Muscle Contraction

Motor Unit

Sensory motor neuron and all the muscle fibers in innervates.

Sodium-Potassium Pump

Pump 3 Na+ out for 2 K+ in

Depolarization

Inside of membrane becomes less negative than RMP

Repolarization

Membrane returns to RMP from a depolarized state

Hyperpolarization

Inside of membrane becomes more negative than RMP

Neuromuscular Junction

Somatic motor neuron axon terminals and motor end plate of sarcolemma form synaptic clefts

End Plate Potential

Depolarization of the motor end plate due to acetylcholine binding to nicotinic receptors in junctional folds, causing an influx of Na+.

Excitation-Contraction Coupling

Sequence of events by which transmission of an action potential along the sarcolemma leads to the sliding of myofilaments.

Dihydropyridine (DHP) receptors

Voltage sensitive proteins in T-tubule membranes linked to ryanodine receptors in the sarcoplasmic reticulum responsible for calcium release when action potential occurs.

Ryanodine receptors

Calcium release channels in the sarcoplasmic reticulum linked to DHP receptors that release calcium into the sarcolemma when AP occurs.

Troponin

Regulatory protein that calcium binds to to remove the blocking action of tropomyosin and expose myosin-binding sites on thin filaments.

Cross-bridge cycling

Formation and detachment of cross-bridges between actin and myosin that leads to muscle contraction.

Cross Bridge Formation

Step 1 of cross-bridge cycling:

Energized myosin head attaches to an actin filament, forming a cross bridge.

ADP and phosphate group are still attached.

Power Stroke

Step 2 of cross-bridge cycling:

The myosin head pivot and bends back into a low-energy state, pulling the actin filament towards the M line.

ADP and phosphate group are released.

Cross Bridge Detachment

Step 3 of cross-bridge cycling:

ATP binds to myosin, causing the myosin head to detach from actin, breaking the cross bridge.

Myosin is in low-energy state.

Cocking of Myosin Head

Step 4 of cross-bridge cycling:

Myosin hydrolyzes ATP to ADP and phosphate, causing the myosin head to return to its high-energy state

Rigor Mortis

In the absence of ATP, myosin can’t detach from actin, leading to muscle stiffness after death.

Muscle Relaxation

• Motor neuron stops stimulating the sarcolemma

• Acetylcholinesterase breaks down acetylcholine in the synaptic cleft

• Calcium is removed from the sarcoplasm by Ca2+-ATPase at SR membrane

• Troponin-Tropomyosin complex position is reestablished

ATP is required for both contraction and relaxation

Stored ATP

ATP already present in muscle cells

4-6 seconds

Creatine Kinase

Coupled reaction of creatine phosphate and and ADP to form ATP

15 seconds

Anaerobic resiration

Glycolysis and lactic acid formation in the cytoplasm produces 2 ATP per glucose

30-40 seconds

Aerobic respiration

Glycolysis, Krebs Cycle, and ETC in the mitochondria produces 36 ATP in total per glucose

Supplies 95% of ATP for muscle activity

Muscle Fatigue

Inability to maintain force after prolonged contraction

Factors that contribute:

• Insufficient ACh release from motor neuron

• Insufficient calcium release form SR

• Creatine Phosphate depletion

• Lactate buildup

• Insufficient oxygen availability or usage

Slow, oxidative fibers

Slow myosin ATPase activity → slow contraction

Aerobic and many capillaries → high myoglobin content and low glycogen stores

Slow rate of fatigue

Fast, glycolytic fibers

Fast myosin APase activity → fast contraction

Anaerobic glycolysis and fewer capillaries → low myoglobin content and more glycogen stores

Fast rate of fatigue

Load and Muscle Fiber type

Factors influencing velocity and duration of contraction

Muscle Twitch

Mechanical event the result of a single action potential in one muscle fiber

Latent Period

Time between sarcolemma depolarization and muscle contraction; same for all muscles

Excitation-Contraction Coupling

Contraction Period

Increase in muscle tension due to cross bridge formation and movement

Relaxation Period

Decrease in muscle tension because of calcium removal

Regulatory proteins repositioned

Treppe

Successive contractions are greater with repeated low frequency stimulation due to:

• Increased Ca2+ availability

• Increased blood flow

• Increased heat

• Increased efficiency of enzymes

Temporal Summation

Increase in frequency of stimulation results in increased tension development

Twitch

Stimuli delivered after relaxation does not produce summation

Unfused Tetanus

High frequency stimulation resulting in maximal tension with some relaxation between stimulation

Fused Tetanus

At the highest stimulus frequency, maximal tension is generated with no relaxation

Spatial Summation / Recruitment

Stimuli occur at same time from different motor units to activate more motor units, resulting in more tension

Asynchronous Stimulation

Motor units are stimulated at different times, so only some muscle fibers contract at any given time to prevent muscle fatigue with sustained contractions.

Maximum amount of force is generated due to a maximum overlap of actin and myosin in the sarcomere.

Length-Tension Relationship

Hypertrophy

Increase in muscle mass due to more myofibrils and sarcoplasmic content

Disuse Atrophy

Decrease in muscle mass due to lack of use, leading to shrinking muscle fibers (fewer myofibrils); reversible.

Denervation Atrophy

Muscle cell death and replacement with connective tissue due to lack of innervation, caused by nerve or spinal cord damage; irreversible.

Isotonic Contraction

Tension is greater than load, so there’s movement; combination of concentric and eccentric contractions.

Concentric Contraction

Muscle contracts with movement; (e.g. flexion).

Eccentric Contraction

Muscle elongates with movement; (e.g. extension).

Isometric Contraction

Load is greater than tension, so there’s no movement; sarcomeres still shorten but series elastic elements (tends and aponeuroses) stretch so muscle length doesn’t change.