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Article ; Online: Increased tetanic calcium in early fatigue of mammalian muscle fibers is accompanied by accelerated force development despite a decreased force.

Leijding, Cecilia / Viken, Ida / Bruton, Joseph D / Andersson, Daniel C / Cheng, Arthur J / Westerblad, Håkan

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 6, Page(s) e22978

Abstract: During the initial phase of fatigue induced by repeated contractions in fast-twitch muscle fibers, tetanic force decreases despite increasing tetanic free cytosolic [ ... ...

Abstract	During the initial phase of fatigue induced by repeated contractions in fast-twitch muscle fibers, tetanic force decreases despite increasing tetanic free cytosolic [Ca
MeSH term(s)	Humans ; Mice ; Rats ; Animals ; Muscle Fatigue/physiology ; Muscle Contraction/physiology ; Calcium/metabolism ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Creatine Kinase ; Mammals/metabolism
Chemical Substances	Calcium (SY7Q814VUP) ; Creatine Kinase (EC 2.7.3.2)
Language	English
Publishing date	2023-05-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202300401R
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Article ; Online: Sphingomyelinase activity promotes atrophy and attenuates force in human muscle fibres and is elevated in heart failure patients.

Olsson, Karl / Cheng, Arthur J / Al-Ameri, Mamdoh / Tardif, Nicolas / Melin, Michael / Rooyackers, Olav / Lanner, Johanna T / Westerblad, Håkan / Gustafsson, Thomas / Bruton, Joseph D / Rullman, Eric

Journal of cachexia, sarcopenia and muscle

2022 Volume 13, Issue 5, Page(s) 2551–2561

Abstract: Background: Activation of sphingomyelinase (SMase) as a result of a general inflammatory response has been implicated as a mechanism underlying disease-related loss of skeletal muscle mass and function in several clinical conditions including heart ... ...

Abstract	Background: Activation of sphingomyelinase (SMase) as a result of a general inflammatory response has been implicated as a mechanism underlying disease-related loss of skeletal muscle mass and function in several clinical conditions including heart failure. Here, for the first time, we characterize the effects of SMase activity on human muscle fibre contractile function and assess skeletal muscle SMase activity in heart failure patients. Methods: The effects of SMase on force production and intracellular Ca Results: Sphingomyelinase reduced muscle fibre force production (-30%, P < 0.05) by impairing sarcoplasmic reticulum (SR) Ca Conclusions: The present findings implicate activation of skeletal muscle SMase as a mechanism underlying human heart failure-related loss of muscle mass and function. Moreover, our findings strengthen the idea that SMase activation may underpin disease-related loss of muscle mass and function in other clinical conditions, acting as a common patophysiological mechanism for the myopathy often reported in diseases associated with a systemic inflammatory response.
MeSH term(s)	Aged ; Animals ; Atrophy/metabolism ; Heart Failure/metabolism ; Humans ; Mice ; Muscle Fibers, Skeletal/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Ribosomal Proteins/metabolism ; Ribosomal Proteins/pharmacology ; Sphingomyelin Phosphodiesterase/genetics ; Sphingomyelin Phosphodiesterase/metabolism ; Sphingomyelin Phosphodiesterase/pharmacology
Chemical Substances	Ribosomal Proteins ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2022-07-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.13029
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Article ; Online: Enzymatically dissociated muscle fibers display rapid dedifferentiation and impaired mitochondrial calcium control.

Gineste, Charlotte / Youhanna, Sonia / Vorrink, Sabine U / Henriksson, Sara / Hernández, Andrés / Cheng, Arthur J / Chaillou, Thomas / Buttgereit, Andreas / Schneidereit, Dominik / Friedrich, Oliver / Hultenby, Kjell / Bruton, Joseph D / Ivarsson, Niklas / Sandblad, Linda / Lauschke, Volker M / Westerblad, Håkan

iScience

2022 Volume 25, Issue 12, Page(s) 105654

Abstract: Cells rapidly lose their physiological phenotype upon disruption of their extracellular matrix (ECM)-intracellular cytoskeleton interactions. By comparing adult mouse skeletal muscle fibers, isolated either by mechanical dissection or by collagenase- ... ...

Abstract	Cells rapidly lose their physiological phenotype upon disruption of their extracellular matrix (ECM)-intracellular cytoskeleton interactions. By comparing adult mouse skeletal muscle fibers, isolated either by mechanical dissection or by collagenase-induced ECM digestion, we investigated acute effects of ECM disruption on cellular and mitochondrial morphology, transcriptomic signatures, and Ca
Language	English
Publishing date	2022-11-22
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.105654
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Article ; Online: Antioxidant treatments do not improve force recovery after fatiguing stimulation of mouse skeletal muscle fibres.

Cheng, Arthur J / Bruton, Joseph D / Lanner, Johanna T / Westerblad, Håkan

The Journal of physiology

2015 Volume 593, Issue 2, Page(s) 457–472

Abstract: The contractile performance of skeletal muscle declines during intense activities, i.e. fatigue develops. Fatigued muscle can enter a state of prolonged low-frequency force depression (PLFFD). PLFFD can be due to decreased tetanic free cytosolic [Ca(2+) ] ...

Abstract	The contractile performance of skeletal muscle declines during intense activities, i.e. fatigue develops. Fatigued muscle can enter a state of prolonged low-frequency force depression (PLFFD). PLFFD can be due to decreased tetanic free cytosolic [Ca(2+) ] ([Ca(2+) ]i ) and/or decreased myofibrillar Ca(2+) sensitivity. Increases in reactive oxygen and nitrogen species (ROS/RNS) may contribute to fatigue-induced force reductions. We studied whether pharmacological ROS/RNS inhibition delays fatigue and/or counteracts the development of PLFFD. Mechanically isolated mouse fast-twitch fibres were fatigued by sixty 150 ms, 70 Hz tetani given every 1 s. Experiments were performed in standard Tyrode solution (control) or in the presence of: NADPH oxidase (NOX) 2 inhibitor (gp91ds-tat); NOX4 inhibitor (GKT137831); mitochondria-targeted antioxidant (SS-31); nitric oxide synthase (NOS) inhibitor (l-NAME); the general antioxidant N-acetylcysteine (NAC); a cocktail of SS-31, l-NAME and NAC. Spatially and temporally averaged [Ca(2+) ]i and peak force were reduced by ∼20% and ∼70% at the end of fatiguing stimulation, respectively, with no marked differences between groups. PLFFD was similar in all groups, with 30 Hz force being decreased by ∼60% at 30 min of recovery. PLFFD was mostly due to decreased tetanic [Ca(2+) ]i in control fibres and in the presence of NOX2 or NOX4 inhibitors. Conversely, in fibres exposed to SS-31 or the anti ROS/RNS cocktail, tetanic [Ca(2+) ]i was not decreased during recovery so PLFFD was only caused by decreased myofibrillar Ca(2+) sensitivity. The cocktail also increased resting [Ca(2+) ]i and ultimately caused cell death. In conclusion, ROS/RNS-neutralizing compounds did not counteract the force decline during or after induction of fatigue.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Calcium/metabolism ; Female ; Mice ; Mice, Inbred C57BL ; Muscle Fatigue ; Muscle Fibers, Skeletal/drug effects ; Muscle Fibers, Skeletal/metabolism ; Muscle Fibers, Skeletal/physiology ; NADPH Oxidases/antagonists & inhibitors ; Nitric Oxide Synthase/antagonists & inhibitors ; Reactive Oxygen Species/metabolism ; Recovery of Function
Chemical Substances	Antioxidants ; Reactive Oxygen Species ; Nitric Oxide Synthase (EC 1.14.13.39) ; NADPH Oxidases (EC 1.6.3.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2015-01-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2014.279398
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Article ; Online: SR Ca

Ivarsson, Niklas / Mattsson, C Mikael / Cheng, Arthur J / Bruton, Joseph D / Ekblom, Björn / Lanner, Johanna T / Westerblad, Håkan

The Journal of general physiology

2019 Volume 151, Issue 4, Page(s) 567–577

Abstract: Effective practices to improve skeletal muscle fatigue resistance are crucial for athletes as well as patients with dysfunctional muscles. To this end, it is important to identify the cellular signaling pathway that triggers mitochondrial biogenesis and ... ...

Abstract	Effective practices to improve skeletal muscle fatigue resistance are crucial for athletes as well as patients with dysfunctional muscles. To this end, it is important to identify the cellular signaling pathway that triggers mitochondrial biogenesis and thereby increases oxidative capacity and fatigue resistance in skeletal muscle fibers. Here, we test the hypothesis that the stress induced in skeletal muscle fibers by endurance exercise causes a reduction in the association of FK506-binding protein 12 (FKBP12) with ryanodine receptor 1 (RYR1). This will result in a mild Ca
MeSH term(s)	Animals ; Anti-Bacterial Agents/pharmacology ; Calcium/metabolism ; Male ; Mice ; Motor Activity ; Muscle Fatigue/physiology ; Muscle, Skeletal ; Protein Stability ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/physiology ; Signal Transduction ; Sirolimus/pharmacology ; Tacrolimus Binding Protein 1A/pharmacology
Chemical Substances	Anti-Bacterial Agents ; Ryanodine Receptor Calcium Release Channel ; ryanodine receptor 1, mouse ; Tacrolimus Binding Protein 1A (EC 5.2.1.-) ; Calcium (SY7Q814VUP) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2019-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3118-5
ISSN	1540-7748 ; 0022-1295
ISSN (online)	1540-7748
ISSN	0022-1295
DOI	10.1085/jgp.201812152
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Article: Methods to detect Ca(2+) in living cells.

Bruton, Joseph D / Cheng, Arthur J / Westerblad, Håkan

Advances in experimental medicine and biology

2012 Volume 740, Page(s) 27–43

Abstract: Measurements of free cytosolic Ca(2+) concentration ([Ca(2+)](i)) or free Ca(2+) concentration in cellular organelles have become more routine. The primary reason for this is the availability of membrane permeant forms of Ca(2+) indicators that can ... ...

Abstract	Measurements of free cytosolic Ca(2+) concentration ([Ca(2+)](i)) or free Ca(2+) concentration in cellular organelles have become more routine. The primary reason for this is the availability of membrane permeant forms of Ca(2+) indicators that can easily enter cells. In this chapter, the properties required of an ideal Ca(2+) indicator are identified and the advantages and disadvantages of available Ca(2+) indicators are pointed out. The pitfalls associated with usage of Ca(2+) indicators together with the clear advantages of ratiometric over non-ratiometric indicators are discussed. The excitation of Ca(2+) indicators and detection of the emitted fluorescence light require dedicated equipment; epifluorescence or confocal microscopes are most frequently used for this purpose and the advantages and disadvantages of these are discussed. Calibration experiments are required to translate changes in the fluorescence of Ca(2+) indicators into real [Ca(2+)](i) changes, but this procedure is non-trivial and potential sources of error are identified. Future developments in the field of Ca(2+) detection are discussed.
MeSH term(s)	Animals ; Calcium/analysis ; Calcium/metabolism ; Calibration ; Cell Survival ; Cytosol/metabolism ; Fluorescence ; Humans ; Microscopy, Confocal
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2012
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-94-007-2888-2_2
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Article ; Online: Antioxidant treatments do not improve force recovery after fatiguing stimulation of mouse skeletal muscle fibres.

Cheng, Arthur J / Bruton, Joseph D / Lanner, Johanna T / Westerblad, Håkan

The Journal of physiology

2014

Abstract	The contractile performance of skeletal muscle declines during intense activities, i.e. fatigue develops. Fatigued muscle can enter a state of prolonged low-frequency force depression (PLFFD). PLFFD can be due to decreased tetanic free cytosolic [Ca
Language	English
Publishing date	2014-11-14
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2014.279398
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Article ; Online: Skeletal muscle: energy metabolism, fiber types, fatigue and adaptability.

Westerblad, Håkan / Bruton, Joseph D / Katz, Abram

Experimental cell research

2010 Volume 316, Issue 18, Page(s) 3093–3099

Abstract: Skeletal muscles cope with a large range of activities, from being able to support the body weight during long periods of upright standing to perform explosive movements in response to an unexpected threat. This requires systems for energy metabolism ... ...

Abstract	Skeletal muscles cope with a large range of activities, from being able to support the body weight during long periods of upright standing to perform explosive movements in response to an unexpected threat. This requires systems for energy metabolism that can provide energy during long periods of moderately increased energy consumption as well as being able to rapidly increasing the rate of energy production more than 100-fold in response to explosive contractions. In this short review we discuss how muscles can deal with these divergent demands. We first outline the major energy metabolism pathways in skeletal muscle. Next we describe metabolic differences between different muscle fiber types. Contractile performance declines during intense activation, i.e. fatigue develops, and we discuss likely underlying mechanisms. Finally, we discuss the ability of muscle fibers to adapt to altered demands, and mechanisms behind these adaptations. The accumulated experimental evidence forces us to conclude that most aspects of energy metabolism involve multiple and overlapping signaling pathways, which indicates that the control of energy metabolism is too important to depend on one single molecule or mechanism.
MeSH term(s)	Adaptation, Physiological ; Animals ; Energy Metabolism ; Humans ; Muscle Fatigue/physiology ; Muscle Fibers, Skeletal/physiology ; Muscle, Skeletal/physiology
Language	English
Publishing date	2010-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2010.05.019
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Article ; Online: Mechanisms of fatigue induced by isometric contractions in exercising humans and in mouse isolated single muscle fibres.

Place, Nicolas / Bruton, Joseph D / Westerblad, Håkan

Clinical and experimental pharmacology & physiology

2009 Volume 36, Issue 3, Page(s) 334–339

Abstract: 1. Muscle fatigue (i.e. the decrease in muscle performance during exercise) has been studied extensively using a variety of experimental paradigms, from mouse to human, from single cell to whole-body exercise. Given the disparity of models used to ... ...

Abstract	1. Muscle fatigue (i.e. the decrease in muscle performance during exercise) has been studied extensively using a variety of experimental paradigms, from mouse to human, from single cell to whole-body exercise. Given the disparity of models used to characterize muscle fatigue, it can be difficult to establish whether the results of basic in vitro studies are applicable to exercise in humans. 2. In the present brief review, our attempt is to relate neuromuscular alterations caused by repeated or sustained isometric contraction in humans to changes in excitation-contraction (E-C) coupling observed in intact single muscle fibres, where force and the free myoplasmic [Ca(2+)] can be measured. 3. Accumulated data indicate that impairment of E-C coupling, most likely located within muscle fibres, accounts for the fatigue-induced decrease in maximal force in humans, whereas central (neural) fatigue is of greater importance for the inability to continue a sustained low-intensity contraction. Based on data from intact single muscle fibres, the fatigue-induced impairment in E-C coupling involves: (i) a reduced number of active cross-bridges owing to a decreased release of Ca(2+); (ii) a decreased sensitivity of the myofilaments to Ca(2+); and/or (iii) a reduced force produced by each active cross-bridge. 4. In conclusion, data from single muscle fibre studies can be used to increase our understanding of fatigue mechanisms in some, but not all, types of human exercise. To further increase the understanding of fatigue mechanisms in humans, we propose future studies using in vitro stimulation patterns that are closer to the in vivo situation.
MeSH term(s)	Actin Cytoskeleton/physiology ; Animals ; Calcium Signaling ; Central Nervous System/physiology ; Exercise ; Humans ; Isometric Contraction ; Mice ; Muscle Fatigue ; Muscle Fibers, Skeletal/physiology ; Muscle, Skeletal/innervation ; Muscle, Skeletal/physiology ; Recovery of Function
Language	English
Publishing date	2009-03
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	189277-0
ISSN	1440-1681 ; 0305-1870 ; 0143-9294
ISSN (online)	1440-1681
ISSN	0305-1870 ; 0143-9294
DOI	10.1111/j.1440-1681.2008.05021.x
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Article ; Online: Impaired sarcoplasmic reticulum Ca

Olsson, Karl / Cheng, Arthur J / Al-Ameri, Mamdoh / Wyckelsma, Victoria L / Rullman, Eric / Westerblad, Håkan / Lanner, Johanna T / Gustafsson, Thomas / Bruton, Joseph D

The Journal of physiology

2019 Volume 598, Issue 4, Page(s) 773–787

Abstract: Key points: Changes in intramuscular Ca: Abstract: Changes in intracellular ... ...

Abstract	Key points: Changes in intramuscular Ca Abstract: Changes in intracellular Ca
MeSH term(s)	Calcium/physiology ; Calcium Signaling ; Humans ; In Vitro Techniques ; Intercostal Muscles/physiopathology ; Muscle Contraction ; Muscle Fatigue ; Muscle Fibers, Skeletal/pathology ; Sarcoplasmic Reticulum/pathology
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2019-12-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP279090
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