Practice Questions

Spindle-shaped cells (tapered at both ends) are characteristic of smooth muscle. This shape allows them to pack tightly together into continuous sheets (often in circular and longitudinal layers) that form the walls of hollow organs, facilitating functions like peristalsis and regulating vessel diameter.

Mature cardiac muscle cells (cardiomyocytes) are terminally differentiated and generally lose their ability to divide. Skeletal muscle cannot divide but has satellite cells for limited repair. Smooth muscle retains a significant capacity to divide and regenerate (hyperplasia).

Calcium channel blockers prevent the influx of extracellular calcium. Since both cardiac muscle and vascular smooth muscle rely heavily on extracellular calcium for contraction, these drugs decrease heart rate/contractility and cause vasodilation, effectively lowering blood pressure and reducing heart strain.

Cardiac muscle has an absolute requirement for aerobic metabolism to produce ATP. It contains very little glycogen and relies almost entirely on continuous oxygen supply. Skeletal and smooth muscles can rely more heavily on anaerobic glycolysis and can tolerate hypoxia much longer without cell death.

Smooth muscle contractions are characteristically very slow to develop and slow to relax. A single smooth muscle twitch can last anywhere from 1 to 3 seconds, which is up to 30 times longer than a typical skeletal muscle twitch, allowing for prolonged, sustained tension.

In skeletal muscle, calcium binds to troponin on the actin filament to expose binding sites. In smooth muscle, calcium binds to calmodulin in the cytosol, which then directly activates an enzyme (myosin light-chain kinase) that phosphorylates the myosin head to initiate contraction.

Muscle hypertrophy (growth due to exercise) occurs not by cell division (hyperplasia), but by the enlargement of existing individual muscle fibers. The cells synthesize more actin and myosin, creating more myofibrils, which increases the thickness and strength of the fiber.

The plateau phase of the cardiac action potential is caused by the opening of slow voltage-gated L-type calcium channels. The influx of extracellular calcium balances the efflux of potassium, prolonging the depolarization and ensuring a long refractory period that prevents tetanus.

Parasympathetic stimulation via the vagus nerve releases acetylcholine, which binds to muscarinic receptors on the heart's pacemaker cells, slowing the heart rate (decreasing cardiac muscle activity). In contrast, it generally stimulates digestive smooth muscle.

Smooth muscle does contain actin and myosin, and they slide against each other to cause contraction. However, these filaments are not arranged in the highly ordered, repeating, registered units (sarcomeres) that create the alternating light and dark bands (striations) seen in skeletal and cardiac muscle.