Evidence suggests different sections of the arteriolar network supplying muscle can respond independently and this may provide a mechanism for the localized distribution of blood flow. This hypothesis was tested in the microcirculation of the cat sartorius muscle by measurement of arteriolar diameter changes during muscle contraction and sympathetic nerve stimulation in each consecutive section of the network. The diameter changes were referenced to the initial distribution of resistance across the network, as determined from arteriolar pressure measurements and morphometric data. This led to an estimate of the change in network resistance. Unlike previous reports, the most distal arterioles dilated little during muscle contraction and our resistance estimate indicates these vessels play an insignificant role in functional hyperemia. The more proximal, third order arterioles dilated proportionately more than other arteriolar orders and made the largest single contribution to resting resistance. Similarly, these vessels were the largest single site of resistance change during sympathetic stimulation. Together, these findings suggest the third order arterioles play a dominant role in regulating flow to the capillaries that each supplies. Antagonism of sympathetic control during muscle contraction has been attributed to direct inhibition of vascular smooth muscle contraction and to inhibition of sympathetic neurotransmission. Evidence to support the latter mechanism comes from the observation that functional dilation is reduced with exogenous norepinephrine as compared to sympathetic stimulation. However, exogenous norepinephrine may bind to both alpha-1 and alpha-2 adrenergic receptors, whereas that released by sympathetic stimulation may bind primarily to alpha-1 receptors. Since this difference could be significant, functional dilation after systemic injection of norepinephrine or phenylephrine, a selective alpha-1 agonist, was compared to that during sympathetic stimulation. In contrast to the findings with norepinephrine, functional dilation after phenylephrine did not differ from that observed during sympathetic stimulation. This indicates the dilator substance(s) released during exercise may selectively inhibit alpha-1 mediated vasoconstriction but less effectively inhibit vasoconstriction mediated by alpha-2 receptors. Furthermore, these findings suggest that the vasodilator mechanism may act primarily at the level of the vascular smooth muscle, without appreciable pre-junctional inhibition of sympathetic nerves.

No description available.

Recently, it became possible to detect single motor units (MUs) noninvasively via the use of spatial filtering electrode arrays. With these arrays, weighted combinations of monopolar electrode signals recorded from the skin surface provide spatial selectivity of the underlying electrical activity. Common spatial filters include the bipolar electrode, the longitude double differentiating (LDD) filter and the normal double differentiating (NDD) filter. In general, the spatial filtering is implemented in hardware and the performance of the spatial filtering apparatus is measured by its common mode rejection ratio (CMRR). High precision hardware differential amplifiers are used to perform the channel weighting in order to achieve high CMRR. But, this hardware is expensive and all channel weightings must be predetermined. Hence, only a few spatially filtered channels are typically derived. In this project, a distinct software equalization filter was cascaded with each of the hardware monopolar signal conditioning circuits to achieve accurate weighting and high CMRR. The simplest technique we explored was to design an equalization filter by dividing the frequency response of a“reference" (or“ideal") channel by the measured frequency response of the channel being equalized, producing the desired equalization filter in the frequency domain (conventional technique). Simulation and experimental results showed that the conventional technique is very sensitive to broadband background noise, producing poor CMRR. Thus, a technique for signal denoising that is based on signal mixing was pursued and evaluated both in simulation and laboratory experiments. The purpose of the mixing technique is to eliminate the noise as much as possible prior to equalization filter design. The simulation results show that without software equalization, CMRR is only around 30 dB; with conventional technique CMRR is around 50~60 dB. By using mixing technique, CMRR can be around 70~80 dB.

In performing manual tasks, muscles are voluntarily contracted in order to produce force and orient the limb in the desired direction. Many occupational tasks are associated with frequent musculoskeletal disorders. In tasks involving skilful manipulation, very frequently the forces are focused on the upper limb and neck. Upper extremity cumulative trauma disorders are among the more common worker related injuries. These muscle disorders may be related to repetitive exertions, excessive muscle loads and extreme postures. One of the major challenges is to quantify the muscle load and researchers have tried various measures to quantify muscle load. Joint mechanical impedance can be a robust method to quantify muscle load. Joint mechanical impedance characterizes the dynamic torque-angle relationship of the joint. Joint impedance has been measured by earlier researchers, for limited tasks, by imparting force (or angle) perturbations on the joint and relating resultant angular (or force) changes. The joint impedance gives a quantitative measure related to muscle co-contraction level. Measurement of the mechanical impedance at the workplace may provide useful information relevant to the understanding of upper limb disorders. Electromyogram (EMG) is the electrical activity of the muscle. Usually, an estimate of the EMG amplitude is obtained from the raw waveform recorded from the surface of the skin. EMG amplitude estimates can be used to non-invasively estimate torque about joints. Presently, there exists no means by which mechanical impedance can be estimated non-invasively (i.e., without external perturbations). Therefore, we proposed the use of EMG to noninvasively estimate the joint mechanical impedance. Our objective in this project was to determine the extent to which surface EMG can be used to estimate mechanical impedance. Simulation studies were first performed to understand the extent to which this tool could be useful and to determine methods to be used for the experiment. The simulations were followed by evaluating and estimating mechanical impedance using data collected from one experimental subject. Simulations helped to devise processing techniques for the measured signals and also to determine the length of data to be collected. Low pass filters for derivatives (used in the development of impedance estimates) were designed. Subtracting out a polynomial was the best approach to attenuate a low frequency drift (artifact) that occurs in torque measurements. Thirty seconds of data provided impedance estimates with a relative error of 5% when EMG amplitude estimates with SNR of 15 were used. Experimental data from constant-posture, slowly force-varying background torque level showed that the elbow joint system behaved like a second order linear system between 2 Hz and 10 Hz. Co-contraction by subjects during experiments caused impedance estimates to be unexpectedly high even at low background torque. Further experiments would need to be conducted with the subjects being instructed to avoid co-contraction.

Thesis (Ph.D.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1980. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND ENGINEERING. / Vita. / Bibliography: leaves 181-187. / by Ronald Stanton LeFever. / Ph.D.

Mechanical forces regulate biological processes in unique and unexpected ways, but many biochemical methods are unable to reproduce the vectorial stretching experienced by proteins in cells. Force spectroscopy techniques remedy these shortcomings by utilizing microscopic force probes to stretch and relax single protein, DNA, and RNA molecules. The central focus of this thesis is the development and implementation of a custom-built protein magnetic tweezers for unfolding and refolding Ig domains from titin, a critical filament of the sarcomere, and the longest continuous peptide in the human body. Suspended from the Z-disc to the tip of the thick filament, titin sustains the brunt of intracellular forces during muscle elongation. Since the discovery of titin, it has been widely debated whether Ig domain unfolding contributes to muscle mechanics. A combination of single quantum dot tracking in myofibrils extracted from rabbit muscle and single molecule magnetic tweezers experiments on recombinant titin fragments confirms, for the first time, the presence of titin Ig domain unfolding and refolding at physiological sarcomere lengths and stretching forces. The magnetic tweezers experiments show the surprising ability of titin Ig domains to generate piconewton level forces during folding, and we advance the hypothesis that titin folding is an important source of energy during muscle contraction. Muscle elongation recruits Ig domains to the unfolded state, whereby folding is initiated through reduction of force on titin upon actomyosin crossbridges formation. Magnetic tweezers measurements demonstrate that titin Ig folding generates peak work, velocity, and power output of 64 zeptojoules, 1.9 microns per second, and 6,000 zeptowatts, matching or exceeding the equivalent single molecule measurements from single molecule myosin II powerstrokes. The forces generated by protein folding are therefore likely to be an integral part of the contractile process of animal muscle.

One advantage of higher life-forms over less developed organisms is their ability to respond to signals from their environment with motion. This requires highly specialized contractile cells and a whole locomotion apparatus. In vertebrates, the cells responsible for movement are the skeletal muscle cells. They receive signals from the autonomic nervous system in the form of an action potential, and they contract in an appropriate manner. Calcium is a vital intracellular passenger whose role in muscular function is to initiate contraction. It is released via specific channel proteins from an internal Ca++ store, the sarcoplasmic reticulum, and triggers muscular contraction, the actual interplay of actin and myosin filaments. The step that is still not fully understood is the coupling process between arrival of an action potential and the subsequent contraction, called excitation-contraction coupling. Several theories have been proposed to explain this process. Some years ago, our laboratory introduced the hypothesis that an oxidation-reduction reaction of critical sulfhydryls associated with the Ca+t channel protein are involved in the regulation of channel gating. In an effort to understand more about the Ca++ channel gating mechanism at the molecular level, this thesis focuses on the interaction between o-phthalaldehyde, a reagent which specifically forms an isoindole derivative with the amino acids cysteine and lysine, and the Ca++ release channel complex. In this thesis, the planar lipid bilayer technique was used to study the Ca++ release channel protein from skeletal muscle sarcoplasmic reticulum at the single channel level. Utilizing this experimental technique, the direct interaction between OP A and the channel was investigated. In this study, it was shown that the interaction of o-phthalaldehyde with the channel increases the channel's open probability as well as its mean open time. Furthermore, the covalent nature of o-phthalaldehyde binding to the calcium release channel complex is shown and its inhibiting effects on chloride channels are demonstrated.

Muscle contraction is a phenomena which fascinated already the ancient Greeks. People have long sought to understand the mechanism of muscle contraction. Today we know that in order for muscle to contract, an action potential propagates from the nerve cell to the muscle cell. Upon arriving at the muscle cell, via a mechanism called Excitation- Contraction (E-C) coupling, Ca2 + is released from an intracellular membrane system, the sarcoplasmic reticulum (SR), into the intracellular fluid. The increase of intracellular Ca2 + initiates the interaction between the contractile units which results in force development and tension. The least well understood step in the contractile process is mechanism of E-C coupling. During the last 15-20 years various theories have been proposed to describe this process. Our laboratory came up with a theory several years ago, that critical sultbydryl groups on a protein, the ryanodine receptor(RyR)/Ca2 + release channel, are oxidized and subsequently reduced during the process of contraction and relaxation. In this thesis a reagent, o-Phthalaldehyde (OPA), was used to better understand the gating mechanism of the RyR/Ca2 + release channel. This reagent has the ability to form an isoindole derivative with the amino acids cysteine and lysine, if they are separated by not more than 3 A .In this study, it was shown that OP A interacts directly with the Ca2 + release channel by forming a covalent derivative with a critical thiol and a nearby lysine. High affinity [3H]Ryanodine binding to the RyR\Ca2 + release channel is activated by < 130μM OP A, but is inhibited by OPA at concentrations ranging from 200-300 μM OPA. This biphasic behavior indicates that at least two sets of cysteine-lysine pairs regulate Ca2 + channel activity. Moreover, the binding of OP A results in increasing the affinity of the receptor for the binding of ryanodine, in a Ca2 + independent manner, which may indicate that there are two different sets of RyR\Ca2+ release channels present in the SR.

The aim of the thesis was to evaluate the effectiveness of static hand splints for the prevention of muscle contracture during early rehabilitation following acquired brain impairment. Three studies were undertaken and are reported in the research. The aim of the first study was to appraise the existing research on the effects of hand splinting for adults with hemiplegia following acquired brain impairment. The aim of the second study was to evaluate the effectiveness of static hand splints which position the wrists and fingers in the common ‘functional position’ when provided in conjunction with a rehabilitation program which included daily motor training and prolonged stretches. The aim of the final study was to evaluate the effectiveness of two hand splinting positions, the ‘functional position’ and a position of wrist and finger extension, in comparison to a control group that did not receive prolonged stretches. Findings indicate that splinting the hand in the ‘functional’ position or in a position of greater wrist extension did not prevent contracture following acquired brain impairment over the course of the study periods (4 weeks with follow up at 4 and 6 weeks in studies 2 and 3 respectively). / Doctor of Philosophy (PhD)

Thesis (Ph.D.)--University of Delaware, 2006. / Principal faculty advisor: John E . Novotny, Dept. of Mechanical Engineering. Includes bibliographical references.