Ch. 6 Muscle Physiology Flashcards
1
Q
Myofibril
A
- muscle fiber (striated skeletal)
- nucleus, mitochondira, glycogen (glucose)
- structural= contraction proteins
1. myosin: thick
2. Actin: thin
2
Q
Regulatory Proteins
A
- tropomyosin: hides binding sites of actin
- toponin: flips tropomyosin when singaled by Ca+ for myosin to bind to actin
- accessory proteins: titin (stabilize myosin) and Nebulin (stabilizes actin)
3
Q
Sacrorecticulum
A
SR- ER + Calcium- terminal cisternae/ lateral sacs
- lateral sace- float proteins (ryanodine)
+
- T Tubules (transverse tubules), dihydropyridine receptors (DHP)
= Ca+ release
4
Q
Sacromere
A
z-line/disc I- zone: thin filaments (light) A-band: thin and thick (dark) H-band: myosin (tail) M line: center (Mittel)
5
Q
Sacrolemma
A
- covers entire muscle fiber
- forms T tubules
- action potential falls through T tubules; lateral sacs
- release Ca+; troponin
6
Q
Neuromuscular Junction
A
- action potential (ACh initiates)
- role of calcium: bind to troponin (excitable)
tropomyosin “on” position
actin binds to myosin heads
= cross bridge (power stroke; ATP)
7
Q
Sliding Filament Theory
A
- inward pull towards M-line
- shorten sacromere:
Z line shortens
I band shortens
H zone shortens
A band and M line stays the same
8
Q
Power Stroke
A
- break down ATP- ADP+Pi
- energized myosin head
- Ca+ released from lateral sacs
- myosin + actin bind to form cross bridge
- Pi released during binding
- ADP is released after power stroke
- New ATP molecule (cyclic process)
- detachement
9
Q
Relaxation
A
- Ca+ leaves (reuptake) into lateral sacs (uses Ca+ATP pump)
- Tropomyosin “off” position (length restored)
10
Q
Rigor Mortis
A
- stiffness upon death
- metabolism stops (ATP unavailable)
+ - Ca+ ions bound (remain bound)
= muscle stiffness (2-4hrs)
11
Q
Twitch
A
- brief, single action potential
- motor unit
- muscle summation is temporal
- tetanus: infection, continuous contraction (GABA); spasm where bacteria inhibits GABA
12
Q
Isotonic and Isometric
A
- concentric contractions (towards body) and eccentric contractions ( away from body; too fast= injury)
- not moving (eg. yoga); and no change in measurement
13
Q
3 sources of energy…
A
- Creatinophosphate: + ADP and creatine kinase- creatine + ATP
- create externally; side effects: weight gain, GI trouble - Glycolysis: glycolysis (2 ATP)- pyruvic acid- minus oxygen- lactic acid
- Kreb’s cycle (2 ATP)- - Oxidative Phosphorylation (34 ATP)
= total 36 ATP + CO2 + H2O
14
Q
Slow and Fast Twitch
A
- daily activities eg. posture; takes more time
vs. - uses ATP faster, uses Ca+ 9related cycles) faster multiple
- fine movements eg. piano playing (instruments)
- m/sec
15
Q
Glycolytic VS Oxidative Fibers
A
- slow twitch: slow oxidative
- fast twitch: fast glycolytic and fast oxidative glycolytic
Glycolytic: - fewer mitochondira
- fatigues easily
- fewer capillaires
- oxygen poor
- white muscle= white fibers
- myoglobin poor
- ex. sprinting
- anaerobic exercise (lactic acid)
** krebs cycle in oxidative and creatine and glycolytic in
16
Q
Central Fatigue
A
- CNS no longer activates motor neurons supplying working muscles
- psychological based
- boredom
- monotony or tiredness
17
Q
Peripheral (neuromuscular Fatigue)
A
- no longer respond to stimulation with same degree of contractile activity
- defence mechanism
- high-intense activities
- build up of latic acid; depletion of glucose
Neuro: inability of active motor neurons to synthesize ACh rapidly enough to sustain chemical transmission of action potentials from motor neurons to muscles
18
Q
EPOC
A
- replenish creatine-phosphate stores
- remove lactic acid build up
19
Q
Control of Motor Unit
A
- spinal cord: afferent neurons to either somatic neuron or
- Brain stem: RAS (muscle tone) and cerebellum to spinocellum
- Higher Motor Cortex: basal ganglion and thalamus
20
Q
Parkinson’s
A
- abnormal movements; involuntary tremors
- repitlian stare (unable to blink)
- posture; gait
- depression, confusion, sleep disturbances
21
Q
M.S
A
- demylination
22
Q
Muscular Dystrophy
A
- genetic
- cardian and resp. failure
- X- chromosome
- constant leakage of Ca+; damages cell
- protein dystrophin (between 2 lines)
- therapy: gene regeneration
23
Q
ALS/ Lou Geghrig
A
- motor movement stops ( worse than MS)
- cytoskeleton: proteins disorganize
- free radical
24
Q
Muscle Spindle
A
- throughout fleshy part of skeletal muscle and consists of muscle fibres known as i
- ntrafusal fibres: spindle-shaed connective tissue capsules paraellel to extrafusal fibres
- extrafusal fibres contains contractile elements throughout entire length
25
Alpha and Gamma Motor Neuron
- efferent neuron that innervates a muscle spindle intrfusal fibres is known as gamma
- nerves that supply extrafusal fibres are called alpha motor neurons
26
Golgi Tendon Organs
- respond to changes in muscle's tension rather than to changes in its length (sensory neuron)
- adjustments can be made if necessary
- made up of connective tissue and collagen fibers
- warn against excessive tension production
27
Smooth Muscle Structure
- myosin and actin
- intermediate filaments (not involved in contraction)
- tropomyosin but NO troponin
- no z-lines/unstriated
- poorly developed S.R.
- no t-tubules
- calmodulin (binding site with Ca+)
- dense irregular bodies (protein molecules)
* is economical energy-efficient; uses less energy
- use only when needed
28
Role Of Ca+
S.R. and ECF- calmodium + CA+- inactive myosin kinase- becomes active (ATP-ADP+Pi)- myosin cross bridge (energize)- actin
29
Single-unit muscle/ syncytium
eg. digestive
- controlled by gap junctions, cells contract as a unit
- varicosity (carry neurotransmitters)
- excitation
- visceral smooth muscle
- slow and energy efficient
30
Motor-Unit Muscle
- separate units activated on its own
| eg. iris, ciliary muscle and large blood vessels
31
Slow-wave potentials VS Pacemaker Potentials
- gradually alternating hyperpolarizing and depolarizing swings in potential cause by automatic cyclic changes in the rate at which Na+ are actively transported across membrane
- if threshold is reached, burst of action potentials
VS
- membrane potential gradually depolarizes to threshold on a regular periodic basis without any nervous-stimulation; trigger self-induced action potentials
32
Cardiac Muscle Structure
- actin and myosin
- no intermediate
- has tropomyosin and troponin
- Z-lines present
- intercalated disk- gap junctions and desmosomes
- fair amount of S.R.
- large T-Tubules
- no calmodium or dense bodies
- mitochondria
- glycogen granules (glucose): huge amount of ATP
- use O2 (60%) NO ANAEROBIC MODE
33
Heart Structure
- apex is on left side but rest is in the middle
- chordea tenindea: prolapse (not including valve down)
- papillary muscle
** never in SV valves
- pulmonary circuit: superior and inferior vena cave- right atrium- right ventricle- pulmonary artery- lungs
- systemic circulation: lungs- pulmonary veins- left atrium- left ventricle- aorta-
coronary (heart), ascending (upwards), descending (down)
34
Heart Wall
- endothelium: infection site; endocarditis
- myocardium: cardiac muscle
- epicardium: thin external layer
- pericardium: double layered sac + fluid (infection); pericarditis (painful friction)
- autorhymthic: does not contract but sets pace
- contractile cells (99%)
35
Autorythmic
Sinoatrial node: natural pace maker- 70-80 beats
AV node: latent- 40-60 beats
Bundle of His: right and left bundle- 20-40
Purkinje fibres: right and left side- 20-40
- interatrial pathway
- both atria and ventricles contract at same time
- AV node slows down for ventricles to empty
* gap junctions facilitate cell to cell spread (quick)
36
Pacemaker Potential
- 60mV (resting potential)
- funny channels (na+ and k+; HCN)
- Ca+ channels- Ca+ transient
- +0mV
- repolarization- K+ channels
37
Abnormal Pacemaker
SA falls apart: heart beats at AV node (40-60)
SA is normal but AV derails: bundle of His/P. Fibers (20-40)
SA and AV is normal: Bundle of his/P. fibres misbehave (140)= ecotopic focus: abnormally excitable
38
Contractile Cell
- 80mV (resting potential)
- Na+ increases
- +50mV: PK+ and PCa+ increases
- plateau
- PK+ increase (delayed rectifier)
- Ca+ comes from S.R. and ECF
39
Refractory Period
- 250 msec
| - no tetanus (no summation)
40
Heart Sounds
Lub: low pitch; soft
- marks closure of AV valves, onset of ventricular systole
Dup: high pitch; sharp
- closure of Sv valves; start of onset of ventricular diastole
Turbulent: pathology
- heart murmurs
eg. infections: rheumtic fever caused by bacteria (strep)
41
Heart Murmurs
- stenotic valve: narrowed valve (does not open properly); stiff, creates turbulence
* whistle sounds
- insufficient valve: does not close properly; scarred valve
* swishing sound
- Mitral Stenosis: bicupsid or left AV (surgery)
42
Timing of Murmur
1. systolic: between lub- murmur- dup
eg. lub- whistle- dup; lub-swish- dup
2. diastolic: lup- dup- murmur- lub
eg. lub- dup- swishing; lub- dup- whistle
43
ECG Record
P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
PR segment: AV nodal delay
ST segment: time during which ventricles are contracting and emptying
Tp interval: ventricles are relaxing and filling
44
Tachycardia and Bradycardia
- fast; more than 100 beats
| - slower than 60 beats per minute
45
Atrial Fibrillation
- rapid, irregular, uncoordinated depolarizations of the atria with no definite P waves
- QRS complex are normal in shape but occur sporadically
- little filling can occur between beats; less filling= weaker contraction
46
Ventricular Fibrillation
- very serious; ventricular musculature is uncoordinated and choatic conditions
- no detectable pattern
- brain can not get enough blood
47
Heart Block
- ventricles occasionally fail to be stimulated and do not contract following atrial contractions
- 2:1 or 3:1 block
- complete heart block: complete dissociation between atrial and ventricular activity with impulses from the atria not being conducted to the ventricles at all
48
Mid Ventricular Diastole
- atrial pressure is higher
- volume in ventricle is increasing
- AV valves are open
49
Late Ventricular Diastole
- SA node reaches threshold and fires; P wave
- atrial depolarization brings about atrial contraction; atrial pressure is higher
- rise in ventricular pressure occurs stimultaneously with rise in atrial pressure due to additional blood added
- volume of ventricluar increases
- AV is still open because atria pressure is slightly higher
50
End of Ventricular Diastole
- end-diastolic volume (135mL)
51
Ventricular Excitation and Onset of Ventricular Systole
- QRS is ventricular depolarization
- v.p. increases signalling onset of ventricular systole
- slight delay between QRS and ven. systole is required
- v.p exceeds a.p.
- AV valve forced closed
52
Isovolumetric Ventricular Contraction
- v.p. exceeds aortic pressure to force open aortic valve
- ventricle remains a closed chamber for a brief amount of time
- no blood leaving or entering while v.p. rises
53
Ventricular Ejection
- v.p.exceeds aortic pressure aortic valve is forced open and ejection begins
- stroke volume: 70 mLs pumped out
- aoritc pressure continues to rise as well
- ventricular volume decreases
54
End of Ventricular Systole
- end-systolic volume: 65 mLs is left over
| - cardiac output= ESVxSV
55
Ventricular Repolarization and onset of Ventricular Diastole
- T wave at end of ventr. systole
- ventricle starts to relax, on repolarization, ventricular pressure falls below aortic pressure and AV closes
- dicrotic notch: closure of AV causes notch on arotic pressure
56
Isovolumetric Ventricular Relaxation
- ventricular pressure exceeds atrial pressure so AV valve is closed
- all valves closed
- no blood enters or leaves as ventricular relaxs and pressure falls
57
Ventricular Filling
- when v.p. falls below artial pressure the AV valve opens and filling begins
- diastle includes both isovolumetric ventricular relaxtion and filling phase
- atrial repolarization and ventricular depolarization occur stimultaneously
58
Heart Innervation
Sympathetic:
Sa node: increases rate of depolarization to threshold; increases heart rate
AV node: increaes excitability; decreases the AV nodal delay
Ventr. Conduction Pathway: increases excitability; hastens conduction through the bundle of his and p fibres
Atrial Muscle: increases contractility; strengthens contraction
Ventricular Muscle: increases contractility and contraction
Adrenal Medulla: Epinephrin
Veins: increase venous return, increases strength of cardiac contraction through Frank-Starling mechanism
59
Intrinsic Control
increase stroke volume by increasing strength of heart contraction
- extent of venous return
- resting cardiac muscle is less than optimal length; cardiac muscle DOES NOT stretch beyond optimal length
60
Frank-Starling Law of Heart
- length is the degree of diastolic filling
- greater the filling= larger the EDV and more the heart is stretched= greater stroke volume
- intrinsic relationship between stroke volume and EDV
61
Extrinsic Control
- actions of cardiac sympathetic nerves and epinephrine
- enhance heart's contractility
- increased Ca+ influx; more force through greater cross-bridge cycling
- shirt Frank cure to left
- also enhances venus return; constricts veins
62
Heart Failure
- intrinsic ability of heart to develop pressure and eject a stroke volume is decreased
- Frank curve shifts downward and to the right; smaller stroke volume
63
Compensated for Heart Failure
- sympathetic activity to heart is reflexly increased, increases heart contractility to normal
- only for limited time; heart becomes less responsive to norepinephrine
- kidneys retain extra salt and water in body during urine formation to expand blood volume
- increase in circulating blood volume increases EDV
64
Decompensated Heart Failure
- forward failure: occurs as heart fails to pump adequate amount of blood forward to tissues
- backward failure: occurs simultaneously as blood that cannot enter be pumped out by heart continues to dam up the venous system (congestive failure)
- left-sided failure is more serious; backward= pulmonary oedema because blood backs up in lungs
- left-sided failure in forward= inadequate flow to kidneys
65
Nourishing the Heart
- abundance of mitochondria
- O2 dependent energy organelles
- abundance of myoglobin
66
Blood Supply
- coronary circulation
- extra blood is delivered by vasodilation, mainly during diastole
- removes up to 65% of oxygen available
- more oxygen made available by increasing coronary blood flow
- adenosine is released when cardiac activity increases and heart is using more ATP nd needs more oxygen
- adenosine induces dilation to blood vessels
- relies on oxidative process to generate energy
67
Coronary Artery Disease
- coronary blood flow may not be able to keep pace with rising oxygen needs
- pathological changes within the coronary artery walls that diminish blood flow through vessels
- heart attacks
- vascular spasms, atherosclerotic plaques and thromboembolism
68
Vascular Spasm
- narrows coronary vessels
- early stages of CAD and triggered by cold, anxiety or physical exertion
- too less of oxygen; releases platelet-activating factor which exerts a variety of actions
69
Atherosclerosis
- blockage of affected vessels
- lipid rich core + smooth muscle + connective tissue cap + Ca+
1. injury to blood vessle wall which triggers inflammatory response; plaque formation
- oxidized cholesterol, bacteria and free radicals
2. excessive amounts of low-density lipoprotein (bad cholestrol) with protein carrier
- becomes oxidized
3. in response to LDL, produce chemicals that attract monocytes, trigger immune response
4. monocytes settle and enlarge; macrophages become foamy= foam cells
- leave a fatty streak
5. progresses as smooth muscle within blood vessel wall migrate to a position on top of lipid accumulation
- smooth muscle cells divide producing atheromas (benign tumors) of smooth muscle
6. plaque bulges into lumen
7. oxidized LDL inhibits release of nitric oxide which is a local chemical messenger that relaxes smooth muscle cells
8. invaded by fibroblasts which form a connective tissue cap over plaque
9. calcium precipitates in plaque; becomes hard and cannot distend easily
70
Agina Pectoris
agina pectoris: pain of chest
- limited ability to perform anaerobic metabolism
- treated by nitroglycerin; vasodilation by metabolically converted to nitric oxide which relaxes smooth muscle
71
Thromboembolism
- enlarging atherosclerotic plaque can break through endothelial lining exposing blood to underlying collagen
- foam cells release chemicals that weaken cap of a plaque
- embolus= free floating clot may completely plus smaller vessel
