Physiological effects of diaphragm muscle denervation and disuse.
From our studies, it is clear that diaphragm muscle neuromotor control is responsive to alterations in innervation and activation. These adaptations to altered use appear to be most pronounced among fast-twitch motor units composed of type II muscle fibers. Because the plasticity involves diminished contractile strength and a slowing of shortening velocity, it might be considered maladaptive with respect to diaphragm functional demands; however, because ventilatory behaviors of the diaphragm most likely require the recruitment of only type S motor units (type I muscle fibers) that appear to be less adaptive, the functional decrements following disuse may involve only nonventilatory behaviors that require the recruitment of fast-twitch (type II muscle fibers) motor units. In other words, in many circumstances, diaphragm muscle adaptations may reduce the functional reserve capacity of the muscle without affecting normal ventilatory performance. The extent to which these observations can be applied to humans remains speculative. Certainly, the animal models approximate the human condition in that ventilatory requirements of the diaphragm are comparable across mammalian species. It is known that type II fibers comprise approximately 60% of the human diaphragm. Therefore, type II muscle fibers in humans may also be particularly vulnerable to adaptive changes associated with diaphragm disuse. With regard to the functional decrements that might ensue in humans, we have estimated that the forces generated by the human diaphragm during tidal breathing are approximately 10% of maximum. Therefore, as in other species, ventilatory forces generated by the diaphragm in humans most likely do not require the recruitment of fast-twitch (type II) motor units. Normal ventilatory behaviors may therefore be spared from maladaptive changes in diaphragm performance. With the imposition of mechanical loads to breathing associated with certain chronic pulmonary diseases, however, it might be expected that the recruitment of fast-twitch motor units would be required on a more continuous basis. Such diseases are normally progressive and incremental, therefore allowing sufficient time for adaptation. One adaptation that might be expected would be an overall improvement in the fatigue resistance of fast-twitch motor units. This adaptation could be accomplished by altering the metabolic enzyme activities of type II muscle fibers, by affecting the expression of contractile proteins, or both. Improvement of muscle fiber fatigue resistance is usually at the expense of fibre size, contractile strength, or both.(ABSTRACT TRUNCATED AT 400 WORDS)
Sieck
G C
GC
Department of Anesthesiology, Mayo Medical School, Rochester, Minnesota.
D000818:Animals; D001284:Atrophy; D002415:Cats; D006224:Cricetinae; D003964:Diaphragm / Q000294:innervation / Q000473:pathology / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D009121:Muscle Denervation; D018485:Muscle Fibers, Skeletal / Q000145:classification; D051381:Rats; D011999:Recruitment, Neurophysiological; D012133:Respiratory Paralysis / Q000473:pathology / Q000503:physiopathology*