The purpose was to investigate muscle potential during the vibrato motion for successful, healthy violin/viola performers. Electromyography was used to analyze parameters of muscle potentials during performance of a standardized exercise. These parameters were (a) evidence of potentials, (b) patterns of potentials, and (c) timing relationships (24 muscles). This study also sought to replicate and expand performance data from previous studies. Procedures from three pilot studies were used to standardize collection of EMG data. Synchronized video recordings were used to determine vibrato speed and conduct motion analysis. EMG data processing prior to analysis included power spectrum analysis and rectification, low-pass filtering, and smoothing data. Motion analysis findings (£D) were 1.09 for the elbow joints and 3.25 for the wrist joints. which was an indication of range of motion, suggested much greater activity in muscles controlling wrist movement than those moving the elbow. The degree of muscle potential and control were generally related to distance from the vibrating hand. Forearm muscle groups (8) demonstrated the greatest evidence of potential (76.5%) and were 18.1% non-periodic. Muscles of the upper arm (7) were off 59.4% and 57.0% non-periodic. Upper arm muscles had greater individual differences. Muscles of the chest and back (9) were collectively inactive (89.1%) and non-periodic (73.3%). With timing relationships, the forearm muscles demonstrated consistent firing patterns. Inconsistent firing patterns were evident in the upper arm, and to a greater degree in the chest and back muscles. Based on evaluations of performer motion and muscle potentials, it was strongly implied that there are (a) distinct roles for various muscles during vibrato (control vs. stabilization/support), (b) significant differences in potential between variables of rest, playing position, and performing, (c) significant differences in potential between some fingers, and (d) no significant differences between violinists and violists. The vibrato motion appeared to be controlled primarily by forearm muscles.

Extraction and quantitation of myosin light chain two coupled with myograph recordings from Ascaris muscle perfused with calmodulin inhibitors and neurotransmitters in conjunction with their respective agonists and antagonists have been used to establish the regulation of contraction in this muscle. Densitometric tracings of isolectric focusing gels separating the regulatory light chain were used to quantitate phosphorylation in resting, contracted and flaccid muscle. These studies indicated that inhibitory neurostimulation is mediated by a true GABA receptor. Myosin-mediated contraction is responsible for maintaining the level of tension observed in resting actin-mediated muscle. Actin-mediated contraction is responsible for the rapid rise in tension following excitatory stimuli. Both systems function simultaneously and are independant.

shum Wai Chi. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 259-279). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Thesis. 1978. Ph.D.--Massachusetts Institute of Technology. Dept. of Electrical Engineering and Computer Science. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Bibliography: leaves 131-133. / Ph.D.

Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 1979. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Bibliography: leaves 188-195. / Ph.D.

by Jing Xian Li. / Thesis (Ph.D.)--Chinese university of Hong Kong, 1998. / Includes bibliographical references (p. 137-151). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

The global intent of this research was to confirm the validity of the interpolated twitch technique (ITT) to voluntary torque model (first study) and then to utilize this technique in developing definitive criterion measures enhancing the study of training strategies on central fatigue (second study) and velocity specific (third study) voluntary activation (VA) and force production outcomes. The first study assessed the contribution of non-stimulated synergists to the non-linearity of the ITT voluntary torque relationship for elbow flexion contraction. Since multiple synergist stimulation was found not to significantly improve the ITT to voluntary torque relationship, follow-up pilot work was conducted in which the quadriceps femoris was identified as a valid ITT test model muscle. The first training study investigated the effects of high volume, maximum voluntary isometric contraction (MVIC) resistance training of the quadriceps femoris on MVIC levels of force and VA prior to, during, and recovery from a standardized fatigue test protocol. Results showed significant increases in pre-fatigue MVIC VA and force, increases in resistance to early fatigue, but also increased overall rate of fatigue resulting in non-significant changes in total force volume and endurance time. Post-fatigue analysis showed significant training increases in rate and level of recovery for both MVIC VA and force production. The second training study investigated the effects of high resistance ramp versus ballistic type MVIC strength training of the quadriceps femoris on central adaptations in submaximal and maximal levels of MVIC VA and force production. Results showed similar ramp and ballistic group training increases in MVIC force and VA on both ramp and ballistic tests. Ballistic group, ballistic test change scores were significant but not for the ramp test, suggesting ballistic group test-training specificity. The ballistic group showed significant force increases on the submaximal 150ms ballistic test, while the ramp group showed non-significant training changes, further supporting test-training specificity for the ballistic group. Results support utility of the ITT and provide valuable information with regard to training and test-training specificity considerations.

Abstract not available

GLUT4 is the principal insulin-responsive glucose transporter in skeletal muscle. Insulin stimulation leads to exocytosis of intracellular GLUT4-containing vesicles to the cell surface, thereby increasing glucose uptake. Muscle contraction also elevates cell surface GLUT4 by a less understood mechanism. Once at the cell surface, GLUT4 may be subject to additional regulation, such as by modulation of its internalization rate or its intrinsic activity. The objective of this thesis was to identify the mechanism of GLUT4 internalization in muscle cells and to determine whether it is regulated by insulin treatment or by the signals elicited by muscle contraction. Skeletal muscle cells in culture stably expressing myc-tagged GLUT4 were used. We found that GLUT4 internalizes simultaneously through a clathrin-dependent and a clathrin- and caveolae-independent and cholesterol- and dynamin-dependent pathway. Insulin did not regulate GLUT4 internalization. In contrast, mitochondrial uncoupling, which may mimic the heightened energy demand that occurs during muscle contraction, retarded GLUT4 internalization by inhibiting the clathrin-independent route. Activation of both AMP-dependent kinase (AMPK) and protein kinase C (PKC) was necessary and sufficient for this response. We further hypothesized that the intrinsic activity of GLUT4 may be regulated under some conditions, based on a discrepancy between the amount of cell surface transporters and the rate of glucose uptake. In particular, inhibitors of p38 mitogen-activated protein kinase (p38MAPK) lowered insulin-dependent glucose uptake without reducing the number of GLUT4 units at the surface. We found that p38MAPK is activated by insulin through TAB1-dependent autophosphorylation, yet p38MAPK was dispensable for insulin-stimulated glucose uptake. Mechanisms other than p38MAPK must be involved in the regulation of GLUT4 intrinsic activity. In conclusion, in addition to its exocytosis, the activity and endocytosis of GLUT4 are regulated by stimuli that increase the rate of glucose uptake into muscle.

GLUT4 is the principal insulin-responsive glucose transporter in skeletal muscle. Insulin stimulation leads to exocytosis of intracellular GLUT4-containing vesicles to the cell surface, thereby increasing glucose uptake. Muscle contraction also elevates cell surface GLUT4 by a less understood mechanism. Once at the cell surface, GLUT4 may be subject to additional regulation, such as by modulation of its internalization rate or its intrinsic activity. The objective of this thesis was to identify the mechanism of GLUT4 internalization in muscle cells and to determine whether it is regulated by insulin treatment or by the signals elicited by muscle contraction. Skeletal muscle cells in culture stably expressing myc-tagged GLUT4 were used. We found that GLUT4 internalizes simultaneously through a clathrin-dependent and a clathrin- and caveolae-independent and cholesterol- and dynamin-dependent pathway. Insulin did not regulate GLUT4 internalization. In contrast, mitochondrial uncoupling, which may mimic the heightened energy demand that occurs during muscle contraction, retarded GLUT4 internalization by inhibiting the clathrin-independent route. Activation of both AMP-dependent kinase (AMPK) and protein kinase C (PKC) was necessary and sufficient for this response. We further hypothesized that the intrinsic activity of GLUT4 may be regulated under some conditions, based on a discrepancy between the amount of cell surface transporters and the rate of glucose uptake. In particular, inhibitors of p38 mitogen-activated protein kinase (p38MAPK) lowered insulin-dependent glucose uptake without reducing the number of GLUT4 units at the surface. We found that p38MAPK is activated by insulin through TAB1-dependent autophosphorylation, yet p38MAPK was dispensable for insulin-stimulated glucose uptake. Mechanisms other than p38MAPK must be involved in the regulation of GLUT4 intrinsic activity. In conclusion, in addition to its exocytosis, the activity and endocytosis of GLUT4 are regulated by stimuli that increase the rate of glucose uptake into muscle.