Home About us Contact | |||
Reflex Amplitudes (reflex + amplitude)
Selected AbstractsThe changes in neuromuscular excitability with normobaric hyperoxia in humansEXPERIMENTAL PHYSIOLOGY, Issue 1 2010Christelle Brerro-Saby Based on previous observations in hyperbaric hyperoxia, we hypothesized that normobaric hyperoxia, often used during general anaesthesia and resuscitation, might also induce a neuromuscular excitability. In heathy volunteers, we studied the consequences of a 50 min period of pure oxygen breathing on the neuromuscular conduction time (CT), the amplitude of the compound evoked muscle potential (M-wave), the latency and amplitude of the Hoffman reflex (H reflex) and the electromyographic tonic vibratory response (TVR) of the flexor digitorum superficialis muscle to explore the proprioceptive reflex loop. Hyperoxia-induced oxidative stress was measured by the changes in blood markers of lipid peroxidation (thiobarbituric acid reactive substances, TBARS) and antioxidant response (reduced ascorbic acid, RAA). During hyperoxia, the M-wave amplitude increased, both CT and H reflex latency were shortened, and the H reflex amplitude increased. By contrast, TVR significantly decreased. Concomitantly, an oxidative stress was assessed by increased TBARS and decreased RAA levels. This study shows the existence of dual effects of hyperoxia, which facilitates the muscle membrane excitability, nerve conduction and spinal reflexes, but reduces the gain of the proprioceptive reflex loop. The activation of the group IV muscle afferents by hyperoxia and the resulting oxidative stress might explain the TVR depression. [source] Modulation of spinal reflexes by aversive and sexually appetitive stimuliPSYCHOPHYSIOLOGY, Issue 2 2003Stephanie Both Abstract In this study, modulation of spinal tendinous (T) reflexes by sexual stimulation was investigated. T reflexes are augmented in states of appetitive and defensive action and modified by differences in arousal intensity. Reflexes were expected to be facilitated by both pleasant (sexual) and unpleasant (anxiety) stimuli. Subjects were exposed to a sexual, an anxiety-inducing, a sexually threatening, and a neutral film excerpt. Genital arousal, emotional experience, subjective action tendencies, and T reflexes were monitored. Self-report and genital data confirmed the affective states as intended. T reflex amplitude significantly increased during viewing of emotionally arousing film excerpts as compared with a neutral film excerpt. T reflexes were facilitated by the sex stimulus to the same extent as by the anxiety and sexual threat stimuli. The results support the view of sexual arousal as an emotional state, generating sex-specific autonomic and general somatic motor system responses, which prepare the organism for action. [source] Mechanical and neural stretch responses of the human soleus muscle at different walking speedsTHE JOURNAL OF PHYSIOLOGY, Issue 13 2009Neil J. Cronin During human walking, a sudden trip may elicit a Ia afferent fibre mediated short latency stretch reflex. The aim of this study was to investigate soleus (SOL) muscle mechanical behaviour in response to dorsiflexion perturbations, and to relate this behaviour to short latency stretch reflex responses. Twelve healthy subjects walked on a treadmill with the left leg attached to an actuator capable of rapidly dorsiflexing the ankle joint. Ultrasound was used to measure fascicle lengths in SOL during walking, and surface electromyography (EMG) was used to record muscle activation. Dorsiflexion perturbations of 6 deg were applied during mid-stance at walking speeds of 3, 4 and 5 km h,1. At each walking speed, perturbations were delivered at three different velocities (slow: ,170 deg s,1, mid: ,230 deg s,1, fast: ,280 deg s,1). At 5 km h,1, fascicle stretch amplitude was 34,40% smaller and fascicle stretch velocity 22,28% slower than at 3 km h,1 in response to a constant amplitude perturbation, whilst stretch reflex amplitudes were unchanged. Changes in fascicle stretch parameters can be attributed to an increase in muscle stiffness at faster walking speeds. As stretch velocity is a potent stimulus to muscle spindles, a decrease in the velocity of fascicle stretch at faster walking speeds would be expected to decrease spindle afferent feedback and thus stretch reflex amplitudes, which did not occur. It is therefore postulated that other mechanisms, such as altered fusimotor drive, reduced pre-synaptic inhibition and/or increased descending excitatory input, acted to maintain motoneurone output as walking speed increased, preventing a decrease in short latency reflex amplitudes. [source] Time-varying changes in corticospinal excitability accompanying the triphasic EMG pattern in humansTHE JOURNAL OF PHYSIOLOGY, Issue 3 2000Colum D. MacKinnon 1Nine healthy subjects performed single rapid wrist movements from neutral to targets at 20 deg of flexion or extension in response to an auditory cue. Surface EMG was recorded from the wrist flexors and extensors together with wrist position. Movements in both directions were characterised by the usual triphasic pattern of EMG activity in agonist (AG1), antagonist (ANTAG) and again in agonist (AG2) muscles. 2Single pulses of transcranial magnetic stimulation (TMS) were applied over the motor cortex at an intensity of 80 % of resting threshold at random times between 80 and 380 ms after the cue. We measured the peak-to-peak amplitude of the evoked motor potential (MEP) and the integrated EMG (IEMG) activity that preceded the MEP. In a separate set of experiments H reflexes were elicited in the wrist flexors instead of MEPs. 3MEP amplitudes in the agonist muscle increased by an average of 10 ± 8 ms (range ,1 to 23 ms) prior to the onset of the AG1 burst and were associated with an increase of over sevenfold in the MEP:IEMG ratio, irrespective of movement direction. Agonist H reflex amplitudes were linearly related to, and increased at the same time as, changes in agonist IEMG. 4The principal ANTAG burst was not preceded by an increase in the antagonist muscle MEP:IEMG ratio. No relationship was found between the amplitude of the antagonist H reflexes and the preceding antagonist IEMG. 5Five subjects showed an increase in the MEP:IEMG ratio preceding and during the initial part of the AG2 burst. 6Our method of analysis shows that changes in motor cortical excitability mediating the initiation of movement occur much closer to the onset of EMG activity (less than 23 ms) than the 80,100 ms lead time previously reported. The lack of such changes before the onset of the ANTAG burst suggests that this may be initiated by a different, perhaps subcortical, mechanism. [source] |