Home About us Contact
|
Home About us Contact | ||
|
|
||
Contracting Muscle (contracting + muscle)
Selected AbstractsHydrogen Peroxide-Dependent Arteriolar Dilation in Contracting Muscle of Rats Fed Normal and High Salt DietsMICROCIRCULATION, Issue 8 2007Paul J. Marvar ABSTRACT Objective: High dietary salt intake decreases the arteriolar dilation associated with skeletal muscle contraction. Because hydrogen peroxide (H2O2) can be released from contracting muscle fibers, this study was designed to assess the possible contribution of H2O2 to skeletal muscle functional hyperemia and its sensitivity to dietary salt. Methods: The authors investigated the effect of catalase treatment on arteriolar dilation and hyperemia in contracting spinotrapezius muscle of rats fed a normal salt (0.45%, NS) or high salt (4%, HS) diet for 4 weeks. Catalase-sensitive 2,,7,-dichlorofluorescein (DCF) fluorescence was measured as an index of H2O2 formation, and the mechanism of arteriolar dilation to H2O2 was probed in each group using pharmacological inhibitors. Results: DCF fluorescence increased with muscle contraction, but not if catalase was present. Catalase also reduced arteriolar dilation and hyperemia during contraction in both dietary groups. Exogenous H2O2 dilated arterioles in both groups, with greater responses in HS rats. Guanylate cyclase inhibition did not affect arteriolar responses to H2O2 in either group, but KCa or KATP channel inhibition equally reduced these responses, and KATP channel inhibition equally reduced functional hyperemia in both groups. Conclusions: These results indicate that locally produced H2O2 contributes to arteriolar dilation and hyperemia in contracting skeletal muscle, and that the effect of H2O2 on arteriolar tone in this vascular bed is mediated largely through K+ channel activation. High dietary salt intake does not reduce the contribution of H2O2 to active hyperemia, or alter the mechanism through which H2O2 relaxes arteriolar smooth muscle. [source] Motor unit recruitment during lengthening contractions of human wrist flexorsMUSCLE AND NERVE, Issue 11 2001Paula J. Stotz MSc Abstract The purpose of this study was to revisit the question of recruitment of motor units during lengthening contractions because of conflicting views in the literature on this subject. Motor unit activity was recorded from the flexor carpi radialis muscle of four human subjects to compare the patterns of recruitment during lengthening and isometric contractions. Lengthening contractions were produced either when the subject voluntarily stopped opposing a background load or when an additional load was imposed on the already contracting muscle. In both cases, lengthening of the active muscle was produced at a variety of speeds, from quite slow to "as fast as possible." No differences in recruitment order were observed between isometric and lengthening contractions at any speed of lengthening contraction. It is concluded that all contractions in normal humans recruit motor units in an orderly fashion from small to large, according to the size principle of motor unit recruitment. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1535,1541, 2001 [source] Regulation and function of Ca2+,calmodulin-dependent protein kinase II of fast-twitch rat skeletal muscleTHE JOURNAL OF PHYSIOLOGY, Issue 3 2007Adam J. Rose The activation and function of Ca2+,calmodulin-dependent kinase II (CaMKII) in contracting rat skeletal muscle was examined. The increase in autonomous activity and phosphorylation at Thr287 of CaMKII of gastrocnemius muscle in response to contractions in situ was rapid and transient, peaking at 1,3 min, but reversed after 30 min of contractions. There was a positive correlation between CaMKII phosphorylation at Thr287 and autonomous CaMKII activity. In contrast to the rapid and transient increase in autonomous CaMKII activity, the phosphorylation of the putative CaMKII substrate trisk95/triadin was rapid and sustained during contractions. There were no changes in CaMKII activity and phosphorylation or trisk95 phosphorylation in the resting contralateral muscles during stimulation. When fast-twitch muscles were contracted ex vivo, CaMKII inhibition resulted in a greater magnitude of fatigue as well as blunted CaMKII and trisk95 phosphorylation, identifying trisk95 as a physiological CaMKII substrate. In summary, skeletal muscle CaMKII activation was rapid and sustained during exercise/contraction and is mediated by factors within the contracting muscle, probably through allosteric activation via Ca2+,CaM. CaMKII may signal through trisk95 to modulate Ca2+ release in fast-twitch rat skeletal muscle during exercise/contraction. [source] IDENTIFYING ATHLETES AT RISK OF HAMSTRING STRAINS AND HOW TO PROTECT THEMCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2004U Proske SUMMARY 1.,One common soft-tissue injury in sports involving sprinting and kicking a ball is the hamstring strain. Strain injuries often occur while the contracting muscle is lengthened, an eccentric contraction. We have proposed that the microscopic damage to muscle fibres that routinely occurs after a period of unaccustomed eccentric exercise can lead to a more severe strain injury. 2.,An indicator of susceptibility for the damage from eccentric exercise is the optimum angle for torque. When this is at a short muscle length, the muscle is more prone to eccentric damage. It is known that subjects most at risk of a hamstring strain have a previous history of hamstring strains. By means of isokinetic dynamometry, we have measured the optimum angle for torque for nine athletes with a history of unilateral hamstring strains. We also measured optimum angles for 18 athletes with no previous history of strain injuries. It was found that mean optimum angle in the previously injured muscles was at a significantly shorter length than for the uninjured muscles of the other leg and for muscles of both legs in the uninjured group. This result suggests that previously injured muscles are more prone to eccentric damage and, therefore, according to our hypothesis, more prone to strain injuries than uninjured muscles. 3.,After a period of unaccustomed eccentric exercise, if the exercise is repeated 1 week later, there is much less evidence of damage because the muscle has undergone an adaptation process that protects it against further damage. We propose that for athletes considered at risk of a hamstring strain, as indicated by the optimum angle for torque, a regular programme of mild eccentric exercise should be undertaken. This approach seems to work because evidence from a group of athletes who have implemented such a programme shows a significant reduction in the incidence of hamstring strains. [source] Disparity in regional and systemic circulatory capacities: do they affect the regulation of the circulation?ACTA PHYSIOLOGICA, Issue 4 2010J. A. L. Calbet Abstract In this review we integrate ideas about regional and systemic circulatory capacities and the balance between skeletal muscle blood flow and cardiac output during heavy exercise in humans. In the first part of the review we discuss issues related to the pumping capacity of the heart and the vasodilator capacity of skeletal muscle. The issue is that skeletal muscle has a vast capacity to vasodilate during exercise [,300 mL (100 g),1 min,1], but the pumping capacity of the human heart is limited to 20,25 L min,1 in untrained subjects and ,35 L min,1 in elite endurance athletes. This means that when more than 7,10 kg of muscle is active during heavy exercise, perfusion of the contracting muscles must be limited or mean arterial pressure will fall. In the second part of the review we emphasize that there is an interplay between sympathetic vasoconstriction and metabolic vasodilation that limits blood flow to contracting muscles to maintain mean arterial pressure. Vasoconstriction in larger vessels continues while constriction in smaller vessels is blunted permitting total muscle blood flow to be limited but distributed more optimally. This interplay between sympathetic constriction and metabolic dilation during heavy whole-body exercise is likely responsible for the very high levels of oxygen extraction seen in contracting skeletal muscle. It also explains why infusing vasodilators in the contracting muscles does not increase oxygen uptake in the muscle. Finally, when ,80% of cardiac output is directed towards contracting skeletal muscle modest vasoconstriction in the active muscles can evoke marked changes in arterial pressure. [source] Changes in presumed motor cortical activity during fatiguing muscle contraction in humansACTA PHYSIOLOGICA, Issue 3 2010T. Seifert Abstract Aim:, Changes in sensory information from active muscles accompany fatiguing exercise and the force-generating capacity deteriorates. The central motor commands therefore must adjust depending on the task performed. Muscle potentials evoked by transcranial magnetic stimulation (TMS) change during the course of fatiguing muscle activity, which demonstrates activity changes in cortical or spinal networks during fatiguing exercise. Here, we investigate cortical mechanisms that are actively involved in driving the contracting muscles. Methods:, During a sustained submaximal contraction (30% of maximal voluntary contraction) of the elbow flexor muscles we applied TMS over the motor cortex. At an intensity below motor threshold, TMS reduced the ongoing muscle activity in biceps brachii. This reduction appears as a suppression at short latency of the stimulus-triggered average of rectified electromyographic (EMG) activity. The magnitude of the suppression was evaluated relative to the mean EMG activity during the 50 ms prior to the cortical stimulus. Results:, During the first 2 min of the fatiguing muscle contraction the suppression was 10 ± 0.9% of the ongoing EMG activity. At 2 min prior to task failure the suppression had reached 16 ± 2.1%. In control experiments without fatigue we did not find a similar increase in suppression with increasing levels of ongoing EMG activity. Conclusion:, Using a form of TMS which reduces cortical output to motor neurones (and disfacilitates them), this study suggests that neuromuscular fatigue increases this disfacilitatory effect. This finding is consistent with an increase in the excitability of inhibitory circuits controlling corticospinal output. [source] | |||||||||||||