呼吸臨床

【特集】呼吸器科医に役立つ最先端のメカノバイオロジー研究

企画:寺崎泰弘,ゲストエディター:伊藤理


 生体は常に重力,圧力,ずり応力といった機械的刺激(メカニカルストレス)を受けています。これらメカニカルストレスがどのようにして細胞機能や生体の応答を制御するか,疾患の病態生理に関与するかを追究する研究が「メカノバイオロジー」です。呼吸器は多様なメカニカルストレスにさらされていることから,呼吸器の細胞機能・生理機能や呼吸器疾患の病態機序を解明するうえで,呼吸器メカノバイオロジー研究の果たすべき役割は大きいと期待されています。今回の特集では,メカノバイオロジーを紹介し,研究の魅力と課題をお伝えすることを企画しています。

(伊藤理)

2)各論:2.呼吸リハビリテーションと骨格筋機能における
メカノバイオロジー

井上貴行*

*名古屋大学医学部附属病院リハビリテーション部(〒466-8560 愛知県名古屋市昭和区鶴舞町65)


Mechanobiology in relation between respiratory rehabilitation and skeletal muscle function

Takayuki Inoue*
*Department of Rehabilitation, Nagoya University Hospital, Nagoya


Keywords:呼吸リハビリテーション,レジスタンストレーニング,骨格筋,筋萎縮,筋肥大/respiratory rehabilitation,resistance training,skeletal muscle,muscle atrophy,muscle hypertrophy


呼吸臨床 2017年1巻2号 論文No.e00019
Jpn Open J Respir Med 2017 Vol. 1 No. 2 Article No.e00019

DOI: 10.24557/kokyurinsho.1.e00019


掲載日:2017年11月8日


©️Takayuki Inoue. 本論文の複製権,翻訳権,上映権,譲渡権,貸与権,公衆送信権(送信可能化権を含む)は弊社に帰属し,それらの利用ならびに許諾等の管理は弊社が行います。


要旨

 呼吸リハビリテーション(以下,リハビリ)の主たる構成要素は「運動」であり,「運動」によって骨格筋はメカニカルストレスにさらされる。骨格筋はメカニカルストレス増減により筋肥大・萎縮を生じる。メカニカルストレスは細胞内の蛋白質合成・分解のバランスを制御することで筋肥大・萎縮を促進することが明らかになってきた。本稿では,蛋白質合成・分解の制御機構に触れつつ,呼吸リハビリとメカニカルストレス,骨格筋機能の関係について解説する。

文献

  1. 日本呼吸ケア・リハビリテーション学会,ほか編. 呼吸リハビリテーションマニュアル−運動療法第2版. 東京: 照林社, 2012.
  2. Hattori K, et al. Preoperative six-minute walk distance is associated with pneumonia after lung resection. Interact Cardiovasc Thorac Surg. 2017; doi:10.1093/icvts/ivx310. 
  3. Hayashi K, et al. Post-operative delayed ambulation after thymectomy is associated withpre-operative six-minute walk distance. Disabil Rehabil. 2017; doi: 10.1080/09638288.2017.1315182.
  4. Hayashi K, et al. Preoperative 6-minute walk distance accurately predicts postoperative complications after operations for hepato-pancreato-biliary cancer. Surgery. 2017; 161: 525-32. 
  5. Inoue T, et al. Changes in exercise capacity, muscle strength, and health-related quality of life in esophageal cancer patients undergoing esophagectomy. BMC Sports Sci Med Rehabil. 2016; 8: 34. doi: 10.1186/s13102-016-0060-y. 
  6. Mizuno Y, et al. Changes in muscle strength and six-minute walk distance before and after living donor liver transplantation. Transplant Proc. 2016; 48: 3348-55.
  7. Vogiatzis I, et al. The physiological basis of rehabilitation in chronic heart and lung disease. J Appl Physiol. 2013; 115: 16-21.
  8. Gayan-Ramirez G, et al. Mechanisms of striated muscle dysfunction during acute exacerbations of COPD. J Appl Physiol 2013; 114: 1291-9.
  9. Birges RC, et al. Impact of resistance training in chronic obstructive pulmonary disease patients during periods of acute exacerbation. Arch Phys Med Rehabil. 2014; 95: 1638-45.
  10. Troosters T, et al. Resistance training prevents deterioration in quadriceps muscle function during acute exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2010; 181: 1072-7.
  11. Richardson RS, et al. Reduced mechanical efficiency in chronic obstructive pulmonary disease but normal peak VO2 with small muscle mass exercise. Am J Respir Crit Care Med. 2004; 169: 89-96.
  12. Zoncu R, et al. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol. 2011; 12: 21-35.
  13. Ito N, et al. Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy. Nat Med. 2013; 19: 101-6.
  14. Hornberger TA, et al. Mechanical stimuli regulate rapamycin-sensitive signalling by a phosphoinositide 3-kinase-, protein kinase B- and growth factor-independent mechanism. Biochem J. 2004; 380: 795-804.
  15. 井上貴行, ほか. 不動終了後のラットヒラメ筋に対する間歇的伸張運動が関節可動域と筋線維におよぼす影響. 理学療法学. 2007; 34: 1-7.
  16. Bodine SC, et al. Identification of ubiquitin ligases required for skeletal muscle atrophy. Science. 2001; 294: 1704-8.
  17. Lagirand-Cantaloube J, et al. Inhibition of atrogin-1/MAFbx mediated MyoD proteolysis prevents skeletal muscle atrophy in vivo. PLoS One. 2009; 4: e4973.
  18. Csibi A, et al. MAFbx/Atrogin-1 controls the activity of the initiation factor eIF3-f in skeletal muscle atrophy by targeting multiple C-terminal lysines. J Biol Chem. 2009; 284: 4413-21.
  19. Cohen S, et al. During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation. Cell Biol. 2009; 185: 1083-95.
  20. Sartori R, et al. BMP signaling controls muscle mass. Nat Genet. 2013; 45: 1309-18.
  21. Masiero E, et al. Autophagy is required to maintain muscle mass. Cell Metab. 2009; 10: 507-15.
  22. Quy PN, et al. Proteasome-dependent activation of mammalian target of rapamycin complex 1 (mTORC1) is essential for autophagy suppression and muscle remodeling following denervation. J Biol Chem. 2013; 288: 1125-34.
  23. Suzuki N, et al. NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. J Clin Invest. 2007; 117: 2468-76.
  24. Lepper C, et al. An absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration. Development. 2011; 138: 3639-46.
  25. Sambasivan R, et al. Pax7-expressing satellite cells are indispensable for adult skeletal muscle regeneration. Development. 2011; 138: 3647-56.
  26. Keefe AC, et al. Muscle stem cells contribute to myofibres in sedentary adult mice. Nat Commun. 2015; 6: 7087.
  27. Fry CS, et al. Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia. Nat Med. 2014; 21: 1-7.
  28. McCarthy JJ, et al. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle. Development.2011; 138: 3657-66.

文献

  1. 日本呼吸ケア・リハビリテーション学会,ほか編. 呼吸リハビリテーションマニュアル−運動療法第2版. 東京: 照林社, 2012.
  2. Hattori K, et al. Preoperative six-minute walk distance is associated with pneumonia after lung resection. Interact Cardiovasc Thorac Surg. 2017; doi:10.1093/icvts/ivx310. 
  3. Hayashi K, et al. Post-operative delayed ambulation after thymectomy is associated withpre-operative six-minute walk distance. Disabil Rehabil. 2017; doi: 10.1080/09638288.2017.1315182.
  4. Hayashi K, et al. Preoperative 6-minute walk distance accurately predicts postoperative complications after operations for hepato-pancreato-biliary cancer. Surgery. 2017; 161: 525-32. 
  5. Inoue T, et al. Changes in exercise capacity, muscle strength, and health-related quality of life in esophageal cancer patients undergoing esophagectomy. BMC Sports Sci Med Rehabil. 2016; 8: 34. doi: 10.1186/s13102-016-0060-y. 
  6. Mizuno Y, et al. Changes in muscle strength and six-minute walk distance before and after living donor liver transplantation. Transplant Proc. 2016; 48: 3348-55.
  7. Vogiatzis I, et al. The physiological basis of rehabilitation in chronic heart and lung disease. J Appl Physiol. 2013; 115: 16-21.
  8. Gayan-Ramirez G, et al. Mechanisms of striated muscle dysfunction during acute exacerbations of COPD. J Appl Physiol 2013; 114: 1291-9.
  9. Birges RC, et al. Impact of resistance training in chronic obstructive pulmonary disease patients during periods of acute exacerbation. Arch Phys Med Rehabil. 2014; 95: 1638-45.
  10. Troosters T, et al. Resistance training prevents deterioration in quadriceps muscle function during acute exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2010; 181: 1072-7.
  11. Richardson RS, et al. Reduced mechanical efficiency in chronic obstructive pulmonary disease but normal peak VO2 with small muscle mass exercise. Am J Respir Crit Care Med. 2004; 169: 89-96.
  12. Zoncu R, et al. mTOR: from growth signal integration to cancer, diabetes and ageing. Nat Rev Mol Cell Biol. 2011; 12: 21-35.
  13. Ito N, et al. Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy. Nat Med. 2013; 19: 101-6.
  14. Hornberger TA, et al. Mechanical stimuli regulate rapamycin-sensitive signalling by a phosphoinositide 3-kinase-, protein kinase B- and growth factor-independent mechanism. Biochem J. 2004; 380: 795-804.
  15. 井上貴行, ほか. 不動終了後のラットヒラメ筋に対する間歇的伸張運動が関節可動域と筋線維におよぼす影響. 理学療法学. 2007; 34: 1-7.
  16. Bodine SC, et al. Identification of ubiquitin ligases required for skeletal muscle atrophy. Science. 2001; 294: 1704-8.
  17. Lagirand-Cantaloube J, et al. Inhibition of atrogin-1/MAFbx mediated MyoD proteolysis prevents skeletal muscle atrophy in vivo. PLoS One. 2009; 4: e4973.
  18. Csibi A, et al. MAFbx/Atrogin-1 controls the activity of the initiation factor eIF3-f in skeletal muscle atrophy by targeting multiple C-terminal lysines. J Biol Chem. 2009; 284: 4413-21.
  19. Cohen S, et al. During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation. Cell Biol. 2009; 185: 1083-95.
  20. Sartori R, et al. BMP signaling controls muscle mass. Nat Genet. 2013; 45: 1309-18.
  21. Masiero E, et al. Autophagy is required to maintain muscle mass. Cell Metab. 2009; 10: 507-15.
  22. Quy PN, et al. Proteasome-dependent activation of mammalian target of rapamycin complex 1 (mTORC1) is essential for autophagy suppression and muscle remodeling following denervation. J Biol Chem. 2013; 288: 1125-34.
  23. Suzuki N, et al. NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. J Clin Invest. 2007; 117: 2468-76.
  24. Lepper C, et al. An absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration. Development. 2011; 138: 3639-46.
  25. Sambasivan R, et al. Pax7-expressing satellite cells are indispensable for adult skeletal muscle regeneration. Development. 2011; 138: 3647-56.
  26. Keefe AC, et al. Muscle stem cells contribute to myofibres in sedentary adult mice. Nat Commun. 2015; 6: 7087.
  27. Fry CS, et al. Inducible depletion of satellite cells in adult, sedentary mice impairs muscle regenerative capacity without affecting sarcopenia. Nat Med. 2014; 21: 1-7.
  28. McCarthy JJ, et al. Effective fiber hypertrophy in satellite cell-depleted skeletal muscle. Development.2011; 138: 3657-66.