Skeletal muscle adaptations following eccentric contractions are not mediated by keratin 18

被引:0
作者
Ganjayi, Muni Swamy [1 ,2 ]
Frank, Samuel W. [3 ]
Krauss, Thomas A. [1 ]
York, Michael L. [4 ]
Bloch, Robert J. [5 ]
Baumann, Cory W. [1 ,2 ]
机构
[1] Ohio Univ, Heritage Coll Osteopath Med, Dept Biomed Sci, Athens, OH 45701 USA
[2] Ohio Univ, Ohio Musculoskeletal & Neurol Inst, Athens, OH 45701 USA
[3] Univ Toledo, Coll Hlth & Human Serv, Dept Exercise & Rehabil Sci, Toledo, OH USA
[4] Ohio Univ, Sch Appl Hlth Sci & Wellness, Div Exercise Physiol, Athens, OH USA
[5] Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD USA
关键词
damage; exercise; injury; intermediate filaments; strength; RESISTANCE EXERCISE; ELBOW FLEXORS; STRENGTH; MICE; RESPONSES; ADULTS; DYSTROPHIN; FILAMENTS; MYOPATHY; DAMAGE;
D O I
10.1152/japplphysiol.00496.2024
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The molecular mechanisms that drive muscle adaptations after eccentric exercise training are multifaceted and likely impacted by age. Previous studies have reported that many genes and proteins respond differently in young and older muscles following training. Keratin 18 (Krt18), a cytoskeletal protein involved in force transduction and organization, was found to be upregulated after muscles performed repeated bouts of eccentric contractions, with higher levels observed in young muscle compared with older muscle. Therefore, the purpose of this study was to determine if Krt18 mediates skeletal muscle adaptations following eccentric exercise training. The anterior crural muscles of Krt18 knockout (KO) and wild-type (WT) mice were subjected to either a single bout or repeated bouts of eccentric contractions, with isometric torque assessed across the initial and final bouts. Functionally, Krt18 KO and WT mice did not differ prior to performing any eccentric contractions (P >= 0.100). Muscle strength (tetanic isometric torques) and the ability to adapt to eccentric exercise training were also consistent across strains at all time points (P >= 0.169). Stated differently, immediate strength deficits and the recovery of strength following a single bout or multiple bouts of eccentric contractions were similar between Krt18 KO and WT mice. In summary, the absence of Krt18 does not impede the muscle's ability to adapt to repeated eccentric contractions, suggesting it is not essential for exercise-induced remodeling. NEW & NOTEWORTHY The molecular processes that underlie the changes in skeletal muscle following eccentric exercise training are complex and involve multiple factors. Our findings indicate that Krt18 may not play a significant role in muscle adaptations following eccentric exercise training, likely due to its low expression in skeletal muscle. These results underscore the complexity of the molecular mechanisms that contribute to muscle plasticity and highlight the need for further research in this area.
引用
收藏
页码:903 / 909
页数:7
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共 30 条
  • [21] Oxidant-induced atrogin-1 and transforming growth factor-β1 precede alcohol-related myopathy in rats
    Otis, Jeffrey S.
    Brown, Lou Ann S.
    Guidot, David M.
    [J]. MUSCLE & NERVE, 2007, 36 (06) : 842 - 848
  • [22] Resistance exercise for muscular strength in older adults: A meta-analysis
    Peterson, Mark D.
    Rhea, Matthew R.
    Sen, Ananda
    Gordon, Paul M.
    [J]. AGEING RESEARCH REVIEWS, 2010, 9 (03) : 226 - 237
  • [23] Age-dependent Muscle Adaptation after Chronic Stretch-shortening Contractions in Rats
    Rader, Erik P.
    Layner, Kayla N.
    Triscuit, Alyssa M.
    Chetlin, Robert D.
    Ensey, James
    Baker, Brent A.
    [J]. AGING AND DISEASE, 2016, 7 (01):
  • [24] The effects of eccentric versus concentric resistance training on muscle strength and mass in healthy adults: a systematic review with meta-analysis
    Roig, M.
    O'Brien, K.
    Kirk, G.
    Murray, R.
    McKinnon, P.
    Shadgan, B.
    Reid, W. D.
    [J]. BRITISH JOURNAL OF SPORTS MEDICINE, 2009, 43 (08) : 556 - 568
  • [25] Single muscle fiber adaptations to resistance training in old (>80 yr) men:: evidence for limited skeletal muscle plasticity
    Slivka, Dustin
    Raue, Ulrika
    Hollon, Chris
    Minchev, Kiril
    Trappe, Scott
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2008, 295 (01) : R273 - R280
  • [26] Responsiveness of muscle size and strength to physical training in very elderly people: A systematic review
    Stewart, V. H.
    Saunders, D. H.
    Greig, C. A.
    [J]. SCANDINAVIAN JOURNAL OF MEDICINE & SCIENCE IN SPORTS, 2014, 24 (01) : e1 - e10
  • [27] Specific interaction of the actin-binding domain of dystrophin with intermediate filaments containing keratin 19
    Stone, MR
    O'Neill, A
    Catino, D
    Bloch, RJ
    [J]. MOLECULAR BIOLOGY OF THE CELL, 2005, 16 (09) : 4280 - 4293
  • [28] Absence of keratin 19 in mice causes skeletal myopathy with mitochondrial and sarcolemmal reorganization
    StoneO, Michele R.
    O'Neill, Andrea
    Lovering, Richard M.
    Strong, John
    Resneck, Wendy G.
    Reed, Patrick W.
    Toivola, Diana M.
    Ursitti, Jeanine A.
    Omary, M. Bishr
    Bloch, Robert J.
    [J]. JOURNAL OF CELL SCIENCE, 2007, 120 (22) : 3999 - 4008
  • [29] Cloning and characterization of cytokeratins 8 and 19 in adult rat striated muscle - Interaction with the dystrophin glycoprotein complex
    Ursitti, JA
    Lee, PC
    Resneck, WG
    McNally, MM
    Bowman, AL
    O'Neill, A
    Stone, MR
    Bloch, RJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (40) : 41830 - 41838
  • [30] Desmin interacts with STIM1 and coordinates Ca2+ signaling in skeletal muscle
    Zhang, Hengtao
    Bryson, Victoria Graham
    Wang, Chaojian
    Li, TianYu
    Kerr, Jaclyn P.
    Wilson, Rebecca
    Muoio, Deborah M.
    Bloch, Robert J.
    Ward, Christopher
    Rosenberg, Paul B.
    [J]. JCI INSIGHT, 2021, 6 (17)