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61 Cards in this Set

  • Front
  • Back

Functions of the Skeletal system

Locomotion


Facial expression


Posture


Body position


Regulation of temperatureorigin

Origin

The place where the Muscle stars on a bone; stationary

Insertion

The place where the muscle ends on the bone

Muscle Action

The insertion moves towards the origin (bicep curls)

Reverse Muscle Action

When the insertion is anchored, the origin can move towards the insertion (pull ups)

First Class Levers

E^ F L_


Scissors


Neck and maxilla

Second Class Levers

F L_ E^


Wheel barrow


Going on reléve

Third Class Levers

F E^ L_


Tweezers


Elbow joint

Abduction of the arm

Agonist: deltoid


Antagonist: latissimus dorsi


Synergist: supraspinatus


Fixator: trapezius

Flexion of the Forearm

Agonist: brachialis


Antagonist: triceps Branchii


Synergist: biceps Branchii


Fixator: pectoralis major

Organization of Muscle

Groups of muscle (deep fascia)


Muscle (epimysium)


Fascicles (perimysium)


Myofibril (endomysium)

Major Structures of a Muscle Fiber

Sarcolemna: conduction of electrical signals


SR: control of muscle contraction/ calcium storage


Myrofibrils: contraction via sacromeres

Sacromere

Z-discs: define length


h-zone: only thick filament


M-line: down the middle


A band: all thick filament


I band: only thin filament


ZOO: overlap


Titin filament: pulls apart during relaxation

Thin filament

Actin: myosin binding site


Troponin: holds tropomyosin in place, moves when Ca binds


Tropomyosin: covers myosin binding site on actin

Thick filament

Myosin: motor protein, form crossbridges with actin

Sliding Filament Mechanism

Myosin heads form cross bridges, conformational change energized ATP hydrolysis causes power strokes and think filaments slide over thick

Contraction cycle (1)

Myosin binding sites on actin are exposed when Ca binds to troponin

Contraction cycle (2)

Myosin heads form crossbridges

Contraction cycle (3)

Myosin heads pivot towards the center of the sacromere

Contraction cycle (4)

ATP binds to myosin Head, and detaches the from actin

Contraction cycle (5)

ATP hydrolysis and the energy released re-energized the myosin head back to cocked position

Contraction cycle (6)

Repeats until myosin binding site on actin is no longer available

Rigor of Death

Lack of ATP to detach myosin Head from actin

Components of NMJ

Motor Nueron


Synaptic end bulb


Voltage gated calcium channel


Acetylcholine vessels


Synaptic cleft


Acetylcholine receptors


Motor end plate


Sodium


T-tubule


SR


Calcium

NMJ (1)

Action potential arrives at synaptic end bulb and voltage gated calcium channels open

NMJ (2)

Synaptic vessels with acetylcholine go through exocytosis

NMJ (3)

Acetylcholine is released into synaptic cleft and binds to receptors in the motor end plate of sarcolemna

NMJ (4)

Acetylcholine receptors opens and allow sodium to enter the muscle fiber, generating action potential on the sarcolemna

NMJ (5)

Acetylcholine beaks Down into acetylcholine esterase

Acetylcholine Esterase

East remaining acetylcholine in synaptic cleft so that another muscle action potential does not arise unless more acetylcholine is released from the motor neuron

Role of Calcium

Calcium diffuses into sarcoplasmic and myofibrils where it can bind to troponin and initiate contraction

Order of muscle contraction

1 excitation: motor neuron sends signal to sodium influx


2 contraction coupling: action potential on sarcolemna to release of calcium from SR


3 contraction: calcium bind to troponin to detachment of crossbridge


4 relaxation: AP stops to sacromere to resting position

Creatine Phosphate Pool

Fastest way to create ATP


~ 15 sec sustainability

Glycogen (anaerobic)

Glycolysis


Creates pyruvate acid and lactic acid


Occurs in cytoplasm


~ 2 min of sustainability

Glycogen (aerobic)

Cellular respiration with amino acids, fatty acids, pyruvic acid, oxygen


Mitochondria


Slow process


~ 40 min (to several hours) sustainability

Fatigue

Progressive increase in the effort required to maintain a desired force, and progressive inability to maintain this force in sustained or repetitive contractions

Causes of Fatigue

Glycogen depletion


Lactic acid buildup from anaerobic glycolysis


Phosphate build up from creation phosphate metabolism

Most Common Fatigue

Psychological


Nervous


Muscular

Cori Cycle

Muscle creates lactic acid through anaerobic glycolysis


Lactic acid is turned into glucose in the liver


Glucose returns to muscle

O2 Debt

Excess post exercise oxygen consumption


Caused by: Cori cycle, resynthesis of creatine, replace oxygen with myoglobin, repair

Twitch

Arising from a single electrical stimulus

Twitch sequence

Latent period: 2 msec, no change in tension


Contraction period: 10-100 msec, peak tension


Relaxation period: 10-100 msec, tension decreases

Temporal Summation (tetanus)

Increasing frequency of electrical stimulus to increase tension

Motor unit

A motor neuron and all the muscle fibers it innervates

Special Summation

Motor unit recruitment to increase tension

Size Principal

Small fibers are used first and large ones are used last

Isometric

Same length

Isometruc

Same tension; after tension is generated length can change

Concentric contraction

Effort > load

Eccentric Contraction

Load > effort

Nervous Strategies to Increase Tension

1) temporal Summation


2) spatial Summation

Controlled Strategies to increase force

Optimal fiber length at he beginning of contraction. Tension generated is proportional to the number of crossbridges formed. Peak tension is developed by utilizing intermediate fibers

Slow Oxidative fibers

Smaller


Slowly contracting


Aerobic metabolism

Fast Glycolytic

Rapidly contracting


Anaerobic


M

Oxidative-Glycolutic Fibers

Medium in size


Relatively fast


Primarily anaerobic

Hypertrophy

With training, each muscle fiber increases in diameter because it increases the amount of myofibrils

Atrophy

Decreased diameter due to decreased myofibrils but amount of nuclei stay the same

Muscle Adaptations

Increased capillary action


Increased mitochondria


Increased cross sectional area

Cardiac Muscle

Pumps blood


Smaller branched cells


Organized into sacromeres


Longer contraction than skeletal


No sufficient Ca from SR


Extracellular SR


Pacemaker cells


No motor units


No temporal summation

Smooth Muscle

No sacromeres


Crossbridges form


Contraction is very slow


Cytoplasmic Ca binds to calmodulin, myosin light chain kinase, myosin Head group stimulates

Structural proteins

Titin: spans half the sacromere from z-disc to m line, stabilizes thick filament


Dystrophin: cytoskeleton protein that links thin filaments to sarcolemna


Nebulin: spans the length of thin filament, anchors thin filament to z disc


Alpha-actin: found in z disc, binds to actin molecules


Myomesin: found in m-line, binds to titin and thick filaments to connect them together