Peak Twitch Tension Research Articles

Fatigue Resistance of Canine Vocal Fold Muscle

The objective of the experiment was to provide data from dogs, the best nonprimate model for the contractile properties of laryngeal muscles, on the fatigue characteristics of vocal fold muscle. Isometric muscle force was recorded from a transducer attached to the section of the thyroid cartilage on which the muscle inserted. Twitch contractions were recorded during supramaximal indirect electrical stimulation by DC pulses for at least 30 minutes. At 5 pulses per second (p/s), potentiation was observed in all records, peaking at an average of 7.5 minutes after stimulation onset. At 10 p/s, the peak of the potentiated average trace was earlier. One third of these records did not show potentiation. Where moderate or large potentiation was observed, the peak twitch tension declined and reached an asymptote above the initial tension, while when potentiation was small or absent, the final force was smaller than initially. Canine vocal fold muscle was observed to be fatigue-resistant, but in phonation other factors may produce fatigue.

Staircase potentiation in isolated frog skeletal muscle: Power spectral analysis of the evoked compound muscle action potential

1. 1. The mechanical and electrophysiological effects of repetitive, low-frequency electrical stimulation on paired sartorii muscles from small male frogs have been investigated, in vitro. 2. 2. Stimulation for 90 sec at 5 Hz resulted in a progressive rise (staircase) then fall (fatigue) in peak twitch tension. 3. 3. The root mean square amplitude, peak-to-peak amplitude, conduction velocity and mean power frequency of evoked compound muscle action potentials (CMAPs) decreased over the stimulation period. 4. 4. Results suggest that alterations in the shape of the CMAP during repetitive stimulation may contribute to the staircase phenomenon.

Dependence of contractile responses by some calcium antagonists on external calcium in the skeletal muscle.

Dependence of contractile potentiation by calcium antagonists on external calcium was investigated on the frog's twitch muscle. Low concentrations (10(-6) to 10(-5) M) of nicardipine and verapamil enhanced the peak tension of both twitch and electrically induced contracture in the presence of calcium. In the calcium-free media the drugs suppressed the contractile tension. Caffeine contracture was inhibited by the calcium antagonists at 20 degrees C. This inhibition was caused by an early onset of relaxation, which was not observed at 7 degrees C. The results suggest that some interaction between calcium ions and drug molecules at the voltage sensor on the transverse tubular membrane, which regulates E-C coupling but is not directly related to the functional calcium channel, may play an important role for the phenomena. The inhibitory action of calcium antagonists on the caffeine contracture in the presence of calcium is probably independent of the potentiating effect seen in the depolarization-induced contractions.

The relationship between post-tetanic potentiation of motor units and myosin isoforms in mouse soleus muscle

Post-tetanic potentiation was measured in motor units, isolated functionally by ventral root splitting, of soleus and extensor digitorum longus muscles of mouse. All motor units from the extensor digitorum longus had times to peak twitch tension less than 13 ms; there was a linear relationship between time to peak tension and post-tetanic potentiation, with the faster units exhibiting greater potentiation. When soleus motor units were similarly analyzed, it appeared that there may be two distinct populations of units. Those units with times to peak tension less than 13 ms were virtually indistinguishable from those of extensor digitorum longus. On the other hand, the slope of the relationship between post-tetanic potentiation and time to peak tension was significantly lower for soleus units with times to peak tension of 13 ms or more. Approximately three-quarters of the soleus units were of the latter slow type, whereas only one-half of the muscle fibres could be classified as type I by means of immunohistochemistry, suggesting that the myosin heavy chain may not be the major determinant of post-tetanic potentiation. Single, chemically skinned fibres of soleus were analyzed for myosin heavy and light chain components by polyacrylamide gel electrophoresis. All fibres with type I heavy chain contained only the two slow light chains. On the other hand, almost all of the fibres with type IIA myosin heavy chain contained both fast and slow light chains. It is suggested that the discrepancy between the proportions of physiologically "fast" motor units and histochemical type IIA fibres may be the consequence of variable amounts of slow light chain associated with the fast IIA myosin heavy chain.

Extracellular calcium and the inotropic effect of epinephrine on frog skeletal muscle.

The purpose of these experiments was to determine if extracellular calcium plays an important role in mediating the inotropic effect of epinephrine in isolated frog sartorius muscle. Initial experiments indicated that epinephrine potentiated the muscle twitch in a concentration-dependent manner with concentrations of 10 microM to 1 mM, increasing peak tension by approximately 33%. To inhibit the influx of extracellular calcium, muscles were incubated for 20 min in media containing epinephrine in which calcium had been removed and replaced by magnesium or EDTA, or in experimental media containing epinephrine and the calcium channel blockers D-600 or diltiazem (5 microM). Each experimental condition was found to antagonize the effects of epinephrine such that peak twitch tensions were not significantly different from the control. When muscles were returned to normal Ringer's solution containing epinephrine, twitches exhibited progressive potentiation. Muscles were also incubated for 20 min in epinephrine without stimulation. Once stimulation was resumed, twitches were not immediately potentiated but rather gradually increased over time. These results suggest that the inotropic effects of epinephrine are influenced by the influx of extracellular calcium, an event that is dependent on muscle activation.

Influence of isoproterenol on myocardial energetics. Experimental and clinical investigations.

The influence of isoproterenol on myocardial performance and energetics was investigated in normal guinea pig myocardium and in patients with normal left ventricular function. The in vitro experiments were performed by simultaneous isometric force and heat measurements using sensitive antimony-bismuth thermopiles. Following the application of isoproterenol (10(-8) M) isometric peak twitch tension and tension-time integral increased significantly by 185% and 142%, respectively. Tension-independent heat which reflects high energy phosphate hydrolysis of excitation-contraction coupling increased by 183%. Tension-dependent heat reflecting the high energy phosphate hydrolysis of the crossbridges increased by 417%. The ratio of tension-dependent heat to tension-time integral increased by 131%. The recovery/initial heat ratio, reflecting the efficiency of the recovery metabolism, and the resting metabolism did not significantly change. In the patients the effect of isoproterenol on myocardial energetics was evaluated in terms of myocardial efficiency. Following isoproterenol administration, left ventricular systolic stress-time integral decreased by 49% due to reductions in end-diastolic pressure, end-diastolic volume and duration of systole. Pressure-volume work remained unchanged. Myocardial oxygen consumption per minute increased in proportion to heart rate. The ratio of myocardial oxygen consumption per beat to left ventricular systolic stress-time integral increased significantly by 95%. External myocardial efficiency was unaltered. Thus, isoproterenol increases the energy turnover of excitation-contraction coupling and increases the energy consumption of the crossbridges disproportionately to developed tension-time integral in the guinea pig heart.

Protection of human left ventricular myocardium from cutting injury with 2,3-butanedione monoxime.

To prevent dissection injury when cutting strip preparations from human left ventricular papillary muscle tissue, dissections were carried out with 2,3-butanedione monoxime (30 mM) added to Krebs-Ringer solution and followed by washout with normal solution. Eleven muscle strip preparations were dissected from left ventricular papillary muscle tissue of five patients undergoing mitral valve replacement surgery. The average muscle strip length was 6.8 +/- 1.4 mm, and cross-section area was 0.49 +/- 0.16 mm2. Peak twitch tension was 2.02 +/- 1.33 g/mm2 and ranged from 0.67 to 5.5 g/mm2 at an extracellular calcium concentration of 2.5 mM (21 degrees C, 0.16 Hz). In one muscle strip, which was stored in Krebs-Ringer plus 2,3-butanedione monoxime solution for 20 hours, peak twitch tension in normal Krebs-Ringer solution was 1.85 g/mm2. When temperature was increased from 21 degrees C, there was a continuous increase in peak twitch tension (by 38%) up to about 28 degrees C; then peak twitch tension decreased so that at 37 degrees C (n = 3) average peak twitch tension was lower than at 21 degrees C by 47%. The force-frequency relation exhibited a broad force plateau between 40 and 120 beats/min at 37 degrees C. The plateau was markedly narrowed at 30 degrees C and 24 degrees C. Thermopile heat measurements revealed appropriate waveform characteristics in high-resolution single-beat heat records indicating minimal surface cell damage. Thus, cardioplegia with 2,3-butanedione monoxime protects human left ventricular myocardium from dissection injury facilitating dissection and preservation of strip preparations with extraordinarily low cross-sectional areas and high peak twitch tensions. These preparations are suitable for myothermal and mechanical measurements.

Contractile properties of cardiac papillary muscle in streptozotocin-diabetic rats and the effects of aldose reductase inhibition

This study examined the preventative effect of an aldose reductase inhibitor, ponalrestat, on contractile properties of heart left ventricular papillary muscles in rats having streptozotocin induced diabetes for 13 weeks. Both contraction and relaxation were slowed by diabetes. The time to reach peak twitch tension was increased by 21%, and the time to relax to half peak tension was increased by 29% (p less than 0.01, respectively compared to normal control animals). With ponalrestat treatment, the increase in contraction time was only 11%, and relaxation was only slowed by 4% (p less than 0.05 and p less than 0.01, respectively compared to diabetic controls). Diabetes also reduced maximum rates of contraction (13%) and relaxation (19%) and prolonged the time taken to reach peak relaxation rate (36%, p less than 0.01). Ponalrestat had no effect on maximum contraction rates but was particularly effective in normalising relaxation rates (p less than 0.01). Deficiencies with diabetes were noted over a range of stimulation frequencies (0.1-4.0 Hz), and ponalrestat treatment was beneficial except at the highest rates. Diabetes and ponalrestat effects were observed over a temperature range of 25-37 degrees C. Ventricular sorbitol levels showed a 17-fold increase with diabetes (p less than 0.01) and this was reduced by 67% with ponalrestat (p less than 0.01). There were no changes in ventricular myo-inositol. It is possible that ponalrestat treatment prevented a defect in sarcoplasmic reticulum calcium handling which could be responsible in part for the deficits in contraction ability and mainly for the deficits in relaxation ability in diabetic cardiomyopathy, although this remains to be tested directly.

Dissociation of changes in apparent myofibrillar Ca2+ sensitivity and twitch relaxation induced by adrenergic and cholinergic stimulation in isolated ferret cardiac muscle.

In isolated, aequorin-injected ferret cardiac muscle we measured the apparent myofilament Ca2+ sensitivity and its relationship to twitch relaxation time in the presence of autonomic perturbations. The Ca2+-tension relation was determined from the peak aequorin luminescence and peak twitch tension measured in muscles across a broad range of bathing [Ca2+] in the presence and absence of acetylcholine (ACh) (1 microM) or isoproterenol (ISN) (1 microM), or both drugs. ACh shifted the relationship of peak tension to (peak) aequorin light leftward, which suggests an increase in myofilament Ca2+ sensitivity, but it did not alter relaxation, which was measured as the time for peak tension to decay by 50% (t 1/2 R). ISN produced its previously documented effects, i.e., a rightward shift of the relationship of peak tension to peak aequorin light and a decrease in t1/2R. ACh abolished the ISN effect on the peak tension-aequorin light relationship but did not reverse the effect of ISN to decrease t1/2R. The effects of ACh and ISN of modulating the apparent myofilament Ca2+ sensitivity in intact muscles, corroborate findings of previous studies in isolated myofibrillar preparations. However, these perturbations of myofilament Ca2+ sensitivity in the intact muscle do not relate to twitch relaxation, measured as t1/2R, since (a) ACh affects the former but not the later and (b) the effect of ISN on the Ca2+-tension relationship is abolished by ACh, while the relaxant effect persists.

Mechanical properties of muscle units in the cat diaphragm.

1. Muscle units in the right sternocostal region of the cat diaphragm (DIA) were isolated in situ by dissecting filaments of the C5 ventral root. Isometric contractile and fatigue properties of DIA units were then measured. Contractile properties included: twitch contraction time (CT), peak twitch tension (Pt), maximum tetanic tension (P0), and the frequency dependence of tension production. Muscle-unit fatigue resistance was estimated using a 2-min fatigue test. 2. DIA muscle units were classified as fast (F) or slow (S) based on the presence or absence of sag in their unfused tetanic force responses. Muscle-unit fatigue indices (FI) were used to further classify DIA units as slow-twitch fatigue-resistant (S), fast-twitch fatigue-resistant (FR) fast-twitch fatigue-intermediate (FInt), or fast-twitch fatigable (FF) types. 3. Based on a total of 47 completely characterized DIA muscle units, 21% were classified as S, 4% as FR, 28% as FInt, and 47% as FF. In contrast to the distribution of unit types in other mixed appendicular muscles, the DIA was composed of a very low proportion of FR units and a relatively high proportion of FInt units. An interval of FIs between 0.50 and 0.75 separated units into fatigue-resistant and fatigable groups. The distribution of FIs for FF and most FInt units was continuous, indicating that they formed a single fatigable group. Relatively few FF units in the DIA had FIs less than 0.10. 4. A wide range of contractile properties was observed for DIA muscle units. Type S units had longer CTs and lower Pt and P0 values than type F units. The mean Pt and P0 of FF and FInt units were comparable, whereas the mean Pt and P0 of the two FR units were lower. Type S units produced a greater proportion of their P0 at lower frequencies of activation than type F units. The lower P0S produced by type F units in the DIA indicated that they were smaller than similar units in appendicular muscles. It was concluded that in meeting most normal ventilatory requirements, adequate force could be generated by the recruitment of only type S and FR units. The recruitment of the more fatigable FF and FInt units may occur only during more forceful respiratory and nonrespiratory behaviors of the DIA.

Low-frequency diaphragmatic fatigue in spontaneously breathing humans.

We used transdiaphragmatic peak twitch tension (PTT) elicited by bilateral phrenic nerve stimulation to ascertain whether low-frequency (LF) diaphragmatic fatigue (DF) can be induced in spontaneously breathing humans by a combination of an inspiratory resistive load (IRL) and graded treadmill exercise (GXT). Our subjects were 10 young males with normal cardiopulmonary function. Before exercise we measured PTT in each subject by administering supramaximal electrical pulses of 100-microseconds duration at a frequency of 1 Hz to each phrenic nerve with the subjects breath holding at functional residual capacity at a given thoracoabdominal configuration. A minimum of six satisfactory PTT measurements were made in each subject, and we computed the 95% confidence limits (CL) for each subject. The subjects then inspired through a resistive load of 38 cmH2O.1(-1).s-1 while carrying out the GXT until exhaustion. After the GXT, PTT was remeasured in all subjects. In five of the subjects, the post-GXT mean PTT fell below the 95% CL of the pre-GXT mean PTT. However, post-GXT PTT means for the other five subjects were within the 95% CL of the pre-GXT means. In conclusion, using PTT as a measure of LFDF, these results demonstrate that LFDF can be produced in 50% of spontaneously breathing young normal males.

Effects of immobilization on the isometric contractile properties of embryonic avian skeletal muscle

Chicken embryos were chronically immobilized by applying a neuromuscular blocking agent, curare, to the chorioallantoic membrane from day 8 through day 16 of incubation to study the effects of a deficit in motor activity on the development of contractile properties of skeletal muscle. Compared with control embryos, spontaneous embryonic motor activity was depressed by 60 to 90% in the curare-treated animals during the treatment period. Growth of the posterior latissimus dorsi muscle, a fast-twitch muscle in the adult, was greatly affected by immobilization. The average blotted mass of the muscles from curare-treated 18- to 19-day embryos was approximately 20% of that from control embryos. The isometric contractile properties of posterior latissimus dorsi muscles isolated from control and curare-treated embryos were compared at 18 to 19 days of incubation. The times to peak tension and to one-half relaxation of the twitch and tetanic responses were significantly greater for the muscles from the immobilized embryos. The peak twitch and tetanic tensions, normalized for muscle cross-sectional area, were significantly less than control values for the muscles from curare-treated embryos. The maximal rate of tetanic tension production was, however, unaffected by immobilization. The results of this study demonstrate that the development of isometric contractile properties of embryonic skeletal muscle is significantly altered by an experimentally induced reduction of spontaneous motor activity. A disruption in the functional development of the sarcoplasmic reticulum following a similar decrease in motor activity, as reported by others, is discussed as a potential mechanism for the altered contractile properties of muscles from the curare-treated embryos.

The effects of isoproterenol, UDCG 115, and caffeine on the heart related to excitation-contraction coupling in heart muscle.

A myothermal technique was used to measure initial heat and tension independent heat from isometrically contracting papillary muscles taken from the right ventricle of rabbits. Tension independent heat produced by the muscle at Lo was isolated with a 2,3-butanedione monoxime (diacetyl monoxime)--hyperosmotic Krebs solution. The effects of the inotropic drugs isoproterenol (1 X 10(-7) M), UDCG 115 (2 X 10(-4) M), and caffeine (2 X 10(-3) M) on heat and mechanical output were measured. We tested the hypothesis that these drugs alter peak twitch tension by increasing the total amount of Ca2+ cycled during the twitch, assuming that net tension independent heat is proportional to total Ca2+ cycled. The hypothesis was rejected for each drug as the positive inotropic effects of isoproterenol and UDCG 115 on twitch tension were not accompanied by increases in net tension independent heat. Net tension independent heat was actually depressed by UDCG 115. The negative inotropic effect of caffeine on twitch tension was accompanied by an increase in tension independent heat at times between the end of mechanical relaxation and the next stimulus. Possible mechanisms to account for these results are discussed.

Effects of caffeine on intracellular calcium concentrations in frog skeletal muscle fibres.

1. The mechanism of twitch potentiation by caffeine was studied in single muscle fibres dissected from m. tibialis anterior of Rana temporaria. Fibres were injected with a Ca2+-sensitive photo-protein, aequorin, and the resultant light signal and tension were simultaneously recorded. 2. In twitch responses triggered every 60 s, peaks of light and tension were maintained at a constant level. Low concentrations of caffeine (0.2-0.4 mM) potentiated twitch tension accompanied by a slight increase in light signal. 3. Although peak twitch tension was dose-dependently potentiated by caffeine, light peaks were suppressed at relatively higher concentrations of caffeine (0.6-1.5 mM) with prolonged decay of the light and tension signals. 4. Light intensity in the resting muscle (resting glow) was elevated by caffeine (0.2-1.5 mM) dose-dependently without detectable tension development. This effect of caffeine was suppressed by 0.5-1.0 mM-procaine or 10 mM-adenine, inhibitors of Ca2+-induced Ca2+ release. 5. In caffeine-treated preparations, peaks of light and tension were augmented by application of procaine (0.5-1.0 mM). Adenine (10 mM) affected the light signal in essentially the same way as procaine, but the effect varied from fibre to fibre. 6. From these results, the following hypothesis is proposed: low concentrations of caffeine directly induce Ca2+ release from sarcoplasmic reticulum (s.r.) in in the resting state, and facilitates Ca2+ release from s.r. induced by the action potential during twitch. At relatively higher concentrations of caffeine (0.6-1.5 mM), rise of resting [Ca2+]i (intracellular free Ca2+ concentration) before activation might be an important factor in twitch potentiation by caffeine. If the rise of resting [Ca2+]i induced by caffeine is inhibited by procaine and the content of Ca2+ in s.r. is well maintained, caffeine could facilitate Ca2+ release by depolarization and thus potentiate twitch tension.

The effects of acute and chronic inotropic interventions on tension independent heat of rabbit papillary muscle.

We have used the myothermal method to noninvasively monitor the amount of calcium cycled during a single isometric twitch of rabbit papillary muscle. Experiments were designed to test the working hypothesis that changes in peak twitch tension caused by pharmacological agents or changing haemodynamic conditions are accompanied by parallel changes in the tension independent heat (TIH) signal associated with Ca2+ cycling. We isolated the TIH signal by eliminating the tension dependent component of initial heat with a hyperosmotic Krebs solution containing 2,3-butanedione monoxime. Contrary to the working hypothesis, positive or negative inotropic effects on twitch tension caused by pressure overload hypertrophy, thyrotoxic hypertrophy, isoproterenol, and UDCG115 were not accompanied by parallel changes in TIH. Alternative explanations for the relation between peak twitch tension and TIH are explored.

Functional property of the masseter muscle in man

The purpose of this paper is to investigate the functional property of the masseter muscle at the motor unit level in man. The responses of the surface EMG and the bite force were studied by averaging technique, with the following results.1. The higher threshold units with large twitch tensions were found in the superficial layer of the muscle, the lowers were throughout the muscle.2. Positive correlation was found between voluntary threshold force and peak twitch tension, linear correlation coefficient was 0.76.3. The motor units with a larger twitch tension tended to have shorter contraction time, but those of smaller had the wide range.4. There was a tendency for deeper-layer units to contribute less to the wave form of the surface EMG than did the superficial units.5. There was a significant tendency for the units recruited with larger forces to contribute extensively to the surface EMG. The linear correlation coefficient was 0.70.6. In 106 force records, DEM (the discrepancy between electrical activity and mechanical contraction) was observed. It seemed that DEM was similar phenomenon to the latency relaxation.

Thermal dependence of contractile properties of skeletal muscle from the lizard Sceloporus occidentalis with comments on methods for fitting and comparing force-velocity curves.

The isometric and isotonic contractile properties of fast-twitch glycolytic fibres of the iliofibularis muscle (FG-IF) in the lizard Sceloporus occidentalis were measured in vitro at 5 degrees C intervals form 10 to 40 degrees C. The mean isometric parameters at 35 degrees C, the preferred body temperature of this species, were as follows: maximum isometric force (Po), 187 +/- 8 (S.E.M.) kNm-2; ratio of twitch force to tetanic force (PTW/Po), 0.46 +/- 0.02; time to peak twitch tension (tPTW), 7.0 +/- 0.3 ms; and time from peak twitch force to 50% relaxation (t50% ), 8.2 +/- 0.3 ms. From 20 to 35 degrees C Po was almost constant (within 8% of the value at 35 degrees C). At 10 and 15 degrees C C. Po dropped to approximately 80% of the value at 35 degrees C. Po was very unstable at 40 degrees C. PTW/Po was almost constant at all temperatures. The time-related isometric parameters were positively modified by temperature at all temperatures measured (Q10 greater than 1.9). The force-velocity curves of the FG-IF deviated from the simple hyperbolic relation of A. V. Hill's characteristic equation. We present two alternative equations for fitting these data. These equations resulted in residual sums of squares from nonlinear least-squares analysis that were at least seven-fold lower than those from Hill's equation. The equation that best describes our data is a hyperbola modified by the addition of a linear component: V = B(1 - P/Po)/(A + P/Po) + C(1 - P/Po). To describe the curvature of this or any other force-velocity relationship, we propose the power ratio, Wmax/VmaxPo (where Wmax is the maximum power calculated from the force-velocity relationship and Vmax is the predicted maximum velocity of shortening at zero force). Vmax of the FG-IF was 21.9LoS-1 at 35 degrees C (where Lo is muscle length). This parameter was directly related to temperature between 10 and 35 degrees C with Q10 greater than 1.8. The shape of the force-velocity curve is not influenced by temperature (Wmax/VmaxPo = 0.11).

The effect of electrical stimulation on reinnervation of rat muscle: contractile properties and endplate morphometry

Denervated extensor digitorum longus muscles of Wistar rats were electrically stimulated in vivo for 4 days (2 h per day) after peroneal nerve crush 1 cm from the muscle. Isometric contractile properties and endplate ultrastructure were measured on days 11 and 18. On day 11, the time to peak (116% of control) and 1/2-relaxation time (136% of control) for the twitch tensions of stimulated muscles measured in vivo were significantly less than those (127% and 157% of controls, respectively) of non-stimulated muscles. Peak twitch and tetanic tensions were not significantly different. The postsynaptic area of endplates for stimulated muscles were closer in size to controls than those for the non-stimulated ones. On day 18, no difference was found in the contractile responses between stimulated and non-stimulated groups. Similarly, the postsynaptic areas were the same for both groups. These results demonstrate that denervated muscle stimulated electrically for 4 days prior to reinnervation can preserve the structure of the endplate as well as accelerate recovery of normal function in reinnervated muscle fibers after 11 days of denervation.

Effects of aminophylline and salbutamol on diaphragmatic force during compensated metabolic acidosis.

We investigated the effects of aminophylline and salbutamol on tetanic force generated by the diaphragm during compensated metabolic acidosis in dogs. Anesthetized, mechanically ventilated animals were prepared with an open thorax. A cast was placed around the abdomen to maintain length and geometry of the diaphragm during contractions. A thin-walled latex balloon was positioned beneath the diaphragm to measure transdiaphragmatic pressure (Pdi). Pdi served as the index of diaphragmatic force of contraction. We measured Pdi during supramaximal phrenic stimulation at low and high frequencies and also during spontaneous inspiratory efforts for a constant diaphragmatic EMG activity. Compensated metabolic acidosis significantly reduced Pdi at all stimulation frequencies (p less than 0.05). The mean percent decrease at low frequencies was greater than at high (p less than 0.05). Pdi was decreased during spontaneous contractions as well (p less than 0.05). Administration of aminophylline significantly improved Pdi at all frequencies of phrenic stimulation (p less than 0.05) and during spontaneous inspiratory efforts (p less than 0.05). Infusion of salbutamol did not have a significant effect on Pdi at any frequency of stimulation but did produce a small potentiating effect during spontaneous contractions (p less than 0.05). We also recorded and analyzed the Pdi response to a single supramaximal impulse to the phrenic nerve, referred to as a twitch, to gain insight into possible cellular mechanisms underlying alterations in tetanic force of contraction. Compensated metabolic acidosis led to a significant reduction in peak twitch tension (PTT) (p less than 0.05) and half relaxation time (1/2RT) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Submaximal sodium-lack contractures in rapidly perfused frog ventricular strips.

Rapid perfusion of strips of frog ventricular muscle (width less than or equal to 8 mm) by sodium-free Ringer yielded contractures with very fast rates of rise (half time approximately equal to 2 s) and flat plateaus. Tension in lithium Ringer was 0.64 (0.38-0.77) of the maximal tension the muscle could produce [i.e., for an extracellular potassium concentration ([K]o) of 160 mM, and an [Na]o of 0 mM at less than 15 degrees C], showing that intracellular calcium concentration ([Ca]i) in zero [Na]o and normal [K]o was insufficient to saturate the myofilaments. Tension was related to [Ca]o in an S-shaped manner (apparent Km = 1.3 microM), was rapidly increased by electrical depolarization, high potassium, or low temperature, but was unaffected by up to 10(-5) M dihydroouabain. From these data was derived the working hypothesis that the value of [Ca]i during the contracture plateau is a steady-state value due to influx through a sodium-dependent mechanism and calcium uptake or efflux via a sodium-independent mechanism. Also, 1 microM dihydroouabain increased peak twitch tension by 60% but did not potentiate tension during the plateaus of contractures obtained by partial replacement of Nao. This result supports the working hypothesis and suggests that the potentiating effect of raising Nai may depend on the membrane potential (D. A. Eisner, W. J. Ledener, and R. D. Vaughan-Jones. J. Physiol. Lond. 335: 723-743, 1983).