[b said:
Quote[/b] (NWlifter @ May 20 2005,4:50)]
[b said:
Quote[/b] ]That's exactly what I've been thinking with regards to eccentric rep speed. A faster speed, if stopped at the end of ROM by your muscles and not joint max or bouncing off your body, puts extreme loading in a stretched position, basically a loaded stretched pulse.
Now what I read was that 'during' the eccentric contraction, if the rep speed is faster, since the cross bridges release 'out of sync' with each other, you will incurr lateral strain between the sarcomeres.
You couldn't increase 'per fiber' tension by 'braking suddenly', the fibers can only display their maximum tension no matter what the action so in effect, the braking is just a higher recruitment/synchronization of the fibers displaying their tension at once which if is enough, will stop the lengthening of the muscle and transfer the tension to the connective tissues, like the tendons.
Ron
Heres some stuff you guys might enjoy, it's on sarcomeres and non-uniform lengthening
Single muscle fiber contraction is dictated by inter-sarcomere dynamics.
Denoth J, Stussi E, Csucs G, Danuser G.
Laboratory for Biomechanics, Department of Materials, Swiss Federal Institute of Technology (ETH), Wagistrasse 4, CH-8952 Schlieren, Switzerland.
[email protected]
This paper presents first results from a study where we developed a generic framework for analysing inter-sarcomere dynamics. Our objective is to find an accurate description of a muscle as a linear motor composed of parallel and series coupled subunits. The quality of theoretical models can be tested through their ability to predict experimental observations. With the current method we have found rigorous mathematical explanations for mechanisms such as sarcomere popping, extra tension and homogenization. These phenomena have been observed for many years in single fibers experiments, yet have never been completely understood in terms of a mechanical model. Now they can be explained on a theoretical basis. Interestingly, rather simplistic descriptions of each of the various molecular components in the sarcomere (actin-myosin cross-bridges, titin and contributions from passive elastic components) are sufficient to predict these behaviors. The complexity of a real muscle fiber is addressed through rigorous coupling of the single component models in a system of differential equations. We examine the properties of the differential equations, based on a down-stripped model, which permits the derivation of analytical solutions. They suggest that the contraction characteristics of inter-connected sarcomeres are essentially dictated by the initial distribution of the sarcomeres on the force-length curve and their starting velocities. The complete model is applied to show the complexity of inter-sarcomere dynamics of activated fibers in stretch-release experiments with either external force or length control. Seemingly contradictory and unexpected observations from single fiber experiments, which have hitherto been discussed with the argument of uncontrollable biological variability, turn out to be a consistent set of possible fiber responses. They result from a convolution of multiple relatively simple rules each of them defining a certain characteristics of the single sarcomere. Copyright 2002 Elsevier Science Ltd. All rights reserved.
Characteristics of isometric and dynamic strength loss following eccentric exercise-induced muscle damage.
Byrne C, Eston RG, Edwards RH.
School of Sport, Health and Exercise Sciences, University of Wales, Bangor, Gwynedd, UK.
Angle-specific isometric strength and angular velocity-specific concentric strength of the knee extensors were studied in eight subjects (5 males and 3 females) following a bout of muscular damaging exercise. One hundred maximal voluntary eccentric contractions of the knee extensors were performed in the prone position through a range of motion from 40 degrees to 140 degrees (0 degrees = full extension) at 1.57 rads(-1). Isometric peak torque was measured whilst seated at 10 degrees and 80 degrees knee flexion, corresponding to short and optimal muscle length, respectively. Isokinetic concentric peak torque was measured at 0.52 and 3.14 rad x s(-1). Plasma creatine kinase (CK) activity was also measured from a fingertip blood sample. These measures were taken before, immediately after and on days 1, 2, 4, and 7 following the eccentric exercise. The eccentric exercise protocol resuited in a greater relative loss of strength (P< 0.05) at short muscle length (76.3 +/- 2.5% of pre-exercise values) compared to optimal length (82.1 +/- 2.7%). There were no differences in the relative strength loss between isometric strength at optimal length and isokinetic concentric strength at 0.52 and 3.14 rad x s(-1). CK activity was significantly elevated above baseline at days 4 (P < 0.01) and 7 (P < 0.01). The greater relative strength loss at short muscle length appeared to persist throughout the seven-day testing period and provides indirect evidence of a shift in the angle-torque relationship towards longer muscle lengths. The results lend partial support to the popping sarcomere hypothesis of muscle damage, but could also be explained by an impairment of activation at short muscle lengths.
Quantitative analysis of sarcomere non-uniformities in active muscle following a stretch.
Talbot JA, Morgan DL.
Department of Physiology, Monash University Clayton, Victoria, Australia.
Electron microscopy of toad (Bufo marinus) muscle fixed without relaxing after a single eccentric contraction at muscle lengths greater than optimum showed over-stretched half-sarcomeres in sufficient numbers to account for more than half of the imposed stretch. Such sarcomeres were absent in another muscle fixed without relaxing after an isometric contraction at the same length and largely absent in a third muscle that underwent eccentric contraction at muscle lengths less than optimum. This provides direct evidence in support of the hypothesis that lengthening of muscles at long length involves lengthening of a few half sarcomeres to beyond filament overlap, while most half sarcomeres are extended much less than in proportion to muscle extension.
Effects of repeated eccentric contractions on structure and mechanical properties of toad sartorius muscle.
Wood SA, Morgan DL, Proske U.
Department of Physiology, Monash University, Clayton, Victoria, Australia.
It has been proposed that lengthening of active muscle at long lengths is nonuniformly distributed between sarcomeres, with a few being stretched beyond overlap and most hardly being stretched at all. A small fraction of the overstretched sarcomeres may fail to reinterdigitate on subsequent relaxation, leading to progressive changes in the muscle's mechanical properties. Sartorius muscles of the toad Bufo marinus were subjected to repeated lengthening (eccentric) contractions at long lengths, while controls were passively stretched and then contracted isometrically or stretched at short lengths. The muscles undergoing eccentric contractions showed a progressive shift to the right of the length-tension curve, a fall in the yield point during stretch, an increase in slope of the tension response during stretch, and a fall in isometric tension. In control muscles, changes, if any, were significantly less. In electron micrographs, muscle fibers that had been subjected to a series of eccentric contractions showed sarcomeres with A bands displaced toward one half-sarcomere, leaving no overlap in the other half. Adjacent regions often looked normal. These results are all in agreement with the predictions of the nonuniform stretch of sarcomeres hypothesis.
Muscle damage is not a function of muscle force but active muscle strain.
Lieber RL, Friden J.
Department of Orthopedics, University of California, San Diego.
Contractile properties of rabbit tibialis anterior muscles were measured after eccentric contraction to investigate the mechanism of muscle injury. In the first experiment, two groups of muscles were strained 25% of the muscle fiber length at identical rates. However, because the timing of the imposed length change relative to muscle activation was different, the groups experienced dramatically different muscle forces. Because muscle maximum tetanic tension and other contractile parameters measured after 30 min of cyclic activity with either strain timing pattern were identical (P > 0.4), we concluded that muscle damage was equivalent despite very different imposed forces. This result was supported by a second experiment in which the same protocol was performed at one-half the strain (12.5% muscle fiber length). Again, there was no difference in maximum tetanic tension after cyclic 12.5% strain with either strain timing. Data from both experiments were analyzed by two-way analysis of variance, which revealed a highly significant effect of strain magnitude (P < 0.001) but no significant effect of stretch timing (P > 0.7). We interpret these data to signify that it is not high force per se that causes muscle damage after eccentric contraction but the magnitude of the active strain (i.e., strain during active lengthening). This conclusion was supported by morphometric analysis showing equivalent area fractions of damaged muscle fibers that were observed throughout the muscle cross section. The active strain hypothesis is described in terms of the interaction between the myofibrillar cytoskeleton, the sarcomere, and the sarcolemma.
