Isometric force development of single horizontal eye muscles in esotropia and exotropia

2020 ◽  
pp. 57-61
Author(s):  
C. Schiavi ◽  
R. Bolzani ◽  
G. Lennerstrand ◽  
S. Tian ◽  
M.G. Benassi ◽  
...  
Keyword(s):  
Isometric Force ◽  
Force Development ◽  
Eye Muscles

scholarly journals Isometric force development in human horizontal eye muscles and pulleys during saccadic eye movements

2009 ◽  
Vol 87 (8) ◽  
pp. 837-842 ◽  
Author(s):  
Gunnar Lennerstrand ◽  
Roberto Bolzani ◽  
Mariagrazia Benassi ◽  
Suna Tian ◽  
Costantino Schiavi
Keyword(s):  
Eye Movements ◽  
Isometric Force ◽  
Saccadic Eye Movements ◽  
Force Development ◽  
Eye Muscles

Contractile responses to ouabain and K+-free solution in aorta from hypertensive rats

1986 ◽  
Vol 250 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
R. S. Moreland ◽  
T. C. Major ◽  
R. C. Webb
Keyword(s):  
Channel Blocker ◽  
Isometric Force ◽  
Maximal Response ◽  
Na Channel ◽  
Free Solution ◽  
Contractile Responses ◽  
Spontaneously Hypertensive ◽  
Force Development ◽  
Monensin A ◽  
Wistar Kyoto

This study characterizes isometric force development in response to ouabain and K+-free solution in isolated aortic strips from spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. SHR aortas were more sensitive to ouabain than those from WKY (threshold: SHR, 3.1 X 10(-5) M; WKY, 25.6 X 10(-5) M), and force development in response to 10(-3) M ouabain was greater in SHR (SHR, 586 +/- 51 mg; WKY, 245 +/- 24 mg). Monensin, a Na+ ionophore, potentiated contractile responses to ouabain, whereas amiloride, a Na+ channel blocker, and low Na+ solutions depressed contractile responses to ouabain. Contractile responses of SHR aortic strips to K+-free solution were faster than those of WKY aortic strips [time to half-maximal response (t1/2): SHR, 24 +/- 5 min; WKY, 47 +/- 4 min]. Maximal force development by aortic strips from SHR in response to K+-free solution was not different from that of WKY aortic strips (SHR, 808 +/- 34 mg; WKY, 750 +/- 37 mg). Monensin (10(-5) M) increased the rate of force development to K+-free solution to a greater extent in WKY aortic strips than in those from SHR (t1/2: SHR, 3 +/- 1 min; WKY, 4 +/- 2 min). Amiloride and low Na+ solution depressed contractile responses to K+-free solution in both SHR and WKY aortic strips. These observations demonstrate that SHR aortas are more responsive to ouabain and K+-free solution compared with WKY aortas. Contractile responses to ouabain and K+-free solution were sensitive to experimental interventions that alter transmembrane Na+ movements.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Physiological Response to Light- and Heavy-load Power-oriented Exercise in Older Adults

2021 ◽  
Author(s):  
Carlos Rodriguez-Lopez ◽  
Julian Alcazar ◽  
Jose Losa-Reyna ◽  
JuanManuel Carmona-Torres ◽  
Aurora Maria Cruz-Santaella ◽  
...  
Keyword(s):  
Older Adults ◽  
Creatine Kinase ◽  
Resistance Training ◽  
Isometric Force ◽  
Rate Of Force Development ◽  
Heavy Load ◽  
Force Development ◽  
Sit To Stand ◽  
Light Load ◽  
Maximal Isometric Force

AbstractThis study investigated the acute responses to volume-load-matched heavy-load (80% 1RM) versus light-load (40% 1RM) power-oriented resistance training sessions in well-functioning older adults. Using a randomized cross-over design, 15 volunteers completed each condition on a leg press. Neuromuscular (maximal isometric force and rate of force development) and functional performance (power during sit-to-stand test), lactate, and muscle damage biochemistry (creatine kinase, lactate dehydrogenase and C-reactive protein serum concentration) were assessed pre- and post-exercise. Performance declines were found after heavy-load (Cohen’s d effect size (d); maximal isometric force=0.95 d; rate of force development=1.17 d; sit-to-stand power =0.38 d, all p<0.05) and light-load (maximal isometric force=0.45 d; rate of force development=0.9 d; sit-to-stand power=1.17 d, all p<0.05), while lactate concentration increased only after light-load (1.7 d, p=0.001). However, no differences were found between conditions (all p>0.05). Both conditions increased creatine kinase the day after exercise (marginal effect=0.75 d, p<0.001), but no other blood markers increased (all, p>0.05). Irrespective of the load used, power training induced non-clinically significant decreases in sit-to-stand performance, moderate declines in maximal isometric force, but pronounced decreases in the rate of force development. Furthermore, the metabolic stress and muscle damage were minor; both sessions were generally well tolerated by well-functioning older adults without previous experience in resistance training.

Dynamics of cardiac muscle: analysis of isotonic, isometric, and isochronal curves

1987 ◽  
Vol 253 (3) ◽  
pp. H645-H653
Author(s):  
O. N. Nwasokwa
Keyword(s):  
Muscle Force ◽  
Isometric Force ◽  
Impedance Matching ◽  
Time Intervals ◽  
Cross Sectional ◽  
Contraction Coupling ◽  
Force Development ◽  
Pentobarbital Sodium Anesthesia ◽  
Matching Transformer ◽  
Isotonic Shortening

Canine papillary muscle force-length-time relation (F-L-t) was investigated under pentobarbital sodium anesthesia. The time intervals taken from end diastole to any point (P) on the force-length plane was determined for isometric (t1) and isotonic (t2) systole and corrected for excitation contraction coupling duration. The ratio t1/t2, designated km, was approximately constant for widely scattered positions of P chosen systematically. The km in the 10 dogs ranged from 0.36 to 0.94 with means +/- SD of 0.66 +/- 0.16; km correlated negatively with muscle average cross-sectional area (r = -0.82; P less than 0.005). Assuming constancy of km, a general relationship was derived between (delta F/delta t)t1L, the rate of isometric force development at P; (delta L/delta t)t2F, the velocity of isotonic shortening at P; (delta F/delta L)(t1,t2)t, the stiffness; and (delta L/delta F)(t1,t2)t, the compliance of the myocardium (all taken at P) as follows (delta F/delta L)t1,t2t = -km(delta F/delta t)t1L/(delta L/delta t)t2F and (delta L/delta F)t1,t2t = -km-1(delta L/delta t)t2F/(delta F/delta t)t1t. The ratio of (delta F/delta t)t1L to (delta L/delta t)t2F defines functional proclivity and measures the differential propensity to force development relative to shortening. Thus myocardial stiffness or compliance determines functional proclivity by acting as an impedance-matching transformer that steps up or steps down force development of shortening as warranted by the loading conditions.

[Ca2+]i signaling in pregnant human myometrium

1994 ◽  
Vol 267 (1) ◽  
pp. E77-E87 ◽  
Author(s):  
S. E. Szal ◽  
J. T. Repke ◽  
E. W. Seely ◽  
S. W. Graves ◽  
C. A. Parker ◽  
...  
Keyword(s):  
Cesarean Section ◽  
Calcium Concentration ◽  
Isometric Force ◽  
Full Term ◽  
Ionized Calcium ◽  
Human Myometrium ◽  
Term Pregnancy ◽  
Force Development ◽  
Calcium Indicator

The purpose of the present study was to determine the changes in intracellular ionized calcium concentration ([Ca2+]i) or [Ca2+]i sensitivity accompanying spontaneous and agonist-induced contraction of human myometrium at term pregnancy, as well as to quantify the response to three prototypical agonists: 1) oxytocin, 2) vasopressin, and 3) phenylephrine. Uterine biopsies were obtained at the time of cesarean section from patients who delivered at or near full-term gestation. These preparations were used to measure isometric force development and [Ca2+]i levels with the luminescent calcium indicator aequorin. Concentration-response relationships were determined with respect to isometric force development in the presence of the agonist. [Ca2+]i-force relationships were determined with respect to spontaneous phasic contractions, as well as agonist-induced phasic and tonic contractions. The results provide evidence that the phasic nature of term human myometrium is due to 1) the resting [Ca2+]i level being less than the calcium threshold for contractions and 2) the inability of the tissue to maintain high [Ca2+]i levels for prolonged periods of time. In addition, calcium-independent mechanisms of regulation were suggested by the relatively minor calcium sensitizing action of oxytocin and the observation that relaxation of tonic contractions preceded the fall in [Ca2+]i levels.

The Frank-Starling mechanism is not mediated by changes in rate of cross-bridge detachment

1997 ◽  
Vol 273 (5) ◽  
pp. H2428-H2435 ◽  
Author(s):  
Thomas Wannenburg ◽  
Paul M. L. Janssen ◽  
Dongsheng Fan ◽  
Pieter P. De Tombe
Keyword(s):  
Cardiac Muscle ◽  
Maximum Rate ◽  
Sarcomere Length ◽  
Myosin Head ◽  
Isometric Force ◽  
Force Development ◽  
Cross Bridge ◽  
Average Slope ◽  
The Cross ◽  
Kinetics Of

We tested the hypothesis that the Frank-Starling relationship is mediated by changes in the rate of cross-bridge detachment in cardiac muscle. We simultaneously measured isometric force development and the rate of ATP consumption at various levels of Ca2+ activation in skinned rat cardiac trabecular muscles at three sarcomere lengths (2.0, 2.1, and 2.2 μm). The maximum rate of ATP consumption was 1.5 nmol ⋅ s−1 ⋅ μl fiber vol−1, which represents an estimated adenosinetriphosphatase (ATPase) rate of ∼10 s−1 per myosin head at 24°C. The rate of ATP consumption was tightly and linearly coupled to the level of isometric force development, and changes in sarcomere length had no effect on the slope of the force-ATPase relationships. The average slope of the force-ATPase relationships was 15.5 pmol ⋅ mN−1 ⋅ mm−1. These results suggest that the mechanisms that underlie the Frank-Starling relationship in cardiac muscle do not involve changes in the kinetics of the apparent detachment step in the cross-bridge cycle.

Excitatory pathways in smooth muscle investigated by phase-plot analysis of isometric force development

1991 ◽  
Vol 261 (1) ◽  
pp. R138-R144
Author(s):  
G. A. Van Koeveringe ◽  
R. Van Mastrigt
Keyword(s):  
Smooth Muscle ◽  
Time Constant ◽  
Isometric Force ◽  
Force Development ◽  
Phase Plot ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Plot Analysis ◽  
Excitatory Pathways ◽  
Rate Limiting

Excitatory pathways in the smooth muscle of the pig urinary bladder were investigated using phase-plot analysis of isometric contractions. The phase plots, plots of the rate of change of the force as a function of the force itself, were dominated by a straight line described by the horizontal intercept (Fiso) and the vertical intercept (U). The quotient Fiso/U is a time constant that characterizes the rate-limiting step in isometric force development in the muscle. Bladder strips of 1 mm diameter were activated by electrical field stimuli, acetylcholine, potassium, and ATP in combination with selective pathway inhibitors such as verapamil, atropine, or a calcium-free solution containing ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. When pathways that depended significantly on depolarization or intracellular calcium release were selected, the time constant was significantly smaller, indicating a faster process. The results indicated that the rate-limiting step in force development was determined by the influx of extracellular calcium.

Nickel inhibits endothelin-induced contractions of vascular smooth muscle

1990 ◽  
Vol 258 (6) ◽  
pp. C1025-C1030 ◽  
Author(s):  
K. Blackburn ◽  
R. F. Highsmith
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Isometric Force ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Porcine Coronary Artery ◽  
Force Development ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Endothelin (ET)-induced contractions of vascular smooth muscle (VSM) are dependent on extracellular Ca2+ yet display only partial sensitivity to L-type Ca2+ antagonists. The purpose of this study was to evaluate the effect of nickel (Ni2+), a Ca2+ channel antagonist with clearly documented differential potency toward L- vs. T-type Ca2+ currents on ET-mediated contractions in VSM. Treatment of rings of left anterior descending porcine coronary artery (LAD) with Ni2+ produced a profound dose-dependent inhibition of isometric force development in response to porcine ET (ET-1). At a concentration of 360 microM, Ni2+ exerted a significant inhibitory effect on contracture in response to doses of ET-1 ranging from 3 to 100 nM. In contrast, the same concentration of Ni2+ failed to significantly affect peak force development in response to KCl depolarization (5-77 mM) or to phenylephrine (0.3-30 mM). In addition, 360 microM Ni2+ significantly inhibited the contractile response of rat aorta to 10 nM ET-1. We conclude that ET-1 activates a Ni2(+)-sensitive process in VSM which may signal an additional Ca2+ influx pathway that appears to be functionally distinct from the L-type Ca2+ channel.

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