C. J. de Ruiter

The force-velocity relationship of human adductor pollicis muscle during stretch and the effects of fatigue

1 We have examined the force‐velocity characteristics of tetanically activated human adductor pollicis working in vivo, in the fresh and fatigued states. 2 The increase in force in response to stretch was divided into two major components. The first, steady, component persisted after the stretch and is concluded not to be a function of active cycling cross‐bridges because it was not affected by either the velocity of the stretch or the level of muscle activation. 3 The origin of the second, transient, component of the increased force seen during stretch is consistent with cross‐bridge activity since it increased with increasing velocity of stretch and was proportional to the level of activation. 4 It is likely that both components of the stretch response make a significant contribution to muscle performance when acting to resist a force. For the fastest stretch used, the contributions of cross‐bridge and non‐cross‐bridge mechanisms were equal. For the slowest stretch, lasting 10 s and over the same distance, the force response was attributed almost entirely to non‐cross‐bridge mechanisms. 5 As a result of acute fatigue (50 % isometric force loss) there were only small reductions in the non‐cross‐bridge component of the force response to stretch, while the cross‐bridge component decreased in absolute terms. 6 The transient component of the stretch response increased as a result of fatigue, relative to the isometric force, while the force during shortening decreased. The results are consistent with a decrease in cross‐bridge turnover in fatigued muscle.

Shortening induced force depression in human adductor pollicis muscle

1 The effects of single isovelocity shortening contractions on force production of the electrically stimulated human adductor pollicis muscle were investigated in seven healthy male subjects. 2 Redeveloped isometric force immediately following isovelocity shortening was always depressed compared with the isometric force recorded at the same muscle length but without preceding shortening. The maximal isometric force deficit (FD) was (mean ± s.e.m.) 37 ± 2 % after 38 deg of shortening at 6.1 deg s−1. 3 The FD was positively correlated with angular displacement (r2 > 0.98) and decreased with increasing velocity of the shortening step. Stimulation at 20 Hz instead of 50 Hz reduced absolute force levels during the contractions to about 73 % and the FD was decreased to a similar extent. Eighty‐nine per cent of the velocity‐related variation in the FD could be explained by the absolute force levels during shortening. 4 FD was largely abolished by allowing the muscle to relax briefly (approximately 200 ms), a time probably too short for significant metabolic recovery. 5 At all but the highest velocities there was a linear decline in force during the latter part of the isovelocity shortening phase, suggesting that the mechanisms underlying FD were active during shortening. 6 Our results show that shortening‐induced force deficit is a significant feature of human muscle working in situ and is proportional to the work done by the muscle‐tendon complex. This finding has important implications for experimental studies of force‐velocity relationships in the intact human.

No acute effects of short-term creatine supplementation on muscle properties and sprint performance.

Abstract In a double-blind, placebo, controlled study, we investigated the acute effects of short-term oral creatine supplementation (20 g · day−1 for 6 days) on muscle activation, fatigue and recovery of the m. quadriceps femoris during electrical stimulation, and on maximal performance during sprint cycling. The quadriceps muscles of 23 well-trained rowers were stimulated at different frequencies (10, 20, 50, 100, 150 and 200 Hz). Furthermore, 40 repetitive, electrically stimulated (duration 220 ms, stimulation frequency 150 Hz) concentric contractions were imposed at a constant angular velocity of 180° · s−1 over a range of 50° (from 90 to 140° knee angle), each extension/flexion cycle lasting 1200 ms. To determine recovery, torque was measured at 20, 50, 80, 120, 180 and 300 s after the last contraction. In addition, two maximal 30-s sprints were performed on a cycle ergometer with 4 min rest in between. Following short-term creatine supplementation, body mass [mean (SEM)] increased (P < 0.05) from 85.7 (2.7) kg to 87.3 (2.9) kg. Creatine supplementation had no effect on maximal voluntary isometric torque and muscle activation, or on fatigue and recovery of dynamic exercise. There was also no significant effect on peak power, time to peak power and work to peak power, or total work during both sprints on the cycle ergometer. It was concluded that short-term oral creatine supplementation resulted in increased body mass, but did not enhance muscle performance or maximal output during sprint cycling.

Change in contractile properties of human muscle in relationship to the loss of power and slowing of relaxation seen with fatigue.

Slow relaxation from an isometric contraction is characteristic of acutely fatigued muscle and is associated with a decrease in the maximum velocity of unloaded shortening (Vmax) and both these phenomena might be due to a decreased rate of cross bridge detachment. We have compared the change in relaxation rate with that of various parameters of the force–velocity relationship over the course of an ischaemic series of fatiguing contractions and subsequent recovery using the human adductor pollicis muscle working in vivo at approximately 37°C in nine healthy young subjects. Maximal isometric force (F0) decreased from 91.0 ± 1.9 to 58.3 ± 3.5 N (mean ±s.e.m.). Maximum power decreased from 53.6 ± 4.0 to 17.7 ± 1.2 (arbitrary units) while relaxation rate declined from −10.3 ± 0.38 to −2.56 ± 0.29 s−1. Vmax showed a smaller relative change from 673 ± 20 to 560 ± 46 deg s−1 and with a time course that differed markedly from that of slowing of relaxation, showing very little change until late in the series of contractions. Curvature of the force–velocity relationship increased (a/F0 decreasing from 0.22 ± 0.02 to 0.11 ± 0.02) with fatigue and with a time course that was similar to that of the loss of power and the slowing of relaxation. It is concluded that for human muscle working at a normal physiological temperature the change in curvature of the force–velocity relationship with fatigue is a major cause of loss of power and may share a common underlying mechanism with the slowing of relaxation from an isometric contraction.

The measurement of force/velocity relationships of fresh and fatigued human adductor pollicis muscle

Abstract The purpose of the study was to obtain force/velocity relationships for electrically stimulated (80 Hz) human adductor pollicis muscle (n = 6) and to quantify the effects of fatigue. There are two major problems of studying human muscle in situ; the first is the contribution of the series elastic component, and the second is a loss of force consequent upon the extent of loaded shortening. These problems were tackled in two ways. Records obtained from isokinetic releases from maximal isometric tetani showed a late linear phase of force decline, and this was extrapolated back to the time of release to obtain measures of instantaneous force. This method gave usable data up to velocities of shortening equivalent to approximately one-third of maximal velocity. An alternative procedure (short activation, SA) allowed the muscle to begin shortening when isometric force reached a value that could be sustained during shortening (essentially an isotonic protocol). At low velocities both protocols gave very similar data (r2 = 0.96), but for high velocities only the SA procedure could be used. Results obtained using the SA protocol in fresh muscle were compared to those for muscle that had been fatigued by 25 s of ischaemic isometric contractions, induced by electrical stimulation at the ulnar nerve. Fatigue resulted in a decrease of isometric force [to 69 (3)%], an increase in half-relaxation time [to 431 (10)%], and decreases in maximal shortening velocity [to 77 (8)%] and power [to 42 (5)%]. These are the first data for human skeletal muscle to show convincingly that during acute fatigue, power is reduced as a consequence of both the loss of force and slowing of the contractile speed.

Extramuscular myofascial force transmission for in situ rat medial gastrocnemius and plantaris muscles in progressive stages of dissection

SUMMARY The aim of this study was to establish the extent of extramuscular myofascial force transmission for dissected rat medial gastrocnemius (GM) and plantaris (PL) muscles. Initially, this was done with GM still connected to extramuscular connective tissue (general fascia, neuro-vascular tract and compartmental fascia). Neighbouring muscles were also connected to these tissues. In a later stage, it was dissected progressively until finally a fully dissected in situ GM was obtained, for which the neuro-vascular tract (i.e. the nerves, bloodvessels and the surrounding connective tissue) was the only extramuscular tissue left intact. Force of GM was measured not only at its distal tendon in progressive stages of dissection, but also at its dissected proximal tendon. In the stage where GM was still connected to extramuscular tissues, the experiments showed that up to 40.5±5.9% (mean ± s.e.m.) of the force exerted by the neighbouring PL muscle was transmitted onto the calcaneal bone, even when the PL tendon was not connected to this bone. After distal PL-tenotomy, a difference between proximally and distally measured forces of GM constituted evidence for myofascial force transmission. In the fully dissected in situ GM muscle, no relevant myofascial force transmission occurred in the reference position (the position of the GM origin corresponding to a knee angle of 120°). However, some myofascial force transmission occurred when the relative position of the origin of the fully dissected GM muscle was changed with respect to the neuro-vascular tract.

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)

Relative torque contribution of vastus medialis muscle at different knee angles

Aim:  We investigated the relative contribution of the vastus medialis (VM) muscle to total isometric knee extension torque at 10°, 30°, 60° and 90° knee flexion. In the past a more prominent role of the VM muscle at more extended knee angles has been put forward. However, different components of the quadriceps muscle converge via a common distal tendon. We therefore hypothesized that the relative contribution of the VM to total knee extension torque would be similar across angles.

Low-frequency fatigue, post-tetanic potentiation and their interaction at different muscle lengths following eccentric exercise

SUMMARY Low-frequency fatigue (LFF) and post-tetanic potentiation (PTP) were quantified at different muscle lengths in rat medial gastrocnemius (GM) muscle. In situ experiments were performed on GM muscle-tendon complexes of anaesthetised (urethane, 1.5 g kg-1 i.p.) Wistar rats (N=8). Force-length characteristics were determined at maximal (200 Hz) and submaximal (60 Hz) stimulation. Data for submaximally stimulated muscle were obtained in a non-potentiated and in a potentiated condition. LFF was induced by a series of 40 eccentric contractions. Post-exercise (40-80 min), data for the force-length relationships were obtained once more. Whereas force loss at 200 Hz-stimulation was least at optimum muscle length, L0,200Hz, (17.0±1.4%, mean ± s.e.m.), force loss at 60 Hz-stimulation was maximal near L0,200Hz (55.1±4.3% at L0,200Hz-1 mm). When the muscle was potentiated, force loss at 60 Hz-stimulation was maximal at short muscle length: L0,200Hz-4 mm (53.5±3.8%). The extent of LFF, quantified by a decrease in the 60:200 Hz force ratio, varied with muscle length: LFF increased with decreasing muscle lengths when muscles were potentiated. However, in the non-potentiated condition, LFF was maximal at a length just below L0,200Hz; the 60:200 Hz force ratio had decreased to 54.6±5.9% of the pre-exercise ratio at L0,200Hz-1 mm. Compared with the non-potentiated condition, LFF was less pronounced in the potentiated condition. PTP counteracted LFF particularly at long muscle lengths. However, at short muscle lengths, LFF was still observed in potentiated muscles.

Muscle function during repetitive moderate-intensity muscle contractions in myoadenylate deaminase-deficient Dutch subjects.

We investigated whether the capacity for repetitive submaximal muscle contraction was reduced in a group of subjects (n=8) with a primary deficiency of myoadenylate deaminase (MAD). Quadriceps femoris muscle fatigue was evaluated using voluntary and electrically stimulated contractions during 20 min of repetitive voluntary isometric contractions at 40% of maximal force-generating capacity (MFGC). After 5 min of exercise, MFGC had declined significantly to 70.6+/-4.1% (mean+/-S.E.M.) and 87.2+/-1.6% of baseline values in MAD-deficient and sedentary control subjects (n=8) respectively (P=0.002 between groups). After 5 min of exercise, the half-relaxation time had increased significantly to 113.4+/-6.1% of baseline in MAD-deficient muscle, but had decreased significantly to 94.1+/-1.3% in control subjects (P=0.003 between groups). All control subjects completed the 20-min exercise test. Five of the MAD-deficient subjects had to stop exercising due to early muscle fatigue; however, three of the MAD-deficient subjects were able to complete the 20-min exercise test. In conclusion, although the capacity for repetitive submaximal isometric muscle contractions for the group of MAD-deficient subjects was significantly decreased, it remains uncertain whether MAD deficiency is the sole cause of pronounced muscle fatigue.