Spinal cholinergic inhibition of the pressor response to skeletal muscle activation

1999 ◽  
Vol 837 (1-2) ◽  
pp. 143-151 ◽  
Author(s):  
Gregory A. Hand ◽  
Peter J. Vrettakos ◽  
Brian S. Treuhaft ◽  
Wendi D. Shealy ◽  
L.Britt Wilson
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activation ◽  
Pressor Response

scholarly journals Caffeine-Induced Effects on Human Skeletal Muscle Contraction Time and Maximal Displacement Measured by Tensiomyography

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 815
Author(s):  
Przemysław Domaszewski ◽  
Paweł Pakosz ◽  
Mariusz Konieczny ◽  
Dawid Bączkowicz ◽  
Ewa Sadowska-Krępa
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activation ◽  
Electric Pulse ◽  
Professional Athletes ◽  
Mechanical Activity ◽  
The Novel ◽  
Contraction Time ◽  
Novel Approach ◽  
Skeletal Muscle Contraction ◽  
Maximal Displacement

Studies on muscle activation time in sport after caffeine supplementation confirmed the effectiveness of caffeine. The novel approach was to determine whether a dose of 9 mg/kg/ body mass (b.m.) of caffeine affects the changes of contraction time and the displacement of electrically stimulated muscle (gastrocnemius medialis) in professional athletes who regularly consume products rich in caffeine and do not comply with the caffeine discontinuation period requirements. The study included 40 professional male handball players (age = 23.13 ± 3.51, b.m. = 93.51 ± 15.70 kg, height 191 ± 7.72, BMI = 25.89 ± 3.10). The analysis showed that in the experimental group the values of examined parameters were significantly reduced (p ≤ 0.001) (contraction time: before = 20.60 ± 2.58 ms/ after = 18.43 ± 3.05 ms; maximal displacement: before = 2.32 ± 0.80 mm/after = 1.69 ± 0.51 mm). No significant changes were found in the placebo group. The main achievement of this research was to demonstrate that caffeine at a dose of 9 mg/kg in professional athletes who regularly consume products rich in caffeine has a direct positive effect on the mechanical activity of skeletal muscle stimulated by an electric pulse.

Hypertrophy, Resistance Training, and the Nature of Skeletal Muscle Activation

1995 ◽  
Vol 9 (3) ◽  
pp. 155-159 ◽  
Author(s):  
Christine L. Ruther ◽  
Catherine L. Golden ◽  
Robert T. Harris ◽  
Gary A. Dudley
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Activation

Internal defibrillation with minimal skeletal muscle activation: A new paradigm toward painless defibrillation

Heart Rhythm ◽  
2005 ◽  
Vol 2 (10) ◽  
pp. 1108-1113 ◽  
Author(s):  
Vinod Jayam ◽  
Menekhem Zviman ◽  
Venku Jayanti ◽  
Ariel Roguin ◽  
Henry Halperin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activation ◽  
New Paradigm ◽  
Internal Defibrillation

Effects of activation pattern on nonisometric human skeletal muscle performance

2007 ◽  
Vol 102 (5) ◽  
pp. 1985-1991 ◽  
Author(s):  
Ryan D. Maladen ◽  
Ramu Perumal ◽  
Anthony S. Wexler ◽  
Stuart A. Binder-Macleod
Keyword(s):  
Skeletal Muscle ◽  
Instantaneous Frequency ◽  
Muscle Activation ◽  
Motor Units ◽  
Muscle Performance ◽  
Variable Frequency ◽  
Constant Frequency ◽  
Muscle Activation Patterns ◽  
Activation Rate ◽  
Discharge Patterns

During volitional muscle activation, motor units often fire with varying discharge patterns that include brief, high-frequency bursts of activity. These variations in the activation rate allow the central nervous system to precisely control the forces produced by the muscle. The present study explores how varying the instantaneous frequency of stimulation pulses within a train affects nonisometric muscle performance. The peak excursion produced in response to each stimulation train was considered as the primary measure of muscle performance. The results showed that at each frequency tested between 10 and 50 Hz, variable-frequency trains that took advantage of the catchlike property of skeletal muscle produced greater excursions than constant-frequency trains. In addition, variable-frequency trains that could achieve targeted trajectories with fewer pulses than constant-frequency trains were identified. These findings suggest that similar to voluntary muscle activation patterns, varying the instantaneous frequency within a train of pulses can be used to improve muscle performance during functional electrical stimulation.

Hemodynamic actions of insulin

1994 ◽  
Vol 267 (2) ◽  
pp. E187-E202 ◽  
Author(s):  
A. D. Baron
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Pressor Response ◽  
Physiological Role ◽  
Oxide System ◽  
Maximal Response ◽  
Insulin Resistant ◽  
The Right

There is accumulating evidence that insulin has a physiological role to vasodilate skeletal muscle vasculature in humans. This effect occurs in a dose-dependent fashion within a half-maximal response of approximately 40 microU/ml. This vasodilating action is impaired in states of insulin resistance such as obesity, non-insulin-dependent diabetes, and elevated blood pressure. The precise physiological role of insulin-mediated vasodilation is not known. Data indicate that the degree of skeletal muscle perfusion can be an important determinant of insulin-mediated glucose uptake. Therefore, it is possible that insulin-mediated vasodilation is an integral aspect of insulin's overall action to stimulate glucose uptake; thus defective vasodilation could potentially contribute to insulin resistance. In addition, insulin-mediated vasodilation may play a role in the regulation of vascular tone. Data are provided to indicate that the pressor response to systemic norepinephrine infusions is increased in obese insulin-resistant subjects. Moreover, the normal effect of insulin to shift the norepinephrine pressor dose-response curve to the right is impaired in these patients. Therefore, impaired insulin-mediated vasodilation could further contribute to the increased prevalence of hypertension observed in states of insulin resistance. Finally, data are presented to indicate that, via a yet unknown interaction with the endothelium, insulin is able to increase nitric oxide synthesis and release and through this mechanism vasodilate. It is interesting to speculate that states of insulin resistance might also be associated with a defect in insulin's action to modulate the nitric oxide system.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals PPADS does not block contraction-induced prostaglandin E2 synthesis in cat skeletal muscle

2008 ◽  
Vol 295 (5) ◽  
pp. H2043-H2045 ◽  
Author(s):  
Jennifer L. McCord ◽  
Shawn G. Hayes ◽  
Marc P. Kaufman
Keyword(s):  
Skeletal Muscle ◽  
Pyridoxal Phosphate ◽  
Pressor Response ◽  
Triceps Surae ◽  
Prostaglandin E ◽  
Exercise Pressor Reflex ◽  
Before And After ◽  
Pressor Reflex ◽  
Response To Exercise

Pyridoxal-phosphate-6-azophenyl-2′-4-disulfonate (PPADS), a purinergic 2 (P2) receptor antagonist, has been shown to attenuate the exercise pressor reflex in cats. In vitro, however, PPADS has been shown to block the production of prostaglandins, some of which play a role in evoking the exercise pressor reflex. Thus the possibility exists that PPADS blocks the exercise pressor reflex through a reduction in prostaglandin synthesis rather than through the blockade of P2 receptors. Using microdialysis, we collected interstitial fluid from skeletal muscle to determine prostaglandin E2 (PGE2) concentrations during the intermittent contraction of the triceps surae muscle before and after a popliteal arterial injection of PPADS (10 mg/kg). We found that the PGE2 concentration increased in response to the intermittent contraction before and after the injection of PPADS (both, P < 0.05). PPADS reduced the pressor response to exercise ( P < 0.05) but had no effect on the magnitude of PGE2 production during contraction ( P = 0.48). These experiments demonstrate that PPADS does not block the exercise pressor reflex through a reduction in PGE2 synthesis. We suggest that PGE2 and P2 receptors play independent roles in stimulating the exercise pressor reflex.

Oxygen delivery to skeletal muscle fibers: effects of microvascular unit structure and control mechanisms

2003 ◽  
Vol 285 (3) ◽  
pp. H955-H963 ◽  
Author(s):  
Arthur Lo ◽  
Andrew J. Fuglevand ◽  
Timothy W. Secomb
Keyword(s):  
Skeletal Muscle ◽  
Muscle Activation ◽  
Tissue Oxygenation ◽  
Oxygen Sensing ◽  
Full Range ◽  
Muscle Fibers ◽  
Motor Units ◽  
Threshold Value ◽  
Control Mechanisms ◽  
Capillary Perfusion

The number of perfused capillaries in skeletal muscle varies with muscle activation. With increasing activation, muscle fibers are recruited as motor units consisting of widely dispersed fibers, whereas capillaries are recruited as groups called microvascular units (MVUs) that supply several adjacent fibers. In this study, a theoretical model was used to examine the consequences of this spatial mismatch between the functional units of muscle activation and capillary perfusion. Diffusive oxygen transport was simulated in cross sections of skeletal muscle, including several MVUs and fibers from several motor units. Four alternative hypothetical mechanisms controlling capillary perfusion were considered. First, all capillaries adjacent to active fibers are perfused. Second, all MVUs containing capillaries adjacent to active fibers are perfused. Third, each MVU is perfused whenever oxygen levels at its feed arteriole fall below a threshold value. Fourth, each MVU is perfused whenever the average oxygen level at its capillaries falls below a threshold value. For each mechanism, the dependence of the fraction of perfused capillaries on the level of muscle activation was predicted. Comparison of the results led to the following conclusions. Control of perfusion by MVUs increases the fraction of perfused capillaries relative to control by individual capillaries. Control by arteriolar oxygen sensing leads to poor control of tissue oxygenation at high levels of muscle activation. Control of MVU perfusion by capillary oxygen sensing permits adequate tissue oxygenation over the full range of activation without resulting in perfusion of all MVUs containing capillaries adjacent to active fibers.

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