Question

7. Having begun and enjoyed resistance training, Emily is looking at ways that she can get stronger. Describe the factors that increase the force of muscle contraction .

8. List and compare the three different types of muscle .

9. Describe the events that occur at the neuromuscular junction that result in a muscle contraction .

Answer 1

Muscle cell structure	Characteristics
Sarcolemma	Serves as the cell membrane Has membrane invaginations In striated muscle cells: transverse tubules (T-tubules) Transmit the action potential (AP) to sarcoplasmic reticulum (see below) The close proximity of T-tubules to adjacent terminal cisternae allows direct transmission of APs to the sarcoplasmic reticulum, which enables a quick release of Ca2+ for contraction. Responsible for synchronization of AP transmission and contraction In smooth muscle cells: caveolae
Sarcoplasm	Serves as the cytoplasm of striated muscle cells Notable contents: Myofibrils consisting of myofilaments Glycosomes (granules of stored glycogen) Myoglobin Ca2+ to initiate contraction by binding troponin
Sarcoplasmic reticulum (SR)	Serves as the endoplasmic reticulum Stores calcium that needs to be released into the sarcoplasm for contraction Consists of a network of longitudinal tubules (L-tubules) In skeletal muscle, L-tubules extend longitudinally into the terminal cisternae, which encircle myofibrils and lie adjacent to T-tubules
Myofilaments	Protein fibers consisting of thick (myosin) and thin (actin) filaments Achieve contraction through their interaction together, which is regulated by special proteins such as troponin

2.types of muscle fibre

	Type 1 fibers (e.g. postural muscles)	Type 2 fibers (extraocular muscles)
Appearance	Rich in mitochondria and myoglobin → dark, red appearance	Poor in mitochondria and myoglobin → light, white appearance
Energy production	Predominantly from aerobic oxidation (oxidative phosphorylation)	Predominantly from anaerobic glycolysis
Myosin ATPase activity	Low	High
Contraction velocity	Slow-twitch	Fast-twitch
Activity period	Long-term activity	Short-term activity

3.types of muscles

	Skeletal muscle	Cardiac muscle	Smooth muscle
Cell morphology	Large elongated cells with multiple nuclei located at the periphery	Branched cells with a central nucleus	Spindle-shaped with a central nucleus
Invaginations of the sarcolemma	One T-tubule and two terminal cisternae form a triad	One broad T-tubule and one terminal cistern of the SR form a dyad	Caveolae

4.

Arrangement of myofilaments

Types

Actin myofilaments

• Contain regulatory proteins : Prevent permanent interaction between myosin and actin.
  • Proteins that block myosin binding sites:
    • In both striated and smooth muscle: tropomyosin

Myosin filaments

• Function: Thick filament that slides along actin filaments, which is driven by ATP hydrolysis
• Structure
  • The myosin molecule is composed of a tail and a head, which are formed from several heavy and light chains depending on the myosin type.
    • Myosin heads have an affinity both for actin and ATPase activity.

5.Two types of arrangement of myofilaments
Sarcomeres of striated muscle
Components on electron microscopy
Lines
Z lines:
M lines:
Bands
I bands: zone containing only (thin) actin filaments
The I bands decrease in size during contraction, when actin slides over myosin towards the M-line.
A bands
The length of a myosin filament, which may contain overlapping actin filaments (keeps its length during contraction!)
Composed of three segments
H zone:
Dark bands of the outer segments (between H and I bands): overlapping actin and myosin filaments; contain myosin heads
Anchorage by:
Dystrophin-glycoprotein complex: links (noncontractile) actin of the cytoskeleton with the sarcolemma and extracellular matrix:
Duchenne muscular dystrophy and Becker muscular dystrophy involve genetic defects of the dystrophin gene.

6.

Initiation of muscle contraction

• Steps: Stimulus (e.g., action potential) from efferent neuron opens presynaptic voltage-gated calcium channels → ACh released into the synaptic gap → ACh binds to postsynaptic ACH receptors → causes muscle cell depolarization that diffuses across the sarcolemma and into T-tubules or caveolae → Depolarization opens voltage-sensitive dihydropyridine receptors (DHPR) and the mechanically coupled ryanodine receptors (RR) in the SR → SR releases calcium → ↑ intracellular calcium

Skeletal muscle contraction results from an increase in intracellular calcium from stores in the sarcoplasmic reticulum. This explains the ability of skeletal muscle to contract despite treatment with calcium channel blockers, which can block an influx of extracellular calcium through DHPRs but cannot affect DHPR voltage-sensing capabilities and the resulting intracellular calcium release.

Steps of the contraction cycle (sliding filament theory)

1. Orientation of the myosin head: hydrolysis of ATP to ADP and Pi (both remain on the myosin head) → myosin head alters its confirmation (“cocked state”) → it is ready to bind actin once
2. Crossbridge formation: intracellular calcium binds troponin and causes a conformational change → moves tropomyosin out of the myosin binding site on actin → myosin head binds actin at a 90° angle, forming a crossbridge
3. Powerstroke of the myosin head: Myosin head releases ADP and Pi → myosin head turns by 45°, pulling myosin along actin → muscle shortens
4. Loosening of the crossbridge: ATP binds myosin head → detaches from the actin filament → myosin head returns to its starting position
5. Replication of the cycle: If calcium concentration in the muscle cell remains elevated → a new cycle begins with reorientation of the myosin head.

When a person dies and breathing and circulation stop, muscle cells lack oxygen and cannot use aerobic respiration to efficiently produce ATP anymore. Without ATP, the crossbridges between myosin and actin filaments cannot be resolved and muscles become tense, which is referred to as rigor mortis.