No description available.

No description available.

No description available.

No description available.

The intent of this investigation was to determine the effects of contractile velocity on muscle glycogen depletion patterns during maximal isokinetic contractions.Three physically active male subjects performed maximal knee extensions and flexions using the Cybex II. Work was performed with one leg at a contractile volecity of 60 degs./sec. (1.05 rads./sec.) and the other at 300 degs./sec. (5.23 rads./sec.). Histochemical data was collected from muscle samples taken from the vastus lateralis m. of each leg. Gylcogen depletion patterns were later observed from a periodic-acid Schiffs stain (PAS) on the muscle sections. Additional muscle samples were freeze-dried for single fiber evaluation, of glycogen content. Both fast twitch (FT) and slow twitch (ST) muscle fibers were depleted of glycogen equally during each of the contractile velocities. Observations from FAS staining suggest that most of the FT fibers were depleted before the ST fibers. The results of this study indicate that the glycogen depletion pattern is independent of the velocity of contraction. This study also supports previous investigations in suggesting that the intensity of muscular contraction is one of the major determinants of the glycogen depletion pattern.

No description available.

Thesis (Master of Science)--University of the Witwatersrand, Faculty of Health Sciences, 1963. / The rapid progress of the last decade has made possible the synthesis of the molar and molecular approaches to the mechanism of muscle contraction. It is now possible to offer a molecular explanation for many of the gross mechanical properties of muscle. As a result there is a necessity to re-examine the validity of the classical terminology used to describe these properties, and to define them more accurately. Since Pick (1882), various "types” of contraction have been ascribed to muscle, according to the changes in length and tension of the activated muscle. These are dependent upon the load opposing the muscle. If the load is less than the force developed in the muscle, shortening occurs at a constant tension just exceeding the load. This process is termed isotonic contraction. If, on the other hand, the load is equal to the tension developed in the muscle,there is no overall change in length, although tension in the system rises. This constitutes an isometric contraction. Recently, studies of the ultra-structure and mechanical properties of muscle have revealed inherent difficulties in the classical terminology. / WHSLYP2017

When active skeletal muscle is stretched, it generally responds with a contraction which resists the stretch. This response is termed the muscle stretch reflex. The size (gain) and timing (phase) of the response has been found to depend on many factors including the characteristics of the applied stretch, the muscle contraction level and the subject's intention. Investigations of this stretch reflex have often involved stretches to muscle which contained frequencies either beyond the range of voluntary movement or else which could be consciously tracked. This study sought to characterise the frequency response of the stretch reflex, in terms of its gain and phase, under a variety of conditions while using stretches to the muscle which were relevant to voluntary movement, yet which were too irregular to be tracked. The types of stretch which satisfied these criteria had first to be determined by an investigation of tracking performance under different conditions of peripheral feedback. Having established the types of stretch which could be used to guarantee reflex rather than voluntary responses, the stretch reflex was investigated using stretches of different amplitude and bandwidth and spanning the full range of contraction level. Research was also undertaken to determine whether the gain and phase of the reflex response could be decoupled from the background contraction level of the muscle and to examine any associated effects on the mechanical properties of the limb. Explanatory models for some of these reflex responses were developed. An interaction between normal physiological tremor and the stretch reflex response was also investigated.

Thesis (M.S.E.S.)--University of Toledo, 2005. / Typescript. "Submitted as partial fulfillment of the requirements for the Master of Science degree in Exercise Science." Bibliography: leaves 71-87.

Force generation and the ability of the heart muscle to contract and correspondingly to beat depends upon multiple interactions between myosin and actin-tropomyosin-troponin, the key proteins of the contractile apparatus. The myosin molecule consists of two heavy chains and two types of light chains, two essential (ELC) and two regulatory (RLC) light chains. We hypothesize that mutations in myosin ELC may affect the ability of myosin to bind to actin, thus producing structurally and/or functionally abnormal sarcomeres effecting heart muscle contraction and relaxation. We believe that this pathological process underlies the basis of Familial Hypertrophic Cardiomyopathy (FHC), a genetic disorder caused by mutations in the genes encoding the major myofilament proteins, including the myosin ELC. I have investigated the effects of two FHC ELC mutations, A57G and E143K, on the actin-myosin interaction and generation of contractile force. Here, I show evidence that mutations in the ELC may cause disruptions in sarcomeric structure which then may cause abnormal muscle contraction and lead to compensatory hypertrophy.