Long-term BTX-A effects on bi-articular muscle: higher passive force, limited length range of active force production and unchanged intermuscular interactions

2021 ◽  
pp. 110627
Author(s):  
Evrim O. Yılmaz ◽  
Cemre S. Kaya ◽  
Zeynep D. Akdeniz-Doğan ◽  
Can A. Yucesoy
2008 ◽  
Vol 294 (1) ◽  
pp. C74-C78 ◽  
Author(s):  
V. Joumaa ◽  
D. E. Rassier ◽  
T. R. Leonard ◽  
W. Herzog

The aim of the present study was to test whether titin is a calcium-dependent spring and whether it is the source of the passive force enhancement observed in muscle and single fiber preparations. We measured passive force enhancement in troponin C (TnC)-depleted myofibrils in which active force production was completely eliminated. The TnC-depleted construct allowed for the investigation of the effect of calcium concentration on passive force, without the confounding effects of actin-myosin cross-bridge formation and active force production. Passive forces in TnC-depleted myofibrils ( n = 6) were 35.0 ± 2.9 nN/ μm2 when stretched to an average sarcomere length of 3.4 μm in a solution with low calcium concentration (pCa 8.0). Passive forces in the same myofibrils increased by 25% to 30% when stretches were performed in a solution with high calcium concentration (pCa 3.5). Since it is well accepted that titin is the primary source for passive force in rabbit psoas myofibrils and since the increase in passive force in TnC-depleted myofibrils was abolished after trypsin treatment, our results suggest that increasing calcium concentration is associated with increased titin stiffness. However, this calcium-induced titin stiffness accounted for only ∼25% of the passive force enhancement observed in intact myofibrils. Therefore, ∼75% of the normally occurring passive force enhancement remains unexplained. The findings of the present study suggest that passive force enhancement is partly caused by a calcium-induced increase in titin stiffness but also requires cross-bridge formation and/or active force production for full manifestation.


2007 ◽  
Vol 131 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Jun Udaka ◽  
Shintaro Ohmori ◽  
Takako Terui ◽  
Iwao Ohtsuki ◽  
Shin'ichi Ishiwata ◽  
...  

Persistent muscle weakness due to disuse-associated skeletal muscle atrophy limits the quality of life for patients with various diseases and individuals who are confined to bed. Fibers from disused muscle exhibit a marked reduction in active force production, which can exacerbate motor function, coupled with the well-known loss of muscle quantity. Despite recent understanding of the signaling pathways leading to the quantity loss, the molecular mechanisms of the depressed qualitative performance still remain elusive. Here we show that long-term disuse causes preferential loss of the giant sarcomere protein titin, associated with changes in physiologic muscle function. Ca2+ sensitivity of active force decreased following 6 wk of hindlimb immobilization in the soleus muscle of the rat, accompanied by a shift in the length-active force relationship to the shorter length side. Our analyses revealed marked changes in the disused sarcomere, with shortening of thick and thin filaments responsible for altered length dependence and expansion of interfilament lattice spacing leading to a reduction in Ca2+ sensitivity. These results provide a novel view that disuse-induced preferential titin loss results in altered muscle function via abnormal sarcomeric organization.


2006 ◽  
Vol 101 (1) ◽  
pp. 23-29 ◽  
Author(s):  
M. B. MacNaughton ◽  
B. R. MacIntosh

Relative force depression associated with muscle fatigue is reported to be greater when assessed at short vs. long muscle lengths. This appears to be due to a rightward shift in the force-length relationship. This rightward shift may be caused by stretch of in-series structures, making sarcomere lengths shorter at any given muscle length. Submaximal force-length relationships (twitch, double pulse, 50 Hz) were evaluated before and after repetitive contractions (50 Hz, 300 ms, 1/s) in an in situ preparation of the rat medial gastrocnemius muscle. In some experiments, fascicle lengths were measured with sonomicrometry. Before repetitive stimulation, fascicle lengths were 11.3 ± 0.8, 12.8 ± 0.9, and 14.4 ± 1.2 mm at lengths corresponding to −3.6, 0, and 3.6 mm where 0 is a reference length that corresponds with maximal active force for double-pulse stimulation. After repetitive stimulation, there was no change in fascicle lengths; these lengths were 11.4 ± 0.8, 12.6 ± 0.9, and 14.2 ± 1.2 mm. The length dependence of fatigue was, therefore, not due to a stretch of in-series structures. Interestingly, the rightward shift that was evident when active force was calculated in the traditional way (subtraction of the passive force measured before contraction) was not seen when active force was calculated by subtracting the passive force that was associated with the fascicle length reached at the peak of the contraction. This calculation is based on the assumption that passive force decreases as the fascicles shorten during a fixed-end contraction. This alternative calculation revealed similar postfatigue absolute active force depression at all lengths. In relative terms, a length dependence of fatigue was still evident, but this was greatly diminished compared with that observed when active force was calculated with the traditional method.


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Josefina Bertoli ◽  
Ewertton de Souza Bezerra ◽  
Andréa Dias Reis ◽  
Êmili Amice da Costa Barros ◽  
Luis Alberto Gobbo ◽  
...  

2018 ◽  
Vol 315 (3) ◽  
pp. C310-C318 ◽  
Author(s):  
V. Joumaa ◽  
F. Bertrand ◽  
S. Liu ◽  
S. Poscente ◽  
W. Herzog

The aim of this study was to determine the role of titin in preventing the development of sarcomere length nonuniformities following activation and after active and passive stretch by determining the effect of partial titin degradation on sarcomere length nonuniformities and force in passive and active myofibrils. Selective partial titin degradation was performed using a low dose of trypsin. Myofibrils were set at a sarcomere length of 2.4 µm and then passively stretched to sarcomere lengths of 3.4 and 4.4 µm. In the active condition, myofibrils were set at a sarcomere length of 2.8 µm, activated, and actively stretched by 1 µm/sarcomere. The extent of sarcomere length nonuniformities was calculated for each sarcomere as the absolute difference between sarcomere length and the mean sarcomere length of the myofibril. Our main finding is that partial titin degradation does not increase sarcomere length nonuniformities after passive stretch and activation compared with when titin is intact but increases the extent of sarcomere length nonuniformities after active stretch. Furthermore, when titin was partially degraded, active and passive stresses were substantially reduced. These results suggest that titin plays a crucial role in actively stretched myofibrils and is likely involved in active and passive force production.


2008 ◽  
Vol 131 (3) ◽  
pp. 275-283 ◽  
Author(s):  
Takako Terui ◽  
Munguntsetseg Sodnomtseren ◽  
Douchi Matsuba ◽  
Jun Udaka ◽  
Shin'ichi Ishiwata ◽  
...  

We investigated the molecular mechanism by which troponin (Tn) regulates the Frank-Starling mechanism of the heart. Quasi-complete reconstitution of thin filaments with rabbit fast skeletal Tn (sTn) attenuated length-dependent activation in skinned porcine left ventricular muscle, to a magnitude similar to that observed in rabbit fast skeletal muscle. The rate of force redevelopment increased upon sTn reconstitution at submaximal levels, coupled with an increase in Ca2+ sensitivity of force, suggesting the acceleration of cross-bridge formation and, accordingly, a reduction in the fraction of resting cross-bridges that can potentially produce additional active force. An increase in titin-based passive force, induced by manipulating the prehistory of stretch, enhanced length-dependent activation, in both control and sTn-reconstituted muscles. Furthermore, reconstitution of rabbit fast skeletal muscle with porcine left ventricular Tn enhanced length-dependent activation, accompanied by a decrease in Ca2+ sensitivity of force. These findings demonstrate that Tn plays an important role in the Frank-Starling mechanism of the heart via on–off switching of the thin filament state, in concert with titin-based regulation.


2011 ◽  
Vol 111 (6) ◽  
pp. 1654-1663 ◽  
Author(s):  
Satoshi Haramizu ◽  
Noriyasu Ota ◽  
Tadashi Hase ◽  
Takatoshi Murase

Catechins have a great variety of biological actions. We evaluated the potential benefits of catechin ingestion on muscle contractile properties, oxidative stress, and inflammation following downhill running, which is a typical eccentric exercise, in senescence-accelerated prone mice (SAMP). Downhill running (13 m/min for 60 min; 16° decline) induced a greater decrease in the contractile force of soleus muscle and in Ca2+-ATPase activity in SAMP1 compared with the senescence-resistant mice (SAMR1). Moreover, compared with SAMR1, SAMP1 showed greater downhill running-induced increases in plasma CPK and LDH activity, malondialdehyde, and carbonylated protein as markers of oxidative stress; and in protein and mRNA expression levels of the inflammatory mediators such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in muscle. SAMP1 exhibited aging-associated vulnerability to oxidative stress and inflammation in muscle induced by downhill running. Long-term (8 wk) catechin ingestion significantly attenuated the downhill running-induced decrease in muscle force and the increased inflammatory mediators in both plasma and gastrocnemius muscle. Furthermore, catechins significantly inhibited the increase in oxidative stress markers immediately after downhill running, accompanied by an increase in glutathione reductase activity. These findings suggest that long-term catechin ingestion attenuates the aging-associated loss of force production, oxidative stress, and inflammation in muscle after exercise.


1997 ◽  
Vol 01 (02) ◽  
pp. 95-109 ◽  
Author(s):  
W. Herzog ◽  
T. R. Leonard

The dynamic properties of the cat soleus muscle were studied in freely walking animal preparations. The force and EMG responses of the soleus following supramaximal, ins tants of the step cycle. The sensorimotor interactions of soleus with the medial head of the gastrocnemius (a functional agonist of the soleus at the ankle) and the tibialis anterior (a functional antagonist of soleus at the ankle) were studied by measuring their force and EMG responses following the artifical stimulation of the soleus nerve. Supramaximal nerve stimulation showed distinct increases in the soleus forces during the entire swing phase and the second part (after peak forces had been reached) of the stance phase. Soleus forces could only be increased slightly in the first part of stance (from paw contact to peak force). These results suggest that force production of the soleus is virtually maximal during the early phases of stance but is submaximal for the remainder of the step cycle. Forces and EMGs of the medial gastrocnemius muscle were affected by the soleus nerve stimulation only in the latter part of the swing phase. In these cases, the force and EMG of the medial gastrocnemius were reduced significantly for the step cycle following the perturbation. The active force production of soleus during late swing causes an inhibition of medial gastrocnemius activity and force. Forces and EMGs of the tibialis anterior muscle were always affected by the soleus nerve stimulation during the swing phase of the step cycle. In these case, the force EMG of the medial gastrocnemius were reduced significantly for the step cycle following the perturbation. The active force production of soleus during late swing causes an inhibition of medial gastrocnemius activity and force. Forces and EMGs of the tibialis anterior muscle were always affected by the soleus nerve stimulation during the swing phase of the step cycle. In these instances, forces and EMGs of the tibialis anterior were significantly increased compared to step cycles preceding or following the perturbation. Part of the force enhancement is caused by the stretch of the activated tibialis anterior by the soleus, and part of the enhancement is caused by reflex activation. No effects on forces or EMGs of the tibialis anterior were observed when the soleus nerve stimulation showed its effects during the stance phase of the step cycle. The results of theis study suggest that the magnitude and the quality of ensorimotor interactions of soleus with medial gastrocnemius and tibialis anterior depend on the phase of the step cycle. The strongest interactions appear to exist during the swing phase; no observable interactions were found during stance.


Sign in / Sign up

Export Citation Format

Share Document