Effect of cycle frequency and excursion amplitude on work done by rat diaphragm muscle

1989 ◽  
Vol 67 (10) ◽  
pp. 1294-1299 ◽  
Author(s):  
D. A. Syme ◽  
E. D. Stevens

Strips of isolated rat diaphragm muscle were attached to a servomotor–transducer apparatus, and the muscle length was cycled in a sinusoidal fashion about the length at which maximum isometric twitch force was developed, Lo. The amplitude of the length displacement (excursion amplitude) and rate of cycling were varied between 3 and 13% Lo and 1–4 Hz respectively. The muscle was tetanically stimulated (100 Hz, supramaximal voltage, stimulus duration (duty cycle) 20% of the length cycle period) during the shortening stage of the imposed length cycle at the phase that yielded maximum net positive work. The force and displacement of the muscle were recorded. Work per cycle was calculated from the area of the loop formed by plotting force against length for one full stretch–shorten cycle. Work per cycle decreased, but power increased, as cycle frequency was increased from 1 to 4 Hz. Maximum work done per cycle was about 12.8 J/kg at a cycle frequency of 1 Hz. Maximum mean power developed was about 27 W/kg and occurred at a cycle frequency of 4 Hz. Work and power were maximum at an excursion amplitude of 13% of Lo (i.e., Lo ± 6.5%). Measured work and power output are considerably less than values estimated from length–tension and force-velocity curves.Key words: rat, diaphragm, work, power, duty cycle.

1993 ◽  
Vol 71 (12) ◽  
pp. 910-916 ◽  
Author(s):  
E. D. Stevens ◽  
D. A. Syme

Isolated rat diaphragm muscle was stimulated repetitively to induce fatigue, and the work done during each contraction was measured. Work per cycle was calculated by measuring force as the activated muscle was subjected to sinusoidal length changes (from 97 to 103% of L0, where L0 is rest length). Work was calculated from the loop formed when force was plotted against length. Work done was positive when the muscle was shortening and was negative when it was lengthening; net work was the difference. Work output was varied by changing the stimulus duty cycle (4, 8, or 16% of the total cycle duration) and cycle frequency (1, 2, or 4 Hz). The rate and extent of the decrease in power was influenced much more by changes in cycle frequency than by changes in duty cycle. Duty cycle and cycle frequency combinations that resulted in greater power in the prefatigue trials were associated with a more rapid rate of fatigue. However, net positive power at the end of the 15-min fatigue period was greater under these same conditions (i.e., high duty cycle and high cycle frequency). Fatigue in working diaphragm muscle depends more on cycle frequency than on duty cycle.Key words: skeletal muscle, muscle power, respiratory muscle, muscle lengthening.


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.


1998 ◽  
Vol 85 (2) ◽  
pp. 525-529 ◽  
Author(s):  
H. F. M. Van Der Heijden ◽  
W. Z. Zhan ◽  
Y. S. Prakash ◽  
P. N. R. Dekhuijzen ◽  
G. C. Sieck

The effects of the β2-adrenoceptor agonist salbutamol (Slb) on isometric and isotonic contractile properties of the rat diaphragm muscle (Diamus) were examined. A loading dose of 25 μg/kg Slb was administered intracardially before Diamus excision to ensure adequate diffusion. Studies were then performed with 0.05 μM Slb in the in vitro tissue chamber. cAMP levels were determined by radioimmunoassay. Compared with controls (Ctl), cAMP levels were elevated after Slb treatment. In Slb-treated rats, isometric twitch and maximum tetanic force were increased by ∼40 and ∼20%, respectively. Maximum shortening velocity increased by ∼15% after Slb treatment, and maximum power output increased by ∼25%. During repeated isotonic activation, the rate of fatigue was faster in the Slb-treated Diamus, but both Slb-treated and Ctl Diamusfatigued to the same maximum power output. Still, endurance time during repetitive isotonic contractions was ∼10% shorter in the Slb-treated Diamus. These results are consistent with the hypothesis that β-adrenoceptor stimulation by Slb enhances Diamus contractility and that these effects of Slb are likely mediated, at least in part, by elevated cAMP.


1999 ◽  
Vol 202 (23) ◽  
pp. 3369-3375 ◽  
Author(s):  
R.K. Josephson

The primary determinants of muscle force throughout a shortening-lengthening cycle, and therefore of the net work done during the cycle, are (1) the shortening or lengthening velocity of the muscle and the force-velocity relationship for the muscle, (2) muscle length and the length-tension relationship for the muscle, and (3) the pattern of stimulation and the time course of muscle activation following stimulation. In addition to these primary factors, there are what are termed secondary determinants of force and work output, which arise from interactions between the primary determinants. The secondary determinants are length-dependent changes in the kinetics of muscle activation, and shortening deactivation, the extent of which depends on the work that has been done during the preceding shortening. The primary and secondary determinants of muscle force and work are illustrated with examples drawn from studies of crustacean muscles.


1993 ◽  
Vol 265 (2) ◽  
pp. R310-R319 ◽  
Author(s):  
D. A. Syme

Shortening, lengthening, and net work done by frog (Rana pipiens) heart trabeculae were measured over a range of strain amplitudes (length change) and cycle frequencies. Net work, the product of muscle strain and force over a full lengthening/shortening cycle, increased with strain to strains well over 25% of the muscle's rest length, a value greater than optimum strains reported for most skeletal muscles. A distinct optimum strain for net work was not found. Maximum net work per cycle averaged 7.5 J/kg for ventricular muscle and 2.0 J/kg for atrial muscle. Isometric twitch stress was maximal at 0.4-0.6 Hz twitch frequency in ventricular trabeculae (average 51 kN/m2) and 0.6-1.4 Hz in the atrium (average 14 kN/m2). The twitch duration decreased with increasing twitch frequency. Shortening and net work were maximal at 0.7-Hz cycle frequency in ventricular trabeculae and 0.9 to 1.4 Hz in the atrium. The decline in work per cycle at slower frequencies was due in part to a decline in twitch force. Maximum power for the ventricle was approximately 5 W/kg and occurred at 0.8 Hz and 26% strain, and was 1/3 to 1/4 the power of most skeletal muscles studied at similar temperatures.


1995 ◽  
Vol 79 (3) ◽  
pp. 738-747 ◽  
Author(s):  
E. Van Lunteren ◽  
M. Moyer ◽  
A. Torres

K+ channel blockers increase skeletal muscle force during twitch contractions; the present study determined whether K+ channel blockade also modulates force during longer term and higher frequency stimulation. 4-Aminopyridine (4-AP; 0.3 mM) increased rat diaphragm force during twitch, 5-Hz and 20-Hz but not 100-Hz stimulation, and prolonged isometric contraction but not half-relaxation time. In response to continuous 5-Hz stimulation, the rate of force decline was accelerated by 4-AP so that over time force dropped below that of control muscle strips. In response to intermittent 20-Hz stimulation, 4-AP produced an early force potentiation; the 4-AP-induced force increase was maintained throughout repetitive stimulation despite an accelerated rate of force decline. In response to continuous 100-Hz stimulation, 4-AP did not affect rate of force decline. During 5- and 20-Hz stimulation, there was an interaction between 4-AP and duration of stimulation in prolonging contraction and especially half-relaxation time. Tetraethylammonium (10 mM) augmented diaphragm force less than did 4-AP, did not affect rate of force decline during 5-Hz stimulation, and did not interact with fatigue to prolong isometric twitch kinetics. These data indicate that K+ channel blockade with 4-AP increases diaphragm force at low to intermediate stimulation frequencies, may increase early force potentiation during repetitive contraction, and depending on stimulation pattern either accelerates or has no effect on rate of fatigue.


1995 ◽  
Vol 269 (3) ◽  
pp. C713-C724 ◽  
Author(s):  
R. W. Grange ◽  
C. R. Cory ◽  
R. Vandenboom ◽  
M. E. Houston

Two studies were conducted to examine the effect of myosin regulatory light chain (R-LC) phosphorylation on the rate and extent of shortening in submaximally activated mouse extensor digitorum longus muscles in vitro at 25 degrees C. For each study, R-LC phosphate content was increased fivefold by application of a 5-Hz, 20-s conditioning stimulus (CS) to 0.65-0.68 mol phosphate/mol R-LC; this level was sustained between 10 and 40 s after the CS. Maximum isometric twitch force and the maximum rate of force development (+dF/dtmax) were potentiated in the range 13-17% and 9-17% (P < 0.05), respectively, after the CS. In study 1, the maximal rate and extent of shortening were significantly enhanced by 10 and 21% (P < 0.001), respectively, when measured using a twitch zero-load clamp technique. In study 2, the force-velocity and force-displacement relationships were both augmented when determined with the twitch afterload technique. Displacement was enhanced between 20 and 82% for loads that ranged from 3 to 75% of active peak twitch force, whereas velocity was increased 6-8% over the same range (P < 0.05), including the predicted maximum velocity (Vmax; 5.08 vs. 4.69 muscle length/s). In both studies the increase in velocity likely represents a shift along the force-velocity relationship toward true Vmax that reflects a decrease in relative load due to force potentiation. Furthermore, with the decrease in relative load, displacement at a given load was also increased. Potentiated displacement and extent of R-LC phosphorylation also decreased in parallel when studied for 5 min after the CS. The increase in muscle shortening is a novel finding and suggests a function for R-LC phosphorylation with respect to movement because both peak work and power were also enhanced by up to 22%. These effects are consistent with an R-LC phosphorylation-induced increase in fapp, the apparent rate constant that describes the cross-bridge transition from the non-force-generating to the force-generating state.


1988 ◽  
Vol 65 (5) ◽  
pp. 1950-1956 ◽  
Author(s):  
P. Herve ◽  
Y. Lecarpentier ◽  
F. Brenot ◽  
M. Clergue ◽  
D. Chemla ◽  
...  

Relaxation of rat diaphragm was shown to be sensitive to load, as previously described for adult mammalian ventricular muscle, because the time course of isotonic relaxation could be changed by changing the load: the lighter the load, the greater the shortening, the quicker the relaxation. Maximum velocity of isotonic relaxation was linearly related to the extent of shortening (r = 0.90). To quantify the degree of load sensitivity, we measured the tRi, i.e., the ratio of time at which the isometric relaxation of the twitch afterloaded at 50% of the isometric peak active tension began to time at which the isometric twitch was relaxed to 50% of the isometric peak active twitch tension. tRi was 0.76 +/- 0.03 (SE) in control conditions but significantly increased to 0.91 +/- 0.02 after ryanodine, which is an inhibitor of the sarcoplasmic reticulum (SR) function, and to 0.89 +/- 0.03 after fatigue. These results suggest that in adult rat diaphragm, as in cardiac muscle, the load sensitivity of relaxation requires a well-functioning SR and that the relaxation abnormalities observed in fatigued diaphragm are related to a dysfunction of the SR.


1997 ◽  
Vol 82 (2) ◽  
pp. 404-412 ◽  
Author(s):  
Catherine Coirault ◽  
Denis Chemla ◽  
Jean-Claude Pourny ◽  
Francine Lambert ◽  
Yves Lecarpentier

Coirault, Catherine, Denis Chemla, Jean-Claude Pourny, Francine Lambert, and Yves Lecarpentier. Instantaneous force-velocity-length relationship in diaphragmatic sarcomere. J. Appl. Physiol. 82(2): 404–412, 1997.—The simultaneous analysis of muscle force, length, velocity, and time has been shown to precisely characterize the mechanical performance of isolated striated muscle. We tested the hypothesis that the three-dimensional force-velocity-length relationship reflects mechanical properties of sarcomeres. In hamster diaphragm strips, instantaneous sarcomere length (S L) and muscle length were simultaneously measured during afterloaded twitches. S L was measured by means of laser diffraction. We also studied the influence of initial S L, abrupt changes in total load, and 2 × 10−7 M dantrolene. Baseline resting S L at the apex of the length-active tension curve was 2.2 ± 0.1 μm, whereas S L at peak shortening was 1.6 ± 0.1 μm in the preloaded twitch and 2.1 ± 0.1 μm in the “isometric” twitch. Over the whole load continuum and at any given level of isotonic load, there was a unique relationship between instantaneous sarcomere velocity and instantaneous S L. Part of this relationship was time independent and initial S L independent and was markedly downshifted after dantrolene. When five different muscle regions were considered, there were no significant variations of S L and sarcomere kinetics along the muscle. These results indicate that the time- and initial length-independent part of the instantaneous force-velocity-length relationship previously described in muscle strips reflects intrinsic sarcomere mechanical properties.


1990 ◽  
Vol 69 (2) ◽  
pp. 740-746 ◽  
Author(s):  
B. T. Ameredes ◽  
T. L. Clanton

A comparison of fatigue as a loss of force with repeated contractions over time was performed in canine respiratory muscle by isometric (nonshortening) and isovelocity (shortening) contractions. In situ diaphragm muscle strips were attached to a linear ergometer and electrically stimulated (30 or 40 Hz) via the left phrenic nerve to produce either isometric (n = 12) or isovelocity (n = 12) contractions (1.5 s) from optimal muscle length (Lo = 8.8 cm). Similar velocities of shortening between isovelocity experiments [0.19 +/- 0.02 (SD) Lo/S] were produced by maximizing the mean power output (Wmax = 210 +/- 27 mW/cm2) that could be developed over 1.5 s when displacement was approximately 0.30 Lo. Initial peak isometric tension was 1.98 kg/cm2, whereas initial peak isovelocity tension was 1.84 kg/mc2 (P less than 0.01) or 93% of initial isometric tension. Fatigue trials of 5 min were conducted on muscles contracting at a constant duty cycle (0.43). At the end of the trials, peak isovelocity tension had fallen to 50% of initial isometric tension (P less than 0.01), whereas peak isometric tension had only fallen by 27%. These results indicate that muscle shortening during force production has a significant influence on diaphragm muscle fatigue. We conclude that the effects of shortening on fatigue must be considered in models of respiratory muscle function, because these muscles typically shorten during breathing.


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