Question 6 of 6

Question 6

Question text not reproduced: the examination questions are © Engineers and Geoscientists BC. Open the official past paper (linked at the top of this page) to read the question, then follow the worked solution below.

(a) From nerve impulse to muscle twitch: excitation–contraction coupling

The chain of events is: (1) the action potential reaches the motor nerve terminal at the neuromuscular junction and depolarises it, opening voltage-gated Ca$^{2+}$ channels; (2) Ca$^{2+}$ influx triggers fusion of acetylcholine (ACh)-containing vesicles with the presynaptic membrane and ACh is released into the synaptic cleft; (3) ACh diffuses across the cleft and binds nicotinic receptors on the motor end-plate, opening ligand-gated cation channels and depolarising the end-plate (the end-plate potential, EPP); (4) the EPP is normally large enough to trigger a propagated action potential in the surrounding sarcolemma, which spreads along the fibre and inward along the transverse (T) tubules; (5) depolarisation of the T-tubule membrane is sensed by dihydropyridine receptors (DHPRs), which are mechanically/electrically coupled to ryanodine receptors (RyRs) on the adjacent terminal cisternae of the sarcoplasmic reticulum (SR), triggering a large, rapid release of Ca$^{2+}$ from the SR into the sarcoplasm; (6) the released Ca$^{2+}$ binds troponin C on the thin filament, shifting the troponin–tropomyosin complex and exposing the myosin-binding sites on actin; (7) energised myosin heads (ATP hydrolysed to ADP+P$_i$) bind actin and undergo the power stroke, sliding the thin filament past the thick filament (the sliding-filament mechanism), and this repeated cross-bridge cycling — as long as Ca$^{2+}$ and ATP remain available — generates the tension that constitutes the onset of the muscle twitch. Relaxation follows once the SERCA Ca$^{2+}$ pump returns Ca$^{2+}$ to the SR faster than it is released, allowing tropomyosin to re-cover the binding sites.

(b) Isometric vs. isotonic contraction

In an isometric contraction, the muscle develops tension without shortening (its overall length stays constant) because the load exceeds, or is fixed and immovable relative to, the force generated — e.g. pushing against a wall, or a postural muscle holding the body upright against gravity without any joint movement. In an isotonic contraction, the muscle develops enough tension to move a load, and shortens (concentric) or is controlled while lengthening (eccentric) at essentially constant tension once that tension exceeds the load — e.g. lifting a dumbbell through a curl (concentric isotonic) or slowly lowering that same dumbbell back down under control (eccentric isotonic). The key distinction is therefore whether the muscle changes length while contracting (isotonic) or not (isometric), not whether a load is present at all.

(c) Fibre type with the largest glycogen stores, and its functional role

The largest glycogen stores are found in type II (fast-twitch, glycolytic) skeletal muscle fibres, particularly the fast-glycolytic type IIb/IIx subtype. Functionally, this glycogen serves as a rapidly mobilisable substrate for anaerobic glycolysis, letting these fibres generate ATP quickly enough to sustain the very high, rapid cross-bridge cycling rates needed for brief, powerful contractions (sprinting, jumping, heavy lifting) when oxidative phosphorylation (which is comparatively slow to up-regulate and depends on adequate O$_2$ delivery) cannot keep pace with ATP demand. The trade-off is rapid fatigability, since anaerobic glycolysis is far less efficient in ATP yield per glucose and produces lactate; by contrast, type I (slow-twitch, oxidative) fibres store comparatively little glycogen, rely more on triglycerides and oxidative phosphorylation, and are built for sustained, fatigue-resistant, lower-power activity.