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PubMedDate not supplied

The influence of voluntary muscle contractions upon the onset and modulation of tinnitus.

OBJECTIVE: To evaluate the frequency of tinnitus onset (in normal subjects) and modulation (in tinnitus patients) during muscle contractions, estimating possible risk factors. MATERIAL AND METHOD: This case-control study enrolled 121 tinnitus patients and 100 healthy volunteers who underwent medical history, ENT examination and 16 maneuvers of muscular contraction (head, neck and limbs). Modulation data were compared between patients with and without normal audiometry, well-defined diagnosis and symptoms of craniomandibular disorders. RESULTS: The ability to modulate tinnitus (65.3%) was significantly higher than that to originate tinnitus (14.0%). The head and neck musculature was significantly more efficient than that of the limbs. Audiometric pattern, well-defined etiology and symptoms of craniomandibular disorders showed no relation to tinnitus modulation. CONCLUSIONS: Somatic modulation is a characteristic aspect of tinnitus.

Adolescent↗
PubMed1989

Desensitization of alpha-1 adrenergic receptor mediated smooth muscle contraction in aorta from endotoxic rats.

Desensitization of vascular smooth muscles in endotoxemia was studied using the aorta from intraperitoneally endotoxin-injected rats. The KCl- and phenylephrine-induced contractions were significantly decreased in the endotoxic aorta compared to the control. In the endotoxic aorta the phenylephrine-induced contracture showed a gradual tension decrease after reaching a plateau and was attenuated by prior exposure to high concentration of phenylephrine, while KCl produced a sustained contraction and it was not affected by prior exposure to phenylephrine. The phenylephrine- and KCl-induced contractures of the control aorta showed stable plateaus and were not affected by prior exposure to phenylephrine. Neither diminished contractile force nor in vitro desensitization of phenylephrine contracture of isolated aorta was prevented by pretreatment of endotoxic rats with an alpha-adrenergic antagonist, phentolamine. These findings suggest that the contractile response to phenylephrine is easily desensitized in the endotoxic aorta compared to the control and neither this in vitro desensitization nor the diminution of contractile force is caused by in vivo exposure of aorta to a high concentration of catecholamines during endotoxemia.

Animals↗
PubMed1987

Possible role of helix-coil transitions in the microscopic mechanism of muscle contraction.

Local helix-coil transitions in the coiled coil portion of myosin have long been implicated as a possible origin of tension generation in muscle. From a statistical mechanical theory of conformational transitions in coiled coils, the free energy required to form a randomly coiled bubble in the hinge region of myosin of the type conjectured by Harrington (Harrington, W. F., 1979, Proc. Natl. Acad. Sci. USA, 76:5066-5070) is estimated to be approximately 25 kcal/mol. Unfortunately this is far more than the free energy available from ATP hydrolysis if the crossbridges operate independently. Thus, in solution such bubbles are predicted to be absent, and the theory requires that the rod portion of myosin be a hingeless, continuously deforming rod. While such bubble formation in vivo cannot be entirely ruled out, it appears to be unlikely. We further conjecture that in solution the swivel located between myosin subfragments 1 and 2 (S-2 and S-1) is due to a locally random conformation of the chains caused by the presence of a proline residue at the point that physically separates the coiled coil from the globular portion of myosin. On attachment of S-1 to actin in the strong binding state, the configurational entropy of the random coil in the swivel region is greatly reduced relative to the case where the ends are free. This produces a spontaneous coil-to-helix transition in the swivel region that causes rotation of S-1 and the translation of actin. Thus, the model predicts that the actin filaments are pushed rather than pulled past the thick filaments by the crossbridges. The specific mechanism of force generation is examined in detail, and a simple statistical mechanical realization of the model is proposed. We find that the model gives a substantial number of qualitative and at times quantitative predictions in accord with experiment, and is particularly appealing in that it provides a simple means of free energy transduction--the well known fact that topological constraints shift the equilibrium between helical and random coil states.

Actins↗
PubMed2004

The motor mechanism of myosin V: insights for muscle contraction.

It is 50 years since the sliding of actin and myosin filaments was proposed as the basis of force generation and shortening in striated muscle. Although this is now generally accepted, the detailed molecular mechanism of how myosin uses adenosine triphosphate to generate force during its cyclic interaction with actin is only now being unravelled. New insights have come from the unconventional myosins, especially myosin V. Myosin V is kinetically tuned to allow movement on actin filaments as a single molecule, which has led to new kinetic, mechanical and structural data that have filled in missing pieces of the actomyosin-chemo-mechanical transduction puzzle.

Actins↗
PubMed2002

MMG and EMG responses during fatiguing isokinetic muscle contractions at different velocities.

The purpose of this study was to determine mechanomyographic (MMG) and electromyographic (EMG) responses of the superficial quadriceps muscles during repeated isokinetic contractions in order to provide information about motor control strategies during such activity, and to assess uniformity in mechanical activity (MMG) between the investigated muscles. Ten adults performed 50 maximal concentric muscle contractions at three randomly selected contraction velocities (60, 180, and 300 degrees.s(-1)) on different days. Surface electrodes and an MMG sensor were placed on the vastus lateralis (VL), rectus femoris (RF), and vastus medialis (VM). EMG and MMG amplitude and peak torque (PT) were calculated for each contraction, normalized, and averaged across all subjects. The results demonstrated that MMG amplitude more closely tracked the fatigue-induced decline in torque production at each velocity than did EMG amplitude. This indicates that MMG amplitude may be useful for estimating force production during fatiguing dynamic contractions when a direct measure is not available, such as during certain rehabilitative exercises. MMG amplitude responses of the VL, RF, and VM were not uniform for each velocity or across velocities, indicating that it may be possible to detect the individual contribution of each muscle to force production during repeated dynamic contractions. Therefore, MMG amplitude may be clinically useful for detecting abnormal force contributions of individual muscles during dynamic contractions, and determining whether various treatments are successful at correcting such abnormalities.

Adult↗