Increase In Peak Tension Research Articles

Peak and Per-Step Tibial Bone Stress During Walking and Running in Female and Male Recreational Runners

Background: Athletes, especially female athletes, experience high rates of tibial bone stress injuries (BSIs). Knowledge of tibial loads during walking and running is needed to understand injury mechanisms and design safe running progression programs. Purpose: To examine tibial loads as a function of gait speed in male and female runners. Study Design: Controlled laboratory study. Methods: Kinematic and kinetic data were collected on 40 recreational runners (20 female, 20 male) during 4 instrumented gait speed conditions on a treadmill (walk, preferred run, slow run, fast run). Musculoskeletal modeling, using participant-specific magnetic resonance imaging and motion data, was used to estimate tibial stress. Peak tibial stress and stress-time impulse were analyzed using 2-factor multivariate analyses of variance (speed*sex) and post hoc comparisons (α = .05). Bone geometry and tibial forces and moments were examined. Results: Peak compression was influenced by speed (P < .001); increasing speed generally increased tibial compression in both sexes. Women displayed greater increases in peak tension (P = .001) and shear (P < .001) than men when transitioning from walking to running. Further, women displayed greater peak tibial stress overall (P < .001). Compressive and tensile stress-time impulse varied by speed (P < .001) and sex (P = .006); impulse was lower during running than walking and greater in women. A shear stress-time impulse interaction (P < .001) indicated that women displayed greater impulse relative to men when changing from a walk to a run. Compared with men, women displayed smaller tibiae (P < .001) and disproportionately lower tibial forces (P≤ .001-.035). Conclusion: Peak tibial stress increased with gait speed, with a 2-fold increase in running relative to walking. Women displayed greater tibial stress than men and greater increases in stress when shifting from walking to running. Sex differences appear to be the result of smaller bone geometry in women and tibial forces that were not proportionately lower, given the womens’ smaller stature and lower mass relative to men. Clinical Relevance: These results may inform interventions to regulate running-related training loads and highlight a need to increase bone strength in women. Lower relative bone strength in women may contribute to a sex bias in tibial BSIs, and female runners may benefit from a slower progression when initiating a running program.

Cardiac Inotropic Effect of Long-Term Administration of Oral Thymoquinone.

Back Ground Long-term administration of Nigella sativa showed cardiac hypertrophic and positive inotropic effects. Thymoquinone (TQ) is an active ingredient in Nigella sativa. Therefore, we aimed to test the cardiac effects of long-term TQ administration. Materials and Methods Twenty adult Wistar rats weighing (150-250 g) were divided into two groups: control and TQ. A TQ-olive oil solution was administered orally to the TQ group (dose 10 mg/kg) for two months. An equivalent volume of olive oil was given to the control group. Langendorff isolated hearts were studied. Peak tension, time to peak tension, half relaxation time, and myocardial flow rate were determined. Heart and left ventricle weights and ratios were recorded. Results The TQ group exhibited significantly higher peak tension than the control group. There were no significant differences between the two groups in time to peak tension, half relaxation time, and myocardial flow rate. Likewise, there were no signs of cardiac hypertrophy. Conclusions Long-term administration of oral TQ induced a positive inotropic effect in the form of an increase in peak tension. TQ administration did not result in cardiac hypertrophy or an increased cardiac metabolic demand at the studied dose. TQ may be a promising inotropic agent.

Timing and Magnitude of Prestretch Strongly Affect Cardiac Muscle Tension Development

Ectopic ventricular pacing leads to regional myocardial prestretch. In-vivo studies suggest that the timing of prestretch determines the effect on pump function and can lead to regional wall remodeling. Here we measure the direct effects of prestretch timing on the magnitude of tension development in isolated cardiac muscle. Prestretch strongly affected tension development but primarily during a brief interval of the twitch. The effects of prestretch were simulated using excised murine right ventricular papillary muscles. A high-speed computer-controlled motor was used to impose precisely timed stretches, while a force transducer measured force output and strain was monitored using a CCD camera and topical markers. The timing of the stretches greatly influenced tension production. A critical stretch timing interval was observed to begin 25 ms after stimulation and extending until 100 ms after stimulation, where stretches occurring in this interval exhibited statistically significant increases in peak tension of as much as 500%. Muscle shortening occurring in the critical interval (from stretches initiated prior to stimulation) showed the opposite effect of stretching in the interval, with peak tension inhibited significantly by as much as 40%. A simple model showed that the varying impact of stretch timing could not be explained by time-varying elastance alone. Therefore, a more detailed and mechanistic myofilament model that included cooperative activation (Campbell et al 2010) was refined to include length dependence and strain-dependent cross-bridge kinetics. By comparing model results and experimental measurements, the strain history dependent mechanisms of these observations was evaluated. These evaluations have led us to the conclusion that even prestretches performed at slow physiologic velocities cause alterations in twitch kinetics that cannot be explained by time varying elastance.

Structure, Property, and Relaxation Behavior of Mulberry (Bombyx Mori) and Tasar (Antheraea Mylitta) Silk

ABSTRACT Mechanical properties of fully degummed filaments of mulberry and tasar silk have been investigated and correlated with structure and morphology. The tensile behavior of mulberry silk filament was different from tasar, which demonstrated characteristic yield point, lower modulus, and breaking extension twice as high as that of mulberry. Stress relaxation and inverse relaxation/stress recovery were observed for both varieties of silk. The magnitude of inverse relaxation increases with the increase in peak tension and reduction in retraction also observed with the decrease in peak tension. Tensile properties and relaxation behavior were correlated with density, birefriengence, orientation index, and sonic modulus.

Study of creep, stress relaxation, and inverse relaxation in mulberry (Bombyx mori) and tasar (Antheraea mylitta) silk

AbstractThe phenomena of creep, stress relaxation, and inverse relaxation/stress recovery were observed for mulberry and tasar silk. Instantaneous extension and secondary creep are both higher for tasar than for mulberry. The magnitude of inverse relaxation increases with the increase in peak tension and reduction in retraction for both varieties of silk. The extent of inverse relaxation was found to reduce because of cycling stressing. © 2006 Wiley Periodicals, Inc. J Appl Polym Sci 99: 3077–3084, 2006

Is the blood flow response to a single contraction determined by work performed?

Nine healthy volunteers performed a series of single handgrip isometric contractions to test the hypothesis that the blood flow response to a contraction is determined solely by the tension-time index (isometric analog of work). Contractions were performed in duplicate at 15, 30, and 60% of maximal voluntary contraction (MVC) at durations of 0.5, 1, and 2 s. Forearm blood flow (FBF) was measured beat by beat by using Doppler ultrasound. Peak FBF responded in a graded fashion to graded increases in peak tension with contraction time held constant (35, 56, and 90 ml/min for 15, 30, and 60% MVC for 1 s, respectively). When tension was kept constant, peak FBF responded in a graded fashion to graded increases in duration (77, 90, and 97 ml/min for 60% MVC for 0.5, 1, and 2 s). With a constant tension-time index, peak FBF responded in a graded fashion to graded increases in peak tension (48, 56, and 77 ml/min for 15% MVC/2 s, 30% MVC/1 s, and 60% MVC/0.5 s). Similar trends were also observed for total postcontraction hyperemia. Blood flow increased regardless of whether the change in tension-time index was accomplished by an increase in tension or duration of contraction. However, with a constant tension-time index, the change in blood flow was related to the peak tension developed. Our results suggest that the blood flow response to a single muscle contraction is not determined solely by the work performed (tension-time index) but also by the number of muscle fibers recruited.

Nitric oxide is not involved in the endotoxemia-induced alterations in Ca2+ and ryanodine responses in mouse diaphragms.

Lipopolysaccharide (LPS, endotoxin)-induced diaphragmatic contractile dysfunction and sarcolemmal injury in animals has been identified. However, the precise nature of sepsis-related alterations in diaphragm myofiber function and the activity of Ca(2+) release from sarcoplasmic reticulum of skeletal muscle remain unclear. The present study investigated the in vivo effects of LPS on the Ca(2+)-dependent mechanical activity and ryanodine response in mouse diaphragm and Ca(2+) release from isolated sarcoplasmic reticulum membrane vesicles, and aimed to examine the role of nitric oxide (NO) in these responses. When diaphragms were bathed in a solution that was Cl(-)-free, Na(+)-free, but contained high K(+), a Ca(2+)-induced contracture was elicited. Increases in external Ca(2+) concentration produced increases in peak tension of Ca(2+)-induced contracture in control diaphragm, while a decrease was seen in endotoxemic diaphragm. Ryanodine induced a marked contracture in control diaphragms, which was diminished after endotoxemia. This finding is correlated with the decrease of ryanodine-induced Ca(2+) release and the suppression of [(3)H]ryanodine binding on the isolated SR of the skeletal muscle from LPS-treated rats. In mice treated with LPS significantly increased levels of plasma nitrite and serum TNF-alpha were observed, changes inhibited by aminoguanidine [an inhibitor of inducible NO synthase (iNOS)] and pentoxifylline (an inhibitor of tumor necrosis factor-alpha formation), respectively. Moreover, LPS treatment resulted in a significant expression of mRNA for iNOS in mouse diaphragms. The inhibitory effects on Ca(2+)- and ryanodine responses by LPS could be prevented by treatment with polymyxin B (LPS neutralizer) and pentoxifylline, but not by treatment with dexamethasone, N(G)-nitro- L-arginine or aminoguanidine (NOS inhibitors). These results imply that the NO-related pathway may not be involved in the dysfunction of the Ca(2+) release mechanism in the sarcoplasmic reticulum of mouse diaphragm during endotoxemia.

Cardiac twitch properties simulated by three-states model.

We examined whether the three states model can explain the systolic and relaxation properties of cardiac muscle to clarify what factors affect these properties. Changing the values of the parameters describing the calcium transient and calcium sensitivity, we estimated the effects of these parameters on the systolic and relaxation properties of twitch contraction. The simulations showed the following four features: 1) An increase in the maximum calcium concentration and calcium sensitivity, and a prolongation of the calcium transient led to an increase in peak tension associated with an increase in the time to peak tension. 2) An increase in myosin ATPase activity led to an increase in peak tension associated with a decrease in the time to peak tension. 3) An increase of peak tension was accompanied by a prolongation of the late systolic period. 4) The constant of the late tension relaxation from 25% to 10% of the peak tension was altered when the crossbridge cycling rate, the resting calcium concentration or the late decline of the calcium transient was changed. The simulation were not contradictory to the experimental results and showed that three state muscle model can provide qualitative descriptions on the systolic and relaxation characteristics of cardiac muscle.

Action potential control of cardiac contractility.

The transient and/or sustained trans-sarcolemmal voltage induced zero to peak tension changes in cardiac contractility at any given level of diastolic dimensions and associated physical-chemical conditions establish the action potential as the predominant controller of cardiac contractility. Demonstration that the inotropic increases in peak tension effects of extra cellular [Ca++] occur and are determined by the duration and degree of positivity of the plateau phase of the action potential document the predominant role of this phase of the action potential relative to control of cardiac contractility. The large increases in peak tension induced by prolongation of the plateau phase of the action potential by interpolated stimuli (i.e., extrasystolic potentiation) and the immediate maximal peak tension following sustained contracture induced by sarcolemmal depolarization highlight this fact. The demonstration that this prolonged action potential induced maximal tension capability (peak inotropic state) of ventricular fibers can be achieved within a single cycle suggests an analogous technic would provide objective noninvasive measurements of the cardiac reserve of humans in health and disease. A potentially valuable measurement, the temporal resolution requirements of which, although beyond the scope of current three-dimensional imaging systems, is achievable with current state of the art technology. The unique experimental and clinical diagnostic value of such a system for noninvasive analogous measurements in humans with congenital and acquired cardiac abnormalities is as yet, however, not widely recognized. Hence, objective confirmation of the unique potential value of such a system awaits development of the required high fidelity [X,Y,Z (1 mm3 voxel) spatial and (10 ms)] temporal resolution capability system.

Mechanisms of positive inotropic action of flosequinan, hydralazine, and milrinone on mammalian myocardium

Flosequinan is an arterial and venous dilator that also has a positive inotropic effect at relatively higher doses. The purpose of this study was to determine the mechanism of this positive inotropic effect in ferret papillary muscles loaded with the Ca 2+ indicator, aequorin. Over the range of doses from 10 −6 to 10 −3 M, flosequinan produced a 61±9% increase in peak tension that was accompanied by a corresponding increase in [Ca 2+] i. This positive inotropic effect was not selectively blocked by addition to the perfusate of procaine 0.6 μM, tetrodotoxin 10 −6 M or by verapamil, 5×10 −8 M. In contrast, the positive inotropic effect of flosequinan, but not milrinone or hydralazine, was potentiated by prior addition of ouabain 3 nM to enhance intracellular Ca 2+ via reduction of the Na +/Ca 2+ exchange. Moreover, antagonists of Na +/Ca 2+ exchange, including cadmium 10 μM, amiloride 600 μM and choline substitution for 1/3 Na + in the perfusate, blocked the response to flosequinan but not hydralazine or milrinone. These results indicate that flosequinan produces a positive inotropic effect by reduction of Na +/Ca 2+ exchange in mammalian myocardium. Moreover, flosequinan has the potential to interact synergistically with other positive inotropic agents such as digoxin that affect Na +/Ca 2+ exchange by direct or indirect actions.

Mechanisms of the inotropic effects of UD-CG 212 Cl, an active metabolite of pimobendan, on ferret papillary muscles.

We investigated the effects of an active metabolite of pimobendan, UD-CG 212 Cl, on Ca(2+) transients and tension using the aequorin method. When extracellular [Ca(2+)] ([Ca2+]o) in the Tyrode's solution was 2 mM, UD-CG 212 C1 (10(-7)-10(-4)M) increased the peak of Ca(2+) transients, accompanying a slight increase in peak tension. When [Ca(2+)]o was decreased to 0.5 mM, the twitch-potentiating effect of UD-CG 212 C1 was more remarkable, but the increase in the Ca(2+) transients at low concentrations of UD-CG 212 C1 (10(-7)-10(-6)M) was not significant as it was at 2 mM [Ca2+]o. The effects of UD-CG 212 Cl on the time courses of Ca(2+) transients and tension were evaluated at 0.5 mM [Ca2+]o. UD-CG 212 Cl shortened the decay time of Ca(2+) transients and the time to peak tension. However, the relaxation time was not significantly altered. UD-CG 212 C1 (10(-6)M) did not significantly change the relation between [Ca(2+)]i and tension in tetanic contraction. Therefore, the twitch-potentiating effect of UD-CG 212 Cl might not be due to an increase in the Ca(2+) sensitivity of the contractile elements. The slight increase in cyclic AMP due to the inhibition of phosphodiesterase type III by UD-CG 212 Cl could explain the twitch-potentiating effect and the faster time courses of Ca(2+) transients and tension.

Mechanism of the positive inotropic action of cocaine in the guinea pig atrium

We studied the mechanism of the positive inotropic action of cocaine in isolated guinea pig atria superfused with Tyrode's solution at 31 °C while attached to a force transducer to measure peak tension developed, maximum velocity of development of tension, and time to peak tension. Cocaine 2.9 μM enhanced peak tension developed and velocity of development of tension, and prolonged time to peak tension. The increase in peak tension developed produced by cocaine was not affected by propranolol. On the other hand, the cocaine-induced increase in velocity of development of tension was reduced, but not abolished. In the presence of propranolol and phentolamine combined, the cocaine-induced prolongation of time to peak tension was abolished and the increases of both peak tension developed and velocity of development of tension were significantly smaller than those observed in the absence of the two adrenergic blockers. For all practical purposes, nifedipine completely abolished the increase in peak tension developed induced by cocaine. It is concluded that the positive inotropic effect of cocaine in the guinea pig atrial muscle is predominantly the result of adrenergic-dependent, both α- and β- receptor mediated, as well as adrenergic-independent increases in calcium influx through the L-type calcium channels in the sarcolemma.

Cellular mechanism of the positive inotropic effect of hydralazine in mammalian myocardium

1. The purpose of this study was to elucidate the cellular mechanism of the positive inotropic effect of hydralazine, a vasodilator widely used for afterload reduction in patients with heart failure that has also been reported to have positive inotropic effects on the heart. After isolation, right ventricular papillary muscles from the ferret were maintained in bicarbonate-buffered salt solution (30 degrees C). A concentration-response relationship was obtained for hydralazine (10(-6) to 10(-3) M). In order to mimic different levels of catecholamine release found in heart failure, we utilized two methods of stimulation: (a) threshold punctate pulses and (b) suprathreshold punctate stimulation with voltage approximately 10% above threshold. 2. In a first group of muscles (n = 16), a maximally effective concentration of hydralazine (10(-3) M) increased peak isometric tension by 39 +/- 9% (P < 0.05). Doses lower than 10(-5) M had no significant effect. The bioluminescent Ca2+ indicator, aequorin, was loaded into a subset of these muscles (n = 7). A significant increase in peak light (i.e., intracellular Ca2+) developed, concurrently with an increase in peak tension (38 +/- 5% to 66 +/- 8%). This inotropic response was associated with a decrease in time to peak tension (ms), 221 +/- 7 to 186 +/- 5 (P < 0.05), and time to peak light, 65 +/- 4 to 52 +/- 2 (P < 0.05). These effects were markedly attenuated by pretreatment with autonomic blocking agents. 3. In a second group of muscles (n = 12), histamine was used to stimulate cyclic AMP production in the presence of propranolol. Hydralazine (3 x 10-4 M) led to a shift in the pD2 (i.e. the negative log of the concentration of histamine producing 50% of the maximal response) from 6.1 +/- 0.1 to 5.9 +/- 0.1(P <0.05), thus increasing the sensitivity of the muscles to histamine. Hydralazine also increased maximum tension from 160 +/- 77% to 195 +/- 57% (P <0.05) above baseline. Thus, hydralazine altered the potency and efficacy of histamine despite the presence of beta-adrenoceptor blockade.4. A third group of muscles were chemically skinned to examine the effects of hydralazine on myofilament Ca2+ responsiveness. Pretreatment of ferret papillary muscles with hydralazine (10-3 M)before skinning did not shift the force-pCa curve after skinning (n = 16). However, hydralazine added to previously skinned fibres desensitized the myofilaments, as indicated by a rightward shift of the force-pCa curve (n = 12). Maximum tension development was not changed.5. The pharmacological effects of hydralazine are characteristic of inotropic drugs that act mainly via cyclic AMP; however, the increase in peak tension demonstrated with histamine in the presence of hydralazine also suggests an effect on cyclic AMP-independent second messenger pathways. These data are consistent with reports that large doses of hydralazine may increase cellular levels of cyclic AMP, as well as other second messengers, by direct cardiac and indirect neuronal mechanisms.

The pH dependence of the contractile response of fatigued skeletal muscle.

Following a period of intense repetitive stimulation (e.g., brief tetanic stimuli every second for 3 min), muscle isometric tension development is reduced by about 80%. This suppression is reversible at a high external pH (8.0) with a half time of 15-20 min, but if the external pH is low (6.4) or the buffer concentration is low, recovery is prevented. Inhibition of recovery is associated with a slowed rate of lactate loss, which may suggest that intracellular lactacidosis is the cause of the inhibition. Alternatively, a low external pH may affect recovery from fatigue quite independently of its effect on lactate efflux. The possibility that surface membrane properties are changed by fatigue in a pH-dependent fashion was examined by measuring the cable properties and action potentials of fatigued fibres at different external pH values. A low external pH during recovery from fatigue was shown to result in a prolonged membrane depolarization of 10-12 mV, an increased transmembrane resistance, and a prolonged action potential. At a high external pH transmembrane resistance is lowered by fatigue, the depolarization lasts only about 10-15 min, and there is a smaller effect on the action potential. While the fatigued fibre membrane does show a changed response that is dependent on external pH, it is not clear that this could be related to the suppression of contraction. Direct measurements of intracellular pH show a fall of about 0.4 to 0.5 pH units in the surface fibres following fatigue. This results from the lactic acid generated during activity. It is now clear that lactate crosses the membrane in association with protons and at least part of this flux is mediated by a specific carrier mechanism. Efflux is limited by the transmembrane pH gradient, which in turn depends on the extracellular buffer concentration in the diffusion limited space around the fibres. Intracellular lactacidosis in resting muscles can be generated by a reversal of the normal flux. Fibres can be loaded with lactate (L) by increasing the extracellular [H+][L-] product with a resultant fall in intracellular pH. Lactate loads similar to those seen in fatigued muscle simulate some but not all of the responses seen in the postfatigue state. The twitch is prolonged with a slow relaxation phase, an increased time to peak tension but with an increase in peak tension. The effects are reversible but usually result in a reduced contractile response following the washout.(ABSTRACT TRUNCATED AT 400 WORDS)

Electrophysiological and mechanical studies of frog heart adrenoceptor stimulation by epinine

Electrophysiological and mechanical effects of epinine, an alpha- and beta-agonist, were investigated in frog atrial fibres. From dose-response curves it was demonstrated that epinine produced an increase in amplitude and duration of the plateau, and in duration of the action potential. Corresponding increases in peak tension, rate of tension development, time to peak tension and rate of relaxation were noted. The positive inotropic effect of epinine was mediated only by myocardial beta-adrenoceptor stimulation; over the whole range of concentrations, the inotropic action of epinine was not influenced by phentolamine (3.10(-6) mol . litre-1), but was inhibited by propranolol (3.10(-8) mol . litre-1). The mechanism of epinine action involved an important increase in slow calcium current Isi responsible for the changes in the action potential, while the positive inotropic effect of the drug was attributed to the resulting increase in intracellular calcium concentration. The action of epinine seemed independent of cAMP concentration, because the effects of epinine on contraction were not significantly increased by papaverine (10(-5) mol . litre-1). In frog heart, a beta-stimulation induced specific effects on action potential and tension. The positive inotropic effect of beta-catecholamines resulted directly from electrical changes induced by an increase in slow calcium current.

Calcium Source for Contractile Response of Guinea Pig Taenia Caecum to Carbachol in a Calcium Deficient, Potassium Rich Solution

The Ca storing site for the carbachol-induced contraction in a high-K medium without adding CaCl2 was further investigated in the guinea pig taenia caecum. La3+ (0.05–0.5 mM) caused an increase in peak tension and relaxation rate in the carbachol contraction but reduced or abolished the response to CaCl2. Simultaneous application of carbachol and CaCl2 produced tension development the trace of which was comparable to the curve obtained by adding graphically the respective traces of the carbachol-induced and Ca-induced tensions. La3+ (0.5 mM) abolished the late, sustained component without appreciable change in the initial, transient contraction. The carbachol contraction persisted after 5 min perfusion of solution containing 0.25 mM EGTA (estimated free Ca2+ concentration less than 10−8 M). The intracellular Ca content was little changed before and after exposure to carbachol. Histamine induced a transient contraction with a dose-dependent amplitude and resulted in a decrease in tension development produced by subsequently applied carbachol. There was an inversely proportional relationship in amplitude between the histamine contraction and the following carbachol contraction, while the sum of tensions raised by both drugs showed little variation. These results favour an intracellular site for the carbachol-sensitive Ca store. Histamine appears to release Ca2+ from the carbachol-sensitive store.

Electrophysiologic correlates of the inotropic effects of Isoproterenol in canine myocardium

The action of l-isoproterenol was studied in isolated canine papillary muscles. The simultaneous action potential and contraction traces were first recorded in digital form on magnetic tape and later measured and analyzed by a computer program. The data were controlled and grouped to permit a three-way analysis of variance in order to test significant effects and correlations. Complete dose-response curves were performed both before and after beta-adrenergic blockade with (±)propranolol. It was demonstrated that isoproterenol produced and increase in the peak potential, the height and duration of the plateau (phase 3), and the rate of repolarization of the action potential (phase 4). Corresponding increases in peak tension, time to peak tension, rate of tension development, and rate of relaxation of the contraction were noted. At the highest isoproterenol concentrations, occasional after-potentials and after-contractions occurred. The changes in the action potential were explained by changes in the inward calcium current, while the inotropic effect on the contraction was attributed to the resulting increase in intracellular calcium concentration. These effects were all blocked by the addition of propranolol, but the blockade could be overcome by increasing the isoproterenol concentration of the perfusate.

Tension prolongation during recovery from myocardial hypoxia.

The mechanical behavior of isolated cat, rat, and dog ventricular muscle was examined during hypoxia and after reoxygenation. During hypoxia, an early abbreviation of tension duration was followed by a decline in the rate of tension development. After reoxygenation, a marked, early prolongation of tension development and relaxation time was invariably observed with little, if any, increase in peak tension. As recovery progressed, the duration of contraction gradually shortened as tension returned to control levels. This phenomenon was also observed in the intact dog heart after release of a coronary artery ligature. Isometric tension gauges sewn to ischemic portions of the left ventricle demonstrated that after reinstitution of coronary flow, segment tension duration "outlasts" the duration of left ventricular pressure development and is associated with ventricular irritability. Epicardial electrograms showed shortening of the QT interval within the ischemic segment with prolongation of the QT interval after release of the coronary ligature. Prolongation of tension development during recovery from hypoxia was not observed in experiments with rat skeletal muscle. These observations identify localized mechanical abnormalities during recovery from myocardial ischemia which may be important in the syndrome of acute coronary heart disease.