Physiology Exam 2
atrial systole/atrial contraction
"active filling" of the ventricle, or "atrial kick"
S2
"dub" - vibrations created by closing of semilunar valves -after T wave
S1
"lub" - vibrations following closure of the AV valves -top of QRS complex
isometric contraction
("Same length") if the load on the muscle is not overcome by the tension generated by the sarcomere shortening, the muscle fiber does not shorten and the load is not moved
isotonic contraction
("same tension") if the tension generated by the muscle fiber is greater than the load placed across the muscle fiber, it will shorten and move the load; once the tension in the muscle fiber exceeds the load, the muscle fiber shortens and the amount of tension remains the same
pacemaker action potential
**unstable -subthreshold "funny" channels, either an increase of Ca into the cell or a decrease of K out of the cell -depolarizing phase: L type VG Ca channels open -repolarizing phase: VG K channels open
skeletal muscle ec-c
-DHPR is a voltage SENSOR that mechanically gates Ca from RYR on the SR
pacemaker cells
-autorhythmic -signal for contraction (have their own electrical activity) -sped up by SNS, slowed down by PNS
smooth muscle (cardiac) action potential
-depolarizing: L type VG Ca -plateau: L type VG Ca -repolarizing: VG K channels
fast oxidative-glycolytic fiber
-fast myosin ATPase -greatest amount of tension **most likely to fatigue rapidly! (motor unit 3)
fast-glycolytic fiber
-fast myosin ATPase -moderate amount of tension *moderately likely to fatigue (motor unit 2)
slow-oxidative fiber
-slow myosin ATPase -least amount of tension *fatigue resistant! (motor unit 1)
cardiac muscle ec-c
-the DHPR is a L-type voltage gated Ca CHANNEL (Ca enters the cytoplasm via the DHPR, binding to the ryanodine receptor to open it) -most of (80%) the Ca needed comes from SR -about 20% comes from ECF via L type Ca channel in the Ttubule
smooth muscle activation
1. Ca binds to calmodulin in cytoplasm 2. Ca-calmodulin complex binds to and activates Myosin Light Chain Kinase (MLCK) 3. Activated MLCK phosphorylates the myosin regulatory light chain (RLC) by transferring a phosphate from ATP 4. Phosphorylated myosin heads bind to actin and begin contraction by crossbridge cycling 5. crossbridge cycle produces tension and shortening
skeletal muscle activation
1. Ca binds to troponin on thin filaments 2. conformational change in troponin moves tropomyosin out of the blocking position 3. myosin crossbridges bind to actin 4. crossbridge cycle produces tension and shortening
guidelines for Wiggers Diagram
1. an electrical event is first 2. a contractile (or relaxing) event is second 3. a pressure change is third 4. a volume or valve event is fourth
stroke volume is regulated by...
1. preload 2. contractility 3. afterload
K concentration inside cell
150mL
K concentration outside of cell
5mL
where does Ca come from for smooth muscle?
Ca can enter cell via: -VG Ca channels -Ligand gated Ca channels -stretch activated cation (Na and Ca)
role of Ca in smooth muscle contraction
Cytosolic Ca concentration can change by different amounts depending on the stimulus -tension is determined by amount of Ca in cytosol -many ways in which cytosolic Ca can be increased -the SR does not contain as much Ca as in skeletal muscle, providing only a small percentage of the Ca required for contraction
cardiac output
FLOW! (amount of blood pumped out by the heart to the body per minute) CO = SV X HR ~3 to 5 L per min
smooth muscle depolarization
L type VG Ca channels open
pacemaker depolarization
L type voltage gated Ca channels open
pacemaker repolarization
VG K channels open
smooth muscle repolarization
VG K channels open
whole muscle
a bundle of muscle fascicles
muscle fascicle
a bundle of muscle fibers (cells)
inotrope
a chemical that affects contractility -positive inotropes: increase contractility by increasing intracellular Ca, such as epinephrine, norepinephrine, and digitalis; -negative inotropes decrease contractility such as beta blockers, calcium channel blockers, and acetylcholine)
muscle fiber
a muscle cell
electrical excitability
a property of both neurons and muscle cells; ability to respond to stimuli by producing action potentials
contractility
ability of muscle to contract forcefully when adequately stimulated
extensibility
ability of muscle to stretch without being damaged
contractile proteins
actin and myosin
end plate potential (EPP)
action potential generated at the muscle membrane
desmosomes
allow FORCE to be transferred between myocytes
AV valves
between atria and ventricles
calmodulin
calcium sensor in smooth muscle (replaces troponin) -Ca bound calmodulin complex binds to myosin light-chain kinase, activating the kinase
angiotensin
causes vasoconstriction
myofibril
contractile assemby of proteins in a muscle cell
sarcomere
contracting subunits that make up each myofibril (source of the striations)
kinase
contraction
systole
contraction of the ventricle
somatic motor neurons
control skeletal muscles; includes all conscious actions and "subconscious" reflexive actions
tropomyosin
covers myosin binding sites on the actin molecules until moved by troponin
muscle action potential
depolarized by VG Na channels, repolarized by VG K channels
phosphate
dilation
cellular basis of contractility
force generated is proportional to number of active crossbridges
cardiac action potential (contraction cells)
have plateau phase
Golgi organ reflex
increased TENSION stimulates sensory receptor (tendon organ), excites sensory neuron which sends info to integrating center in spinal cord, which excites motor neurons, which cause effector to RELAX AND RELIEVE EXCESS TENSION
aldosteron
increases water absorption, increasing blood pressure (without changing the radius)
sarcoplasmic reticulum
intracellular storehouse of calcium ions (internal organelle)
auscultation
listening to the heart thorugh the chest wall through a stethescope
M line
middle of sarcomere
smooth muscle ec-c
most Ca comes from ECF
vasoconstriction
narrowing of blood vessels; decreases flow
transverse tubules
network of tubular passages within striated muscle that are an extension of the plasma membrane
Rigor mortis
no ATP in body (stiffness after death)
mechanism of fatigue
not lactic acid! a few other theories: -high extracellular K concentration? -
calcium induced calcium release (CICR)
occurs in cardiac muscle; as the AP causes Na influx, when that current flow reaches the DHP receptor, instead of letting in Na, it lets in Ca which then attaches to RYR which then causes an influx of Ca to move from the SR to the cytoplasm
motor unit
one motor neuron plus the muscle fibers it innervates
gap junctions
provide ELECTRICAL connection between myocytes
Golgi tendon organ
provides information about changes in muscle tension (FORCE) -how much strain is being put on this muscle/organ? -protects against excess tension (if you're lifting something too heavy) -responds to both too much flexion and too much extension
diastole
relaxation of the ventricle
muscle spindle
sensory receptor that provides information about changes in muscle LENGTH -ends are contractile but middle is not
three types of muscle
skeletal, cardiac, smooth
length-tension relationship
The resting length of a muscle and the tension the muscle can produce at this resting length. (sarcomeres have an optimal length)
intercalated discs
specialized connections between myocardial cells containing gap junctions and desmosomes
Frank-Starling law of the heart
stroke volume increases as EDV increases -stretch adjusts sarcomeres to an optimal length "The more you fill, the more you eject, the more forceful the ejection"
autonomic neurons
sympathetic and parasympathetic neurons; control cardiac and smooth muscle, exocrine glands/cells, some endocrine glands/cells, some adipose tissue
neuromuscular junction (NMJ)
synapse between a somatic motor neuron and a skeletal muscle fiber
role of Ca in skeletal muscle contraction
the amount of Ca released from the SR as a result of an action potential is sufficient to briefly saturate all of the troponin Ca binding sites resulting in a twitch
stroke volume
the amount of blood pumped out of your heart with each heartbeat ~60-70 ml/heartbeat
cardiac myocyte
the contractile cell of the heart (rod shaped, small) -single nucleus -branch and join at intercalated disks -t tubules branch -SR is smaller -mitochondria occupy one third of cell volume
preload
the degree of stretch on the heart before it contracts (amount heart fills with blood before ventricular systole) -EDV
what prevents tetany in cardiac tissue?
the plateau phase (refractory)
afterload
the pressure that must be exceeded before ejection of blood from the ventricles can occur (wall tension required to open the semilunar valves and overcome pressure of the arteries -systolic blood pressure
regulatory proteins
troponin and tropomyosin
recruitment
two motor units can generate more tension than one; when a large amount of tension is needed, more motor neurons are recruited; one muscle group in the body may have many motor units of many different types
high O2 levels
vasoconstriction
high CO2 levels
vasodilation
where is smooth muscle found?
walls of hollow organs; arteries, arterioles, airways, stomach, intestines, urinary bladder, uterus
troponin
when stimulated by calcium, undergoes a conformational change that moves tropomyosin out of the way
vasodilation
widening of blood vessels, increases flow
knee jerk reflex
STRETCHING stimulates the muscle spindle sensory receptor, exciting the sensory neuron, sending info to integrating center in spinal cord, which excites motor neuron and effector CONTRACTS TO RELIEVE STRETCHING
z disc
Separates the sarcomeres from each other