Effect of nutritional deprivation on diaphragm contractility and muscle fiber size

Lewis, Michael I.; Sieck, Gary C.; Fournier, Mario; Belman, Michael J.

doi:10.1152/jappl.1986.60.2.596

Cited by 120 publications

(86 citation statements)

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“…The fiber compositions and the fiber areas of type I and II muscle fibers in this study were almost consistent with the previous studies (Close 1972;Lewis et al 1986). The present data of the decrement of both fiber area and percentage in type II, in other words, the relative increment of type I muscle fiber, seem to be very compatible with muscle contractile profiles after denervation.…”

Section: Discussionsupporting

confidence: 92%

Effects of Unilateral Phrenic Nerve Denervation on Diaphragm Contractility in Rat.

Shindoh

Hida

Kurosawa

et al. 1994

Tohoku J. Exp. Med.

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We examined the early effects of phrenic nerve denervation on the diaphragm muscle 1, 3, 7 and 14 days after unilateral denervation in rats. In the denervated hemidiaphragms, force frequency curves at 3, 7 and 14 days decreased significantly by 51%, 50% and 38% respectively of the peak tension of the force frequency curves of the diaphragms of rats with sham operation. Twitch tensions increased significantly at 14 days, and contraction times and half relaxation times slowed significantly at 3, 7 and 14 days. The tensions of denervated diaphragms at 5 min during the fatigue runs was significantly increased at 14 days. As determined by histological staining, the mean cross sectional area of fast-twitch fibers (type II) decreased significantly from 2,742 (sham) to 1,599,um2 (14 days), but that of the slow-twitch fibers (type I) did not change significantly during the same period. These findings suggest that, during the first two weeks of denervation, fast twitch fibers (type II) atrophy more rapidly than slow twitch fatigue resistant fibers (type I), as confirmed by the contractile properties and histological findings. twitch kinetics; muscle atrophy; muscle plasticity Hemidiaphragmatic paralysis due to acute phrenic nerve injury is well known as a cause of respiratory muscle failure. Concerning the denervation of skeletal muscles, previous studies have shown that denervation of the skeletal muscles induced muscle fiber atrophy, with an increase in cell membrane resistance (Albuquerque et al. 1971), an enhanced extrajunctional acetylcholine (ACh) sensitivity (Axelsson and Thesleff 1959) and a depolarization of the resting membrane potential in the myocyte (Redfern and Thesleff 1971). Furthermore, recent studies have shown that denervation induces changes in the messenger RNA

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Section: Discussionsupporting

confidence: 92%

Effects of Unilateral Phrenic Nerve Denervation on Diaphragm Contractility in Rat.

Shindoh

Hida

Kurosawa

et al. 1994

Tohoku J. Exp. Med.

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“…Therefore, it is not surprising that type IIx and lib fibers displayed a similar pattern of atrophy in response to CS treatment. In the Sham Diam, there was a generalized atrophy of all fiber types, which has also been previously observed (2,10,11,17,20,22 2, 3 ,10, 13, 22). The reasons for these discrepant results are unclear but may relate to the type, dose, and duration of CS treatment used.…”

Section: Discussionsupporting

confidence: 80%

“…The final body weight of the CS-treated animals was ~15% lower than that of Ctl rats. Because alter ations in nutritional status alone can affect morphology and function of the rat Diam (2,11,17), interpretation of the direct effects of CS treatm ent is confounded. How ever, the morphological and contractile adaptations of the Diam in the Sham group, where body weight was matched to that of the CS group by food restriction, were generally dissimilar to those observed in the CS-treated animals.…”

Section: Discussionmentioning

confidence: 99%

Corticosteroid effects on isotonic contractile properties of rat diaphragm muscle

Balkom

Zhan²,

Prakash³

et al. 1997

Journal of Applied Physiology

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Van Balkom, Roland H. H., Wen-Zhi Zhan, Y. S. Prakash, P. N. Richard Dekhuijzen, and Gary C. Sieck. Corticosteroid effects on isotonic contractile properties of rat diaphragm muscle. J. Appl. Physiol. 83(4): 1062–1067, 1997.—The effects of corticosteroids (CS) on diaphragm muscle (Diam) fiber morphology and contractile properties were evaluated in three groups of rats: controls (Ctl), surgical sham and weight-matched controls (Sham), and CS-treated (6 mg ⋅ kg−1 ⋅ day−1prednisolone at 2.5 ml/h for 3 wk). In the CS-treated Diam, there was a selective atrophy of type IIx and IIb fibers, compared with a generalized atrophy of all fibers in the Sham group. Maximum isometric force was reduced by 20% in the CS group compared with both Ctl and Sham. Maximum shortening velocity in the CS Diamwas slowed by ∼20% compared with Ctl and Sham. Peak power output of the CS Diam was only 60% of Ctl and 70% of Sham. Endurance to repeated isotonic contractions improved in the CS-treated Diam compared with Ctl. We conclude that the atrophy of type IIx and IIb fibers in the Diam can only partially account for the CS-induced changes in isotonic contractile properties. Other factors such as reduced myofibrillar density or altered cross-bridge cycling kinetics are also likely to contribute to the effects of CS treatment.

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“…Critical illness-associated phenomena, such as mechanical ventilation (MV)-induced diaphragm inactivity (15)(16)(17)(18)(19)(20), malnutrition (21), and inflammation (22), are associated with weakness of diaphragm fibers and activation of proteolytic pathways in animal models. Whether these findings translate to humans is unknown, although several studies (23)(24)(25), but not all (26), in braindead organ donors who received MV before organ harvest revealed atrophy and activation of the ubiquitin-proteasome pathway in diaphragm muscle fibers.…”

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confidence: 99%

Diaphragm Muscle Fiber Weakness and Ubiquitin–Proteasome Activation in Critically Ill Patients

Hooijman

Beishuizen²,

Witt³

et al. 2015

Am J Respir Crit Care Med

172

180

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Rationale: The clinical significance of diaphragm weakness in critically ill patients is evident: it prolongs ventilator dependency, and increases morbidity and duration of hospital stay. To date, the nature of diaphragm weakness and its underlying pathophysiologic mechanisms are poorly understood.Objectives: We hypothesized that diaphragm muscle fibers of mechanically ventilated critically ill patients display atrophy and contractile weakness, and that the ubiquitin-proteasome pathway is activated in the diaphragm.Methods: We obtained diaphragm muscle biopsies from 22 critically ill patients who received mechanical ventilation before surgery and compared these with biopsies obtained from patients during thoracic surgery for resection of a suspected early lung malignancy (control subjects). In a proof-of-concept study in a muscle-specific ring finger protein-1 (MuRF-1) knockout mouse model, we evaluated the role of the ubiquitin-proteasome pathway in the development of contractile weakness during mechanical ventilation.Measurements and Main Results: Both slow-and fast-twitch diaphragm muscle fibers of critically ill patients had approximately 25% smaller cross-sectional area, and had contractile force reduced by half or more. Markers of the ubiquitin-proteasome pathway were significantly up-regulated in the diaphragm of critically ill patients. Finally, MuRF-1 knockout mice were protected against the development of diaphragm contractile weakness during mechanical ventilation.Conclusions: These findings show that diaphragm muscle fibers of critically ill patients display atrophy and severe contractile weakness, and in the diaphragm of critically ill patients the ubiquitin-proteasome pathway is activated. This study provides rationale for the development of treatment strategies that target the contractility of diaphragm fibers to facilitate weaning.

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Effect of nutritional deprivation on diaphragm contractility and muscle fiber size

Cited by 120 publications

References 0 publications

Effects of Unilateral Phrenic Nerve Denervation on Diaphragm Contractility in Rat.

Effects of Unilateral Phrenic Nerve Denervation on Diaphragm Contractility in Rat.

Corticosteroid effects on isotonic contractile properties of rat diaphragm muscle

Diaphragm Muscle Fiber Weakness and Ubiquitin–Proteasome Activation in Critically Ill Patients

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