exam 3

Transverse Tubules (T-tubules)

Invaginations of the sarcolemma that facilitate action potential conduction

Triad

Structure formed by one T-tubule and two adjacent terminal cisternae of the SR

Glycogen granules

Immediate energy source for ATP production during muscle contraction

Titin

Elastic protein providing elasticity, stabilizing myosin, and maintaining sarcomere structure

Nebulin

Regulates thin filament alignment

A band

Dark region containing thick filaments (myosin)

H zone

Central part of A band with only thick filaments

I band

Light region containing only thin filaments

M line

Middle of sarcomere anchoring thick filaments

Z disk

Anchors thin filaments and marks sarcomere boundaries

Muscle tension

Force generated during contraction

Load

External force on a muscle

Contraction

Activation of muscle fibers to generate force

Relaxation

Reduction of tension as filaments return to resting position

Sliding Filament Theory

Contraction occurs as thin filaments slide over thick filaments, Z disks move closer, A band remains constant, I band and H zone shorten

Power stroke

Myosin pulls actin toward M line

Contractile cycle

Rigor state → ATP binds → Myosin detaches → ATP hydrolysis → Myosin reattaches → Power stroke

E-C Coupling

ACh binds → Na+ influx → AP propagates → Ca2+ released from SR → Contraction begins

Latent period

Time between AP and contraction onset

Phosphocreatine

Short-term ATP source

Aerobic respiration

Produces 32 ATP per glucose

Anaerobic respiration

Produces 2 ATP per glucose

Muscle fatigue

Caused by metabolic depletion, ion imbalance, and neural factors

Type I fibers

Slow-twitch oxidative, fatigue-resistant, aerobic, high myoglobin

Type IIa fibers

Fast-twitch oxidative-glycolytic with intermediate properties

Type IIx fibers

Fast-twitch glycolytic that fatigue quickly

Smooth muscle types

Vascular, gastrointestinal, urinary, respiratory, reproductive, ocular

Single-unit smooth muscle

Cells connected via gap junctions forming functional syncytium

Multi-unit smooth muscle

Independent cells (e.g., iris, airways)

Smooth muscle contraction

Ca2+ → Calmodulin → MLCK → Myosin phosphorylation → Contraction

Base of heart

The top where major blood vessels attach, not the pointed end

Ventricles

Lower chambers of the heart with thicker walls

Atria

Upper chambers of the heart

Right atrium

Receives deoxygenated blood from superior and inferior vena cava

Right ventricle

Pumps blood through pulmonary artery to lungs

Left atrium

Receives oxygenated blood from pulmonary veins

Left ventricle

Pumps oxygenated blood through aorta to body

Coronary arteries

Supply oxygenated blood to heart muscle

Coronary veins

Drain deoxygenated blood from heart muscle

AV valves

Between atria and ventricles; tricuspid (right) has three cusps, bicuspid/mitral (left) has two

Semilunar valves

Between ventricles and arteries; pulmonary valve connects right ventricle to pulmonary artery, aortic valve connects left ventricle to aorta

Intercalated disks

Specialized connections between cardiac cells with desmosomes for anchoring and gap junctions for electrical signal passage

Calcium in cardiac muscle

Enters from both extracellular fluid and sarcoplasmic reticulum, crucial for myocardial action potentials

Ca2+-induced Ca2+ release

Calcium enters cardiac muscle cell triggering release of more calcium from sarcoplasmic reticulum

Myocardial contractile cells

Have unstable membrane potential

Rapid repolarization phase

Due to potassium (K+) efflux

SA Node

Generates electrical impulses in the heart

AV Node

Briefly delays electrical signal to allow ventricles to fill with blood

Bundle of His

Transmits electrical signal from AV node through interventricular septum

Purkinje Fibers

Spread electrical impulse throughout ventricles causing contraction from bottom up

P wave

Represents atrial depolarization and associated with atrial contraction

QRS complex

Represents ventricular depolarization and associated with ventricular contraction

T wave

Represents ventricular repolarization and associated with ventricular relaxation

End-diastolic volume (EDV)

Volume of blood in ventricles at end of diastole, typically around 120 mL

End-systolic volume (ESV)

Volume of blood left in ventricles after systole, typically around 50 mL

Stroke volume (SV)

Amount of blood pumped by left ventricle in one contraction; calculated as EDV−ESV

Cardiac output (CO)

Volume of blood pumped per minute; calculated as SV×HR, typically 4.9 L/min

Parasympathetic control of heart

ACh binds to muscarinic receptors opening K+ channels, decreasing depolarization rate and slowing heart rate

Sympathetic control of heart

NE binds to beta-1 receptors activating cAMP and PKA, opening Na+ and Ca2+ channels, increasing depolarization rate and heart rate

Contractility

Intrinsic ability of heart muscle to contract forcefully at given fiber length

Frank-Starling law

More the heart muscle is stretched, greater the force of contraction; ensures balanced output of ventricles

Venous return

Volume of blood returned to heart via veins; determines EDV

Inotropic agent

Substance affecting heart muscle contractility

Catecholamines mechanism

Bind to beta-1 receptors, activate adenylyl cyclase, increase cAMP and PKA, phosphorylate calcium channels increasing Ca2+ influx

Cardiac glycosides

Increase contractility by inhibiting Na+/K+ ATPase pump, leading to increased intracellular calcium

Aorta and major arteries

Have thick walls with high proportion of smooth muscle and elastic tissue to withstand high blood pressure

Arterioles

Small vessels with thick muscular walls that regulate blood flow into capillaries

Metarterioles

Connect arterioles to capillaries and allow blood to bypass capillaries through arteriovenous shunt

Capillary walls

Single layer of endothelial cells allowing exchange of gases, nutrients, and waste products

Pericytes

Contractile cells around capillaries that help regulate blood flow and stabilize walls

Systolic pressure

Pressure in arteries during heart contraction, averaging 120 mm Hg

Diastolic pressure

Pressure in arteries during heart relaxation, averaging 80 mm Hg

Venous blood flow against gravity

Assisted by skeletal muscle pump and valves in veins that prevent backflow

Mean arterial pressure (MAP)

Average pressure in arteries during one cardiac cycle; calculated as Diastolic + 1/3(Systolic - Diastolic)

MAP relation

MAP = Cardiac Output x Total Peripheral Resistance

Radius-resistance relationship

R=(8ηL)/(πr^4); resistance inversely proportional to fourth power of radius

Myogenic autoregulation

Increased blood pressure stretches arteriole, activates ion channels causing calcium influx and vasoconstriction

Active hyperemia

Increased tissue metabolism leads to metabolite build-up causing vasodilation in arterioles

Reactive hyperemia

After blood flow restriction, accumulated metabolites cause arteriole dilation when flow resumes

Catecholamine receptors

Alpha-1 (high affinity for NE, vasoconstriction), Beta-2 (high affinity for epinephrine, vasodilation), Alpha-2 (inhibit NE release)

Baroreceptors

Located in carotid sinus and aortic arch to monitor systemic blood pressure

Baroreceptor reflex for increased BP

Baroreceptors detect increased BP, sensory neurons signal medulla, parasympathetic output increases, sympathetic decreases, causing decreased heart rate and vasodilation

Orthostatic hypotension

Blood pressure drop when standing due to blood pooling in lower extremities

Capillary density

Determined by tissue's metabolic activity; highest in muscles, liver, and kidneys

Tissues without traditional capillaries

Bone marrow (sinusoids), liver (sinusoids), brain (modified capillaries with blood-brain barrier)

Colloid osmotic pressure

Pressure exerted by plasma proteins that draws water back into capillaries from interstitial fluid

Net fluid flow in capillaries

Arterial end has higher hydrostatic than osmotic pressure causing filtration; venous end has higher osmotic than hydrostatic pressure causing absorption

Flow-resistance relationship

F=ΔP/R; flow decreases when resistance increases and increases when resistance decrease