Fos immunoreactivity in the intermediolateral nucleus induced by tendon vibration of the m. triceps surae in rats pretreated with a nitric oxide blocker or precursor

Crossed effects from group I afferents on reflex excitability and their mechanisms of action are not yet well understood. The current view is that the influence is weak and takes place indirectly via oligosynaptic pathways. We examined possible contralateral effects from group I afferents on presynaptic inhibition of Ia terminals in humans and cats. In resting and seated human subjects the soleus (SO) H-reflex was conditioned by an electrical stimulus to the ipsilateral common peroneal nerve (CPN) to assess the level of presynaptic inhibition (PSI_control). A brief conditioning vibratory stimulus was applied to the triceps surae tendon at the contralateral side (to activate preferentially Ia muscle afferents). The amplitude of the resulting H-reflex response (PSI_conditioned) was compared to the H-reflex under PSI_control, i.e., without the vibration. The interstimulus interval between the brief vibratory stimulus and the electrical shock to the CPN was −60 to 60 ms. The H-reflex conditioned by both stimuli did not differ from that conditioned exclusively by the ipsilateral CPN stimulation. In anesthetized cats, bilateral monosynaptic reflexes (MSRs) in the left and right L7 ventral roots were recorded simultaneously. Conditioning stimulation applied to the contralateral group I posterior biceps and semitendinosus (PBSt) afferents at different time intervals (0–120 ms) did not have an effect on the ipsilateral gastrocnemius/soleus (GS) MSR. An additional experimental paradigm in the cat using contralateral tendon vibration, similar to that conducted in humans, was also performed. No significant differences between GS-MSRs conditioned by ipsilateral PBSt stimulus alone and those conditioned by both ipsilateral PBSt stimulus and contralateral tendon vibration were detected. The present results strongly suggest an absence of effects from contralateral group I fibers on the presynaptic mechanism of MSR modulation in relaxed humans and anesthetized cats.

Download Full-text

Hoffmann reflex is increased after 14 days of daily repeated Achilles tendon vibration for the soleus but not for the gastrocnemii muscles

Applied Physiology Nutrition and Metabolism ◽

10.1139/h11-129 ◽

2012 ◽

Vol 37 (1) ◽

pp. 14-20 ◽

Cited By ~ 11

Author(s):

Thomas Lapole ◽

Chantal Pérot

Keyword(s):

Achilles Tendon ◽

Motor Units ◽

Muscle Spindles ◽

Triceps Surae ◽

Control Group ◽

Tendon Vibration ◽

Hoffmann Reflex ◽

Reflex Excitability ◽

Short Period ◽

Post Test

In a previous study, Achilles tendon vibrations were enough to improve the triceps surae (TS) activation capacities and also to slightly increase TS Hoffmann reflex (H-reflex) obtained by summing up soleus (Sol) and gastrocnemii (GM and GL) EMGs. The purpose of the present study was to analyze separately Sol and GM or GL reflexes to account for different effects of the vibrations on the reflex excitability of the slow soleus and of the gastrocnemii muscles. A control group (n = 13) and a vibration group (n = 16) were tested in pre-test and post-test conditions. The Achilles tendon vibration program consisted of 1 h of daily vibration (frequency: 50 Hz) applied during 14 days. Maximal Sol, GM and GL H-reflexes, and M-waves were recorded, and their Hmax/Mmax ratios gave the index of reflex excitability. After the vibration protocol, only Sol Hmax/Mmax was enhanced (p < 0.001). The enhanced Sol reflex excitability after vibration is in favor of a decrease in the pre-synaptic inhibition due to the repeated vibrations and the high solicitation of the reflex pathway. Those results of a short period of vibration applied at rest may be limited to the soleus because of its high density in muscle spindles and slow motor units, both structures being very sensitive to vibrations.

Download Full-text

Role of neuronal nitric oxide in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats

Journal of Applied Physiology ◽

10.1152/japplphysiol.00250.2013 ◽

2013 ◽

Vol 115 (1) ◽

pp. 97-106 ◽

Cited By ~ 21

Author(s):

Nicholas G. Jendzjowsky ◽

Darren S. DeLorey

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Muscle Contraction ◽

Triceps Surae ◽

Sympathetic Stimulation ◽

Sprague Dawley ◽

Sympathetic Vasoconstriction ◽

In Series ◽

Nnos Inhibition

Isoform-specific nitric oxide (NO) synthase (NOS) contributions to NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle are incompletely understood. The purpose of the present study was to investigate the role of neuronal NOS (nNOS) in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats. We hypothesized that acute pharmacological inhibition of nNOS would augment sympathetic vasoconstriction in resting and contracting skeletal muscle, demonstrating that nNOS is primarily responsible for NO-mediated inhibition of sympathetic vasoconstriction. Sprague-Dawley rats ( n = 13) were anesthetized and instrumented with an indwelling brachial artery catheter, femoral artery flow probe, and lumbar sympathetic chain stimulating electrodes. Triceps surae muscles were stimulated to contract rhythmically at 60% of maximal contractile force. In series 1 ( n = 9), the percent change in femoral vascular conductance (%FVC) in response to sympathetic stimulations delivered at 2 and 5 Hz was determined at rest and during muscle contraction before and after selective nNOS blockade with S-methyl-l-thiocitrulline (SMTC, 0.6 mg/kg iv) and subsequent nonselective NOS blockade with Nω-nitro-l-arginine methyl ester (l-NAME, 5 mg/kg iv). In series 2 ( n = 4), l-NAME was injected first, and then SMTC was injected to determine if the effect of l-NAME on constrictor responses was influenced by selective nNOS inhibition. Sympathetic stimulation decreased FVC at rest (−25 ± 7 and −44 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−7 ± 3 and −19 ± 5%FVC at 2 and 5 Hz, respectively). The decrease in FVC in response to sympathetic stimulation was greater in the presence of SMTC at rest (−32 ± 6 and −49 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−21 ± 4 and −28 ± 4%FVC at 2 and 5 Hz, respectively). l-NAME further increased ( P < 0.05) the sympathetic vasoconstrictor response at rest (−47 ± 4 and −60 ± 6%FVC at 2 and 5 Hz, respectively) and during muscle contraction (−33 ± 3 and −40 ± 6%FVC at 2 and 5 Hz, respectively). The effect of l-NAME was not altered by the order of nNOS inhibition. These data demonstrate that NO derived from nNOS and endothelial NOS contribute to the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.

Download Full-text

Mediators of contraction-evoked skeletal muscle depressor response in anesthetized rats

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.2.578 ◽

1996 ◽

Vol 81 (2) ◽

pp. 578-585 ◽

Cited By ~ 17

Author(s):

G. M. Toney ◽

S. W. Mifflin

Keyword(s):

Nitric Oxide ◽

Cardiovascular Responses ◽

Atropine Sulfate ◽

Bilateral Adrenalectomy ◽

Triceps Surae ◽

Induced Response ◽

Beta Adrenoceptor ◽

Depressor Response ◽

Anesthetized Rats ◽

Before And After

In the present study, mediators of muscle contraction-evoked cardiovascular responses were examined in anesthetized rats. Rhythmic contractions of the hindlimb triceps surae muscle were produced by stimulating the tibial nerve (motor threshold 22.7 +/- 2.3 microA; n = 10) by using a 1 s on-1 s off pattern. Mean arterial pressure (MAP) and heart rate (HR) responses were recorded before and after 1) muscarinic receptor blockade (atropine sulfate; 2.0 mg/kg i.v., n = 5); 2) nitric oxide synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME; 300 microM/kg i.v., n = 7); 3) beta-adrenoceptor blockade (propranolol; 2.0 mg/kg i.v., n = 10); and 4) bilateral adrenalectomy (n = 4). Rhythmic stimulation (10-s) significantly reduced MAP (P < 0.05) and elicited small decreases in HR that were abolished by neuromuscular blockade (n = 4). Atropine had no effect on MAP or HR responses to contraction. L-NAME increased baseline MAP (112.2 +/- 2.2 to 137.1 +/- 4.6 mmHg, P < 0.05) and attenuated contraction-evoked reductions of MAP (P < 0.05) without affecting HR. L-NAME-induced response deficits were mimicked in four separate rats by elevating MAP with phenylephrine (7–10 micrograms.kg-1.h-1 iv) to a level not different from that produced by L-NAME. Bilateral adrenalectomy and propranolol did not significantly affect HR responses but reduced contraction-evoked decreases in MAP from 14.3 +/- 2.9 to 7.7 +/- 2.2 mmHg and from 13.4 +/- 1.3 to 6.3 +/- 3.1 mmHg, respectively (P < 0.05). Baseline MAP was unchanged. We conclude that adrenal catecholamines, acting at beta-adrenoceptors, contribute significantly to the contraction-evoked depressor response in rats. No role for muscarinic receptors is evident in this response. Furthermore, attenuation of depressor responses to contraction after nitric oxide inhibition could result from an indirect effect of the pressor actions of L-NAME.

Download Full-text

Involuntary sustained firing of plantar flexor motor neurones: effect of electrical stimulation parameters during tendon vibration

European Journal of Applied Physiology ◽

10.1007/s00421-020-04563-7 ◽

2021 ◽

Author(s):

Ricardo N. O. Mesquita ◽

Janet L. Taylor ◽

Benjamin Kirk ◽

Anthony J. Blazevich

Keyword(s):

Electrical Stimulation ◽

Pulse Width ◽

Neuromuscular Electrical Stimulation ◽

Voluntary Contraction ◽

Triceps Surae ◽

Tendon Vibration ◽

Plantar Flexor ◽

Intensity Pattern ◽

Simultaneous Application ◽

Motor Neurones

Abstract Purpose Simultaneous application of tendon vibration and neuromuscular electrical stimulation (NMES) induces an involuntary sustained torque. We examined the effect of different NMES parameters (intensity, pattern of stimulation and pulse width) on the magnitude of the evoked involuntary torque. Methods Plantar flexor torque was recorded during 33-s Achilles tendon vibration with simultaneous 20-Hz NMES bouts on triceps surae (n = 20; 13 women). Intensity was set to elicit 10, 20 or 30% of maximal voluntary contraction torque (MVC), pulse width was narrow (0.2 ms) or wide (1 ms), and the stimulus pattern varied (5 × 2-s or 10 × 1-s). Up to 12 different trials were performed in a randomized order, and then repeated in those who produced a sustained involuntary torque after the cessation of vibration. Results Six of 7 men and 5 of 13 women produced a post-vibration sustained torque. Eight of 20 participants did not complete the 30% trials, as they were perceived as painful. Torque during vibration at the end of NMES and the increase in torque throughout the trial were significantly higher in 20 than 10% trials (n = 11; 9.7 ± 9.0 vs 7.1 ± 6.1% MVC and 4.3 ± 4.5 vs 3.6 ± 3.5% MVC, respectively). Post-vibration sustained torque was higher in wide pulse-width trials (5.4 ± 5.9 vs 4.1 ± 4.3% MVC). Measures of involuntary torque were not different between 20 and 30% trials (n = 8). Conclusion Bouts of 5 × 2-s NMES with wide pulse width eliciting 20% MVC provides the most robust responses and could be used to maximise the production of involuntary torque in triceps surae.

Download Full-text

Pressor reflex evoked by static muscle contraction: role of nitric oxide in the dorsal horn

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.6.r1639 ◽

1999 ◽

Vol 276 (6) ◽

pp. R1639-R1646 ◽

Cited By ~ 6

Author(s):

L. Britt Wilson ◽

John Engbretson ◽

Angela D. Crews

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Dorsal Horn ◽

Time Course ◽

Pressor Response ◽

Triceps Surae ◽

No Production ◽

Static Contraction ◽

Pressor Reflex ◽

Ventral Roots

In this study, we tested the hypothesis that nitric oxide (NO) production in the dorsal horn is involved in producing the pressor reflex elicited by static contraction of skeletal muscle. Cats were anesthetized with α-chloralose (80 mg/kg) and urethane (100 mg/kg), and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L7 and S1 ventral roots. Dialysis of the NO synthase inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 50 mmol/l syringe concentration, based upon dose-response data) into the dorsal horn at L6 and S1 failed to attenuate the peak change in mean arterial pressure (MAP) evoked by static contraction (ΔMAP in mmHg: 57 ± 5 before and 50 ± 6 after 2 h of l-NAME). However, this dialysis of l-NAME reduced the magnitude of the initial pressor response as the MAP at 10 s of the contraction fell from 27 ± 4 to 17 ± 4 mmHg. On the other hand, 2 h of l-arginine dialysis (50 mmol/l) shifted the curve representing the time course of the pressor response upward and increased the peak pressor response to static contraction from 51 ± 9 to 68 ± 9 mmHg. A 2-h dialysis of d-NAME (50 mmol/l), the inactive enantiomer of l-NAME, had no effect on the time course or the peak pressor response (ΔMAP in mmHg: 78 ± 12 before and 72 ± 15 after). These data suggest that NO production in the dorsal horn has a modulatory influence on the pressor reflex evoked by static contraction of skeletal muscle and that increasing the level of NO in the dorsal horn enhances the excitability of dorsal horn cells to muscle afferent input.

Download Full-text

Effects of repeated Achilles tendon vibration on triceps surae stiffness and reflex excitability

Journal of Electromyography and Kinesiology ◽

10.1016/j.jelekin.2010.10.011 ◽

2011 ◽

Vol 21 (1) ◽

pp. 87-94 ◽

Cited By ~ 13

Author(s):

Thomas Lapole ◽

Chantal Pérot

Keyword(s):

Achilles Tendon ◽

Triceps Surae ◽

Tendon Vibration ◽

Reflex Excitability

Download Full-text

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100166397 ◽

1996 ◽

Vol 54 ◽

pp. 786-787

Author(s):

Chi-Ming Wei ◽

Margarita Bracamonte ◽

Shi-Wen Jiang ◽

Richard C. Daly ◽

Christopher G.A. McGregor ◽

...

Keyword(s):

Nitric Oxide ◽

Heart Failure ◽

Nitric Oxide Synthase ◽

Endothelial Nitric Oxide Synthase ◽

Cardiac Tissues ◽

Mammalian Tissues ◽

End Stage Heart Failure ◽

End Stage ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Download Full-text