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
Q
Alpha and Gamma Motor Neuron
A
- efferent neuron that innervates a muscle spindle intrfusal fibres is known as gamma
- nerves that supply extrafusal fibres are called alpha motor neurons
26
Q
Golgi Tendon Organs
A
- 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
Q
Smooth Muscle Structure
A
- 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
Q
Role Of Ca+
A
S.R. and ECF- calmodium + CA+- inactive myosin kinase- becomes active (ATP-ADP+Pi)- myosin cross bridge (energize)- actin
