Is curvature of the force-velocity relationship affected by oxygen availability? Evidence from studies in ex vivo and in situ rat muscles.

The power of shortening contractions in skeletal muscle is determined by the force-velocity relationship. Fatigue has been reported to either increase or decrease the force-velocity curvature depending on experimental circumstances. These discrepant findings may be related to experimental differences in oxygen availability. We therefore investigated how the curvature of the force-velocity relationship in soleus and gastrocnemius rat muscles is affected during fatigue, in both an ex vivo setup without an intact blood perfusion and in an in situ setup with an intact blood perfusion. Furthermore, we investigated the effect of reduced oxygen concentrations and reduced diffusion distance on the curvature of the force-velocity relationship in ex vivo muscles, where muscle oxygen uptake relies on diffusion from the incubation medium. Muscles were electrically stimulated to perform repeated shortening contractions and force-velocity curves were determined in rested and fatigued conditions. The curvature increased during fatigue in the soleus muscles (both in situ and ex vivo), and decreased for the gastrocnemius muscles (in situ) or remained unchanged (ex vivo). Furthermore, under ex vivo conditions, neither reduced oxygen concentrations nor reduced diffusion distance conferred any substantial effect on the force-velocity curvature. In contrast, reduced oxygen availability and increased diffusion distance did increase the loss of maximal power during fatigue, mainly due to additional decreases in isometric force. We conclude that oxygen availability does not influence the fatigue-induced changes in force-velocity curvature. Rather, the observed variable fatigue profiles with regard to changes in curvature seem to be linked to the muscle fiber-type composition.

Blood lactate accumulation decreases during the slow component of oxygen uptake without a decrease in muscular efficiency.

Pulmonary oxygen uptake ([Formula: see text]) slowly increases during exercise above the anaerobic threshold, and this increase is called the slow component of [Formula: see text]. The mechanism of the increase in [Formula: see text] is assumed to be due to increasing energy cost associated with increasingly inefficient muscle contraction. We hypothesized that the increase in [Formula: see text] would be accompanied by a constant or increasing rate of accumulation of blood lactate, indicating sustained anaerobic metabolism while [Formula: see text] increased. Ten male subjects performed cycle ergometry for 3, 6, and 9 min at a power output representing 60% of the difference between lactate threshold and maximal [Formula: see text] while [Formula: see text] and blood lactate accumulation were measured. Blood lactate accumulation decreased over time, providing the energy equivalent of (mean ± SD) 1586 ± 265, 855 ± 287, and 431 ± 392 ml of [Formula: see text] during 0-3, 3-6, and 6-9 min of exercise, respectively. As duration progressed, [Formula: see text] supplied 86.3 ± 2.0, 93.6 ± 1.9, and 96.8 ± 2.9% of total energy from 0 to 3, 3 to 6, and 6 to 9 min, respectively, while anaerobic contribution decreased. There was no change in total energy cost after 3 min, except that required by ventilatory muscles for the progressive increase in ventilation. The slow component of [Formula: see text] is accompanied by decreasing anaerobic energy contribution beyond 3 min during heavy exercise.

Optimal pacing strategy: from theoretical modelling to reality in 1500-m speed skating.

PURPOSE: Athletes are trained to choose the pace which is perceived to be correct during a specific effort, such as the 1500-m speed skating competition. The purpose of the present study was to "override" self-paced (SP) performance by instructing athletes to execute a theoretically optimal pacing profile. METHODS: Seven national-level speed-skaters performed a SP 1500-m which was analysed by obtaining velocity (every 100 m) and body position (every 200 m) with video to calculate total mechanical power output. Together with gross efficiency and aerobic kinetics, obtained in separate trials, data were used to calculate aerobic and anaerobic power output profiles. An energy flow model was applied to SP, simulating a range of pacing strategies, and a theoretically optimal pacing profile was imposed in a second race (IM). RESULTS: Final time for IM was ∼2 s slower than SP. Total power distribution per lap differed, with a higher power over the first 300 m for IM (637.0 (49.4) vs 612.5 (50.0) W). Anaerobic parameters did not differ. The faster first lap resulted in a higher aerodynamic drag coefficient and perhaps a less effective push-off. CONCLUSION: Experienced athletes have a well-developed performance template, and changing pacing strategy towards a theoretically optimal fast start protocol had negative consequences on speed-skating technique and did not result in better performance.

Force-frequency and force-length properties in skeletal muscle following unilateral focal ischaemic insult in a rat model.

AIM: Our purpose was to quantify skeletal muscle properties following unilateral focal ischaemic insult (stroke) in a rat model. METHODS: Male rats were divided into two groups: stroke and 2 weeks recovery (n = 8) and control group (n = 7). Stroke was induced in the area of the motor neocortex containing hind limb corticospinal neurones. Contractile properties of the medial gastrocnemius muscle were measured in situ in both limbs. Force-length and force-frequency properties were measured before and 35 min after 5 min fatiguing stimulation. RESULTS: Stroke resulted in bilateral tetanic fade during 200 Hz stimulation. When normalized to 100 Hz contractions, force at 200 Hz was 95.4 +/- 0.9% for the paretic muscles, 96.7 +/- 1.7% for non-paretic muscles and 102.2 +/- 1.0% for muscles of control rats (P = 0.006). Prior to fatiguing contractions, there was no difference in the length dependence of force. During repetitive contractions, active force fell significantly to 19 +/- 4 and 25 +/- 5% of initial force in paretic and non-paretic muscles of animals with a stroke respectively. In control animals active force fell to 37 +/- 5%. During repetitive contractions, fusion index increased in muscles of stroke animals to 1.0 +/- 0 but in control animals it was 0.95 +/- 0.02. There was selective force depression at short lengths for fatigued paretic muscle (significant difference at muscle lengths less than reference length -2 mm). CONCLUSION: The tetanic fade at high stimulation frequencies indicates that there may be activation failure following focal ischaemic insult. The greater magnitude of fatigue and selective depression at short lengths following repetitive contractions should be investigated further.

Low-frequency fatigue at maximal and submaximal muscle contractions

Skeletal muscle force production following repetitive contractions is preferentially reduced when muscle is evaluated with low-frequency stimulation. This selective impairment in force generation is called low-frequency fatigue (LFF) and could be dependent on the contraction type. The purpose of this study was to compare LFF after concentric and eccentric maximal and submaximal contractions of knee extensor muscles. Ten healthy male subjects (age: 23.6 ± 4.2 years; weight: 73.8 ± 7.7 kg; height: 1.79 ± 0.05 m) executed maximal voluntary contractions that were measured before a fatigue test (pre-exercise), immediately after (after-exercise) and after 1 h of recovery (after-recovery). The fatigue test consisted of 60 maximal (100 percent) or submaximal (40 percent) dynamic concentric or eccentric knee extensions at an angular velocity of 60°/s. The isometric torque produced by low- (20 Hz) and high- (100 Hz) frequency stimulation was also measured at these times and the 20:100 Hz ratio was calculated to assess LFF. One-way ANOVA for repeated measures followed by the Newman-Keuls post hoc test was used to determine significant (P < 0.05) differences. LFF was evident after-recovery in all trials except following submaximal eccentric contractions. LFF was not evident after-exercise, regardless of exercise intensity or contraction type. Our results suggest that low-frequency fatigue was evident after submaximal concentric but not submaximal eccentric contractions and was more pronounced after 1-h of recovery.

Low-frequency fatigue at maximal and submaximal muscle contractions.

Skeletal muscle force production following repetitive contractions is preferentially reduced when muscle is evaluated with low-frequency stimulation. This selective impairment in force generation is called low-frequency fatigue (LFF) and could be dependent on the contraction type. The purpose of this study was to compare LFF after concentric and eccentric maximal and submaximal contractions of knee extensor muscles. Ten healthy male subjects (age: 23.6 +/- 4.2 years; weight: 73.8 +/- 7.7 kg; height: 1.79 +/- 0.05 m) executed maximal voluntary contractions that were measured before a fatigue test (pre-exercise), immediately after (after-exercise) and after 1 h of recovery (after-recovery). The fatigue test consisted of 60 maximal (100%) or submaximal (40%) dynamic concentric or eccentric knee extensions at an angular velocity of 60 degrees /s. The isometric torque produced by low- (20 Hz) and high- (100 Hz) frequency stimulation was also measured at these times and the 20:100 Hz ratio was calculated to assess LFF. One-way ANOVA for repeated measures followed by the Newman-Keuls post hoc test was used to determine significant (P < 0.05) differences. LFF was evident after-recovery in all trials except following submaximal eccentric contractions. LFF was not evident after-exercise, regardless of exercise intensity or contraction type. Our results suggest that low-frequency fatigue was evident after submaximal concentric but not submaximal eccentric contractions and was more pronounced after 1-h of recovery.

Is a parallel elastic element responsible for the enhancement of steady-state muscle force following active stretch?

For over 50 years, it has been recognised that muscles from many different species of animals are able to generate a higher steady-state isometric force after active stretch than during a purely isometric contraction at the same length. This is known as ;residual force enhancement' (rFE). The mechanism underlying this phenomenon remains controversial. One proposal is that an elastic element parallel to the cross-bridges becomes stiffer, or is engaged, when the muscle is activated and generates force when stretched. If this is indeed the sole mechanism, then rFE should be eliminated by subsequently shortening the muscle by a distance equal to or greater than the initial stretch. We tested this hypothesis using six intact single fibres from frog lumbrical muscle. The fibres were activated and stretched to generate rFE and then rapidly shortened by between 25% and 700% of the initial stretch distance. In contrast to previous reports, we found that rapid shortening induced a depression of subsequent isometric force. We used two methods to account for this force depression when calculating rFE, thereby obtaining upper and lower bounds for the true rFE. With both methods of calculation, rFE was significantly greater than zero when shortening distance was equal to stretch distance (P=0.0004 and P=0.03, respectively). Therefore, our hypothesis was not supported. We conclude that rFE is unlikely to be generated solely by a parallel elastic element.

The biphasic force-velocity relationship in whole rat skeletal muscle in situ.

Edman has reported that the force-velocity relationship (FVR) departs from Hill's classic hyperbola near 0.80 of measured isometric force (J Physiol 404: 301-321, 1988). The purpose of this study was to investigate the biphasic nature of the FVR in the rested state and after some recovery from fatigue in the rat medial gastrocnemius muscle in situ. Force-velocity characteristics were determined before and during recovery from fatigue induced by intermittent stimulation at 170 Hz for 100 ms each second for 6 min. Force-velocity data were obtained for isotonic contractions with 100 ms of 200-Hz stimulation, including several measurements with loads above 0.80 of measured isometric force. The force-velocity data obtained in this study were fit well by a double-hyperbolic equation. A departure from Hill's classic hyperbola was found at 0.88+/-0.01 of measured isometric force, which is higher than the approximately 0.80 reported by Edman et al. for isolated frog fibers. After 45 min of recovery, maximum shortening velocity was 86+/-2% of prefatigue, but neither curvature nor predicted isometric force was significantly different from prefatigue. The location of the departure from Hill's classic hyperbola was not different after this recovery from the fatiguing contractions. Including an isometric point in the data set will not yield the same values for maximal velocity and the degree of curvature as would be obtained using the double hyperbola approach. Data up to 0.88 of measured isometric force can be used to fit data to the Hill equation.

Reports of the length dependence of fatigue are greatly exaggerated.

Relative force depression associated with muscle fatigue is reported to be greater when assessed at short vs. long muscle lengths. This appears to be due to a rightward shift in the force-length relationship. This rightward shift may be caused by stretch of in-series structures, making sarcomere lengths shorter at any given muscle length. Submaximal force-length relationships (twitch, double pulse, 50 Hz) were evaluated before and after repetitive contractions (50 Hz, 300 ms, 1/s) in an in situ preparation of the rat medial gastrocnemius muscle. In some experiments, fascicle lengths were measured with sonomicrometry. Before repetitive stimulation, fascicle lengths were 11.3 +/- 0.8, 12.8 +/- 0.9, and 14.4 +/- 1.2 mm at lengths corresponding to -3.6, 0, and 3.6 mm where 0 is a reference length that corresponds with maximal active force for double-pulse stimulation. After repetitive stimulation, there was no change in fascicle lengths; these lengths were 11.4 +/- 0.8, 12.6 +/- 0.9, and 14.2 +/- 1.2 mm. The length dependence of fatigue was, therefore, not due to a stretch of in-series structures. Interestingly, the rightward shift that was evident when active force was calculated in the traditional way (subtraction of the passive force measured before contraction) was not seen when active force was calculated by subtracting the passive force that was associated with the fascicle length reached at the peak of the contraction. This calculation is based on the assumption that passive force decreases as the fascicles shorten during a fixed-end contraction. This alternative calculation revealed similar postfatigue absolute active force depression at all lengths. In relative terms, a length dependence of fatigue was still evident, but this was greatly diminished compared with that observed when active force was calculated with the traditional method.

Abdominal muscle activation of elite male golfers with chronic low back pain.

PURPOSE: The purpose of this study was twofold: 1) to determine whether elite male golfers with chronic low back pain (CLBP) exhibit different abdominal muscle activity patterns during the golf swing than asymptomatic control (AC) golfers and 2) to determine whether elite male golfers with CLBP experience greater fatigue in the abdominal muscles than AC golfers after a typical practice session. METHODS: Surface EMG data were collected bilaterally from the rectus abdominis (RA), external oblique (EO), and internal oblique (IO) muscles. Muscle activity during the golf swing was measured using the root mean square (RMS) of the EMG signal in various phases of the golf swing. Fatigue was assessed using the median frequency (MF) and RMS of the EMG signal during a 10-s submaximal isometric contraction. Low back pain was quantified with the McGill Pain Questionnaire before and after the practice session. RESULTS: No differences in the RMS of abdominal muscle activity were noted during the golf swing between AC and CLBP subjects. However, EO (lead) onset times were significantly delayed with respect to the start of the backswing in CLBP subjects. Low back pain in CLBP golfers increased significantly after the practice session. Abdominal muscle fatigue, as measured with MF or RMS, was not evident after the practice session for either AC or CLBP subjects. CONCLUSION: Abdominal muscle activity and muscle fatigue characteristics were quite similar between AC and CLBP subjects after repetitive golf swings. Despite this, it was clear that repetitive golf swings were aggravating some part of the musculoskeletal system in CLBP subjects, which resulted in increased pain in the low back area.

Evaluation of the Monark Wingate ergometer by direct measurement of resistance and velocity.

The purpose of this study was to assess the accuracy of the new basket-loaded Wingate ergometer introduced by Monark (Model 834E). Velocity was measured directly from the pedal switch while tension was measured with transducers on each end of the brake lacing. Moment of inertia of the flywheel was determined and accounted for in the calculation of power. Constant load tests (39.24 to 98.1 N), were done at pedaling speeds from 80 to 140 r x min(-1) (flywheel angular velocity = 30-50 rad x s(-1)). The load transmitted to the lacing at the front and back of the flywheel was 95.5 +/- 0.8% (mean +/- SEM) and 6.71 +/- 0.8%, respectively, of the load in the basket. Thus, the resultant tension (front minus back) was on average 88.8 +/- 0.57% of the applied load. The velocity recorded by the Monark Wingate Ergometer computer program (MWECP) was the same (100.4 +/- 1.56%) as that determined from the pedal switch directly. Five male mountain bikers performed a 30-s all-out test. Peak power calculated by MWECP (1181 +/- 55W) was always higher (p < .01) than that calculated from direct measures of tension and velocity (1102 +/- 66W), when not taking into account the moment of inertia. These experiments suggest that the basket-loaded Monark Wingate ergometer does not provide a correct calculation of power because of incomplete load transmission to the flywheel.

Cadence, power, and muscle activation in cycle ergometry.

PURPOSE: Based on the resistance-rpm relationship for cycling, which is not unlike the force-velocity relationship of muscle, it is hypothesized that the cadence which requires the minimal muscle activation will be progressively higher as power output increases. METHODS: To test this hypothesis, subjects were instrumented with surface electrodes placed over seven muscles that were considered to be important during cycling. Measurements were made while subjects cycled at 100, 200, 300, and 400 W at each cadence: 50, 60, 80, 100, and 120 rpm. These power outputs represented effort which was up to 32% of peak power output for these subjects. RESULTS: When all seven muscles were averaged together, there was a proportional increase in EMG amplitude each cadence as power increased. A second-order polynomial equation fit the EMG:cadence results very well (r2 = 0.87- 0.996) for each power output. Optimal cadence (cadence with lowest amplitude of EMG for a given power output) increased with increases in power output: 57 +/- 3.1, 70 +/- 3.7, 86 +/- 7.6, and 99 +/- 4.0 rpm for 100, 200, 300, and 400 W, respectively. CONCLUSION: The results confirm that the level of muscle activation varies with cadence at a given power output. The minimum EMG amplitude occurs at a progressively higher cadence as power output increases. These results have implications for the sense of effort and preferential use of higher cadences as power output is increased.

Force-frequency relationship and potentiation in mammalian skeletal muscle.

Repetitive activation of a skeletal muscle results in potentiation of the twitch contractile response. Incompletely fused tetanic contractions similar to those evoked by voluntary activation may also be potentiated by prior activity. We aimed to investigate the role of stimulation frequency on the enhancement of unfused isometric contractions in rat medial gastrocnemius muscles in situ. Muscles set at optimal length were stimulated via the sciatic nerve with 50-micros duration supramaximal pulses. Trials consisted of 8 s of repetitive trains [5 pulses (quintuplets) 2 times per second or 2 pulses (doublets) 5 times per second] at 20, 40, 50, 60, 70, and 80 Hz. These stimulation frequencies represent a range over which voluntary activation would be expected to occur. When the frequency of stimulation was 20, 50, or 70 Hz, the peak active force (highest tension during a contraction - rest tension) of doublet contractions increased from 2.2 +/- 0.2, 4.1 +/- 0.4, and 4.3 +/- 0.5 to 3.1 +/- 0.3, 5.6 +/- 0.4, and 6.1 +/- 0.7 N, respectively. Corresponding measurements for quintuplet contractions increased from 2.2 +/- 0.2, 6.1 +/- 0.5, and 8.7 +/- 0.7 to 3.2 +/- 0.3, 7.3 +/- 0.6, and 9.0 +/- 0.7 N, respectively. Initial peak active force values were 27 +/- 1 and 61.5 +/- 5% of the maximal (tetanic) force for doublet and quintuplet contractions, respectively, at 80 Hz. With doublets, peak active force increased at all stimulation frequencies. With quintuplets, peak active force increased significantly for frequencies up to 60 Hz. Twitch enhancement at the end of the 8 s of repetitive stimulation was the same regardless of the pattern of stimulation during the 8 s, and twitch peak active force returned to prestimulation values by 5 min. These experiments confirm that activity-dependent potentiation is evident during repeated, incompletely fused tetanic contractions over a broad range of frequencies. This observation suggests that, during voluntary motor unit recruitment, derecruitment or decreased firing frequency would be necessary to achieve a fixed (submaximal) target force during repeated isometric contractions over this time period.

Coexistence of potentiation and fatigue in skeletal muscle

Twitch potentiation and fatigue in skeletal muscle are two conditions in which force production is affected by the stimulation history. Twitch potentiation is the increase in the twitch active force observed after a tetanic contraction or during and following low-frequency stimulation. There is evidence that the mechanism responsible for potentiation is phosphorylation of the regulatory light chains of myosin, a Ca2+ -dependent process. Fatigue is the force decrease observed after a period of repeated muscle stimulation. Fatigue has also been associated with a Ca2+ -related mechanism: decreased peak Ca2+ concentration in the myoplasm is observed during fatigue. This decrease is probably due to an inhibition of Ca2+ release from the sarcoplasmic reticulum. Although potentiation and fatigue have opposing effects on force production in skeletal muscle, these two presumed mechanisms can coexist. When peak myoplasmic Ca2+ concentration is depressed, but myosin light chains are relatively phosphorylated, the force response can be attenuated, not different, or enhanced, relative to previous values. In circumstances where there is interaction between potentiation and fatigue, care must be taken in interpreting the contractile responses.

Coexistence of potentiation and fatigue in skeletal muscle.

Twitch potentiation and fatigue in skeletal muscle are two conditions in which force production is affected by the stimulation history. Twitch potentiation is the increase in the twitch active force observed after a tetanic contraction or during and following low-frequency stimulation. There is evidence that the mechanism responsible for potentiation is phosphorylation of the regulatory light chains of myosin, a Ca2+-dependent process. Fatigue is the force decrease observed after a period of repeated muscle stimulation. Fatigue has also been associated with a Ca2+-related mechanism: decreased peak Ca2+ concentration in the myoplasm is observed during fatigue. This decrease is probably due to an inhibition of Ca2+ release from the sarcoplasmic reticulum. Although potentiation and fatigue have opposing effects on force production in skeletal muscle, these two presumed mechanisms can coexist. When peak myoplasmic Ca2+ concentration is depressed, but myosin light chains are relatively phosphorylated, the force response can be attenuated, not different, or enhanced, relative to previous values. In circumstances where there is interaction between potentiation and fatigue, care must be taken in interpreting the contractile responses.

Length dependence of staircase potentiation: interactions with caffeine and dantrolene sodium.

In skeletal muscle, there is a length dependence of staircase potentiation for which the mechanism is unclear. In this study we tested the hypothesis that abolition of this length dependence by caffeine is effected by a mechanism independent of enhanced Ca2+ release. To test this hypothesis we have used caffeine, which abolishes length dependence of potentiation, and dantrolene sodium, which inhibits Ca2+ release. In situ isometric twitch contractions of rat gastrocnemius muscle before and after 20 s of repetitive stimulation at 5 Hz were analyzed at optimal length (Lo), Lo - 10%, and Lo + 10%. Potentiation was observed to be length dependent, with an increase in developed tension (DT) of 78 +/- 12, 51 +/- 5, and 34 +/- 9% (mean +/- SEM), at Lo - 10%, Lo, and Lo + 10%, respectively. Caffeine diminished the length dependence of activation and suppressed the length dependence of staircase potentiation, giving increases in DT of 65+/-13, 53 +/- 11, and 45 +/- 12% for Lo - 10%, Lo, and Lo + 10%, respectively. Dantrolene administered after caffeine did not reverse this effect. Dantrolene alone depressed the potentiation response, but did not affect the length dependence of staircase potentiation, with increases in DT of 58 +/- 17, 26 +/- 8, and 18 +/- 7%, respectively. This study confirms that there is a length dependence of staircase potentiation in mammalian skeletal muscle which is suppressed by caffeine. Since dantrolene did not alter this suppression of the length dependence of potentiation by caffeine, it is apparently not directly modulated by Ca2+ availability in the myoplasm.

Staircase in mammalian muscle without light chain phosphorylation.

In disuse atrophied skeletal muscle, the staircase response is virtually absent and light chain phosphorylation does not occur. The purpose of the present study was to determine if staircase could be restored in atrophied muscle with continued absence of myosin light chain phosphorylation, by reducing what appears to be an otherwise enhanced calcium release. Control (untreated) and sham-operated female Sprague-Dawley rats were compared with animals after 2 weeks of complete inactivity induced by tetrodotoxin (TTX) application to the left sciatic nerve. In situ isometric contractile responses of rat gastrocnemius muscle were analyzed before and after administration of dantrolene sodium (DS), a drug which is known to inhibit Ca2+ release in skeletal muscle. Twitch active force (AF) was attenuated by DS from 2.2 +/- 0.2 N, 2.7 +/- 0.1 N and 2.4 +/- 0.2 N to 0.77 +/- 0.2 N, 1.05 +/- 0.1 N and 1.01 +/- 0.2 N in TTX (N = 5), sham (N = 11) and control (N = 7) muscles, respectively. Following dantrolene treatment, 10 s of 10-Hz stimulation increased AF to 1.32 +/- 0.2 N, 1.52 +/- 0.1 N and 1.45 +/- 0.2 N for the TTX, sham and control groups, respectively, demonstrating a positive staircase response. Regulatory light chain (R-LC) phosphorylation was lower for TTX-treated (5.5 +/- 5.5%) than for control (26.1 +/- 5.3%) and sham (20.0 +/- 5%) groups. There was no significant change from resting levels for any of the groups after DS treatment (P = 0.88). This study shows that treatment with dantrolene permits staircase in atrophied muscle as well as control muscle, by a mechanism which appears to be independent of R-LC phosphorylation.

Length dependence of active force production in skeletal muscle.

The sliding filament and cross-bridge theories of muscle contraction provide discrete predictions of the tetanic force-length relationship of skeletal muscle that have been tested experimentally. The active force generated by a maximally activated single fiber (with sarcomere length control) is maximal when the filament overlap is optimized and is proportionally decreased when overlap is diminished. The force-length relationship is a static property of skeletal muscle and, therefore, it does not predict the consequences of dynamic contractions. Changes in sarcomere length during muscle contraction result in modulation of the active force that is not necessarily predicted by the cross-bridge theory. The results of in vivo studies of the force-length relationship suggest that muscles that operate on the ascending limb of the force-length relationship typically function in stretch-shortening cycle contractions, and muscles that operate on the descending limb typically function in shorten-stretch cycle contractions. The joint moments produced by a muscle depend on the moment arm and the sarcomere length of the muscle. Moment arm magnitude also affects the excursion (length change) of a muscle for a given change in joint angle, and the number of sarcomeres arranged in series within a muscle fiber determines the sarcomere length change associated with a given excursion.

Caffeine and length dependence of staircase potentiation in skeletal muscle.

Skeletal muscle sensitivity to Ca2+ is greater at long lengths, and this results in an optimal length for twitch contractions that is longer than optimal length for tetanic contractions. Caffeine abolishes this length dependence of Ca2+ sensitivity. Muscle length (ML) also affects the degree of staircase potentiation. Since staircase potentiation is apparently caused by an increased Ca2+ sensitivity of the myofilaments, we tested the hypothesis that caffeine depresses the length dependence of staircase potentiation. In situ isometric twitch contractions of rat gastrocnemius muscle before and after 10 s of 10-Hz stimulation were analyzed at seven different lengths to evaluate the length dependence of staircase potentiation. In the absence of caffeine, length dependence of Ca2+ sensitivity was observed, and the degree of potentiation after 10-Hz stimulation showed a linear decrease with increased length (DT = 1.47 - 0.05 ML, r2 = 0.95, where DT is developed tension). Length dependence of Ca2+ sensitivity was decreased by caffeine when caffeine was administered in amounts estimated to result in 0.5 and 0.75 mM concentrations. Furthermore, the negative slope of the relationship between staircase potentiation and muscle length was diminished at the lower caffeine dose, and the slope was not different from zero after the higher dose (DT = 1.53 - 0.009 ML, r2 = 0.43). Our study shows that length dependence of Ca2+ sensitivity in intact skeletal muscle is diminished by caffeine. Caffeine also suppressed the length dependence of staircase potentiation, suggesting that the mechanism of this length dependence may be closely related to the mechanism for length dependence of Ca2+ sensitivity.

Attenuation of myosin light chain phosphorylation and posttetanic potentiation in atrophied skeletal muscle.

Previously we have demonstrated that the absence of staircase potentiation in atrophied rat gastrocnemius muscle is accompanied by a virtual absence of phosphorylation of the regulatory light chains (R-LC) of myosin. It was our purpose in the present study to determine if posttetanic potentiation and corresponding R-LC phosphorylation were also attenuated in disuse-atrophied muscles. Two weeks after a spinal hemisection (T12), twitch and tetanic contractile characteristics were measured in situ in control, sham-treated and atrophied (hemisected) muscles. Posttetanic potentiation 20 s after a 2 s tetanic contraction (200 Hz) was depressed in atrophied muscles (128.7 +/- 2.6%; mean +/- SEM) when compared to sham-treated (149.9 +/- 2.4%) and control (142.9 +/- 2. 7%) muscles. Atrophied muscles demonstrated a significant increase in R-LC phosphorylation from rest (0.05 +/- 0.04 moles of phosphate/mole of R-LC) to posttetanic conditions (0.21 +/- 0.03 moles of phosphate/mole of R-LC), and less phosphorylation than control and sham-treated muscles (0.43 +/- 0.06 and 0.49 +/- 0.03 moles of phosphate/mole of R-LC, respectively) after tetanic stimulation. The preservation of the potentiation-phosphorylation relationship in atrophied muscles is consistent with the hypothesis that R-LC phosphorylation may be the principal mechanism for twitch potentiation.