Isometric Relaxation Rate Research Articles

Dynamic Skeletal Muscle Exercise and Fatigue Development in Post Infarction Heart Failure Rats and Effect of Warm-Up

Skeletal muscle fatigue develops during physical exercise. Most reports on skeletal muscle fatigue use isometricfatigue protocols with a fall in force production as a measure of fatigue. However, most muscles shorten during normal use and we propose that the fatigue mechanism will be different during dynamic contractions as compared with isometric contractions. Methods: Fatigue was induced in rat soleus muscles from post infarction heart failure (HF) rats and controls (SHAM) by in situ isotonic shortening contractions (1s at 30Hz every 2s for 15min). The muscles were allowed to shorten isotonically against a load (AL) corresponding to 1/3 of maximal isometric force. After 15min recovery period the muscles were stimulated with a similar protocol. MLC2s phosphorylation and metabolites were measured at different points of time. Results: During 1st protocol, fatigue development was confirmed by a significant fall in shortening in both SHAM and HF. After 100s of stimulation soleus from SHAM showed an increase in baseline tension (Tbl) between stimulation trains, which was much less pronounced in HF (p<0.01). At this time there was a significant higher lactate concentration in SHAM muscle compared with HF. The increase in Tbl at 100s was correlated to both isotonic and isometric relaxation rate. At 100s in 2nd protocol, the isotonic and isometric relaxation rates were nearly recovered leading to almost no rise in Tbl in both SHAM and HF. There was a linear correlation (p=0.99) between maximal shortening and MLC2s phosphorylation in protocols with variable AL. We propose that MLC2s phosphorylation participates in the regulation of shortening, while metabolites (especially lactate) may contribute to the reduced relaxation rates leading to increased Tbl.

Causes of fatigue in slow-twitch rat skeletal muscle during dynamic activity

Skeletal muscle fatigue is most often studied in vitro at room temperature and is classically defined as a decline in maximum force production or power output, exclusively linked to repeated isometric contractions. However, most muscles shorten during normal use, and we propose that both the functional correlate of fatigue, as well as the fatigue mechanism, will be different during dynamic contractions compared with static contractions. Under isoflurane anesthesia, fatigue was induced in rat soleus muscles in situ by isotonic shortening contractions at 37 degrees C. Muscles were stimulated repeatedly for 1 s at 30 Hz every 2 s for a total of 15 min. The muscles were allowed to shorten isotonically against a load corresponding to one-third of maximal isometric force. Maximal unloaded shortening velocity (V(0)), maximum force production (F(max)), and isometric relaxation rate (-dF/dt) was reduced after 100 s but returned to almost initial values at the end of the stimulation protocol. Likewise, ATP and creatine phosphate (CrP) were reduced after 100 s, but the level of CrP was partially restored to initial values after 15 min. The rate of isometric force development, the velocity of shortening, and isotonic shortening were also reduced at 100 s, but in striking contrast, did not recover during the remainder of the stimulation protocol. The regulatory myosin light chain (MLC2s) was dephosphorylated after 100 s and did not recover. Although metabolic changes may account for the changes of F(max), -dF/dt, and V(0), dephosphorylation of MLC2s may be involved in the fatigue seen as sustained slower contraction velocities and decreased muscle shortening.

Parvalbumin content in striated muscles of the common shrew (Sorex araneus)

The parvalbumin content of mammalian muscles correlates positively with isometric relaxation rate and fiber type IIB frequency of the muscles but negatively with animal size. Since shrews are small-bodied animals with a relatively low number of type IIB fibers, it is of some interest to know how the parvalbumin content of shrew muscle correlates with the above factors. Parvalbumin content in heart, diaphragm, and gastrocnemius muscle of the common shrew, mouse, and rat was determined electrophoretically. Parvalbumin was not found in heart muscle of any species. Shrew diaphragm (0.29 ± 0.04 g/kg) had significantly less parvalbumin than mouse (0.63 ± 0.11 g/kg) or rat (0.54 ± 0.09 g/kg) diaphragm. Similarly, the parvalbumin content of shrew gastrocnemius muscle (0.28 ± 0.04 g/kg) was significantly lower than in that of mouse (2.88 ± 0.38 g/kg) or rat (0.96 ± 0.25 g/kg) gastrocnemius muscle. The isometric twitch of the gastrocnemius muscle was somewhat faster than the twitch of the diaphragm in all three species. The isometric contractions of shrew and mouse skeletal muscles were generally very similar in duration, with the exception of the relaxation time of the gastrocnemius muscle, which was shorter in the mouse. Diaphragm and gastrocnemius muscle of the rat were clearly slower than the respective muscles in the mouse or shrew with regard to both the contraction and relaxation phases. The half-relaxation time of isometric contractions correlated relatively weakly with parvalbumin content of the muscles (r = 0.40) but more strongly with their fiber IIB content (r = 0.81). The unexpectedly low parvalbumin content and relatively slow rate of contraction in shrew skeletal muscles are attributed to the exceptional fiber type composition, i.e., a high proportion of type IID fibers.

Isometric relaxation of isolated diaphragm muscle: influence of load, length, time, and stimulation

Determinants of the isometric relaxation rate were investigated in isolated rat diaphragm (n = 30). We tested the hypothesis that these determinants could include loading conditions, namely preload and afterload; abrupt changes in load during the contraction phase; stimulation conditions; and time. Two relaxation sequences were studied. When isometric relaxation occurred at initial muscle length (isotonic-isometric sequence), an increase in total load (P) accelerated the negative peak rate of tension decline (-dP/dtmax). Variations in initial length, stimulation, and onset of relaxation did not modify the -dP/dtmax vs. afterload relationship. When isometric relaxation was analyzed after -dP/dtmax, for a given afterload level the instantaneous rate of tension decline (-dP/dt) was a unique function of instantaneous tension, regardless of previous loading conditions, stimulation mode, or time. When the isometric relaxation occurred at end-shortening muscle length (isometric-isotonic sequence), the -dP/dtmax vs. P relationship was flat. The rate of tension decay, as attested by either -dP/dtmax or instantaneous -dP/dt vs. instantaneous tension phase plane, differed markedly depending on stimulation conditions. Thus the regulation of isometric relaxation rate differed according to the relaxation sequence. In muscle isometrically relaxing at initial muscle length, peak isometric relaxation rate was mainly determined by afterload. Conversely, in muscle isometrically relaxing at end-shortening length, isometric relaxation rate was highly dependent on the level of activation and was independent of preload and afterload.

Effect of ethanol on contraction and relaxation of isolated rat ventricular muscle

The effects of ethanol on myocardial mechanical properties were evaluated in isolated rat ventricular muscle preparations. Ethanol reduced peak developed tension by 6.3% at a concentration of 100 mg 100 ml , 11.8% at 200 mg 100 ml and 27.2% at 400 mg 100 ml . A similar degree of depression was observed in dT dt . Time to peak tension was slightly shortened, and isometric relaxation rate was increased at a high concentration of ethanol. The resting tension did not change significantly. Despite biochemical data by others suggesting an alcohol induced delay in calcium sequestration by cardiac microsomes, ethanol at concentrations found in human intoxication depressed the systolic performance of isolated muscle preparations but did not prolong relaxation or alter resting tension.

Rat myocardial mechanics during pressure-induced hypertrophy development and reversal.

Moderate cardiac hypertrophy (CH) was produced in rats by abdominal aorta constriction for 5, 8, 15, 21, and 28 days. Aortic constriction release after 5, 8, and 15 days led to CH regression, which was complete within 15 days. A study of left ventricular papillary muscle mechanics during CH development demonstrated an early but transitory decrease in both maximum isometric force (Po) and maximum muscle shortening velocity (max V); in addition, the time-to-peak tension increased, and there was a decrease in isometric relaxation rate and in force-frequency relationship (negative staircase.) After CH regression, isometric relaxation and negative staircase were similar to controls, whereas the prolonged duration of contraction persisted. After release of the aortic constriction at 8 and 15 days, Po and max V were normal; however, after the earlier release (5 days), Po was higher than control, when muscle thickness was taken into consideration. These findings suggest 1) that an alteration in muscle mechanics may be related to the hypertrophy itself; 2) that anomalous excitation-contraction coupling might persist after CH regression.