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1 nsion cost decreased throughout steady-state isometric force.
2 /s, then was constant at 3.26 +/- 0.06 times isometric force.
3 in small-vessel myographs for measurement of isometric force.
4 initial force was raised to 75-80% of steady isometric force.
5 ording intracellular electrical activity and isometric force.
6 rsal of the power stroke, thereby increasing isometric force.
7 ta-cardiac myosin but a 2-fold lower average isometric force.
8 ivated force in the range 0.3-0.8 of maximum isometric force.
9 Work and power were compromised more than isometric force.
10 , thereby ensuring effective transfer of OHC isometric forces.
11 PD and non-COPD fibres that produced similar isometric forces.
12 o slower components by 50%, in proportion to isometric force, (2) adding a non-relaxing component and
13 electrode, intracellular microelectrode, and isometric force (a surrogate marker for the Ca2+ transie
20 s of BS and OM on the calcium sensitivity of isometric force and filament structural changes suggest
22 creases in fibre number, 20-57% increases in isometric force and no differences in specific force.
23 scle fibers developed greater than twice the isometric force and power output of young fibers, yet cr
24 ated to yield 50% maximal force, after which isometric force and rate constants (k(tr)) of force deve
25 f phosphorylation at Thr(18) on steady-state isometric force and relaxation rate were investigated in
26 microM phalloidin for 1 h, the increases in isometric force and stiffness were not sustained despite
27 s on force and fiber shortening by measuring isometric force and stiffness, the rate of tension decli
29 ed quadriceps and handgrip maximum voluntary isometric force and the relaxation times, force-frequenc
30 rs, as measured by their ability to generate isometric force and to hydrolyze ATP by actomyosin Mg2+
31 TP, 2-deoxy ATP (dATP), CTP, and UTP support isometric force and unloaded shortening velocity (Vu) to
32 ent activation (fractional calcium binding), isometric force, and the rate of force generation in mus
34 ly switched from that for motion to that for isometric force approximately 65 ms before contact (p =
35 G mouse hearts expressing ssTnI and measured isometric force at extracellular pH 7.33 and pH 6.75.
36 -10 degrees C) but much larger than that for isometric force at higher temperature (1.3 at 20-25 degr
37 The average (extrapolated) value of maximum isometric force at low kinesin density was 0.90 +/- 0.14
38 5 degrees C; this was similar to the Q10 for isometric force at low temperature (3.5 at 7-10 degrees
40 lue indicates that the myosin head generates isometric force by a small sub-step of the 11 nm stroke
41 ame assay could be used to determine average isometric force by loading the actin filaments with incr
42 on, RLC phosphorylation enrichment increased isometric force by more than 3-fold and peak power outpu
43 5), the normalised tendon strain at maximum isometric force (c) (varied from 0 to 0.08), the muscle
44 acting as a lever, while the enhancement in isometric force can be directly related to enhancement o
46 nt atrophy and impairment of specific force (isometric force/cross-sectional area) and unloaded short
47 sed from 2.3 microm to 2.0 microm submaximal isometric force decreased approximately 40% in both alph
48 100 pmol/L and 10 nmol/L endothelin-1 raised isometric force, decreased actomyosin ATPase activity, a
50 r decrease in Ca(2+) sensitivity and maximal isometric force development compared with the R141W muta
51 k(tr) measurements underestimate the rate of isometric force development during submaximal Ca2+ activ
53 troponin C (HCTnC), and the Ca(2+) dependent isometric force development of these troponin-replaced f
55 ch lower specific force, and slower rates of isometric force development, slow phase relaxation, and
57 , maximal force and k(tr) and the pCa(50) of isometric force did not differ between WT and cMyBP-C(-/
59 n cost (i.e. ATP hydrolysis rate per unit of isometric force) during Ca2+-induced activation of Trito
64 ases both the unloaded sliding speed and the isometric force exerted by myosin heads on the thin fila
65 rements of the unloaded sliding speed of and isometric force exerted on single thin filaments in in v
66 as calculated as the decrease in the maximum isometric force expressed as a percentage of the maximum
68 ere paralleled by increases of 30% to 80% in isometric force (F(max)), rate of tension redevelopment
73 match a target force at 2% of their maximal isometric force for 35 s with abduction of the index fin
74 of fatigue, induced by production of maximal isometric force for 60 s with four fingers, upon indices
76 egment is stretched and a deficit in maximum isometric force (force deficit) is produced, the regions
81 ized as a force field: the collection of the isometric forces generated at the ankle over different l
83 himpanzees does not stem from differences in isometric force-generating capabilities or maximum short
84 rformance differential have included greater isometric force-generating capabilities, faster maximum
85 on returned nearly to control levels, as did isometric force generation and rate of ATP hydrolysis.
86 end of the latency relaxation (LR) preceding isometric force generation, approximately 10 ms after th
87 end of the latency relaxation (LR) preceding isometric force generation, approximately 10 ms after th
90 a powerful inotropic peptide that increases isometric force in isolated papillary muscle and the ext
92 resting sarcomere length similar to that of isometric force in the range 2.5-4.0 microm, but was les
94 actin filament velocities and higher average isometric forces (in an in vitro motility assay) when co
96 ing stroke responsible for the generation of isometric force is a larger fraction of the total myosin
98 ter value was normalised for the decrease in isometric force, it became 2.56 +/- 0.3 mM s(1), which i
100 ament compliance to sarcomere compliance and isometric force kinetics, the Ca(2+)-activation dependen
101 omycin inhibits myogenic tone and K+-induced isometric force largely by blockade of L-type, dihydropy
104 vasive measurement of airway resistance, and isometric force measurements in isolated bronchial rings
106 ith intracellular microelectrode recordings, isometric force measurements, Kit-like immunohistochemis
108 30% of the velocity and produced 65% of the isometric force of cells reconstituted with the thiophos
109 atin not only increases the mass and maximum isometric force of muscles, but also increases the susce
110 ded in organ chambers for the measurement of isometric force or frozen for isolation of membrane prot
112 ls were reduced to approximately 70% maximal isometric force (P4.5) in cardiac myocyte preparations,
113 ontraction, but as the fibres approached the isometric force plateau they showed little IS sensitivit
116 uced by 27.5 +/- 5.0% (P < 0.05), whilst the isometric force produced by the EDL-TA muscle group was
118 rylation on Ca(2+) dependence of myofilament isometric force production, isometric ATPase rate, and t
121 Elevated levels of phosphate (Pi) reduce isometric force, providing support for the notion that t
122 eshold force of units for recruitment during isometric force ramps in many different directions.
126 ted in a leftward shift of the concentration-isometric force relations for both aorta types, as expec
129 aorta, phenylephrine and KCl concentration- isometric force relations in the presence or absence of
131 of P(i)/mol of LC(20)) and similar levels of isometric force revealed differences in the rates of dep
132 ogether with the increased sliding speed and isometric force seen in the presence of regulatory prote
133 measured the time course of [Ca(2+)](i) and isometric force simultaneously in an intact artery after
134 roM free Ca2+ induced sustained increases in isometric force, stiffness, and rMLC phosphorylation.
137 V0 shortening is superimposed on the maximum isometric force T0 , n decreases progressively with the
139 thin filament sliding speed but reduced the isometric force that heavy meromyosin exerted on regulat
140 lue of the muscle force, F, approximates the isometric force, the muscle stiffness, E, is large, and
141 nt with PI(3,5)P2 increased the magnitude of isometric force, the rate of force development, and the
142 ; (2) rapid movement to position target; (3) isometric force to a target level; and (4) adaptation to
152 rol mice, but no reduction in muscle mass or isometric force was observed in SynTgSod1(-/-) mice comp
154 09 ms (mean +/- s.e.m.) to 113 +/- 17 ms and isometric force was reduced to 63 +/- 3% of the initial
158 at physiological temperatures, a decrease in isometric force, which mainly indicates a reduction in t
159 ng the Ca sensitivity of ATPase activity and isometric force, which were both completely restored by
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