Skin sympathetic nerve activity in humans during exposure to emotionally-charged images : sex differences

While it is known that anxiety or emotional arousal affects skin sympathetic nerve activity (SSNA), the galvanic skin response (GSR) is the most widely used parameter to infer increases in SSNA during stress or emotional studies. We recently showed that SSNA provides a more sensitive measure of emotional state than effector-organ responses. The aim of the present study was to assess whether there are gender differences in the responses of SSNA and other physiological parameters such as blood pressure, heart rate, skin blood flow and sweat release, while subjects viewed neutral or emotionally-charged images from the International Affective Picture System (IAPS). Changes in SSNA were assessed using microneurography in 20 subjects (10 male and 10 female). Blocks of positively-charged (erotica) or negatively-charge images (mutilation) were presented in a quasi-random fashion, following a block of neutral images, with each block containing 15 images and lasting 2 min. Images of both erotica and mutilation caused significant increases in SSNA, with increases being greater for males viewing erotica and greater for females viewing mutilation. The increases in SSNA were often coupled with sweat release and cutaneous vasoconstriction; however, these markers were not significantly different than those produced by viewing neutral images and were not always consistent with the SSNA increases. We conclude that SSNA increases with both positively-charged and negatively-charged emotional images, yet sex differences are present

Intramuscular stimulation of tibialis anterior in human subjects : the effects of discharge variability on force production and fatigue

Continuous intramuscular stimulation of tibialis anterior (TA) was used to test the hypothesis that irregular trains of stimuli can increase force production and offset the magnitude of fatigue when compared with a continuous train of regular stimuli at an identical mean frequency (19 or 24 Hz). To achieve this, tungsten microelectrodes were inserted into the muscle belly into the motor point of the tibialis anterior muscle of able-bodied individuals (aged 19–50) and stimulated at current intensities ranging from 5 to 7 mA. The motor point was stimulated with a continuous train of regular stimulation at either 19 or 24 Hz (n = 11) or until the force declined below 25% of the peak force at the onset of stimulation. For the first seven subjects, no fatigue was exhibited, and thus, we simply compared the forces generated by the regular and irregular segments of the continuous train (120 sec for each segment). For four additional subjects, we delivered a higher frequency train (24 Hz) that elicited some fatigue. Once the force had declined below 25% of the initial peak force (which took between 140 and 210 sec), the continuous irregular train was integrated. Interestingly, for those subjects who exhibited muscular fatigue, force always began to rise again once the irregularity was incorporated into the continuous regular train of stimulation at the identical mean frequency (24 Hz). We conclude that incorporating irregularity into continuous trains of stimuli offers a significant advantage to the human neuromuscular system during both fatigued and nonfatigued states and could offer benefits to therapies such as functional electrical stimulation (FES)

Inhibition of augmented muscle vasoconstrictor drive following asphyxic apnoea in awake human subjects is not affected by relief of chemical drive

Progressive asphyxia, produced by a prolonged voluntary breath hold (end-expiratory apnoea), evokes large bursts of muscle sympathetic nerve activity (MSNA). These bursts increase in amplitude until the asphyxic break point is reached, at which point the bursts are inhibited. We tested the hypothesis that lung inflation, rather than relief from hypoxia and hypercapnia, is responsible for the inhibition of MSNA. Multiunit MSNA was recorded from motor fascicles of the common peroneal nerve in 11 subjects. Following a period of quiet breathing, subjects were instructed to behave as follows: (i) to hold their breath in expiration for as long as they could (mean duration 32.3 +/- 1.9 s); (ii) to take a single breath of room air, 100% N-2 or10% CO2 + 90% N2 at the asphyxic break point; (iii) to exhale and continue the apnoea until the next break point; and then (iv) to resume breathing. All subjects reported relief during inhalation of any gas, and could continue holding their breath for a further 30.7 +/- 2.8 s with room air, 18.6 +/- 1.7 s with N-2 and 11.8 +/- 1.8 s with 10% CO2 + 90% N-2. Despite the exaggerated chemoreceptor drive in the latter two conditions (hence the significantly shorter latencies to the subsequent asphyxic break point), the inhibition still occurred; moreover, there was no significant difference in duration of the inhibition of MSNA following the single breath of room air (7.6 +/- 0.7 s), N-2 (6.2 +/- 0.6 s) or 10% CO2 + 90% N2 (5.5 +/- 0.4 s). Following the resumption of breathing, however, the duration of MSNA inhibition (11.0 +/- 1.0 s) was significantly longer than that following a single breath. To investigate the involvement of chemoreceptors in the respiratory modulation of MSNA further, the same gases were used during an inspiratory-capacity apnoea, which causes a brief inhibition of MSNA during the inflation phase and a sustained increase during the hold phase. The duration of the apnoea was shortest after a breath of 10% O-2 + 90% N-2, but the latency until the bursts resumed after the inspiratory breath hold were similar for all gases, which suggests that there is no chemoreceptor involvement during the sympathetic silence seen during the inflation phase of inspiratory-capacity apnoeas. We conclude that neither peripheral nor central chemoreceptors are responsible for the inhibition of muscle vasoconstrictor drive following an end-expiratory apnoea or an end-inspiratory apnoea. Rather, we suggest that the inhibition is evoked by stretch receptors in the lungs and/or chest wall, which may also contribute to the longer inhibition associated with the hyperventilation following the subsequent resumption of rhythmic breathing

Increases in muscle sympathetic nerve activity, heart rate, respiration, and skin blood flow during passive viewing of exercise

The cardiovascular and respiratory effects of exercise have been widely studied, as have the autonomic effects of imagined and observed exercise. However, the effects of observed exercise in the first person have not been documented, nor have direct recordings of muscle sympathetic nerve activity (MSNA) been obtained during observed or imagined exercise. The aim of the current study was to measure blood pressure, heart rate, respiration, skin blood flow, sweat release, and MSNA (via microelectrodes inserted into the common peroneal nerve), during observation of exercise from the first person point of view. It was hypothesized that the moving stimuli would produce robust compensatory increases in the above-mentioned parameters as effectively as those generated by mental imagery and—to a lesser extent—actual exercise. Nine subjects watched a first-person running video, allowing them to view the action from the perspective of the runner rather than viewing someone else perform the exercise. On average, statistically significant increases from baseline during the running phase were seen in heart rate, respiratory rate, skin blood flow, and burst amplitude of MSNA. These results suggest that observation of exercise in the first person is a strong enough stimulus to evoke “physiologically appropriate” autonomic responses that have a purely psychogenic origin

Autonomic dysreflexia : somatosympathetic and viscerosympathetic vasoconstrictor responses to innocuous and noxious sensory stimulation below lesion in human spinal cord injury

Autonomic dysreflexia is a dangerous elevation in blood pressure in people with spinal cord injury (SCI), produced by a spinally-mediated reflex activation of sympathetic vasoconstrictor neurones supplying skeletal muscle and the gut. Current dogma states that, apart from visceral inputs - such as those originating from a distended bladder or impacted colon - autonomic dysreflexia is triggered by noxious inputs below the lesion. However, while selective stimulation of small-diameter afferents in muscle or skin evokes a sustained increase in muscle sympathetic nerve activity and blood pressure, and a transient increase in skin sympathetic nerve activity and decrease in skin blood flow in able-bodied subjects, such noxious inputs have no effects on blood pressure and skin blood flow in SCI individuals. Conversely, weak electrical stimulation over the abdominal wall, which in able-bodied subjects is not painful and activates large-diameter cutaneous afferents, causes a marked increase in blood pressure in SCI but not in able-bodied subjects. Moreover, vibration of the penis in spinal-injured men, which is not noxious, caused marked vasoconstriction and increases in blood pressure, similar to those produced by non-noxious distension of the bladder during urodynamics procedures. This suggests that activation of large-diameter somatic afferents, not small-diameter afferents, triggers the increases in vasoconstrictor drive that lead to autonomic dysreflexia, arguing against current dogma on the importance of noxious inputs in triggering autonomic dysreflexia

The effect of nitric oxide inhibition in spinal cord injured humans with and without preserved sympathetic control of the vasculature

Systemic pharmacological inhibition of nitric oxide (NO) causes a hypertensive response, which has been attributed both to inhibition of peripheral NO-mediated vasodilatation and to inhibition of central nervous NO-production leading to a later onset sympathetic vasoconstriction. In the present study we aimed to test the importance of these two mechanisms by comparing the time-courses of the hypertensive responses in spinal cord injured (SCI) subjects with varying degrees of loss of sympathetic vascular control depending on level of injury as well as able-bodied controls. We hypothesized that high level SCI with no sympathetic vasoconstrictor control would have an abbreviated time-course of the hypertensive response to the NO-inhibitor L-NAME, because they would lack the late onset sympathetic component to the hypertensive response. NO production was blocked in 12 subjects with SCI and 6 controls by intravenous infusion of L-NAME (1.55-2.7 mg/kg). We measured blood pressure, heart rate and vascular conductance in the carotid, brachial and femoral arteries before, during, and after 1 hour of L-NAME in a 4-hour protocol. Peak increases in mean arterial pressure were significantly larger in high level SCI vs controls: 32 ± 6 vs. 12 ± 2 mmHg (both groups received 1.55 mg/kg). The decreases in vascular conductance in the brachial and femoral vascular beds were also larger in the high level SCI group, whereas decreases in heart rate and carotid conductance were not significantly different between the groups. There were no indications of any abbreviated responses in blood pressure or vascular conductance in the high level SCI compared to control. The mid level and low-level SCI subject had responses similar to controls. These data confirm previous reports that NO inhibition causes a larger increase in blood pressure in high level SCI, and extend these data by providing evidence for differences in vascular conductance in the limbs. The current data do not support an obligatory important role for sympathetic vasoconstriction in maintaining the hypertensive response to L-NAME in humans

Cardiovascular variability in Parkinson's disease and extrapyramidal motor slowing

Objective Parkinson's disease (PD) is a degenerative neurological condition, associated with cardiovascular dysfunction. Many studies have utilised heart rate variability (HRV) to assess the autonomic nervous system in PD, but blood pressure variability (BPV) has received less attention. The purpose of the present study was to compare HRV and BPV between participants with established PD, extrapyramidal motor slowing (EPMS) (not reaching clinical criteria for PD), older healthy controls (OHC), and young healthy controls (YHC), in order to ascertain whether either of these measures can be used as an early marker of non-motor symptoms in PD. Methods HRVwas assessed at rest and during 2 min of slow deep breathing in 97 participants, divided into four groups: YHC (20-30 years; n = 19); OHC (67-83 years; n = 28); EPMS (59-91 years; n = 25) and PD (61-84 years; n = 25). Results Spectral analysis of blood pressure was performed on stable non-invasive recordings of blood pressure obtained in 76 of the participants. Low frequency (LF) and high frequency (HF) components, and the LF/HF ratio, were measured. Significant differences were only seen between the YHC and the three older groups. For HRV this was seen at rest and during 2 min of slow deep breathing, whereas for BPV this was only seen during 2 min of slow deep breathing. Interpretation These data indicate that there are only agerelated changes in HRV and BPV, and that neither technique is sensitive enough to provide an index of pre-clinical PD

Inter-individual responses to experimental muscle pain : baseline anxiety ratings and attitudes to pain do not determine the direction of the sympathetic response to tonic muscle pain in humans

We have recently shown that intramuscular infusion of hypertonic saline, causing pain lasting ~. 60. min, increases muscle sympathetic nerve activity (MSNA) in one group of subjects, yet decreases it in another. Across subjects these divergent sympathetic responses to long-lasting muscle pain are consistent over time and cannot be foreseen on the basis of baseline MSNA, blood pressure, heart rate or sex. We predicted that differences in anxiety or attitudes to pain may account for these differences. Psychometric measures were assessed prior to the induction of pain using the State and Trait Anxiety Inventory (STAI), Pain Vigilance and Awareness Questionnaire (PVAQ), Pain Anxiety Symptoms Scale (PASS) and Pain Catastrophising Scale (PCS); PCS was also administered after the experiment. MSNA was recorded from the common peroneal nerve, before and during a 45-minute intramuscular infusion of hypertonic saline solution into the tibialis anterior muscle of 66 awake human subjects. Forty-one subjects showed an increase in mean burst amplitude of MSNA (172.8. ±. 10.6%) while 25 showed a decrease (69.9. ±. 3.8%). None of the measured psychological parameters showed significant differences between the increasing and the decreasing groups. We conclude that inter-individual anxiety or pain attitudes do not determine whether MSNA increases or decreases during long-lasting experimental muscle pain in healthy human subjects

The effects of audiovisual distraction on the muscle sympathetic responses to experimental muscle pain

Pain elicited by intramuscular infusion of hypertonic saline solution causes muscle sympathetic nerve activity (MSNA) to increase in some subjects, yet decrease in others. Although the direction of the response is not predictable based on baseline physiological and psychological parameters, we know that it results from sustained functional changes in specific brain regions that are responsible for the behavioral and cardiovascular responses to psychological stressors, as well as those involved in attention. The aim of this study was to investigate whether MSNA responses to experimental muscle pain in humans could be altered with an audiovisual stimulus that served to distract them from the pain. MSNA was recorded from the left common peroneal nerve of 20 young healthy individuals during a 45-min intramuscular infusion of hypertonic saline solution into the ipsilateral tibialis anterior muscle. The distracting stimulus commenced 15 min after the start of the infusion and lasted for 15 min. Fifteen subjects showed an increase in mean burst amplitude of MSNA (to 176.4 ± 7.9% of baseline), while five showed a decrease (to 73.1 ± 5.2% of baseline); distraction had no effect on these profiles. These results indicate that even though the subjects were attending to the audiovisual stimulus, and were presumably distracted from the pain, it failed to alter the MSNA responses to muscle pain

Sympathetic baroreflex sensitivity is inversely related to vascular transduction in men but not women

Sympathetic baroreflex sensitivity (BRS) is a measure of how effectively the baroreflex buffers beat-to-beat changes in blood pressure through the modulation of muscle sympathetic nerve activity (MSNA). However, current methods of assessment do not take into account the transduction of sympathetic nerve activity at the level of the vasculature, which is known to vary between individuals. In this study we tested the hypothesis that there is an inverse relationship between sympathetic BRS and vascular transduction. In 38 (18 men) healthy adults, continuous measurements of blood pressure, MSNA and superficial femoral artery diameter and blood flow (Doppler ultrasound) were recorded during 10 min of rest. Spontaneous sympathetic BRS was quantified as the relationship between diastolic pressure and MSNA burst incidence. Vascular transduction was quantified by plotting the changes in leg vascular conductance for 10 cardiac cycles following each burst of MSNA, and taking the nadir. In men, sympathetic BRS was inversely related to vascular transduction (r= -0.49; P = 0.04). However, this relationship was not present in women (r= -0.17; P = 0.47). To conclude, an interaction exists between sympathetic BRS and vascular transduction in healthy men, such that men with high sympathetic BRS have low vascular transduction and vice versa. This may be to ensure that blood pressure is regulated effectively, although further research is needed to explore what mechanisms are involved and examine why this relationship was not apparent in women