Hypercapnic impairment of neuromuscular function is related to afferent depression.

Acetazolamide (ACZ), a carbonic anhydrase inhibitor, results in altered neuromuscular function secondary to depressed afferent transmission in intact humans. One effect of ACZ is hypercapnia. Thus, to test if the neuromuscular depression observed following ACZ treatment is related to elevated CO(2), human subjects ( n=10) were exposed to 15 min of room air (0% CO(2)) or hypercapnia (7% inspired CO(2)), and neuromuscular function was evaluated. Isometric force (36.8 to 31.1 N) and peak-to-peak electromyographic amplitude (EMG, 1.5 to 1.0 mV) associated with an Achilles tendon tap, and soleus H(max):M(max) ratio (69.0 to 62.2%) were depressed, while EMG latency (34.8 to 39.8 ms) was increased by hypercapnia. Reflex recovery profiles (following a conditioning tap to the contralateral Achilles tendon), motor nerve conduction velocity, amplitude of the maximum M-wave, and peak twitch tension at M(max) were unaltered by hypercapnia. We conclude that elevated CO(2) impairs neuromuscular function through effects on afferent transmission or synaptic integrity between type Ia fibers of the muscle spindle and the alpha motor neuron, without affecting the muscle spindle, efferent conduction or skeletal muscle force-generating capacity.