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A 34-year-old man is undergoing rehabilitation after a prolonged ICU stay. During isometric testing, his quadriceps generate normal passive tension but markedly reduced active tension at all muscle lengths. Which of the following mechanisms best explains this finding?
A. Reduced preload causing loss of optimal sarcomere overlap
B. Impaired cross-bridge formation due to loss of actin and myosin filaments
C. Excessive afterload preventing muscle shortening
D. Increased Golgi tendon organ firing inhibiting α-motor neurons
E. Failure of Ca²⁺ reuptake by the sarcoplasmic reticulum
B
B. Impaired cross-bridge formation due to loss of actin and myosin filaments — Correct.
Prolonged ICU stay → disuse atrophy → loss of contractile proteins. Passive tension (elastic components) remains intact, but active tension falls at all lengths because fewer cross-bridges can form.
A. Preload affects length–tension positioning, not uniform loss of active tension.
C. Afterload affects velocity, not isometric force.
D. Golgi inhibition is reflex-based and transient, not structural.
E. SERCA failure affects relaxation, not selective loss of active tension.
A patient with a spinal cord injury retains voluntary movement but cannot smoothly grade muscle force when lifting objects of increasing weight. He can lift light loads but drops heavier ones abruptly. Injury to which structure best explains this deficit?
A. Muscle spindle intrafusal fibers
B. Type Ia afferent neurons
C. Type Ib afferent neurons
D. γ-motor neurons
E. α-motor neurons
C
C. Type Ib afferent neurons — Correct.
Type Ib afferents from Golgi tendon organs provide graded feedback about active muscle tension, allowing smooth force modulation. Loss → inability to sustain heavier loads.
A. Intrafusal fibers detect length, not force.
B. Type Ia fibers mediate stretch reflex, not force grading.
D. γ-motor neurons adjust spindle sensitivity, not load control.
E. α-motor neuron injury would cause paralysis, which is not present.
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