Maximal Rate Of Force Development Research Articles

The effect of endurance exercise on muscle force generating capacity of the lower limbs

The purpose of this study was to investigate the recovery of muscle force generating capacity (FGC) of the lower limbs following a session of cycle exercise (CE). Fourteen male cyclists (mean +/- SD age 25 +/- 4 yrs and VO2max 65.8 +/- 5 ml x kg(-1)min(-1)) performed tests assessing lower limb muscle FGC at rest (pre-test), as well as 6 and 24 hrs following CE performed on a mechanically-braked cycle ergometer. The CE consisted of 30 min at a workload corresponding to the lactate (Dmax) threshold (+/-15 W), and four 60 s rides at 120% VO2max with one min rest between each ride. At the completion of the CE a 6 or 24 hr recovery period was initiated, after which, each subject's muscle FGC was measured. The analysis of lower limb muscle FGC included, (1) 6 s all-out cycle test; (2) a maximal isokinetic leg extension at 60, 120 and 180 degrees x s(-1); and (3) a maximal concentric squat jump. Statistical analysis showed that compared to pre-test levels, a significant reduction in both isokinetic peak torque at 60 degrees x s(-1) and isoinertial maximum force occurred after 6 hrs of recovery. Although not significant, reductions also occurred at 6 hrs of recovery in isokinetic peak torque at 120 and 180 degrees x s(-1), as well as maximum rate of force development (RFD) during the squat jumps. No significant differences were observed between isokinetic peak torque, maximum force or RFD pre-test and following the 24 hr recovery period, indicating these tests had returned to normal by this time. No significant differences were found between peak power (PP) during the 6 s cycle test, pre-test and following either 6 or 24 hrs of recovery. These findings confirm earlier research that maximal voluntary strength is reduced for at least 6 hours following exhaustive dynamic exercise. The reduction in muscle FGC should be considered when resistance training is scheduled after endurance exercise.

Effects of anoxia, acidosis and temperature on the contractile properties of turtle cardiac muscle strips.

The responses to anoxia and acidosis of cardiac ventricular muscle strips from the anoxia-tolerant turtle Chrysemys picta bellii were investigated at 10 degrees C and 20 degrees C. Force-velocity curves were determined by quick isotonic releases at 85% of the time to peak isometric force under control, anoxia, lactate acidosis and anoxic lactate acidosis conditions. The isotonic forces during quick releases spanned 5-95% of the measured isometric force at each conditions. Superfusion solution pH was 7.8 and 7.95 for non-acidosis experiments, and 7.0 and 7.15 for acidosis experiments, at 20 degrees C and 10 degrees C, respectively. After normalizing force data to control isometric force, the values of maximum isometric force (P0), maximum velocity of shortening (Vmax) and maximal power output (Powermax) were evaluated by fitting the curves using the hyperbolic Hill equation. The maximum rate of force development (dF/dtmax), time-to-peak force (TPF) and half-relaxation time (T1/2) were also determined. At 20 degrees C, during acidosis, anoxia and anoxic acidosis, P0 decreased significantly to 81%, 40% and 24% of control values, dF/dtmax decreased significantly to 67%, 53% and 23% of control values, and Powermax decreased significantly to 75%, 40% and 14% of control values, respectively. Vmax, however, was not significantly affected by acidosis, anoxia or even anoxia acidosis. TPF was significantly shortened by anoxia, but prolonged by acidosis. The effects were similar at 10 degrees C, Temperature did not affect P0, but Vmax decreased by a factor of 1.6-1.8 at all corresponding conditions when temperature was reduced from 20 degrees C to 10 degrees C. We conclude that acidosis and anoxia inhibit isometric force production and Powermax of turtle cardiac muscle, but have no effect on Vmax, and the insensitivity of Vmax indicates that the rate of cross-bridge cycling is not affected by these conditions. Our observations indicate that the reduced power outputs of the hearts of submerged anoxic turtles at low temperature are due in part to inhibition of force production by anoxia and acidosis, and to a reduction of contraction velocity at low temperature.

Differences between contractions of fast and slow muscles after nerve grafting.

The nature of reinnervation of fast- and slow-twitch skeletal muscles, as assessed by contractile characteristics, was determined in a rat sciatic-nerve graft model. The isometric contractile function of the fast-twitch plantaris and slow-twitch soleus muscles from hindlimbs of adult male Lewis rats (225 to 250 g) was assessed at 16 weeks after sciatic-nerve grafting. A 3-cm interposition sciatic-nerve graft was performed in the following groups: fresh syngeneic (n = 10), fresh allogeneic (n = 11), 3-week stored allogeneic (n = 9), and freeze-thawed allogeneic (n = 9). A control group consisted of 8 normal unoperated rats. Contractile properties were assessed by stimulating the muscles indirectly via the sciatic nerve. At 16 weeks, soleus and plantaris muscle masses were 40 and 52 percent of controls, while their respective absolute tetanic forces (N) were less than 65 and 45 percent of controls. Analysis of time-dependent contractile parameters showed that the soleus/plantaris ratios for time to peak tension (TTP) and maximum rate of force development (df/dt) were not significantly altered following grafting. However, the ratio for half relaxation time (1/2RT) was significantly reduced from 4.44 +/- 0.62 toward a value of 1 following grafting. In this study, the authors found that, when fast and slow muscles were reinnervated from a common nerve, maintenance of differences in rate of force development supported selective reinnervation, while loss of differences in time of force relaxation supported random reinnervation.

ESTROGEN EFFECTS ON MOUSE MUSCLE CONTRACTILE PARAMETERS 538

Studies on the effects of estrogen on muscle contractile parameters in humans have been contradictory. This study investigated the effects of estrogen on contractile parameters of fast and slow mouse skeletal muscles. Adult male and female C57-BL mice were injected with sham or 17β-estradiol 3-benzoate (E2) for 14 days. Females were either sham injected (olive oil) or given a “high dose” of E2(10μg E2/100 g BW in olive oil). Males received either sham,“high dose” or “low dose” of E2 (5μg E2/100 g BW). Circulating E2 levels were determined in all animals. Isolated extensor digitorum longus (EDL) and soleus (SOL) muscles were studied during in vitro fatiguing contractions and 50 min of recovery. E2 administration had no effect on fatigue rate or recovery contractile parameters in EDL muscles from male or female mice. However, gender had a significant (P<0.05) main effect on EDL recovery contractile parameters. Female EDL muscles recovered peak tetanic tension (P0), maximal rate of force development (+dFo/dtmax), peak twitch tension (Pt), and maximal rate of twitch force development (+dFt/dtmax) sooner than males. Conversely, E2 level had a significant (P<0.05) main effect on contractile parameters of SOL muscles during post-fatigue recovery. SOL muscles from “high dose” male and female mice recovered Po, +dFo/dtmax, Pt, and +dFt/dtmax sooner than mice with lower E2 levels. The antioxidant or membrane stabilizing properties of E2 may result in improved post-fatigue recovery parameters in SOL muscles. This suggests that E2 may protect and enhance recovery primarily in slow oxidative muscle.

Electrophoretic Separation of Myosin Heavy Chain Isoforms in the Human M. Vastus Lateralis: References to Reproducibility and Relationships with Force, Electromechanical Delay, Fibre Conduction Velocity, Endurance and Electromyography

The aim of this investigation was to determine the relationship between muscle performance and the myosin heavy chain (MHC) composition and the reliability of electrophoretically determined MHC compositions. A total of thirty-one male subjects participated in the experiments. Maximal voluntary isometric contractions (MVC) of the knee extensors were performed at an arbitrary knee angle of 90° and the following variables were recorded : maximal isometric force, muscle fibre conduction velocity (MFCV), electromechanical delay (EMD), maximal rate of force development (MRFD), median frequency of EMG (MF) and iEMG. Static isometric contractions of the knee extensors were held at an angle of 90° using contractile forces of 10%, 50% and 100% MVC, respectively. These tests were conducted on separate days. Muscle biopsy samples were obtained from the left m. vastus lateralis before MVC and static endurance tests. MHC protein isoform differences were determined through sodium dodecyl–polyacrylamide gel electrophoresis (SDS-PAGE) followed by densitometric analysis. Type I-MHC compositions of the m. vastus lateralis ranged from 20–68% with a mean of 49 ± 18%, mean type IIa-MHC and type IIb-MHC percentages were 35 ± 16% and 16 ± 10%, respectively. MHC compositions of duplicate biopsy samples were not significantly different from that of original samples. The coefficients of variation calculated for duplicate biopsy samples suggested reasonable reproducibility for MHC isoform differentiation for type I-MHC and type-II MHC composition (CV=12.6%). Differentiation between type IIa-MHC and type IIb-MHC was not always clear using the densitometric traces. Subjects with higher percentages of type II-MHC displayed significantly faster MFCV (r=0.67, P<0.1), isometric force development (r=0.68, P<0.1) and shorter periods of EMD (r=–0.72, P<0.05). There was also a tendency toward faster MRFD in these subjects although results did not reach significance. Endurance times for isometric contractions held at 10%, 50% and 100% MVC to exhaustion were not correlated with MHC composition. No relationships between II-MHC composition and MF or iEMG were observed. It was suggested that surface electromyographic recordings obtained during isometric MVC did not reflect underlying differences in muscle fibre composition.

Myocardial Depressant Effects of Sevoflurane

The effects of anesthetic concentrations of sevoflurane were studied in isolated myocardial tissue to delineate the mechanisms by which cardiac function is altered. Isometric force of isolated guinea pig ventricular papillary muscle was studied at 37 degrees C in normal and 26 mM K+ Tyrode's solution at various stimulation rates. Normal and slow action potentials were evaluated using conventional microelectrodes. Effects of sevoflurane on sarcoplasmic reticulum function in situ were also evaluated by its effect on rapid cooling contractures, which are known to activate Ca2+ release from the sarcoplasmic reticulum, and on concentrations of rat papillary muscle. Finally, Ca2+ and K+ currents of isolated guinea pig ventricular myocytes were examined using the whole-cell patch clamp technique. Sevoflurane equivalent to 1.4% and 2.8% depressed guinea pig myocardial contractions to approximately 85 and approximately 65% of control, respectively, although the maximum rate of force development at 2 or 3 Hz and force in rat myocardium after rest showed less depression. In the partially depolarized, beta-adrenergically stimulated myocardium, sevoflurane selectively depressed late peak force without changing early peak force, whereas it virtually abolished rapid cooling contractures. Sevoflurane did not alter the peak amplitude or maximum depolarization rate of normal and slow action potentials, but action potential duration was significantly prolonged. In isolated guinea pig myocytes at room temperature, 0.7 mM sevoflurane (equivalent to 3.4%) depressed peak Ca2+ current by approximately 25% and increased the apparent rate of inactivation. The delayed outward K+ current was markedly depressed, but the inwardly rectifying K+ current was only slightly affected by 0.35 mM sevoflurane. These results suggest that the direct myocardial depressant effects of sevoflurane are similar to those previously described for isoflurane. The rapid initial release of Ca2+ from the sarcoplasmic reticulum is not markedly decreased, although certain release pathway, specifically those induced by rapid cooling, appear to be depressed. Contractile depression may be partly related to the depression of Ca2+ influx through the cardiac membrane. The major electrophysiologic effect of sevoflurane seems to be a depression of the delayed outward K+ current, which appears to underlie the increased action potential duration.

Force development of dynamic and static contractions in children and adults.

There are still unclarified points remaining in regard to the characteristics of force development in children who are immature in their basic activities in daily living. Moreover, there are morphological, histological, and biochemical differences between immature and mature muscles. In the present study, dynamic elbow flexion and static contractions which were performed by elbow flexors with maximum effort were examined by force-velocity and force-time relationships and electromyograms (EMG) in six-year-old children and in adults. In dynamic contractions with various loads, the force-velocity relationship for children was (P + 5.65) (v + 1.48) = 19.51, and (P + 14.65) (v + 2.26) = 96.21 for adults. The maximum power in children and adults was 22.8 watts and 160.8 watts, respectively. The contraction delay in children was greater than that in adults for every relative load. In static contractions, the maximum rate of force development for children was significantly lower than that for adults at each pre-tension. With an increase in pre-tension, the adult rate showed a tendency to decrease, whereas the rate for children showed no change. The electromechanical delay observed in children was significantly greater than that in adults. For dynamic and static contractions, the contractile speed in children was lower than that in adults.

Assessing Dynamic Performance

The purpose of this study was to quantify the rate of force development (RFD) and maximum force in isometric, concentric, and stretch-shorten cycle contraction modes and to determine their relationships to sprint running performance. Fifteen athletic subjects performed a series of isometric, concentric, and stretch-shorten cycle RFD tests in an upright squat position using a modified Smith machine positioned over a force platform. The concentric and isometric tests were performed at both 110° and 150° knee angles. From the force data recorded, the maximum force, maximum RFD, force at 30 ms, and impulse at 100 ms were used as test variables. Subjects also ran a 30-m indoor sprint from a crouched start. Of the 20 force-time variables calculated, the concentric tests were the only ones significantly correlated to performance and able to effectively discriminate between good and poor performers. Isometric tests were unrelated to dynamic performance. This was suggested to be due to the large neural and mechanical differences between isometric and dynamic muscular actions. The results are strongly supportive of the use of concentric RFD tests but not isometric ones.

Fatigue and recovery of voluntary and electrically elicited dynamic force in humans.

1. Percutaneous electrical stimulation of the human quadriceps muscle has been used to assess the loss of central activation immediately after a bout of fatiguing exercise and during the recovery period. 2. Fatigue was induced in eight healthy males by a maximal effort lasting 25 s performed on an isokinetic cycle ergometer at a constant pedal frequency of 60 revolutions per minute. The cranks of the ergometer were driven by an electric motor. Before and after the sprint, subjects allowed their legs to be passively taken round by the motor. During the passive movement the knee extensors were stimulated (4 pulses; 100 Hz). Peak voluntary force (PVF) during the sprint and peak stimulated forces (PSF) before and in recovery were recorded via strain gauges in the pedals. Recovery of voluntary force was assessed in a series of separate experiments in which subjects performed a second maximal effort after recovery periods of different durations. 3. Peak stimulated forces were reduced to 69.8 +/- 9.3% immediately after the maximal effort, (P < 0.05), but had returned to pre-exercise values after 3 min. The maximum rate of force development (MRFD) was also reduced following fatigue to 68.8 +/- 11.0% (P < 0.05) of control and was fully recovered after 2 min. PVF was reduced to 72.0 +/- 9.4% (P < 0.05) of the control value following the maximal effort. After 3 min voluntary force had fully recovered. 4. The effect of changing the duration of the fatiguing exercise (10, 25 and 45 s maximal effort) resulted in an increased degree of voluntary force loss as the duration of the maximal effort increased.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of K+ on the recovery of the twitch and tetanic force following fatigue in the sartorius muscle of the frog, Rana pipiens.

The goal of this study was to investigate how an increase in the extracellular K+ (K0+) concentration immediately after fatigue affects the recovery of the resting potential, the twitch and tetanic contraction of frog sartorius muscle to further understand the role of K+ in the mechanism of fatigue. Resting potentials were measured with conventional microelectrodes. Twitch and tetanic contractions were elicited by field stimulation. All muscles were fatigued with tetanic contractions at a rate of one contraction per second for 3 min while being exposed to 3 mmole l-1 K0+. During fatigue development the resting potential decreased by 16 mV (control group and pH0 7.2, extracellular pH), while the decrease in the twitch force was 32.8%, compared to 79.3% for the tetanic force, and 84.6% for the maximum rate of force development of the tetanus. Fatigued muscles were also unable to maintain a plateau phase during a tetanus: force declined by 14.8% during this phase. During the recovery period under control conditions (3 mmole l-1 K0+), all four parameters returned to their pre-fatigue values, the recovery of the plateau phase was the fastest (10 min), while that of the twitch force was the slowest (80 min). When K0+ was increased to 7.5 or 9.5 mmole l-1 immediately after fatigue, the recovery rate of the tetanic force and plateau phase was reduced. The maximum rate of force development of the tetanus, however, recovered at a faster rate than control muscles. The recovery of the twitch force was also increased above that of control when K0+ was increased to 9.0 mmole l-1 (a concentration which maximally potentiates the twitch force of unfatigued muscle). Frog sartorius muscles were also tested at pH0 6.4, a pH0 which inhibits force recovery. At that pH0 the effects of K0+ were similar to those observed at pH0 7.2. It is concluded that the role of K+ in muscle fatigue is more complex and may not involve just a contribution to the decrease in force during fatigue development, but may also contribute to an increase in force development under some conditions.

Premovement electromyographic silent period and α-motoneuron excitability

The purpose of this study was to investigate the possible neurophysiological mechanism of EMG signal silence (premovement silence (PMS)) preceding a ballistic movement in 10 healthy volunteers. The subjects were asked to respond to a flashing light signal by performing a plantar flexion in the ankle as strongly and quickly as possible. The EMG signals from agonists lateral gastrocnemius (LG) and soleus (SO), and antagonist tibialis anterior (TA) were simultaneously recorded together with the force signal. The excitability of spinal α-motoneuron pools was also determined at various phases of the movement execution by means of H-reflex analysis. Our results indicated that: (a) the maximal rate of force development (dF/dt) was significantly greater in the group of subjects demonstrating clear PMS than that without PMS; and (b) the significant decrease in H-reflex amplitude was observed approximately 40 ms prior to the appearance of PMS of both LG and SO muscles, which preceded the force development by about 50–60 ms. These data suggest that PMS is associated with an enhancement of rapid force development due possibly to optimal motor unit synchrony. The decreased H-reflex amplitude (decreased monosynaptic reflex gain) in the absence of parallel decrease in the surface EMG recording (maintained α-motoneuron activity) prior to PMS and complete disappearance of selected motor unit activities during PMS also suggest that the presynaptic inhibition and/or disfacilitation are mainly involved for PMS during a ballistic movement.

Aminophylline increases submaximum power but not intrinsic velocity of shortening of frog muscle.

We hypothesized that methylxanthines, such as aminophylline, increase the power developed by submaximally activated frog skeletal muscles by increasing the force developed at any given velocity of shortening. Frog semitendinosus muscles were excised and tested at 20 degrees C in oxygenated control and aminophylline Ringer solutions. Force-velocity relationships were determined and power was calculated from muscles stimulated at frequencies of 80 and 300 Hz. The 300-Hz frequency of stimulation produced a maximum rate of force development. In 50 and 500 microM aminophylline, twitch force increased by 25 +/- 12 and 75 +/- 13%, respectively. Aminophylline did not affect maximum isometric force generation or the shortening velocity at any relative load. At 80-Hz stimulation and in the presence of 500 microM aminophylline, power increased by an average of 11% at 10 of 14 relative loads. At maximum frequencies of stimulation, aminophylline had no effect on any measured parameter. We conclude that aminophylline increases the power developed by submaximally activated frog muscles through an increase in the force generated particularly at the lower velocities of shortening.

The Influence of Temperature on Ryanodine Sensitivity and the Force-Frequency Relationship in the Myocardium of Rainbow Trout

The relationship between stimulation frequency and contraction was established for ventricular strips from rainbow trout heart at 5, 15 and 25 degrees C. Compared to mammalian species, changes in temperature had little impact on force development in trout ventricle at physiologically relevant stimulation frequencies. However, the force-frequency relationship was changed from a biphasic response with a minimum around 0.2 Hz at 5 and 15 degrees C to a monophasic decline in force with increasing frequency at 25 degrees C. Ryanodine reversed the negative force-frequency relationship at 25 degrees C. Potentiation of twitch force after a 5 min rest period was increased from 121 +/- 4% at 15 degrees C to 209 +/- 12% at 25 degrees C. A similar augmentation was seen for the maximal rate of force development. Rest potentiation of both force and maximal rate of force development (dF/dT) was abolished by ryanodine at both 15 and 25 degrees C. The ryanodine concentration causing a half-maximal reduction in rest potentiation of force was 51 nmol l-1 at 25 degrees C and 483 nmol l-1 at 15 degrees C. Rest potentiation was maximally reduced by 10 mumol l-1 ryanodine to 50 and 79% of the value in the absence of ryanodine at 25 and 15 degrees C, respectively. At 5 degrees C, rest potentiation was similar to that at 15 degrees C. At 5 degrees C, there was no rest potentiation of dF/dT and ryanodine did not reduce rest potentiation of force. Instead, rest potentiation was correlated with a potentiation of time to peak tension (TPT) at 5 degrees C. Thus, in trout ventricle, force correlates with TPT at 5 degrees C and seems to be regulated by a ryanodine-insensitive mechanism, while at 25 degrees C force is correlated with the maximal rate of force development and the sarcoplasmic reticulum appears to contribute significantly to excitation-contraction coupling.

Measurement of Platelet-Mediated Force Development During Plasma Clot Formation

We have developed an instrument that measures force development during clot retraction. Clots are formed between an aluminum plate and cup. The plate is coupled to a strain gauge transducer. Force generated by platelets is transmitted to the upper plate and the resulting voltage change is recorded. Calibration using standard weights allows conversion of the voltage signal to dynes/cm2. Study parameters include lag phase prior to force development, maximum rate of force development (MRFD), and maximum force generated (MFG). When controlled for platelet count, ionic strength (0.15), pH (7.4), calcium concentration (10mM), thrombin concentration (1.5 u/ml), temperature, and gap distance (1 mm), measurements are reproducible. Control of each variable is critical since clot retraction depends on platelet function and fibrin structure. At 37 degrees C and 26 x 10(3) platelets/microL, the lag phase was 300 seconds, the MRFD was 0.69 dynes/(cm2 sec), and the force at 1000 seconds (MFG) was 2450 dynes. At 7.5 x 10(4) platelets/microL, the lag phase was 160 seconds, the MRFD was 1.06 dyne/(cm2 sec), and the MFG was 4400 dynes. Decreasing the sample temperature from 37 degrees C to 27 degrees C (75 x 10(3) platelets/microL) increases the lag phase from 170 to 300 seconds, decreases MRFD from 1.06 to 0.66 dynes/(cm2 sec), and decreases the MFG at 1000 seconds from 4,400 to 2,800 dynes. At 15 degrees C, retraction is totally inhibited. This instrument provides a simple way to quantify the impact of altered fibrin structure and platelet function on clot retraction. Measurement of force development during clot retraction may offer a new approach to the study of qualitative platelet dysfunction.

Pharmacology of an Indian-snuff obtained from Amazonian Maquira sclerophylla

The powdered bark of Maquira sclerophylla is consumed as snuff in north Brazil. Both the crude and the purified hydrosoluble extract (WP) injected i.p. in the dose range of 0.05–0.5 g kg induced hyperexcitability, tremors, motor incoordination, ataxia, quietness and muscle relaxation in rats. The effects were progressive, dose-related and reversed after 30 min. Anesthetized rats, guinea-pigs and dogs injected with the purified extract (10–50 mg kg i.v.) showed a biphasic change of carotid blood pressure. The early and transient hypotension was blocked by atropine but not by vagotomy: the secondary hypertension was long lasting and sustained for over 30 min. The hypertension was shortened but not blocked after ganglionic blockade or reserpine treatment. Either pithing or alpha receptor blockade with yohimbine reduced both effects of the extract. Guinea-pigs and dogs were more responsive than rats and died by heart arrest. Incubation of WP (20 μg ml ) increased both the rate and force of contraction of isolated guinea-pig right atria by 2 and 5 times, respectively. Propranolol (4 μg ml ) blocked the chronotropic effect but did not decrease the inotropic effect. In electrically driven guinea-pig left atria, WP (10 μg ml ) increased the force of contraction by 80% and the maximum rate of force development by 60%, but did not change the time to peak tension, the time to 50% relaxation, or the rate of relaxation. These cardiovascular effects resemble those of digitalis-like drugs. Cardenolides were detected in WP by phytochemical screening.

Experimental studies on the oxygen tension in the myocardium and changes of cardiac function in hypoxia.

Using adult mongrel dogs, experiments were performed to elucidate the relationship between the changes in the myocardial oxygen tension (PmO2) in anoxia and disturbances of cardiac function. Dogs, forced to inspire 100% N2, suffered from a respiratory arrest after 5 min, and developed acute anoxia. However, by 100% O2 inhalation 2 min after the onset of the respiratory arrest, the anoxia rapidly resolved. The arterial oxygen tension (PaO2), left intra ventricular oxygen tension (PLVO2) and PmO2 showed the most pronounced fall 2 min after the respiratory arrest induced by N2 inhalation. The arterial carbon deoxide tension (PaCO2) decreased until the respiratory arrest, after which it started to rise. When inhalation of 100% O2 was initiated at the anoxia, the PaO2, PLVO2 and PmO2 recovered within 1 min followed by a rise beyond the baseline value. Left ventricular end-diastolic pressure (LVEDP), left atrial mean pressure (LAm), left ventricular systolic pressure (LVSP), aortic mean pressure (Aom), maximum rate of force development by left ventricle (LVmax.dp/dt), total peripheral resistance (TPR), cardiac output (CO) and heart rate (HR) were measured. At the onset of anoxia, these parameters decreased sharply. When inhalation of 100% O2 was initiated within 2 min of the respiratory arrest, these disturbances of cardiac function recovered rapidly. The fall of PmO2 plays an important role in the impairment of cardiac function.

Hypoxia-induced fibre type transformation in rat hindlimb muscles

Twelve male Sprague-Dawley rats (21 days old) were randomly assigned into two experimental groups: sea level control (CONT) and hypobaric hypoxia (HYPO). The HYPO rats were kept in an hypobaric chamber maintaining a simulated altitude of 4000 m (61.1 kPa). After 10 weeks of treatment, the rat hindlimb muscles [soleus (SOL) and extensor digitorum longus (EDL)] were subjected to histochemical and electro-mechanical analyses. Results indicated that compared to CONT the HYPO SOL muscle had a significantly greater relative distribution of fast-twitch-oxidative-glycolytic (FOG) fibres (28.9% SEM 2.0 vs 18.3% SEM 1.8, P less than 0.01) with a significant decrease in slow twitch oxidative fibre distribution (69.5% SEM 2.4 vs 82.9% SEM 3.1, P less than 0.01). Compared to CONT the HYPO EDL muscle also manifested a significant increase in FOG fibre distribution (51.6% SEM 0.8 vs 46.6% SEM 1.1, P less than 0.01), but this was accompanied by a significant decrease in fast twitch glucolytic fibres (44.3% SEM 0.9 vs 49.2% SEM 1.7, P less than 0.05). These histochemical fibre type transformations accompanied significant and expected changes in the electro-mechanical parameters tested in situ, e.g. maximal twitch force, maximal rate of force development, contraction time, half relaxation time, force: frequency curve, and fatigability. It was concluded that chronic hypobaric hypoxia could have a potent influence upon the phenotype expression of muscle fibres.

Isometric contractile function recovery following tourniquet ischemia

The purpose of this study was to document the recovery of isometric contractile function following tourniquet ischemia. Male Wistar rats ( N = 27) were subjected to unilateral hindlimb tourniquet ischemia of 0 hr (control, N = 6), 1 hr ( N = 5), 2 hr ( N = 5), 3 hr ( N = 5) and 4 hr ( N = 3). Following a 2-week recovery period, isometric force measurements were made from both gastrocnemii of each rat with the contralateral limb acting as the control side. Each muscle was analyzed for maximal twitch ( P t , N/g), maximal rate of rise of twitch tension ( DP/dt, N/sec), time to peak tension (TPT, msec), half relaxation time (RT 1 2 , msec), maximal tetanus ( P O, N/g, at 100 Hz), and fatigue (Burke Fatigue Protocol). P t, P O, and DP/dt were significantly different from control values ( P < 0.05) for all hours of tourniquet ischemia. A strong negative correlation ( P < 0.001) was found for twitch ( R = −0.84), tetanus ( R = −0.78), and maximal rate of force development ( R = −0.83) with respect to increasing hours of ischemia. The recovery of isometric twitch and tetanic function following tourniquet ischemia is inversely related to the ischemic interval. This study quantified the relationship between muscle ischemia and recovery of function following a 2-week interval and stresses the functional physiological changes which occur in skeletal muscle following tourniquet ischemia.

Effects of organophosphorus agents on sarcoplasmic reticulum in skinned skeletal muscle fibers

These experiments were designed to determine whether skinned skeletal muscle fibers could be useful in screening new antidotes to organophosphorus poisons. Isometric force and fiber diameter were measured in mechanically skinned fibers from mice and frogs. Fibers were depleted of calcium and placed in a calcium loading solution that contained 0.5 m m EGTA with pCa 6.25. The elapsed time (zero time) before a contracture began and the maximum rate of force development (slope) were measured and divided by the square of the diameter (normalized zero time, normalized slope). The zero time was assumed to be the time required for the sarcoplasmic reticulum to attain a threshold concentration for calcium-induced calcium release, and the slope was assumed to indicated primarily the rapidity of the release of calcium from the sarcoplasmic reticulum. Organophosphorus agents, sarin, soman, tabun, and VX were also placed in the loading solutions. Only sarin failed to shorten the normalized zero times of mouse fibers compared to controls, and all agents decreased the normalized slopes. The normalized zero times of frog fibers were not altered by the agents, but the normalized slopes were altered by some agents. Pralidoxime chloride (PAM) and 3-Cl-2,5,6-trimethylbenzoic acid (TBA) were also added to the loading solution for mouse fibers; PAM was marginally effective in moderating some actions of the organophosphates. Because the effects of the agents on the fibers were so definite, we concluded that the skinned muscle fiber might indeed be useful as a screening tool for developing and testing new antidotes to organophosphorus poisons.

Effects of neuropeptide Y (NPY) on isolated guinea-pig heart.

Neuropeptide Y (NPY) is present in nerve fibres throughout the mammalian heart. We have elucidated the effects of NPY on the isolated papillary muscle and heart (Langendorff) from the guinea-pig. The paced papillary muscle was studied with regard to duration of the action potential, peak force, maximum rate of force development, time to peak force, and time from peak force to half relaxation; all these parameters were identical whether or not NPY (5 X 10(-7) M) was present in the medium. When a stimulation with trains of pulses was superimposed, the paced papillary muscle exhibited enhanced contractions. This increase in contractility was not observed in the presence of the beta-adrenoceptor antagonist propranolol (10(-6) M) and was thus considered to be adrenergically mediated. The latter (adrenergic) response was markedly attenuated by NPY. Since NPY did not interfere with the response to exogenous noradrenaline (NA) it is suggested that the peptide exerts a pre-junctional inhibitory affect on adrenergic nerve-mediated positive inotropy. Neuropeptide Y did not influence the electrocardiogram from the spontaneously beating heart (Lagendorff), nor did the peptide modify the positive chronotropic effect of exogenously applied NA. In conclusion, the results indicate that NPY is without effect on the heart muscle proper but that the sympathetic terminals of the heart possess pre-junctional receptors for NPY (and/or related peptides) related to suppression of stimulated NA release.