peristalsis

for maintaining posture

Semester 2 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions