Effect of Muscle Stretching on Tension Development and Mechanical Threshold during Contractures

1973 ◽  
Vol 246 (155) ◽  
pp. 221-222 ◽  
Author(s):  
H. GONZALEZ-SERRATOS ◽  
R. VALLE ◽  
A. CILLERO
1990 ◽  
Vol 259 (5) ◽  
pp. C709-C714 ◽  
Author(s):  
T. Oba ◽  
M. Yamaguchi

To examine the molecular mechanism underlying contractile activation, we studied effects of a sulfhydryl reagent, N-(7-dimethylamino-4-methylcoumarinyl)maleimide (DACM), on twitch, Ag(+)-induced contraction, and K+ and caffeine contractures in single toe muscle fibers of frog. DACM suppressed twitch and Ag(+)-induced contraction, dose dependently, but not caffeine contracture. K+ contracture also was decreased appreciably by exposure to 40 microM DACM for 10 min. DACM elicited no shift of the mechanical threshold or inhibition of resting potential but slightly inhibited action potential. Increase of the fluorescence intensity produced by binding of 10 microM DACM to sulfhydryl groups was depressed by brief pretreatment with 100 microM Ag+. When exposed to 1 mM dithiothreitol (DTT) within 5 s of the rising phase of 5 microM Ag(+)-induced contraction, the fiber rapidly decreased the tension to the resting level. In this case, reapplication of 5 microM Ag+ after washing out DTT elicited a new contraction similar to the first Ag(+)-induced contraction. The second contraction amplitude depended on the time between the onset of the first Ag(+)-induced contraction and DTT application. If DTT was applied after more than 16 s, tension no longer developed on the second exposure to Ag+ or K+. The experiments provide evidence that crucial sulfhydryl groups participate in muscle activation. The possible role of the sulfhydryl group on the transverse tubular membrane in tension development is discussed.


1972 ◽  
Vol 50 (3) ◽  
pp. 179-187 ◽  
Author(s):  
E. C. Vos ◽  
G. B. Frank

Small bundles of fibers of the semitendinosus of Rana pipiens were subjected to rapid stretches in normal Ringer solution and solutions containing potassium in concentrations just below the mechanical threshold for tension development. The resistance to stretch (R.T.S.) increased with increasing [K+]0. The increase in R.T.S. was dependent on the duration of exposure; the maximum occurred after about 30 s while longer exposures led to a decrease in the R.T.S. The maximum increase in the R.T.S. varied from two to six times the normal R.T.S. The increase in the R.T.S was hyperbolically related to [K+]0. An attempt was made to correlate the mechanical activation and the increase in respiration in muscles exposed to elevated [K+]0 (Solandt effect) by continuously measuring the oxygen consumption [Formula: see text] of toe muscles. Following exposure to an elevated [K+]0 just below the mechanical threshold, the [Formula: see text] started to increase after about 30 s and took 2–3 min to reach a new steady level. The results suggest that: (a) a low level of activation of the contractile elements occurs just below the mechanical threshold for tension development, (b) the excitation–contraction coupling process of frog striated muscle is one of continuous change, i.e. without a sharply defined threshold, and (c) the Solandt effect is probably the expression of a continuous relaxation-type process.


1990 ◽  
Vol 68 (12) ◽  
pp. 1503-1509 ◽  
Author(s):  
Alexandre Bouron ◽  
Michèle Rivet ◽  
Mohammad Nasri-Sebdani ◽  
Joel Guillemain ◽  
Philippe Durbin ◽  
...  

The effect of LCB29 was tested on twitch characteristics, tetanic tension, and K+ and voltage-clamp contractures of rat soleus muscle fibers. In concentrations ranging from 10−6 to 5 × 10−4 M, LCB29 simultaneously inhibited the twitch amplitude, the maximum rate of tension development, and the maximum rate of relaxation. In concentrations ranging from 10−5 to 10−4 M, tetanic tension (100 Hz, 1 s) was inhibited by the same amount. The effect of 5 × 10−5 M LCB29 was studied on K+ contractures and contractures induced, under voltage-clamp conditions, by long-lasting depolarizations. Its effect was significantly stronger than those on twitch and tetanic tension. In addition, LCB29 had a dual effect on strength–duration curves for mechanical threshold. It increased both the rheobasic potential and the steepness of the curve. It is concluded that LCB29 exerts a direct myorelaxant effect on rat soleus muscle; two sites of action are probably involved.Key words: myorelaxants, skeletal muscle, K+ contractures, voltage clamp, mammalian.


1969 ◽  
Vol 54 (3) ◽  
pp. 352-368 ◽  
Author(s):  
Stuart R. Taylor ◽  
Hanna Preiser ◽  
Alexander Sandow

I-, CH3SO4-, and ClO4-, like other previously studied type A twitch potentiators (Br-, NO3-, SCN-, and caffeine), lower the mechanical threshold in K depolarization contractures of frog skeletal muscle. In potentiated twitches, I-, Br-, CH3SO4-, ClO4, and SCN, as already reported for NO3- and caffeine, slightly shorten the latent period (L) and considerably increase the rate of tension development (dP/dt) during the first few milliseconds of the contraction period. Divalent cations (8 mM Ca2+, 0.5–1.0 mM Zn2+ and Cd2+) raise the mechanical threshold of contractures, and correspondingly affect the twitch by depressing the tension output, increasing L, and decreasing the early dP/dt, thus acting oppositely to the type A potentiators. These various results form a broad, consistent pattern indicating that electromechanical coupling in the twitch is conditioned by a mechanical threshold as it is in the contracture, and suggesting that the lower the threshold, in reference to the raised threshold under the action of the divalent cations, the more effective is a given action potential in activating the twitch as regards especially both its early rate and peak magnitude of tension development. The results suggest that the direct action by which the various agents affect the level of the mechanical threshold involves effects on E-C coupling processes of the T tubular and/or the sarcoplasmic reticulum which control the release of Ca for activating contraction.


Circulation ◽  
1997 ◽  
Vol 95 (9) ◽  
pp. 2312-2317 ◽  
Author(s):  
Dongsheng Fan ◽  
Thomas Wannenburg ◽  
Pieter P. de Tombe

Author(s):  
Timothy S. Pulverenti ◽  
Gabriel S. Trajano ◽  
Benjamin J. C. Kirk ◽  
Vanesa Bochkezanian ◽  
Anthony J. Blazevich

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A45-A46
Author(s):  
Skyler Kanegi ◽  
Armen Akopian

Abstract Introduction The combination of artificial light and lack of exposure to natural light can delay the circadian clock, dysregulate the circadian cycle, and decrease alertness upon waking. This effect has been especially significant during the COVID-19 pandemic, where overexposure to artificial light at improper hours has contributed to increased rates of clinical insomnia. Artificial light may also contribute to concomitant neurological conditions such as primary headache, but the mechanisms by which light triggers sleep deprivation-induced headache are not well-understood. Methods To measure pain sensitivity, we habituated 13 wild-type male mice to von Frey filaments applied to the periorbital area until there was no response to 0.6g stimulus. We then applied 5 lux of continuous dim light to mice during their usual 12-hour dark cycle. The 12-hour light cycle remained unchanged with 200 lux continuous light. Three groups of mice experienced the dim light stimulus for one, three, or five consecutive days. Ambulation and rest activity were measured using SOF-812 Activity Monitor machines. After the experiment concluded, we waited 24 hours and measured mechanical threshold using von Frey filaments at 1, 3, 5, 8, and every 3 days subsequently until mice no longer responded to 0.6g stimulus. Results Artificial light triggered changes in circadian behavior including increased number of rest periods during 12-hour dark (dim light) cycle and shortened sleep duration during 12-hour light cycle. Following the artificial light stimulus, there was a significant decrease in mechanical threshold (P<0.05), representing allodynia. The one-day group displayed one day of significant allodynia. The three-day group displayed three days of significant allodynia. The five-day group displayed five days of significant allodynia. Conclusion Artificial light may trigger circadian dysregulation, and the duration of artificial light exposure seemed to be directly correlated to the duration of allodynia up to one week after the stimulus was removed. We will repeat these experiments and analyze CNS and PNS tissue samples to understand the underlying physiological and biochemical bases of how artificial light triggers sleep deprivation-induced headache. This knowledge could increase our understanding of the pathophysiology and comorbidity of sleep deprivation and headache. Support (if any) Funding was received from the National Institute of Health (NS104200).


2020 ◽  
Vol 11 (1) ◽  
pp. 307
Author(s):  
Carla Stecco ◽  
Carmelo Pirri ◽  
Caterina Fede ◽  
Can A. Yucesoy ◽  
Raffaele De Caro ◽  
...  

Stretching exercises are integral part of the rehabilitation and sport. Despite this, the mechanism behind its proposed effect remains ambiguous. It is assumed that flexibility increases, e.g., action on muscle and tendon, respectively, but this is not always present in the stretching protocol of the exercises used. Recently, the fasciae have increased popularity and seems that they can have a role to define the flexibility and the perception of the limitation of the maximal range of motion (ROM). Deep fascia is also considered a key element to transmit load in parallel bypassing the joints, transmitting around 30% of the force generated during a muscular contraction. So, it seems impossible dividing the action of the muscles from the fasciae, but they have to be considered as a “myofascial unit”. The purpose of this manuscript is to evaluate the mechanical behavior of muscles, tendons, and fasciae to better understand how they can interact during passive stretching. Stress-strain values of muscle, tendon and fascia demonstrate that during passive stretching, the fascia is the first tissue that limit the elongation, suggesting that fascial tissue is probably the major target of static stretching. A better understanding of myofascial force transmission, and the study of the biomechanical behavior of fasciae, with also the thixotropic effect, can help to design a correct plan of stretching.


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