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PubMed1996

Force-velocity and force-power properties of single muscle fibers from elite master runners and sedentary men.

Gastrocnemius muscle fiber bundles were obtained by needle biopsy from five middle-aged sedentary men (SED group) and six age-matched endurance-trained master runners (RUN group). A single chemically permeabilized fiber segment was mounted between a force transducer and a position motor, subjected to a series of isotonic contractions at maximal Ca2+ activation (15 degrees C), and subsequently run on a 5% polyacrylamide gel to determine myosin heavy chain composition. The Hill equation was fit to the data obtained for each individual fiber (r2 > or = 0.98). For the SED group, fiber force-velocity parameters varied (P < 0.05) with fiber myosin heavy chain expression as follows: peak force, no differences: peak tension (force/fiber cross-sectional area), type IIx > type IIa > type I; maximal shortening velocity (Vmax, defined as y-intercept of force-velocity relationship), type IIx = type IIa > type I; a/Pzero (where a is a constant with dimensions of force and Pzero is peak isometric force), type IIx > type IIa > type I. Consequently, type IIx fibers produced twice as much peak power as type IIa fibers, whereas type IIa fibers produced about five times more peak power than type I fibers. RUN type I and IIa fibers were smaller in diameter and produced less peak force than SED type I and IIa fibers. The absolute peak power output of RUN type I and IIa fibers was 13 and 27% less, respectively, than peak power of similarly typed SED fibers. However, type I and IIa Vmax and a/Pzero were not different between the SED and RUN groups, and RUN type I and IIa power deficits disappeared after power was normalized for differences in fiber diameter. Thus the reduced absolute peak power output of the type I and IIa fibers from the master runners was a result of the smaller diameter of these fibers and a corresponding reduction in their peak isometric force production. This impairment in absolute peak power production at the single fiber level may be in part responsible for the reduced in vivo power output previously observed for endurance-trained athletes.

Adult↗
PubMed1997

Optimal shortening velocities for in situ power production of rat soleus and plantaris muscles.

Force-velocity (FV) relationships have been used previously to calculate maximal power production and to identify an optimal velocity of shortening (V(opt)-fv) to produce such power in skeletal muscle. The cyclical nature of muscle position during locomotion for muscles such as the soleus and plantaris is such that either constant force or velocity is rarely attained. In the present study, the work loop technique, a technique developed to measure maximal attainable power output from muscles undergoing cyclic length changes, was undertaken to determine whether simulating in vivo function alters the power-velocity relationship of the soleus and plantaris and, in particular, the velocity of shortening that produces maximal power (V(opt)-wl). FV relationships were determined for both soleus (n = 4) and plantaris (n = 4) muscles in situ from adult female Sprague-Dawley rats by measuring shortening velocities during afterloaded isotonic contractions. The velocity that produced maximal power using FV relationships, V(opt)-fv, was 54.6 +/- 0.7 mm/s for the plantaris vs. 20.2 +/- 1.2 mm/s for the soleus. Then, the work loop technique was employed to measure net power from these same muscles at multiple cycling frequencies (1.5 to 4.0 Hz for the soleus; 4.0 to 8.0 Hz for the plantaris). Multiple power-velocity curves were generated (one at each cycle frequency) by varying the strain (1-8 mm). Thus, at each cycle frequency, V(opt)-wl could be identified. For both the plantaris and soleus, V(opt)-wl at each cycle frequency was not different from their respective V(opt)-fv value. Thus both fast and slow skeletal muscles have inherent optimal shortening velocities, identifiable with FV relationships, that dictate their respective maximal attainable mechanical power production using the work loop technique.

Animals↗
PubMed1980

Effect of damaged ends in papillary muscle preparations.

The mechanical characteristics of the central segment of isolated cat papillary muscle were determined with recently developed equipment. Two small sharpened stainless steel pins, inserted transversely through the muscle, were used to mark the ends of a segment not damaged by attachments. Installation of the pins did not affect the performance of the muscle. The distance between the pins was measured and controlled to produce isometric and afterloaded isotonic contractions of the segment of the muscle between the pins. Data from such contractions were compared with traditional whole muscle measurements made on the same preparation. The isometric length-tension curve of the central segment was significantly higher than that of the whole muscle, and there was no plateau of developed force at long lengths in five of six muscles studied. In the resting state, the segment was more compliant than the whole muscle for physiologic lengths and much stiffer for longer lengths. Segment velocity and shortening were significantly higher than whole muscle velocity and shortening at comparable loads.

Animals↗
PubMed1981

Myocardial mechanical alterations during gradual onset long-term hypertension in rats.

Although a suddenly produced load leads to depressed myocardial contractility, the effects of a slowly induced physiological overload have not been defined. Therefore, a more gradual pressure overload was produced in female Wistar rats by hypertension due to constriction of the left renal artery. Hypertension (systolic blood pressure greater than or equal to 150 mmHg) developed within 3 wk, and blood pressure continued to increase for the next 5 wk. Heart weights in hypertensive animals were elevated by 34% after the onset of hypertension. Isometric and isotonic contractions from left ventricular papillary muscles were recorded at 5, 10, 20, and 30 wk after the onset of hypertension. Total and actively developed isometric tension at all initial muscle lengths were significantly greater in hypertensive animals throughout the 30-wk period. Time to peak tension and time to half relaxation were significantly prolonged. Force-velocity curves demonstrated a significant depression in velocity of shortening at all relative loads in hypertensive muscles that progressed with the duration of hypertension. These studies suggest that myocardial hypertrophy may impart the ability to maintain ventricular performance in terms of force development while speed of shortening decays.

Animals↗
PubMed1985

Altered myocardial mechanics in diabetic rabbits.

Diabetes mellitus may lead to congestive heart failure in humans, independent of atherosclerotic coronary artery disease. Previous studies have explored the myocardial effects of chronic diabetes in dogs and rats with somewhat divergent results. Therefore the current study examined papillary muscle function in rabbits made diabetic with 140-150 mg/kg intravenous alloxan compared with that of age-matched controls. The period of diabetes was 3 days (study 1), 1 mo (study 2), 3 mo (study 3), and 6 mo (study 4). The duration of isometric and isotonic contraction and relaxation were markedly prolonged in diabetes from studies 2, 3, and 4. Shortening velocity was diminished in diabetics from studies 1, 3, and 4. A blunted inotropic response to increasing stimulus frequency was observed in diabetics. Changes in resting tension were not consistently observed, suggesting that passive muscle stiffness is not altered. These findings indicate that previous work on diabetic rats can be extended to diabetic rabbits and suggest that chronic diabetes diminishes contractility and prolongs the duration of contraction in mammalian hearts.

Animals↗
PubMed1987

Myocardial adaptation to chronic propranolol therapy in normal rats.

The intrinsic myocardial adaptation to chronic beta-blockade was explored in normal male Wistar rats. Propranolol was administered by subcutaneous infusion using osmotic minipumps for 3-4 wk (P group). Heart rate fell by approximately 100 beats/min. A second group of animals was similarly treated but had their pumps removed several days before study (P-R group). Heart rate rose, but remained below base line. Study of isolated ventricular papillary muscle from P, P-R, and age-matched controls (C group) revealed prolonged contraction duration in P and P-R groups, but no change in shortening velocity. A greater shortening of time to peak tension and time to one-half relaxation in response to norepinephrine was demonstrated in P and P-R groups. Acute in vivo or in vitro administration of propranolol had no effect on base-line mechanical performance. No changes in the Ca2+, actin-activated Mg2+ myosin adenosine triphosphatase (ATPase) activity, or myosin isoenzyme distribution were found. Free thyroxine levels were decreased in P but not P-R groups. These findings indicate that chronic propranolol therapy in normal rats slows contraction and relaxation without altering contractility. The greater shortening of contraction duration in response to norepinephrine is partly offset by the prolongation of the base-line contraction.

Adaptation, Physiological↗
PubMed1994

Role of sarcoplasmic reticulum in loss of load-sensitive relaxation in pressure overload cardiac hypertrophy.

The loss of load-sensitive relaxation observed in the pressure-overloaded heart may reflect a strategy of slowed cytosolic Ca2+ uptake to yield a prolongation of the active state of the muscle and a decrease in cellular energy expenditure. A decrease in the potential of the sarcoplasmic reticulum (SR) to resequester cytosolic Ca2+ during diastole could contribute to this attenuated load sensitivity. To test this hypothesis, both in vitro mechanical function of anterior papillary muscles and the SR Ca2+ sequestration potential of female guinea pig left ventricle were compared in cardiac hypertrophy (Hyp) and sham-operated (Sham) groups. Twenty-one days of pressure overload induced by coarctation of the suprarenal, subdiaphragmatic aorta resulted in a 36% increase in left ventricular mass in the Hyp. Peak isometric tension, the rate of isometric tension development, and the maximal rates of isometric and isotonic relaxation were significantly reduced in Hyp. Load-sensitive relaxation were significantly reduced in Hyp. Load-sensitive relaxation quantified by the ratio of a rapid loading to unloading force step in isotonically contracting papillary muscle was reduced 50% in Hyp muscles. Maximum activity of SR Ca(2+)-adenosinetriphosphatase (ATPase) measured under optimal conditions (37 degrees C; saturating Ca2+) was unaltered, but at low free Ca2+ concentrations (0.65 microM), it was decreased by 43% of the Sham response. Bivariate regression analysis revealed a significant (r = 0.84; P = 0.009) relationship between the decrease in SR Ca(2+)-ATPase activity and the loss of load-sensitive relaxation after aortic coarctation. Stimulation of the SR Ca(2+)-ATPase by the catalytic subunit of adenosine 3',5'-cyclic monophosphate-dependent protein kinase resulted in a 2.6-fold increase for Sham but only a 1.6-fold increase for Hyp. Semiquantitative Western blot radioimmunoassays revealed that the changes in SR Ca(2+)-ATPase activity were not due to decreases in the content of the Ca(2+)-ATPase protein or phospholamban. Our data directly implicate a role for decreased SR function in attenuated load sensitivity. A purposeful downregulation of SR Ca2+ uptake likely results from a qualitative rather than a quantitative change in the ATPase and possibly one of its key regulators, phospholamban.

Animals↗
PubMed1996

Effect of length and contraction on coronary perfusion in isolated perfused papillary muscle of rat heart.

We studied the impeding effect of cardiac muscle contraction on coronary arterial inflow in six isolated, perfused papillary muscles of the rat. Special attention was given to the effect of changes in muscle length and contractility on flow impediment in systole. Contractility was changed by resumption of pacing after a quiescent period of 60-100 s or by doubling the calcium concentration in the perfusate and the superfusion fluid from 1 to 2 mM. The vascular bed was maximally dilated with adenosine, and perfusion pressure was kept constant at 69 +/- 3 cmH2O. We found that contractions impede arterial inflow by 29% [from 17.3 +/- 2.2 ml.min-1.g-1 during diastole to 12.4 +/- 1.8 (SE) ml.min-1.g-1 at peak systole, P < 0.001] while the muscle was kept at 90% of maximum muscle length (MLmax). When the muscle was stretched from 80 to 97% of MLmax, diastolic force increased from 0.5 +/- 0.3 to 11.1 +/- 1.2 mN/mm2, systolic force increased from 11.1 +/- 1.5 to 44.6 +/- 4.0 mN/mm2, diastolic flow decreased by 12% (from 18.2 +/- 2.3 to 15.9 +/- 1.9 ml.min-1.g-1, P < 0.05), and systolic flow decreased by 3% (12.4 +/- 2.3 to 12.0 +/- 1.6 ml.min-1.g-1, P = NS). Increased contractility by elevated [Ca2+] did not affect diastolic flow but increased systolic flow impediment from 29 to 39% (systolic flow decreased from 12.4 +/- 1.8 to 10.3 +/- 1.4 ml.min-1.g-1, P < 0.01). The results are qualitatively similar to findings in the intact heart. Limitations on quantitative comparison due to differences in muscle architecture and differences in force vectors in the papillary muscle and the left ventricle are discussed. The results show that ventricular pressure is not essential in systolic coronary arterial flow impediment. The findings are in agreement with the varying elastance concept where the flow impediment is predicted to depend on myocardial elastic properties.

Animals↗
PubMed2000

Force-velocity relationship and biochemical-to-mechanical energy conversion by the sarcomere.

The intracellular control mechanism leading to the well-known linear relationship between energy consumption by the sarcomere and the generated mechanical energy is analyzed here by coupling calcium kinetics with cross-bridge cycling. A key element in the control of the biochemical-to-mechanical energy conversion is the effect of filament sliding velocity on cross-bridge cycling. Our earlier studies have established the existence of a negative mechanical feedback mechanism whereby the rate of cross-bridge turnover from the strong, force-generating conformation to the weak, non-force-generating conformation is a linear function of the filament sliding velocity. This feedback allows the analytic derivation of the experimentally established Hill's equation for the force-velocity relationship. Moreover, it allows us to derive the transient length response to load clamps and the transient force response to sarcomere shortening at constant velocity. The results are in agreement with experimental studies. The mechanical feedback regulates the generated power, maintains the linear relationship between energy liberated by the actomyosin-ATPase and the generated mechanical energy, and determines the efficiency of biochemical-to-mechanical energy conversion. The mechanical feedback defines three elements of the mechanical energy: 1) external work done; 2) pseudopotential energy, required for cross-bridge recruitment; and 3) energy dissipation caused by the viscoelastic property of the cross bridge. The last two elements dissipate as heat.

Animals↗
PubMed1990

Influence of temperature on mechanics and energetics of muscle contraction.

Results gleaned from use of temperature as a probe to study skeletal muscle performance and mechanisms of activation and contraction are reviewed. Steady-state and non-steady-state responses to changes in temperature are considered. Temperature sensitivities, Q10 values, of mechanical and energetic parameters range from nearly 1 to greater than 5 in frog skeletal muscle. Factors that are less temperature sensitive (Q10 less than or equal to 1.5) are peak tetanic force, instantaneous stiffness, curvature of force-velocity relation, magnitude of labile heat, and mechanical efficiency. Rates with intermediate temperature sensitivities (Q10 greater than 2 but less than 3) include rate of isometric force development, maximum shortening velocity, and relaxation from a brief tetanus. Rates with high temperature sensitivities (Q10 greater than 3) include cross-bridge turnover during an isometric tetanus, isometric economy, maximum power output, Ca2+ sequestration by sarcoplasmic reticulum, relaxation from a prolonged tetanus, and recovery metabolism. The observation that the Q10 for relaxation rate depends on tetanic duration can be explained in terms of the possible role of parvalbumin as a soluble relaxing factor.

Animals↗
PubMed1985

Contractile properties of cultured glomerular mesangial cells.

The glomerular mesangium is composed of matrix material and at least two cell types. One is a bone marrow-derived phagocyte and the other is a smooth muscle-like cell. The phagocytic cell represents approximately 3-7% of the total mesangial cell population. The other, more abundant, cell type appears to be contractile and therefore has been proposed to play a role in regulating the surface area for filtration, one component of the ultrafiltration coefficient, Kf. In this review we discuss the contractile properties of cultured mesangial cells as well as the phenotypic alterations that lead to loss of isotonic contraction after prolonged culture.

Angiotensin II↗
PubMed1986

Changes in cross-bridge properties of sensitized airway smooth muscle.

We have reported previously that in ovalbumin-sensitized canine tracheal smooth muscle (TSM) the maximum ability to shorten is increased. This could account for the increased airway narrowing seen in vivo in allergic bronchoconstriction. It was associated with increased velocity of shortening. We now report that, by using an electromagnetic muscle lever system, quick releases were applied to control and sensitized TSM at 0.5-s intervals throughout the course of a lightly preloaded 10-s isotonic contraction. From the records obtained it is possible to determine that, early in contraction, shortening is brought about by relatively rapidly cycling [0.35 optimal muscle length units +/- 0.033/s (SE)] cross bridges. We also report that in the sensitized TSM it is the early bridges that increase their velocity by 26.6% (P less than 0.05) compared with similar bridges in muscles from control animals. Since 70% of the maximum shortening of the muscle occurs when early bridges are operative, it is likely that these bridges are responsible for the major part of the shortening. It is thus probable that increased allergic bronchoconstriction is produced by increased activity of early, rapidly cycling bridges. The bridges that are active late in the shortening show no difference between control and sensitized airway smooth muscles.

Animals↗
PubMed1987

Contractile properties of the shortening rat diaphragm in vitro.

Diaphragmatic fatigue has been defined in terms of the failure of the muscle to continue to generate a given level of tension. Appropriate shortening of the diaphragm is, however, just as important for adequate ventilation. In this study we have examined in vitro the contractile properties of the rat diaphragm under afterloaded isotonic conditions and the effect of fatigue on the ability of the diaphragm to shorten. Shortening of the muscle strips was found to depend on size of afterload, frequency of stimulation, duration of stimulation, and initial length of the muscle. The afterloaded isotonic length-tension relationship coincided with the relationship between length and active isometric tension only for relatively small afterloads. Fatigue of the muscle strips, induced by isometric or afterloaded isotonic contractions, was associated with a decline in the extent of shortening as well as a decrease in active isometric tension. Ability to shorten and ability to develop isometric tension did not decrease to the same extent under all conditions. We conclude that active shortening, as well as active isometric tension, is decreased by muscular fatigue and that changes in these properties can be different depending on experimental conditions. The results suggest that the definition of diaphragmatic fatigue should be expanded to include the ability of the muscle to shorten by an appropriate amount. The results also suggest that measurement of isometric performance may not provide a complete estimate of the overall performance of the fatigued diaphragm.

Animals↗
PubMed1988

Contractile properties of cat skeletal muscle after repetitive stimulation.

The isometric and force-velocity properties of the fast-twitch flexor digitorum longus (FDL) and slow-twitch soleus muscles were investigated immediately after and during recovery from a fatiguing stimulus regime (40 Hz for 330 ms every second for 180 s) in the anesthetized cat. The amplitude of the isometric twitch of FDL was unaffected but in soleus it remained depressed for much of the recovery period. Immediately after stimulation the twitch time to peak of FDL increased to 140% of the control (prefatigue) value and then reverted to control values. The maximum isometric tetanic tension (Po) developed by FDL was reduced to 67% of control values immediately after the stimulus regime, whereas soleus declined to 93% of control. Recovery of maximum force development was achieved after 45 min in FDL and after 15 min in soleus. The maximum speed of shortening of FDL was reduced to 63% of control values immediately after fatigue; despite some recovery within the first 30 min, it remained depressed during the remainder of the recovery period (up to 300 min). Maximum speed of shortening was unaltered in soleus. The a/Po value transiently increased to 176% of control values in FDL immediately after the fatigue regime but promptly returned to control values. Force-velocity properties of soleus were not affected by the stimulus regime. It is concluded that in FDL changes in the maximum speed of shortening and maximum isometric tension as a result of the stimulus regime are attributable to changes in the intrinsic behavior of cross-bridges and the metabolic status of the fibers, particularly in the fast-twitch fatigue-resistant fibers.

Animals↗
PubMed1991

Pulmonary vascular smooth muscle: biochemical and mechanical developmental changes.

To evaluate the developmental changes in pulmonary vascular smooth muscle contractile protein content, mechanical properties, and their contribution to the high resistance characteristic of the fetal and immediate neonatal period, we studied pulmonary vessels of fetal, newborn, and adult sheep, as well as newborn and adult pigs. Strips of the second- through fifth-generation vessels were dissected, and their content of tissue total smooth muscle cell protein, myosin, and actin-to-myosin ratio were measured; the mechanical properties of the second-generation vascular strips were also studied. For all ages the smooth muscle protein and myosin content of the second-generation vessels were significantly greater than for the lower pulmonary vascular orders (P less than 0.05). The myosin content in fetal sheep (0.77 +/- 0.03 micrograms/mg wet tissue) was similar to that of the newborn (0.79 +/- 0.04) and adult (0.86 +/- 0.05). However, the smooth muscle protein content (7.94 +/- 0.21 micrograms/mg wet tissue) and the actin-to-myosin ratio of the pulmonary vascular tissue of the fetus (1.00 +/- 0.04) were lower (P less than 0.01) in the fetal than in the newborn (9.16 +/- 0.26 and 1.60 +/- 0.12) and adult (9.38 +/- 0.3 and 1.60 +/- 0.11, respectively). No differences were observed for these parameters between the newborn and adult pig. Stress (16.5 +/- 1.7 mN/mm2) and the maximum shortening capacity (13.0 +/- 1.5% of optimal length) in the newborn pulmonary vascular strips were significantly greater than for the fetus (6.8 +/- 1.4 and 5.9 +/- 1.0, respectively) but similar to those of the adult sheep.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1992

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.

Aminophylline↗
PubMed1994

Metabolic and work capacity of skeletal muscle of PFK-deficient dogs studied in situ.

Mechanical and metabolic relationships of muscle lacking phosphofructokinase (PFKD) activity were compared with muscle having normal phosphofructokinase (NORM) activity by using the gastrocnemius-plantaris muscle group with isolated circulation in situ. Muscle contractile properties were similar in both groups. Initial power output (W) during repetitive tetanic (200 ms, 50 impulses/s) isotonic contractions was similar in both groups; however, W declined significantly more (30-80%) in PFKD than in NORM muscle over time, with a constant O2 uptake (VO2)/W. Despite similar O2 and substrate delivery, PFKD muscle had a lower VO2 (42-55%), less glucose uptake, similar free fatty acid uptake, and lactic acid uptake rather than output, during contractions. Muscle venous H+ concentration, strong ion difference, and PCO2 increased during contractions, the magnitude of change being smaller in PFKD muscle. Elevating arterial lactate concentration before contractions in PFKD muscle resulted in significant improvements in W and VO2 without altering the acid-base exchange at the muscle. Increasing O2 delivery by increasing arterial O2 concentration in PFKD dogs did not improve W or VO2. We conclude that, despite no inherent mechanical or contractile differences, PFKD muscle has a severely limited oxidative capacity and exaggerated fatigue and blood flow responses to contractions due to limited substrate metabolism resulting from the inability to utilize glycogen and/or glucose.

Acid-Base Equilibrium↗
PubMed1996

Sarcomere relaxation in hamster diaphragm muscle.

We characterized instantaneous sarcomere relaxation over the load continuum in isolated hamster diaphragm muscles by means of laser diffraction. In afterloaded twitches, sarcomere relaxation displayed two consecutive phases. The bulk of sarcomere lengthening occurred during the first phase and corresponded in time to muscle lengthening. The second phase of sarcomere relaxation was slower and corresponded in time to tension decay. At initial muscle length, the peak velocity of sarcomere lengthening (SVL) was linearly related to both the maximum extent of sarcomere shortening (delta SL) and sarcomere length at peak shortening (SLmin; each P < 0.01). Varying preload modified the SVL vs. SLmin relationship but not the SVL vs. delta SL relationship. At a given preload, muscle tension decay began at a similar sarcomere length, regardless of the afterload level. In conclusion, our results support the role played by sarcomere length in regulating the diaphragm muscle-lengthening rate but not the rate of tension decline.

Animals↗