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