Absence of myofibrillar creatine kinase and diaphragm isometric function during repetitive activation

1998 ◽  
Vol 84 (4) ◽  
pp. 1166-1173 ◽  
Author(s):  
John J. Labella ◽  
Monica J. Daood ◽  
A. P. Koretsky ◽  
Brian B. Roman ◽  
Gary C. Sieck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Function ◽  
Isometric Force ◽  
Force Generation ◽  
Fatigue Properties ◽  
Specific Force ◽  
Null Mutant ◽  
Isometric Muscle

Creatine kinase (CK) provides ATP buffering in skeletal muscle and is expressed as 1) cytosolic myofibrillar CK (M-CK) and 2) sarcomeric mitochondrial CK (ScCKmit) isoforms that differ in their subcellular localization. We compared the isometric contractile and fatigue properties of 1) control CK-sufficient (Ctl), 2) M-CK-deficient (M-CK[−/−]), and 3) combined M-CK/ScCKmit-deficient null mutant (CK[−/−]) diaphragm (Dia) to determine the effect of the absence of M-CK activity on Dia performance in vitro. Baseline contractile properties were comparable across groups except for specific force, which was ∼16% lower in CK[−/−] Dia compared with M-CK[−/−] and Ctl Dia. During repetitive activation (40 Hz, [Formula: see text] duty cycle), force declined in all three groups. This decline was significantly greater in CK[−/−] Dia compared with Ctl and M-CK[−/−] Dia. The pattern of force decline did not differ between M-CK[−/−] and Ctl Dia. We conclude that Dia isometric muscle function is not absolutely dependent on the presence of M-CK, whereas the complete absence of CK acutely impairs isometric force generation during repetitive activation.

scholarly journals Taurine supplementation increases skeletal muscle force production and protects muscle function during and after high-frequency in vitro stimulation

2009 ◽  
Vol 107 (1) ◽  
pp. 144-154 ◽  
Author(s):  
Craig A. Goodman ◽  
Deanna Horvath ◽  
Christos Stathis ◽  
Trevor Mori ◽  
Kevin Croft ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
High Frequency ◽  
Muscle Function ◽  
Muscle Force ◽  
High Frequency Stimulation ◽  
Specific Force ◽  
Tetanic Force ◽  
Control Muscle ◽  
Frequency Stimulation

Recent studies report that depletion and repletion of muscle taurine (Tau) to endogenous levels affects skeletal muscle contractility in vitro. In this study, muscle Tau content was raised above endogenous levels by supplementing male Sprague-Dawley rats with 2.5% (wt/vol) Tau in drinking water for 2 wk, after which extensor digitorum longus (EDL) muscles were examined for in vitro contractile properties, fatigue resistance, and recovery from fatigue after two different high-frequency stimulation bouts. Tau supplementation increased muscle Tau content by ∼40% and isometric twitch force by 19%, shifted the force-frequency relationship upward and to the left, increased specific force by 4.2%, and increased muscle calsequestrin protein content by 49%. Force at the end of a 10-s (100 Hz) continuous tetanic stimulation was 6% greater than controls, while force at the end of the 3-min intermittent high-frequency stimulation bout was significantly higher than controls, with a 12% greater area under the force curve. For 1 h after the 10-s continuous stimulation, tetanic force in Tau-supplemented muscles remained relatively stable while control muscle force gradually deteriorated. After the 3-min intermittent bout, tetanic force continued to slowly recover over the next 1 h, while control muscle force again began to decline. Tau supplementation attenuated F2-isoprostane production (a sensitive indicator of reactive oxygen species-induced lipid peroxidation) during the 3-min intermittent stimulation bout. Finally, Tau transporter protein expression was not altered by the Tau supplementation. Our results demonstrate that raising Tau content above endogenous levels increases twitch and subtetanic and specific force in rat fast-twitch skeletal muscle. Also, we demonstrate that raising Tau protects muscle function during high-frequency in vitro stimulation and the ensuing recovery period and helps reduce oxidative stress during prolonged stimulation.

Injury to skeletal muscle fibers of mice following lengthening contractions

1985 ◽  
Vol 59 (1) ◽  
pp. 119-126 ◽  
Author(s):  
K. K. McCully ◽  
J. A. Faulkner
Keyword(s):  
Skeletal Muscle ◽  
Isometric Force ◽  
Muscle Fibers ◽  
Lengthening Contractions ◽  
Control Value ◽  
Skeletal Muscle Fibers ◽  
Maximum Isometric Force ◽  
Distal Tendon ◽  
Shortening Contractions

We tested the hypothesis that lengthening contractions result in greater injury to skeletal muscle fibers than isometric or shortening contractions. Mice were anesthetized with pentobarbital sodium and secured to a platform maintained at 37 degrees C. The distal tendon of the extensor digitorum longus muscle was attached to a servomotor. A protocol consisting of isometric, shortening, or lengthening contractions was performed. After the contraction protocol the distal tendon was reattached, incisions were closed, and the mice were allowed to recover. The muscles were removed after 1–30 days, and maximum isometric force (Po) was measured in vitro at 37 degrees C. Three days after isometric and shortening contractions and sham operations, histological appearance was not different from control and Po was 80% of the control value. Three days after lengthening contractions, histological sections showed that 37 +/- 4% of muscle fibers degenerated and Po was 22 +/- 3% of the control value. Muscle regeneration, first seen at 4 days, was nearly complete by 30 days, when Po was 84 +/- 3% of the control value. We conclude that, with the protocol used, lengthening, but not isometric or shortening contractions, caused significant injury to muscle fibers.

Contractile force of canine airway smooth muscle during cyclical length changes

1983 ◽  
Vol 55 (3) ◽  
pp. 759-769 ◽  
Author(s):  
S. J. Gunst
Keyword(s):  
Muscle Force ◽  
Isometric Force ◽  
Smooth Muscles ◽  
Rate Of Change ◽  
Dynamic Force ◽  
Airway Caliber ◽  
Length Changes ◽  
Isometric Muscle ◽  
Isometric Muscle Force

Strips of tonically contracted canine tracheal and bronchial airway smooth muscles (AWSM) were studied in vitro to compare dynamic muscle force during stretch-retraction cycles with static isometric muscle force at various length points within the cycling range. At any particular rate, a characteristic force-length loop was obtained by cycling over a given range of lengths. Dynamic muscle force dropped well below static isometric muscle force at lengths short of the peak length at all rates of cycling. When stretch or retraction of the muscle was stopped at any point along either path of the cycle, muscle force rose to approach the isometric force at that length. Dynamic force at the peak length of the cycle remained close to, or slightly greater than, the static isometric force. The results suggest that the velocity of shortening of tonically contracted AWSM is very slow relative to the rates of cycling employed. A slow rate of shortening of AWSM relative to the rate of change in airway caliber during breathing could account for well-known effects of volume history on airway tone.

Potentiation of acetylcholine-induced skeletal muscle contractions in vitro by prostaglandin F2α in the lizard, Crotaphytus collaris

1984 ◽  
Vol 62 (11) ◽  
pp. 2188-2191 ◽  
Author(s):  
Louis J. Guillette Jr. ◽  
David A. Dickey
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Striated Muscle ◽  
Prostaglandin F2α ◽  
Sexually Active ◽  
Crotaphytus Collaris ◽  
Male And Female ◽  
Percent Increase ◽  
Prostaglandin F

Acetylcholine-induced in vitro contractions of the puboischiotibialis muscle was potentiated by pretreatment with prostaglandin F2α (1.5 ng/mL). This phenomenon was exhibited by both sexually active male and female Crotaphytus collaris collaris and the degree of response was similar in both sexes. However, females exhibited a greater mean (±SE) percent increase as well as more variation than males (males, 54.6 ± 10.9%; females, 114.7 ± 61.4%). These data suggest that prostaglandin F2α plays a role in the control of striated muscle function in lizards. Moreover, prostaglandin potentiation of muscle contraction may be important during the reptilian reproductive cycle, particularly at the time of oviposition.

scholarly journals Influenza Infection has Fiber Type-Specific Effects on Cellular and Molecular Skeletal Muscle Function in Aged Mice

2020 ◽  
Vol 75 (12) ◽  
pp. 2333-2341
Author(s):  
Chad R Straight ◽  
Olivia R Ringham ◽  
Jenna M Bartley ◽  
Spencer R Keilich ◽  
George A Kuchel ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Contractile Function ◽  
Isometric Force ◽  
Fiber Type ◽  
Influenza Infection ◽  
Fiber Types ◽  
Specific Force ◽  
Mhc Iia ◽  
Mhc Iib ◽  
Maximal Isometric Force

Abstract Skeletal muscle myopathies represent a common non-pulmonary manifestation of influenza infection, leading to reduced physical function and hospitalization in older adults. However, underlying mechanisms remain poorly understood. Our study examined the effects of influenza virus A pulmonary infection on contractile function at the cellular (single fiber) and molecular (myosin-actin interactions and myofilament properties) levels in soleus and extensor digitorum longus muscles of aged (20 months) C57BL/6 male mice that were healthy or flu-infected for 7 (7-days post-infection; 7-DPI) or 12 days (12-DPI). Cross-sectional area (CSA) of myosin heavy chain (MHC) IIA and IIB fibers was reduced at 12-DPI relative to 7-DPI and healthy. Maximal isometric force in MHC IIA fibers was also reduced at 12-DPI relative to 7-DPI and healthy, resulting in no change in specific force (maximal isometric force divided by CSA). In contrast, MHC IIB fibers produced greater isometric force and specific force at 7-DPI compared to 12-DPI or healthy. The increased specific force in MHC IIB fibers was likely due to greater myofilament lattice stiffness and/or an increased number or stiffness of strongly bound myosin-actin cross-bridges. At the molecular level, cross-bridge kinetics were slower in MHC IIA fibers with infection, while changes in MHC IIB fibers were largely absent. In both fiber types, greater myofilament lattice stiffness was positively related to specific force. This study provides novel evidence that cellular and molecular contractile function is impacted by influenza infection in a fiber type-specific manner, suggesting potential molecular mechanisms to help explain the impact of flu-induced myopathies.

scholarly journals Role of TRPC1 channel in skeletal muscle function

2010 ◽  
Vol 298 (1) ◽  
pp. C149-C162 ◽  
Author(s):  
Nadège Zanou ◽  
Georges Shapovalov ◽  
Magali Louis ◽  
Nicolas Tajeddine ◽  
Chiara Gallo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Function ◽  
Transient Receptor Potential ◽  
Force Production ◽  
Receptor Potential ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Skeletal Muscle Function ◽  
Cross Sectional

Skeletal muscle contraction is reputed not to depend on extracellular Ca2+. Indeed, stricto sensu , excitation-contraction coupling does not necessitate entry of Ca2+. However, we previously observed that, during sustained activity (repeated contractions), entry of Ca2+is needed to maintain force production. In the present study, we evaluated the possible involvement of the canonical transient receptor potential (TRPC)1 ion channel in this entry of Ca2+and investigated its possible role in muscle function. Patch-clamp experiments reveal the presence of a small-conductance channel (13 pS) that is completely lost in adult fibers from TRPC1−/−mice. The influx of Ca2+through TRPC1 channels represents a minor part of the entry of Ca2+into muscle fibers at rest, and the activity of the channel is not store dependent. The lack of TRPC1 does not affect intracellular Ca2+concentration ([Ca2+]i) transients reached during a single isometric contraction. However, the involvement of TRPC1-related Ca2+entry is clearly emphasized in muscle fatigue. Indeed, muscles from TRPC1−/−mice stimulated repeatedly progressively display lower [Ca2+]itransients than those observed in TRPC1+/+fibers, and they also present an accentuated progressive loss of force. Interestingly, muscles from TRPC1−/−mice display a smaller fiber cross-sectional area, generate less force per cross-sectional area, and contain less myofibrillar proteins than their controls. They do not present other signs of myopathy. In agreement with in vitro experiments, TRPC1−/−mice present an important decrease of endurance of physical activity. We conclude that TRPC1 ion channels modulate the entry of Ca2+during repeated contractions and help muscles to maintain their force during sustained repeated contractions.

scholarly journals Causes of fatigue in slow-twitch rat skeletal muscle during dynamic activity

2009 ◽  
Vol 297 (3) ◽  
pp. R900-R910 ◽  
Author(s):  
Morten Munkvik ◽  
Per Kristian Lunde ◽  
Ole M. Sejersted
Keyword(s):  
Skeletal Muscle ◽  
Isometric Force ◽  
Force Production ◽  
Maximum Force ◽  
Stimulation Protocol ◽  
Shortening Velocity ◽  
Dynamic Activity ◽  
Initial Values ◽  
Isotonic Shortening

Skeletal muscle fatigue is most often studied in vitro at room temperature and is classically defined as a decline in maximum force production or power output, exclusively linked to repeated isometric contractions. However, most muscles shorten during normal use, and we propose that both the functional correlate of fatigue, as well as the fatigue mechanism, will be different during dynamic contractions compared with static contractions. Under isoflurane anesthesia, fatigue was induced in rat soleus muscles in situ by isotonic shortening contractions at 37°C. Muscles were stimulated repeatedly for 1 s at 30 Hz every 2 s for a total of 15 min. The muscles were allowed to shorten isotonically against a load corresponding to one-third of maximal isometric force. Maximal unloaded shortening velocity (V0), maximum force production (Fmax), and isometric relaxation rate (−dF/d t) was reduced after 100 s but returned to almost initial values at the end of the stimulation protocol. Likewise, ATP and creatine phosphate (CrP) were reduced after 100 s, but the level of CrP was partially restored to initial values after 15 min. The rate of isometric force development, the velocity of shortening, and isotonic shortening were also reduced at 100 s, but in striking contrast, did not recover during the remainder of the stimulation protocol. The regulatory myosin light chain (MLC2s) was dephosphorylated after 100 s and did not recover. Although metabolic changes may account for the changes of Fmax, −dF/d t, and V0, dephosphorylation of MLC2s may be involved in the fatigue seen as sustained slower contraction velocities and decreased muscle shortening.

Effects of cocaine on leakage of creatine kinase from skeletal muscle: In vitro and in vivo studies in mice

Life Sciences ◽  
1995 ◽  
Vol 57 (17) ◽  
pp. 1569-1578 ◽  
Author(s):  
Gayle A. Brazeau ◽  
Anne McArdle ◽  
Malcolm J. Jackson
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
In Vivo Studies
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