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Agonists vs Antagonists: What does an agonist do?

An agonist is an alternative ligand that will activate receptors → it acts like the primary ligand. (Nicotine)

Agonists vs Antagonists: What does an antagonist do?

An antagonist is a ligand that block receptor activity. (Heroin)

Muscle Fibers: Muscle fibers are also referred to as ---.

Muscle fibers are also referred to as muscle cells.

Muscle Fibers: --- = a bundle of muscle fibers.

Fascicles = a bundle of muscle fibers.

Muscle Fibers: Do muscle fibers have on or more nuclei?

Muscle fibers have more than one nuclei.

Muscle Fibers: --- = cell membrane.

Sarcolemma = cell membrane

Muscle Fibers: --- = extensions of the cell membrane.

T-tubules = extensions of the cell membrane.

Muscle Fibers: Anatomy of a myofibril

\
* Is a repeated pattern of thick and thin filaments
* These filaments overlap each other
* Sarcomere = one repeat of the pattern → smallest unit capable of contraction
* Myosin = motor protein that makes up the thick filament (in middle of the sarcomere)
* Actin = globular protein that makes up the thin filament

Muscle Contraction: --- and --- filaments --- across each other so they have more ---.

Thick and thin filaments slide across each other so they have more overlap.

Muscle Contraction: Does the sarcomere length increase of decrease?

The sarcomere length decreases.

Muscle Contraction: --- heads attach to ---.

Myosin heads attach to actin.

End Plate Potential: Na+ influx results in muscle fiber ---.

Na+ influx results in muscle fiber depolarization.

End Plate Potential: Most EEPs lead to --- --- in the cells.

Most EEPs lead to action potentials in the cells.

End Plate Potential: Results in eventual the release of --- ions.

Results in eventual the release of calcium ions.

\

1. Acetylcholine (neurotransmitter) released by somatic motor neuron (via voltage-gated calcium channels) into the neuromuscular junction.
2. EPP followed by action potentials spreads along the sarcolemma, specifically the T-tubules (part of the sarcolemma) → the action potentials alter the conformation of the DHP receptor.
3. DHP receptor activated which causes the release of calcium from the sarcoplasmic reticulum into the cytoplasm.
4. Calcium binds with troponin which results in the release of tropomyosin from actin-binding site of myosin heads → results in strong binding of actin and myosin.


1. Tropomyosin normally blocks myosin from binding with actin.
5. Power Stroke:


1. ATP binds to myosin → results in myosin release from actin and energy moves myosin head to 90 degree angle.
2. Rigor mortis is when there is no ATP so myosin is stuck to actin (stiffness of the muscles).
6. Calcium is pumped back into the sarcoplasmic reticulum using calcium ATPase.
7. Titin restores sarcomere length.

Muscle Fatigue: Central fatigue

\
Central fatigue is when the CNS is overworked or has \n “had enough”.

Muscle Fatigue: Peripheral fatigue

* Depletion of storage of acetylcholine and energy.
* Accumulation of lactate, H+, and phosphate groups.
* Excessive efflux of K+ ions leading to changes in \n membrane potential.

Muscle Fatigue: Phosphocreatine

Backup energy of source in muscles (outside of cellular respiration and glycolysis).

Slow Twitch

* Speed: slowest
* Endurance: Fatigue resistance
* Metabolism: Aerobic
* Mitochondria: High → important for aerobic respiration
* Colour: dark red (myoglobin)

Fast Twitch Oxidative Glycolytic

* Speed: intermediate
* Endurance: Fatigue resistance
* Metabolism: Glycolytic can increase oxidative with training
* Mitochondria: Moderate
* Colour: Red

Fast Twitch Glycolytic

* Speed: Fastest
* Endurance: Easily fatigue
* Metabolism: Anaerobic
* Mitochondria: Low
* Colour: Pale