Influence of hyperthyroidism on maximal shortening velocity and myosin isoform distribution in skeletal muscles

1991 ◽  
Vol 261 (2) ◽  
pp. C285-C295 ◽  
Author(s):  
V. J. Caiozzo ◽  
R. E. Herrick ◽  
K. M. Baldwin

The objectives of this study were 1) to examine the effects of hyperthyroidism on the myosin isoform distribution in slow and fast skeletal muscle, 2) to explore how these effects were manifested with respect to the force-velocity relationship and maximal shortening velocity, and 3) to contrast two different techniques of measuring maximal shortening velocity under normal and hyperthyroid conditions. Adult female Sprague-Dawley rats were randomly assigned to one of two groups: control (n = 8) or hyperthyroid (n = 8). Hyperthyroidism was induced by injections of 3,3',5-triiodo-L-thyronine every other day for 20 wk. We found that hyperthyroidism produced a significant shift in the myosin isoform distribution of the soleus but not the plantaris. The relative amount of the slow myosin isoform was reduced from a control value of 93 to 69% in the hyperthyroid condition. In contrast, both the intermediate and fast myosin-3 isoform pools were substantially increased (P less than 0.001) by approximately fourfold. Hyperthyroidism produced an increase in the maximal shortening velocity of the soleus as measured either by the slack test (+57%; P less than 0.001) or by extrapolation of force-velocity data (+33%; P less than 0.001). The hyperthyroid condition did not, however, affect the mechanical properties of the plantaris.

1992 ◽  
Vol 263 (1) ◽  
pp. C86-C94 ◽  
Author(s):  
V. J. Caiozzo ◽  
R. E. Herrick ◽  
K. M. Baldwin

This study examined both the shortening velocity and myosin isoform distribution of slow- (soleus) and fast-twitch (plantaris) skeletal muscles under hypothyroid conditions. Adult female Sprague-Dawley rats were randomly assigned to one of two groups: control (n = 7) or hypothyroid (n = 7). In both muscles, the relative contents of native slow myosin (SM) and type I myosin heavy chain (MHC) increased in response to the hypothyroid treatment. The effects were such that the hypothyroid soleus muscle expressed only the native SM and type I MHC isoforms while repressing native intermediate myosin and type IIA MHC. In the plantaris, the relative content of native SM and type I MHC isoforms increased from 5 to 13% and from 4 to 10% of the total myosin pool, respectively. Maximal shortening velocity of the soleus and plantaris as measured by the slack test decreased by 32 and 19%, respectively, in response to hypothyroidism. In contrast, maximal shortening velocity as estimated by force-velocity data decreased only in the soleus (-19%). No significant change was observed for the plantaris.


1997 ◽  
Vol 87 (2) ◽  
pp. 354-360 ◽  
Author(s):  
Yumiko Ishizawa ◽  
Shuichiro Ohta ◽  
Hiroyuki Shimonaka ◽  
Shuji Dohi

Background Although hyper- and hypoglycemia induce neurophysiologic changes, there have been no reports on the effects of blood glucose changes on anesthetic requirements. This study examined the effects of hyper- and hypoglycemia on the minimum alveolar concentration (MAC) of halothane in rats. In addition, based on a previous finding that the level of brain acetylcholine was reduced during mild hypoglycemia, the authors examined the influence of physostigmine on MAC during hypoglycemia. Methods In Sprague-Dawley rats, anesthesia was induced and maintained with halothane in oxygen and air. The MAC was determined by observing the response to tail clamping and tested during mild hypoglycemia (blood glucose level, 60 mg/dl) and hyperglycemia (blood glucose level, 300 and 500 mg/dl) induced by insulin and glucose infusion, respectively (experiment 1). The effects of 0.3 and 1.0 mg/kg physostigmine given intraperitoneally on MAC were examined in rats with mild and severe hypoglycemia (blood glucose level, 60 and 30 mg/dl; experiment 2). Results In experiment 1, mild hypoglycemia significantly reduced the MAC of halothane (0.76 +/- 0.03%) compared with the control value (0.92 +/- 0.04%), but hyperglycemia did not change MAC. In experiment 2, mild and severe hypoglycemia reduced MAC of halothane in a degree-dependent manner. Physostigmine (1 mg/kg) had no effect on MAC regardless of blood glucose level, but 0.3 mg/kg reduced MAC. Conclusions Hypoglycemia reduced anesthetic requirements in a degree-dependent manner, whereas hyperglycemia had no effects. Although the mechanism of hypoglycemic MAC reduction needs further investigations, physostigmine studies suggest that this may not be related to inhibition of cholinergic transmission.


2000 ◽  
Vol 89 (6) ◽  
pp. 2215-2219 ◽  
Author(s):  
Bill T. Ameredes ◽  
Wen-Zhi Zhan ◽  
Y. S. Prakash ◽  
Rene Vandenboom ◽  
Gary C. Sieck

We hypothesized that decrements in maximum power output (W˙max) of the rat diaphragm (Dia) muscle with repetitive activation are due to a disproportionate reduction in force (force fatigue) compared with a slowing of shortening velocity (velocity fatigue). Segments of midcostal Dia muscle were mounted in vitro (26°C) and stimulated directly at 75 Hz in 400-ms-duration trains repeated each second (duty cycle = 0.4) for 120 s. A novel technique was used to monitor instantaneous reductions in maximum specific force (Po) andW˙max during fatigue. During each stimulus train, activation was isometric for the initial 360 ms during which Po was measured; the muscle was then allowed to shorten at a constant velocity (30% V max) for the final 40 ms, and W˙max was determined. Compared with initial values, after 120 s of repetitive activation, Po andW˙max decreased by 75 and 73%, respectively. Maximum shortening velocity was measured in two ways: by extrapolation of the force-velocity relationship ( V max) and using the slack test [maximum unloaded shortening velocity ( V o)]. After 120 s of repetitive activation, V max slowed by 44%, whereas V o slowed by 22%. Thus the decrease inW˙max with repetitive activation was dominated by force fatigue, with velocity fatigue playing a secondary role. On the basis of a greater slowing of V max vs. V o, we also conclude that force and power fatigue cannot be attributed simply to the total inactivation of the most fatigable fiber types.


1982 ◽  
Vol 52 (4) ◽  
pp. 930-938 ◽  
Author(s):  
Y. Kikuchi ◽  
H. Sasaki ◽  
K. Sekizawa ◽  
K. Aihara ◽  
T. Takishima

We examined the force-velocity relationship of the respiratory muscles in normal subjects under nearly isotonic conditions, taking into consideration the pleural pressure (Ppl) changes during maximum forced expirations (MFE). We used an electromagnetic valve (EMV) to select the Ppl value at the onset of mouth flow; and both a pressure reservoir and a variable resistance to control the Ppl changes after the opening of the EMV during MFE. To simulate isotonic conditions and to obtain the shortening velocity of the contractile element (CE), we mathematically corrected the velocity of the series elastic component (SEC), using a modified version of Hill's equation. Although the maximum tension at total lung capacity (TLC) [1,156 +/- 215 (SD) g/cm] was larger than that at functional residual capacity (FRC) (782 +/- 97 g/cm) there was no significant difference in the maximum shortening velocity, 3.4 +/- 1.0 and 3.2 +/- 0.8 circumference/s at TLC and FRC, respectively. The mean values of k (slope) for the SEC at TLC and FRC were 19 +/- 4 and 18 +/- 5 circumference-1, respectively, and they were not significantly different. We concluded that the force-velocity relationship of the expiratory muscles exhibited the same mechanical properties as that of the other skeletal muscles.


1992 ◽  
Vol 73 (1) ◽  
pp. 71-74 ◽  
Author(s):  
B. M. Block ◽  
S. R. Barry ◽  
J. A. Faulkner

We hypothesized that methylxanthines, such as aminophylline, increase the power developed by submaximally activated frog skeletal muscles by increasing the force developed at any given velocity of shortening. Frog semitendinosus muscles were excised and tested at 20 degrees C in oxygenated control and aminophylline Ringer solutions. Force-velocity relationships were determined and power was calculated from muscles stimulated at frequencies of 80 and 300 Hz. The 300-Hz frequency of stimulation produced a maximum rate of force development. In 50 and 500 microM aminophylline, twitch force increased by 25 +/- 12 and 75 +/- 13%, respectively. Aminophylline did not affect maximum isometric force generation or the shortening velocity at any relative load. At 80-Hz stimulation and in the presence of 500 microM aminophylline, power increased by an average of 11% at 10 of 14 relative loads. At maximum frequencies of stimulation, aminophylline had no effect on any measured parameter. We conclude that aminophylline increases the power developed by submaximally activated frog muscles through an increase in the force generated particularly at the lower velocities of shortening.


2002 ◽  
Vol 92 (3) ◽  
pp. 1074-1082 ◽  
Author(s):  
Gilles Orliaguet ◽  
Olivier Langeron ◽  
Belaid Bouhemad ◽  
Pierre Coriat ◽  
Yves LeCarpentier ◽  
...  

The effects of maturation on cross-bridge (CB) properties were studied in rat diaphragm strips obtained at postnatal days 3, 10, and 17 and in adults (10–12 wk old). Calculations of muscle energetics and characteristics of CBs were determined from standard Huxley equations. Maturation did not change the curvature of the force-velocity relationship or the peak of mechanical efficiency. There was a significant increase in the total number of CBs per cross-sectional area (m) with aging but not in single CB force. The turnover rate of myosin ATPase increased, the duration of the CB cycle decreased, and the velocity of CBs decreased significantly only after the first week postpartum. There was a linear relationship between maximum total force and m ( r = 0.969, P < 0.001), and between maximum unloaded shortening velocity and m ( r = 0.728, P < 0.001). When this study in the rat and previous study in the hamster are compared, it appears that there are few species differences in the postnatal maturation process of the diaphragm.


2014 ◽  
Vol 111 (12) ◽  
pp. 2614-2623 ◽  
Author(s):  
Anders S. Johansson ◽  
Karl-Gunnar Westberg ◽  
Benoni B. Edin

Although splitting of food items between the incisors often requires high bite forces, rarely do the teeth harmfully collide when the jaw quickly closes after split. Previous studies indicate that the force-velocity relationship of the jaw closing muscles principally explains the prompt dissipation of jaw closing force. Here, we asked whether people could regulate the dissipation of jaw closing force during food splitting. We hypothesized that such regulation might be implemented via differential recruitment of masseter muscle portions situated along the anteroposterior axis because these portions will experience a different shortening velocity during jaw closure. Study participants performed two different tasks when holding a peanut-half stacked on a chocolate piece between their incisors. In one task, they were asked to split the peanut-half only (single-split trials) and, in the other, to split both the peanut and the chocolate in one action (double-split trials). In double-split trials following the peanut split, the intensity of the tooth impact on the chocolate piece was on average 2.5 times greater than in single-split trials, indicating a substantially greater loss of jaw closing force in the single-split trials. We conclude that control of jaw closing force dissipation following food splitting depends on task demands. Consistent with our hypothesis, converging neurophysiological and morphometric data indicated that this control involved a differential activation of the jaw closing masseter muscle along the anteroposterior axis. These latter findings suggest that the regulation of jaw closing force after sudden unloading of the jaw exploits masseter muscle compartmentalization.


2010 ◽  
Vol 88 (10) ◽  
pp. 937-948 ◽  
Author(s):  
Sharon R. Bullimore ◽  
Travis J. Saunders ◽  
Walter Herzog ◽  
Brian R. MacIntosh

The maximal shortening velocity of a muscle (Vmax) provides a link between its macroscopic properties and the underlying biochemical reactions and is altered in some diseases. Two methods that are widely used for determining Vmax are afterloaded and isotonic release contractions. To determine whether these two methods give equivalent results, we calculated Vmax in 9 intact single fibres from the lumbrical muscles of the frog Xenopus laevis (9.5–15.5 °C, stimulation frequency 35–70 Hz). The data were modelled using a 3-state cross-bridge model in which the states were inactive, detached, and attached. Afterloaded contractions gave lower predictions of Vmax than did isotonic release contractions in all 9 fibres (3.20 ± 0.84 versus 4.11 ± 1.08 lengths per second, respectively; means ± SD, p = 0.001) and underestimated unloaded shortening velocity measured with the slack test by an average of 29% (p = 0.001, n = 6). Excellent model predictions could be obtained by assuming that activation is inhibited by shortening. We conclude that under the experimental conditions used in this study, afterloaded and isotonic release contractions do not give equivalent results. When a change in the Vmax measured with afterloaded contractions is observed in diseased muscle, it is important to consider that this may reflect differences in either activation kinetics or cross-bridge cycling rates.


2019 ◽  
Author(s):  
Louvet S.

AbstractAccompanying Paper 1 tests a theoretical relationship between force and shortening velocity of a muscle fiber without justifying its validity. Paper 2 determines the kinematics and dynamics of a myosin II head during the working stroke (WS). Paper 3 imposes the Uniform law as a density representative of the orientation of the levers belonging to the WS heads. By support of these works, Papers 4 and 5 put into equation the evolution of the tension during the four phases of a length step. The present paper closes all six articles by imposing two tasks on itself. The first purpose is to apply the theoretical elements developed for a length step to a succession of identical length steps, otherwise known as shortening staircase. With the values of the geometric and temporal parameters assigned to a myosin head in Papers 1 to 5, a correct adjustment is established between the theoretical tension deduced from our model and the experimental tension published in 1997 by a team of Italian researchers relating to nine shortening staircases performed on the same fiber. In particular, we obtain the equation of the tension reached at the time end of the step (T*) which remains constant step by step as soon as the shortening of a half-sarcomere exceeds 17 nm. The second objective is to find and explain the equation of the Force-Velocity curve introduced ex abrupto into Paper 1: by decreasing the size and duration of the steps, the staircase tends towards a constant slope line corresponding to a continuous speed shortening. By applying the methods of infinitesimal calculus to the different formulations leading to T*, we deduce the Force-Velocity relationship (see Supplement S6.L). And the circle is complete.


Author(s):  
Alf Månsson

Abstract Muscle force and power are developed by myosin cross-bridges, which cyclically attach to actin, undergo a force-generating transition and detach under turnover of ATP. The force-generating transition is intimately associated with release of inorganic phosphate (Pi) but the exact sequence of events in relation to the actual Pi release step is controversial. Details of this process are reflected in the relationships between [Pi] and the developed force and shortening velocity. In order to account for these relationships, models have proposed branched kinetic pathways or loose coupling between biochemical and force-generating transitions. A key hypothesis underlying the present study is that such complexities are not required to explain changes in the force–velocity relationship and ATP turnover rate with altered [Pi]. We therefore set out to test if models without branched kinetic paths and Pi-release occurring before the main force-generating transition can account for effects of varied [Pi] (0.1–25 mM). The models tested, one assuming either linear or non-linear cross-bridge elasticity, account well for critical aspects of muscle contraction at 0.5 mM Pi but their capacity to account for the maximum power output vary. We find that the models, within experimental uncertainties, account for the relationship between [Pi] and isometric force as well as between [Pi] and the velocity of shortening at low loads. However, in apparent contradiction with available experimental findings, the tested models produce an anomalous force–velocity relationship at elevated [Pi] and high loads with more than one possible velocity for a given load. Nevertheless, considering experimental uncertainties and effects of sarcomere non-uniformities, these discrepancies are insufficient to refute the tested models in favour of more complex alternatives.


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