lecture 4 - muscle

MUSCLE PHYSIOLOGY

CH. 9

Biol340 - Mammalian Physiology 1

UNIT OUTLINE:

2 Biol340 - Mammalian Physiology

I. INTRODUCTION i. General Functions of Muscular System ii. Types of Muscle Overview

II. LEVELS OF ORGANIZATION i. Structural Organization of Skeletal Muscle

III. STRUCTURE & FUNCTION i. Excitation-Contraction Coupling ii. Cross-bridge Cycle iii. Sliding Filament Model

IV. HOMEOSTASIS i. Development of Force ii. Fatigue

V. INTEGRATION i. Exercise ii. Clinical

UNIT LEARNING OUTCOMES: Student will be able to

1. Distinguish between thick and thin filaments. 2. Describe the steps in excitation-contraction coupling. 3. Summarize the changes that occur within a sarcomere during contraction. 4. Explain the relationship of skeletal muscle elasticity and muscle relaxation. 5. Explain the length-tension relationship in skeletal muscle contraction. 6. Describe what occurs in a muscle during a single twitch, and relate each event to a graph of a

twitch. 7. Distinguish between isometric and isotonic contractions, and give examples of both. 8. Explain the events that occur in motor unit recruitment as the intensity of stimulation is

increased. 9. Distinguish between treppe, wave summation, incomplete tetany, and tetany that occur with

an increase in frequency of stimulation. 10. Define muscle fatigue, and explain some of its causes. 11. Explain the two primary criteria used to classify skeletal muscle fiber types. 12. Compare and contrast the three muscle fiber types. 13. Compare and contrast the changes in skeletal muscle that occur as a result of an exercise

program or from the lack of exercise.


Remember that these Learning Outcomes make for a great basis for your studying. (Try turning the statements into questions.)

I. INTRODUCTION: Functions of Muscle

Body movement due to contraction of muscles attached to bones produces highly coordinated and localized movements

Maintenance of posture stabilizes joints and helps maintain the bodys posture

Protection and support muscles arranged along the walls of abdominal and pelvic cavity protect the internal organs and support normal position

Storage and movement of materials sphincters, circular muscle bands

contract and relax to regulate passage of material allow voluntary expulsion of feces and urine

Heat production produced by energy required for muscle contraction continuously generate heat to maintain body temperature shiver when cold to generate heat


I. INTRODUCTION:


Characteristics

Excitability responsive to nervous system stimulation neurons secreting neurotransmitters that bind to muscle cells

Conductivity electrical change traveling along plasma membrane initiated in response to neurotransmitter binding

Contractility contractile proteins within muscle cells slide past each other tension used to pull on bones of skeleton

Elasticity due to protein fibers acting like compressed coils when contraction ended, tension in proteins released muscle returns to original length

Extensibility lengthening of a muscle cell e.g., extension of the triceps brachii when flex elbow joint

TYPES OF MUSCLE


I. INTRODUCTION:


I. INTRODUCTION:


II. LEVELS OF ORGANIZATION

General Topics i. Structural Organization of Skeletal Muscle

i. Macroscopic ii. Microscopic

Epimysium

Tendon

Deep fascia

Skeletal muscle

Artery Vein Nerve

Perimysium

Fascicle

Endomysium

Muscle fiber

STRUCTURAL ORGANIZATION OF SKELETAL MUSCLE

Composed of thousands of muscle cells Typically as long as the entire muscle Often referred to as muscle fibers Organized into bundles, termed fascicles Three concentric layers of connective tissue:

epimysium, perimysium, endomysium Provide

protection sites for blood vessel and nerve distribution means of attachment to skeleton or other

structures



MICROSCOPIC ANATOMY

Multinucleated cell Elongated cells extending length of

muscle Myoblasts

embryonic cells which fuse form single skeletal muscle fibers

during development each contributing a nucleus to total

nuclei Thus fibers are multinucleated cells

Satellite cells myoblasts remaining, unfused, in

adult skeletal tissue may be stimulated to differentiate if

tissue injured

Muscle fiber

Myoblasts

Satellite cell

Satellite cell Nuclei

Muscle fiber

Myoblasts fuse to form a skeletal muscle fiber.



Muscle

Fascicle

Muscle fiber Sarcoplasmic

reticulum Triad

Terminal cisternae

T-tubule

Sarcolemma

Myofibrils

Sarcomere

Myofilaments

Nucleus

Openings into T-tubules

Nucleus

Sarcoplasm Mitochondrion Nucleus

Muscle fibers and myofibrils Myofibrils

long cylindrical structures extend length of muscle fiber compose 80% of volume of muscle fiber each fiber with hundreds to thousands

Myofilaments bundles of protein filaments takes many to extend length of myofibril two types: thick and thin




III. STRUCTURE & FUNCTION

General Topics i. Excitation-Contraction Coupling ii. Cross-Bridge Cycle iii. Sliding Filament Model

OVERVIEW OF EVENTS IN SKELETAL MUSCLE CONTRACTION

1 2

3

NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER

Release of neurotransmitter acetycholine (ACh) from synaptic vesicles and subsequent binding of Ach to Ach receptors.

SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC RETICULUM: EXCITATION-CONTRACTION COUPLING

ACh binding triggers propagation of an action potential along the sarcolemma and T-tubules to the sarcoplasmic reticulum, which is stimulated to release Ca2+.

SARCOMERE: CROSSBRIDGE CYCLING

Ca2+ binding to troponin triggers sliding of thin filaments past thick filaments of sarcomeres; sarcomeres shorten, causing muscle contraction.

Ca2+ Sarcomere Sarcolemma

Muscle fiber

Neuromuscular junction

Synaptic vesicle (contains ACh) Action potential

T-tubule

ACh Ach receptor Sarcoplasmic

reticulum

Terminal cisterna of SR

Thick filament Thin filament

Ca2+

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

1 2

3 Ca2+



NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER

Motor end plate

1 NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER Ca2+ entry at synaptic knob

Nerve signal

1a

1a

ACh receptor

Synaptic cleft

Interstitial fluid

Synaptic vesicles (contain ACh)

A nerve signal is propagated down a motor axon and triggers the entry of Ca2+ into the synaptic knob. Ca2+ binds to proteins in synaptic vesicle membrane.

Release of ACh from synaptic knob

Binding of ACh to ACh receptor at motor end plate

ACh diffuses across the fluid-filled synaptic cleft in the motor end plate to bind with ACh receptors.

Ca2+

Ca2+ 1b

ACh 1c

1b

Synaptic vesicle

ACh

1c

Voltage-gated Ca2+ channel


Synaptic knob

Calcium binding triggers synaptic vesicles to merge with the synaptic knob plasma membrane and ACh is exocytosed into the synaptic cleft.



SKELETAL MUSCLE FIBER: EXCITATION-CONTRACTION COUPLING

2

Synaptic cleft

Voltage-gated Na+ channel

2a

Voltage-gated K+ channel

Interstitial fluid

Sarcolemma

2b

EPP

2a

2c

2c

Sarcolemma

Terminal cisterna of sarcoplasmic

reticulum

T-tubule

SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC RETICULUM: EXCITATION-CONTRACTION COUPLING

Development of an end-plate potential (EPP) at the motor end plate

Binding of ACh to ACh receptors in the motor end plate triggers the opening of these chemically gated ion channels. Na+ rapidly diffuses into and K+ slowly diffuses out of the muscle fiber.

The result is a reversal in the electrical charge difference across the membrane of a muscle fiber at the motor end plate, which is called an end-plate potential (EPP). (The inside which was negative is now positive.)

Initiation and propagation of an action potential along sarcolemma and T-tubules An action potential is propagated along the sarcolemma & T-tubules. First, voltage-gated Na+ channels open, and Na+ moves in to cause depolarization. Second, voltage-gated K+ channels open, and K+ moves out to cause repolarization.

Release of Ca2+ from the sarcoplasmic reticulum When the action potential reaches the sarcoplasmic reticulum, it triggers the opening of voltage-gated Ca2+ channels located in the terminal cisternae of the sarcoplasmic reticulum. Ca2+ diffuses out of the cisternae sarcoplasmic reticulum into the sarcoplasm.

Ca2+

Terminal cisterna

Voltage-gated Ca2+ channels

ACh receptor ACh

Na+ +

+ + +

+

+

+ + +

+ +

+ + + + + + + + + + + + + + + + + + +

+ + + + + + + + + + + +

+ + + + + + + + +

+

+ +

+ +

+ +

+ +

+

K+ Sarcoplasm

Motor end plate

2b

Ca2+



ACTION POTENTIALS AND CONTRACTION



QUESTION Thick filaments in skeletal muscle are composed of A.Actin B.Myosin C.Troponin D.Calmodulin E.Tropomyosin



Thick filaments Assembled from bundles of protein molecules, myosin

each myosin protein with two intertwined strands each strand with a globular head and elongated tail tails pointing toward center of thick filaments heads pointing toward edges of thick filaments head with a binding site for actin (thin filaments) head with site where ATP attaches and is split

Myosin molecule

Heads Actin binding site ATP and ATPase binding site

Myosin heads

Tail



Thin filaments Primarily composed of two strands of protein, actin Two strands twisted around each other Many small spherical molecules, globular actin Connected to form a fibrous strand, filamentous actin Globular actin with myosin binding site

where myosin head attaches during contraction

G-actin

Tropomyosin

F-actin Myosin binding site

Troponin Ca2+ binding site

Tropomyosin twistedstringlike protein cover small bands of the actin strands covers myosin binding sites in a noncontracting muscle

Troponin globular protein attached to tropomyosin binding site for Ca2+ together form troponin-tropomyosin complex



ROLES OF TROPONIN, TROPOMYOSIN, AND CA2+ IN CONTRACTION

Biol340 - Mammalian Physiology 20 Biol340 - Mammalian Physiology 20


Crossbridge cycling Four repeating steps

1) Crossbridge formation myosin heads in the ready position attach to exposed myosin binding sites on actin results in formation of a crossbridge between thick and thin filament

2) Power stroke swiveling of the myosin head, termed power stroke pulls thin filaments a small distance past thick filaments ADP and Pi released

3) Release of myosin head binding of ATP to binding site of myosin head causes release of myosin head from actin

4) Reset myosin head ATP split into ADP and Pi by ATPase

enzyme on myosin head provides energy to cock the myosin head



SARCOMERE: SKELETAL MUSCLE CONTRACTION

Crossbridge cycling: Multiple repetitions of attach, pull, release, and reset lead to

fully contracted sarcomere.

Ca2+ binds to troponin in muscle thin filaments, causing a conformational change in troponin. Troponin changes shape and the entire troponin-tropomyosin complex is movedthus, tropomyosin no longer covers the myosin binding site on actin.

Myosin heads, which are in the cocked position, bind to the exposed myosin binding site on actin forming a crossbridge between myosin and actin.

The myosin head swivels toward the center of the sarcomere, pulling along the attached thin filament. This motion is called a power stroke. ADP and Pi are released during this process.

ATP binds to the ATP binding site on the myosin head, which causes the release of the myosin head from the binding site on actin.

ATP is split into ADP and Pi by myosin ATPase. This provides the energy to reset the myosin head.

Pi

3 SARCOMERE: CROSSBRIDGE CYCLING 3a

Myosin binding sites exposed

Ca2+

Relaxed sarcomere (prior to Ca2+ release)

Thin filament

Thick filament

Myosin

Actin Tropomyosin Troponin

Thin filament

Myosin head ADP

3e

3d 3c

Thin filament

Myosin head ADP

Pi

Crossbridge

Thin filament

Thin filament

Myosin head Pi ADP

Myosin head ATP

Actin

3b Attach

Power stroke (pull) Release of myosin head (release)

Reset myosin head (reset)




QUESTION Rigor mortis occurs in a dead person because A.ATP, which is necessary for the detachment of cross bridges, is not being formed B.ATP, which is necessary for the formation of cross bridges, is not being formed C.Calcium, which is necessary for the formation of cross bridges, is not being formed D.Deterioration of muscle proteins prevents detachment of cross bridges E.None of the choices are correct



STRUCTURE OF A SARCOMERE

Muscle fiber

(a)

Sarcomeres

Myofilaments

Myofibril I band A band I band

Z disc H zone Z disc

M line

Sarcomere

I bands region containing only thin filaments extend from both directions of Z disc bisected by Z disc appear light under a microscope disappear at maximal muscle contraction

A band central region of sarcomere contains entire thick filament contains partially overlapping thin filaments appears dark under a microscope

H zone central portion of A band thick filaments only present; no thin filament overlap disappears during maximal muscle contraction

M line protein meshwork structure at center of H zone attachment site for thick filaments




Z disc Thin filaments

Connectin & accessory proteins

I band Thin filaments

Connectin

A band Thick filaments Thin filaments

H zone Thick filaments

M line Thick filaments

& accessory proteins

Transverse sectional plane




Connectin Z disc

Thin filament Thick filament

Sarcomere Z disc

Thin filament

(b)

I band A band H zone

I band

M line




SLIDING FILAMENT MECHANISM



Relaxed sarcomere

Z disc M line Z disc

Relaxed sarcomere Z disc

Connectin Thick filament

Thin filament Z disc

Thin filament M line

(a) Relaxed skeletal muscle

Z disc

Contraction

I band H zone A band I band

Fully contracted sarcomere

A band

M line Z disc

Contraction

Z disc

I band A band H zone

Fully contracted sarcomere

A band

M line Z disc

(b) Fully contracted skeletal muscle

I band

a, b(right): Dr. H. E. Huxley Biol340 - Mammalian Physiology 28


QUESTION During skeletal-muscle contraction, the I band and H zone shorten but the A band stays the same.

A. True B. False



Events in muscle relaxation Termination of the nerve signal in the motor neuron Prevents further release of ACh Continual hydrolysis of ACh from receptor by acetylcholinesterase Closure of ACh receptor Ceasing of end plate potential No further action potential generated Closure of voltage-gated calcium channels in SR Already released calcium continuously returned by calcium pumps Remaining calcium transported back into storage Return of troponin to its original shape Tropomyosin now moving over myosin binding sites on actin

prevents crossbridge formation Returns to original relaxed position

through natural elasticity of muscle fiber



MECHANICS OF SINGLE-FIBER CONTRACTIONS

A muscle fiber generates force called tension in order to oppose a force called the load, which is exerted on the muscle by an object.

The mechanical response of a muscle fiber to a single action potential is known as a twitch.



MUSCLE TWITCH

Mu

scle

ten

sion

Muscle Twitch Relaxation

period Contraction

period Latent period

Muscle Electrodes

Hardware detecting change

of length of muscle Pivot

Weight

Voltage Frequency

Stimulus

Time (msec) Latent period period after stimulus before contraction begins no change in fiber length time needed to initiate tension in fiber Contraction period

begins as power strokes pull thin filaments increasing muscle tension shorter duration than relaxation period

Relaxation period begins with release of cross-bridges decreasing muscle tension



Isometric contraction Muscle tension insufficient to overcome resistance Contraction of muscle and increased tension Muscle length the same E.g., pushing on a wall E.g., holding a weight while arm doesnt move



Isotonic contraction Muscle tension able to overcome resistance Results in movement Tone same but length changes E.g., swinging a tennis racket Concentric contraction, subtype

muscle shortens as it contracts e.g., in the biceps brachii when lifting a load

Eccentric contraction, subtype muscle lengthens as it contracts e.g., in the biceps brachii when lowering a load




IV. HOMEOSTASIS

General Topics i. Development of Force

i. Length-Tension ii. Load & Velocity iii. Motor Units iv. Recruitment

ii. Fatigue

LENGTH-TENSION RELATIONSHIP The amount of active tension a muscle fiber develops during contraction can also be altered by changing the length of the fiber. If you stretch a muscle fiber to various lengths and tetanically stimulate it at each length, the magnitude of the active tension will vary with length. The length at which the fiber develops the greatest isometric active tension is termed the optimal length, L0. When a quarterback throws a pass, he must first bring his arm back. This slightly stretches the triceps and allows for a more forceful throw. Explain the physiology behind the increase in force of muscle contraction.


IV. HOMEOSTASIS

QUESTION


THE MAXIMAL FORCE WILL BE DEVELOPED BY A MUSCLE AT ITS A. shortest length. B. intermediate length. C. maximal length.

IV. HOMEOSTASIS

39

LOAD-SHORTENING RELATIONSHIP


IV. HOMEOSTASIS

40

WHOLE-MUSCLE CONTRACTION


IV. HOMEOSTASIS

MOTOR UNITS A motor unit is defined as the motor neuron

and the skeletal muscle fibers it innervates.

One motor neuron innervates many muscle fibers, but one muscle fiber is innervated by only one motor neuron.

Within a whole muscle there are many motor units.

The number of fibers innervated depends on the muscle, fine motor movements (like typing) rely on motor units with relatively few fibers in contrast to those in the leg muscles, for example.


IV. HOMEOSTASIS

Recruitment Helps explain how muscles can exert varying levels of force Do this in spite of the all-or-none law

muscle fiber contracts maximally or not at all Difference in force and precision

varied by changing number of motor units reduced number of motor unit activated

less force exerted greater number of motor units activated

more force exerted


IV. HOMEOSTASIS

Mus

cle

tens

ion

9 8 7 6 5 4 3 2 1 0

Maximum contractions

Voltage increments (mV) Biol340 - Mammalian Physiology 43

IV. HOMEOSTASIS

Experiments with increased stimulation frequency

Frequency of less than 10 per second muscle contracting and

completely relaxing before next simulation

each tension same M

usc

le te

nsi

on Muscle tension Stimulus

(a) Twitch

Frequency (less than 10 stimuli per second)


IV. HOMEOSTASIS

Experiments with increased stimulation frequency

Frequency between 10 and 20 per second

allows for complete relaxation tension increasing insufficient time to remove all Ca2+ more cross-bridges with

subsequent stimulation heat also increasing enzyme

efficiency

stepwise increase in contraction strength, treppe

Mu

scle

ten

sion

(b) Treppe

Frequency (1020 stimuli per second)


IV. HOMEOSTASIS

Mu

scle

ten

sion Tetany Incomplete tetany

Fatigue Wave

summation

(c) Wave summation, incomplete tetany, and tetany

Frequency (2050 stimuli per second)

Experiments with increased stimulation frequency (continued) Frequency between 20 and 40 per second

relaxation not occurring summation of contractile forces called wave summation or temporal summation with further increases less time for relaxation

tension tracing increasing incomplete tetany At 40 to 50 per second

contractions fused to form continuous contraction called tetany if continues, muscle reaches fatigue

decrease in muscle tension from repetitive stimulation


IV. HOMEOSTASIS

In human body, stimulation < 25 stimuli per second no tetany occurs sustained contraction in the body due to stimulation of different motor units in same muscle

MUSCLE FATIGUE When a skeletal muscle fiber is repeatedly stimulated, the tension the fiber develops eventually decreases even though the stimulation continues.

This decline in muscle tension as a result of previous contractile activity is known as muscle fatigue.


IV. HOMEOSTASIS

MUSCLE FATIGUE CAUSES Many factors can contribute to the fatigue of skeletal muscle. Acute fatigue from high-intensity, short-duration exercise is thought to involve:

decrease in ATP concentration. increase in concentrations of ADP, Pi, Mg2+ , H+ and oxygen free radicals.

These have been shown to:

decrease the rate of Ca2+ release, reuptake and storage by the endoplasmic reticulum. decrease the sensitivity of the thin filament proteins to activation by Ca2+ release. directly inhibit the binding and power-stroke motion of the myosin cross-bridges.

Central Command Fatigue

Another type of fatigue quite different from muscle fatigue occurs when the appropriate regions of the cerebral cortex fail to send excitatory signals to the motor neurons.


IV. HOMEOSTASIS

TYPES OF SKELETAL MUSCLE FIBERS All skeletal muscle fibers do not all have the same mechanical and metabolic characteristics. Fibers are classified on the basis of:

1.Their maximal velocities of shortening (fast or slow) Fast and slow fibers contain forms of myosin that differ in the maximal rates at which they use ATP. This determines the maximal rate of cross-bridge cycling and thus the maximal shortening velocity.

2.The major pathway they use to form ATPoxidative or glycolytic Oxidative: Most of the ATP such fibers produce is dependent upon blood flow to deliver oxygen and fuel molecules to the muscle and contain myoglobin. These fibers appear darker and muscles containing many of these are used for long term contractions (like standing).

Glycolytic: In contrast, these fibers have few mitochondria but possess a high concentration of glycolytic enzymes and a large store of glycogen. This allows for quick bursts of activity.


IV. HOMEOSTASIS

QUESTION


IV. HOMEOSTASIS

MUSCLE FIBERS THAT RELY ON ANAEROBIC GLYCOLYSIS FOR THEIR ATP _____. A. are able to create more force B. fatigue more easily C. have more myoglobin D. have many mitochondria

Type of contraction generated Fiber-types

Fast-twitch fibers have fast variant of myosin ATPase initiate contraction more quickly following stimulation produce contraction of shorter duration produce a strong contraction greater power and speed than slow-twitch fibers

Slow-twitch fibers have slow variant of myosin ATPase


IV. HOMEOSTASIS

Means for supplying ATP Oxidative versus glycolytic fibers

Oxidative fibers use aerobic cellular respiration have features that support this

extensive capillaries large numbers of mitochondria large supply of myoglobin (impart red appearance)

allow to continue contracting for long periods also called fatigue-resistant


IV. HOMEOSTASIS

Means for supplying ATP

Oxidative versus glycolytic fibers (continued) Glycolytic fibers

use anaerobic cellular respiration have fewer structures needed for aerobic cellular respiration

white appearance due to lack of myoglobin large glycogen reserves for anaerobic respiration tire easily after short time of sustained activity also termed fatigable


IV. HOMEOSTASIS

54

On the basis of these two characteristics, three principal types of skeletal muscle fibers can be distinguished:

Note that the fourth theoretical possibilityslow-glycolytic fibersis not found.

Type I

Type IIa Type IIb


IV. HOMEOSTASIS

Mixture of muscle fiber types in skeletal muscle Variation in relative percentage of muscle fibers Most muscles with a mixture of all types E.g., in eye, high percentage of fast glycolytic fibers

requires swift, brief contractions E.g., in postural muscles, high percentage of slow oxidative fibers

need to contract continually to help maintain posture


IV. HOMEOSTASIS

Variation of muscle fiber types in individuals

Long distance runners higher proportion of

slow-oxidative fibers in legs

Sprinters higher percentage of

fast-glycolytic fibers Determined primarily by

genes Determined partially by

training

SO FO

SO FO

FO FO

FG FG

FG SO

FO

SO

FG


Gladden Willis/ Visuals Unlimited


IV. HOMEOSTASIS

COMPARISON OF SKELETAL FIBER TYPES


IV. HOMEOSTASIS

CONTROL OF MUSCLE TENSION


IV. HOMEOSTASIS


V. INTEGRATION

General Topics i. Exercise ii. Clinical Applications

EFFECTS OF EXERCISE ON SKELETAL MUSCLE

Changes in muscle from a sustained exercise program Hypertrophy

increase in skeletal muscle size results from repetitive stimulation of fibers results in

more mitochondria larger glycogen reserves increased ability to produce ATP more myofibrils that contain larger number of myofilaments

Hyperplasia increase in the number of muscle fibers may occur in a limited way with exercise


V. INTEGRATION

Changes in muscle from lack of exercise Atrophy

decreasing muscle fiber size results from lack of exercise can arise from temporary reduction in muscle use

e.g., individuals in a cast causes decrease in muscle tone and power initially reversible, but dead fibers not replaced with extreme atrophy, loss of muscle function permanent

muscle replaced with connective tissue

EFFECTS OF EXERCISE ON SKELETAL MUSCLE


V. INTEGRATION

SKELETAL MUSCLE DISORDERS A number of conditions and diseases can affect the contraction of skeletal muscle.

Many of them are caused by defects in the parts of the nervous system that control contraction of the muscle fibers rather than by defects in the muscle fibers themselves.

For example, poliomyelitis is a viral disease that destroys motor neurons, leading to the paralysis of skeletal muscle, and may result in death due to respiratory failure.


V. INTEGRATION

SKELETAL MUSCLE DISORDERS Myasthenia Gravis Autoimmune disorder where the nAChR has antibodies generated against it, causing receptor destruction.

How would this cause a motor deficit? How would you treat it?

Muscular Dystrophy Defect in the protein dystrophin, which connects the Z-disc to the muscle cell membrane.

How would this cause a motor deficit? Muscle Cramps Involuntary tetanic contraction of muscles due to electrolyte imbalances. Hypocalcemic Tetany Involuntary tetanic contraction of muscles due to low calcium.


V. INTEGRATION

QUESTION


When you attempt to shovel a load of snow that is too heavy, what sort of muscle contraction are you using? A. Isometric Contraction B. Isotonic Contraction

V. INTEGRATION

lecture 4 - muscle

Documents

muscle physiology

muscle fatigue

skeletal muscle contraction

muscle returns

muscle relaxation

types of muscle overview

skeletal muscle fiber

circular muscle bands