Human Physiology Exam 3

Skeletal Muscle

Striated muscle

voluntary

Cardiac

Muscle found only in heart

Involuntary

Striated

Smooth

Organ muscle

Involuntary

Nonstriated

Skeletal Muscle

Number of muscle fibers bound by connective tissue

Muscle fiber is a muscle cell

Linked to bones by tendon

Components of Skeletal muscles

Sarcolemma

Sarcoplasm

Myofibrils

Myofibrils

Contractile elements of muscle fiber

Composed of myofilaments

Myosin

Thick filaments

Heads form cross bridges between thick and thin filaments

Actin

Thin Filament

Contractile filament

A Bands

Lots of Myosin

Dark Bands

I Bands

Light Bands

No myosin

Motor unit

Single motor neuron and all the muscle fibers it innervates

Innervates more than just 1 muscle fiber

Motor end plate

Area of the muscle fiber sarcolemma where a motor neuron stimulates skeletal muscle

Neurotransmitter: Acetylcholine

Sarcomere

Functional unit of contraction

Between 2 Z-discs

Regions: A band, H zone, M line, I band

Myosin Heads

Actin binding site

ATP Bind site

ATPase

Tropomyosin

Resting, covers myosin binding sites blocking interaction

Blocks binding sites on actin for myosin

Troponin

Made of 3 units

Binds to tropomyosin

Binds to actin

Binds with Ca2+

Calcium binds to troponin to move it to allow binding

Sliding filament Mechanism

Contraction is accomplished by thin filaments from opposite sides of each sarcomere sliding closer together between thick filaments

Power Stroke

Sliding filament mechanism

Attachment of a myosin cross bridge to a thin filament

Swiveling of myosin head = power stroke

Detachment of the cross bridge from the thin filament

Reattach to a new actin biding site

Repeat cycle

Cross Bridge Cycle

Asynchronous power stroke of myosin heads

Functions of ATP in Contraction

Energizes X-bridge, providing energy for power stroke

Binding of ATP relaxes muscle

Ca+

the Link between excitation and contraction

During cross bridge cycling

Excitation-Contraction Coupling

At rest low calcium intracellular

-Stored in sarcoplasmic reticulum (intracellular storage)

Increases in intracellular Ca++ leads to contraction

-Release from SR

SR calcium Release

AP propagated into interior by transverse tubules

Voltage gated Ca++ channels in SR

Release of Ca++ from sarcoplasmic reticulum

Binds to Troponin to move Tropomyosin

Neural Activation

Leads to muscle contraction

AP travels down somatic motor neuron axon to axon terminal

Exocytosis of ACh

ACh binds to nicotinic ACh receptors and opens them

End Plate Potential

Induces AP in sarcolemma of muscle fiber

AP results in release of Ca2+ inside muscle fiber

Muscle Relaxation

AP stops

Active reuptake of Ca2+ into SR

Ca++ ATP pump

ATP need

Splitting of ATP by mosin ATPase provides energy

Tension

Force exerted on an object by contracting muscle

Load

Force exerted on the muscle by weight of the object

Twitch

Response of a single muscle fiber to a single AP

Latent period - takes time for everything to get triggered and stimulated to move

Contraction Time

Relaxation Time

Muscle contractions

Force Velocity Curve

For muscles to contract, they must generate force that is greater than the opposing forces

The greater the force, the slower the contraction

Isotonic Contraction

Change in muscle length

Concentric and eccentric

Concentric Contraction

Muscle Shortens

Eccentric

Muscle lengthens

Isometric

Muscles can’t shorten because the load is too great

Can be voluntary

Nervous System

Muscle tension Control in skeletal muscle

Frequency of Stimulation

Motor Unit Recruitment

Muscle

Muscle tension control

Properties of skeletal muscles control tension

Frequency of Stimulation

Because a muscle twitch is fairly slow compared to an action potential many action potentials can arrive before a single twitch is completed

Generation of a force that is greater than a single twitch

Summation

Muscle summation

Muscle is stimulated again before relaxation leads to summation

Tetanus

Contraction is usually 3-4 greater than a single twitch

Max contraction of a muscle releasing max calcium

Summation of many action potentials (lots of calcium being released)

Summation

Increase of AP frequency

How many muscle fibers in each motor unit

High Variation in number of muscle fibers in each motor unit

Precise delicate movements and course powerful movements

Motor Unit Recruitment

Increasing the number of active motor units

Increase tension

Increase velocity to lift a given load

Increasing Tension in Skeletal muscles

In nervous system: frequency of stimulation and motor unit control

In skeletal muscle: Length of fiber at onset of contraction, type of skeletal muscle, extent of fatigue, x-sectional of fiber

Length of Fiber at onset of contraction

Length-tension relationship

Overlap of Actin over myosin - lower tension

Overextension of muscle - lower tension

Optimal Overlap of actin over myosin - Maximal amount of tension

Skeletal Muscle Energy Metabolism

Big energy demand for ATP

-Myosin ATPase and Ca++ pump

Small supply of stored ATP

Formation of ATP by muscle

1. Creatine phosphate

2. Oxidative phosphorylation

3. Glycolysis

Creatine Phosphate

Utilized at onset of contractile activity

Limited by CP stores

Stores used initially in seconds

Types of Skeletal Muscle Fibers

Based on

1. Maximal velocity of shortening

2. Major pathway used to form ATP (oxidative or glycolytic)

All 3 types are represented in a typical skeletal muscle

All muscle fibers in a single motor unit are the same fiber type

3 Types of skeletal muscle fibers

Slow-oxidative (type 1)

Fast-oxidative Glycolytic (type 2a)

Fast-glycolytic (type 2x)

Activates from type 1 → type 2a → type2x based on increasing resistance

Muscle characteristics

Speed of Contraction - fast twitch fibers (type 2)

Fatigue resistance - endurance fibers (type 1)

Myoglobin Content - type 1 fibers

Mitochondria - type 1 fibers

Oxidative Phosphorylation Capacity - type 1

Enzymes - type 2

Glycogen content - type 2

Size Differences - strength differences

Fatigue

Decline in muscle tension as a result of previous contractile activity, even though stimulation continues

Dependent on Type of skeletal muscle, intensity/duration, and individual fitness

Muscle Fatigue Factors

Internal acidity

K+ accumulation

Glycogen Depletion

Reduced SR calcium release

Central fatigue

Skeletal Muscle Tension Factors

1. Frequency of stimulation

2. Length of fiber at onset of contraction

3. Extent of fatigue

4. Cross-sectional area of skeletal muscle

Peak force production is related to the physiological cross-sectional area

Adaptation to Endurance Training

Type 1 Fibers

Increased ability to use fatty acids as fuel and increased intracellular triglyceride storage

Increase capillary density

Increase in number of mitochondria

Increase in Krebs cycle enzymes

Muscle does not change in size

Adaptation of Skeletal Muscle

Resistance training promotes hypertrophy of fast glycolytic fibers

Skeletal muscles atrophy when not used

Control of Motor Movement

Input from primary motor cortex

Input from brain stem

Input from afferent neurons

Muscles need sensory feedback from muscles for optimal function

1. Muscle spindles

2. Golgi tendon organs

Muscle spindle

Parallel to extrafusal muscle fibers

Contains intrafusal muscle fibers

Innervated by gamma motor neurons

Function to sense muscle length

Sensory Info from Muscle Spindles

Purpose is to resist tendency for passive stretch of muscles by gravitation forces when a person is upright

Stretch of muscle - increases firing leads to contraction of muscle

Intrafusal

Muscle spindles own muscles

Gamma motor neuron

Muscle spindles own nervous supply

Alpha-Gamma Co-activation Alpha and Gamma motor neurons activate extrafusal and intrafusal respectively.

Patellar knee-jerk reaction

Muscle spindles mediate this

Golgi Tendon Organs

Found in Tendons

Senses muscle tension

Inhibitory synapses on motor neurons of the contracting muscle

Excitatory synapses on motor neurons of ipsilateral antagonists

Cardiac and Smooth Muscles

Involuntary

Regulated by autonomic nervous system

Contraction is due to myosin/actin cross bridges

Stimulated by rises in intracellular calcium

Cardiac Muscle

Striated

Myosin and actin filaments form sarcomeres

Contraction occurs by means of sliding thin filaments

Unlike skeletal muscle fibers, these fibers are connected via gap junctions found at intercalated discs

Myocardium

A mass of cardiac muscle cells connected to each other via gap junctions

Action potentials that occur at any cell in a myocardium can stimulate all the cells in the myocardium

It behaves as a single function unit

Smooth Muscle

Found in walls of hollow organs and tubes

No striations - Not arranged in sarcomere pattern found in skeletal and cardiac muscle

Spindle-shaped cells with single nucleus

Muscle cells usually arranged in sheets

Smooth Muscle Layers

Thick Myosin Filaments

Thin actin filaments - Contain tropomyosin but lack troponin

Intermediate filaments

Intermediate Filaments

Do not directly participate in contraction

Form part of cytoskeletal framework that supports cell shape

Single unit smooth muscle

Cells electrically linked by gap junctions

act as one unit

Multiunit smooth muscle

Units must be separately stimulated by nerves to contract

Excitation contraction coupling in smooth muscle

Begins with rise in intracellular calcium concentrations

Small amounts come from Sarcoplasmic Reticulum

Most by extracellular following opening of voltage gated calcium channels

Action of Calcium in E-C Coupling

Calcium binds to calmodulin

Activates myosin light chain kinase (MLCK)

MLCK phosphorylates myosin light chains

Phosphorylated myosin forms cross bridges with actin to initiate contraction

Cardiovascular system

Consists of Blood, Heart, and blood vessels

Blood

Transport medium (cells suspended in fluid)

Represents about 8% of total body weight

Average blood volume = 5L

Consists of Erythrocytes, Leukocytes, Platelets, Plasma

Erythrocytes

Red blood cells

Contains hemoglobin for o2 transport

No nucleus or organelles

Biconcave discs - provides larger surface area for diffusion of O2

Flexible membrane - Allows RBCs to travel through narrow capillaries without rupturing

Leukocytes

White blood cells

Platelets

Cell fragments

Lack nuclei

Have organelles

Function in hemostasis

Come from megakaryocyte cells

Also called Thrombocytes

Plasma

90% water

7-9% proteins

Maintain osmotic pressure of blood

Lipid transport

Immunity - Antibodies

Clotting factors

Various enzymes

Erythropoiesis

Erythrocyte product

RBCs survive about 120 days

Spleen removes most of old erythrocytes

Replaced at rate of 2-3 million cells per second

Occurs in bone marrow

Multipotent

Signaled by Erythropoietin

Anemia

Refers to a below-normal O2 carrying capacity of the blood

Caused by dietary deficiencies, blood loss, bone marrow failure, hemolytic anemia

Thrombopoietin

Hormone produced by liver increases number of megakaryocytes and therefore increases platelet production

Hemostasis

Prevents blood loss from a broken blood vessel

1. Vascular spasm

2. Formation of a platelet plug

3. Blood coagulation

Vascular spasm

Reduces blood flow through a damaged vessel

Formation of a platelet plug

Platelets aggregate on contact with exposed collagen in damaged wall of the vessel

Platelets release ADP which causes surface of nearby circulating platelets to become sticky

Blood coagulation

Clotting

Coagulation proteins in blood activate

Platelets at Rest

Inhibited by prostacyclin, and nitric oxide

Formation of platelet plug

Activate clotting factors

Clot Formation

Reinforces platelet plug by formation of clot

Clotting factors are always present in blood plasma in inactive precursor form

Vessel damage that exposes collagen initiates cascade of reactions that involve successive activation of clotting factors

Converts fibrinogen → Fibrin

Intrinsic Pathway

Blood clot formation

Activated by exposed collagen

Extrinsic Pathway

Blood clot formation

Released from damaged formation - Tissue Factor

Fibrinogen

Turns into fibrin during blood clot formation

Leukocytes

White blood cells

Mobile units of body’s immune defense system

Immune system, recognizes and destroys or neutralizes materials within body that are foreign to normal self

Defends against invading pathogens

Identifies and destroys cancer cells that arise in body

Functions as a cleanup crew that removes worn out cells and tissue debris

Heart Structure

Hollow, Muscular organ

Located in thoracic cavity

4 chambers (2 atria and 2 ventricles)

Pumps constantly - variable rate

Pulmonary (right) and systemic (left) blood circuits

Heart valves

Atrioventricular valves from atria to ventricles

Semilunar valves

Used to prevent backflow of blood in heart

Sounds are called murmurs - heart valves closing and opening

Heart Valve Opening

When pressure is greater behind the valve, it opens

Atrium → AV valve → Ventricle → Aortic or Pulmonary Semilunar valve → Aorta or pulmonary system

Heart Valve Closed

When pressure is greater in front of the valve it closes. Note that when pressure is greater in front of the valve, it does not open in the opposite direction, that is, it is a one-way valve

Blood Flow in Heart

Deoxygenated blood enters right side through vena cavae

→right atrium → right AV valve → right ventricle → pulmonary semilunar valve → pulmonary trunk and arteries → lungs (pulmonary circuit)

Cardia Cycle

Consists of 2 phases

Systole - Ventricles Contract, Atria Relaxed

Diastole - Ventricles fill and relax, Atria contract for a portion of Diastole phase

Systole

1. Isovolumertric contraction

2. Ejection

Sequence of events

Isovolumetric contraction

Ventricles contract, but no blood ejected

Blood pressure rises above pressure in atria

Atrioventricular valves shut

Semilunar valves shut

Ejection

Blood pressure in ventricle exceeds pressure in arteries

Blood flows out of ventricles, causing pressure in ventricles to fall