Skin sympathetic nerve activity and effector function during sleep in humans

Multi-unit sympathetic skin nerve activity (SSA) in the peroneal nerve was recorded together with electrical skin resistance, skin blood flow and (in some subjects) finger blood pressure during sleep in 22 sleep-deprived healthy subjects. The average strength of sympathetic activity in different sleep stages was measured during 5-min periods as the area-under-curve of the integrated neurogram. Stage 2 sleep was reached by 15 subjects, stages 3–4 by nine and rapid eye movement (REM) sleep by six subjects. Non-REM sleep was always associated with an increased skin resistance, which was larger in glabrous than in hairy skin (293±48 vs. 175±4% of awake control level, n= 10, P < 0.05). Skin blood flow also increased during sleep, with a mean maximal increase of 397±79% of the awake control level (n= 11, P < 0.05). In spite of these changes of effector function no significant difference in mean SSA was found between the awake control period and periods of non-REM sleep, but during REM sleep SSA increased with 34% (P < 0.05) compared with the immediately preceding stage 2 period. In stage 2 sleep, K-complexes were associated with bursts of SSA followed by transient changes of skin resistance, blood flow and arterial blood pressure. When both skin resistance and blood flow were recorded within the innervation area of the impaled fascicle, single bursts or short periods of increased SSA could be succeeded by increased skin blood flow without concomitant skin resistance change. This indicates the existence of specific sympathetic vasodilator fibres in the skin. Therefore the unchanged strength of multiunit SSA during non-REM sleep in the face of increases of skin resistance and blood flow may be a consequence of an increased sympathetic vasodilator nerve activity combined with decreases of vasoconstrictor and sudomotor traffic.     

Central blood volume influences sympathetic sudomotor nerve traffic in warm humans

The objective of this study was to test whether changes in central blood volume can induce reflex effects on sweating. Multi-unit skin sympathetic nerve activity (SSA) was recorded from the posterior cutaneous nerve of the forearm or radial nerve branches in 11 healthy volunteers. Skin electrical resistance and skin blood flow were recorded in the area innervated by the impaled nerve fascicle. Sudomotor nerve traffic and sweating was induced by whole body heating. Lower body negative pressure (LBNP) and tilting (3d? head up) was used for blood volume displacement from the chest to the lower body. Low levels of LBNP (5 and 10 mmHg) had no effect on blood pressure, heart rate or skin blood flow but induced a prompt inhibition of SSA and a reduced number of transient skin resistance changes (n= 9), both rapidly returning to control levels after cessation of LBNP. Quantitatively, the effect was similar at both levels of LBNP. Head up tilting also reduced SSA (n= 3, tilt manoeuvres). A capacity for mental stress-induced SSA increase remained during LBNP. Spontaneous flucturations in blood pressure did not affect SSA, arguing against arterial (high-pressure) baroreceptors modulating SSA. Consequently, the present results indicate that unloading of cardiopulmonary (low-pressure) volume receptors reduces sympathetic sudomotor nerve traffic and sweating in warm subjects. It is suggested that the reflex contributes to counteracting hypovolaemia.     

Experimental studies on the effects of vibration and noise on sympathetic nerve activity in skin

Summary Multi-unit sympathetic activity was recorded at elbow level from median nerve fascicles supplying glabrous skin of the left hand in five healthy subjects. The resultant vasomotor responses accompanying the neural activity were monitored by simultaneous recordings of skin blood flow using the laser doppler method and skin temperature in the innervation zones. No significant change in sympathetic activity was observed during handgrip exercise of the right hand under a constant gripping force of 2 kg. Subjects maintained the same gripping force of the right hand during exposure in random order to local vibration and/or noise, each type of exposure lasting 5 min with intervals of 20 min. A two-peaked significant increase in outflow from sympathetic nerves was observed during local exposure of the right hand to vibration with a frequency of 60 Hz and an acceleration of 50 m·s^–2, followed by a postexposure period which revealed a relative suppression of sympathetic nerve activity and a significant increase in blood flow. Noise at 100 dB(A) showed only an initial effect on skin sympathetic nerve activity (SSA), whereas when combined with local vibration at 60 Hz, a pronounced increase in neural activity was noticed, indicating a combined effect of vibration and noise. These results from direct recordings of SSA suggest a sympathetic vasomotor reflex mechanism triggered by local vibration stimuli to the hand.     

Mechanisms of cutaneous vasoconstriction during upright posture

The cutaneous circulation is thought to participate in the neurocirculatory adjustments during orthostatic stress, but the underlying mechanisms mediating such reflex cutaneous vasoconstriction are poorly understood. The aim of this study was to assess the relative importance of baroreceptor (cardiopulmonary and arterial) and positional (vestibular, exercise, veno-arteriolar and myogenic) reflexes in triggering cutaneous vasoconstriction during upright posture. First, hypotensive lower body negative pressure (LBNP) was compared with actual postural changes to assess the relative contributions of baroreceptor reflexes and positional reflexes. Then changes in body position were compared with changes in limb position in the absence or presence of proximal (axillary) or distal (local cutaneous) nerve blocks, to assess the relative contributions of vestibular, exercise, veno-arteriolar and myogenic reflexes. Skin sympathetic nerve activity was determined by microneurography, and skin blood flow was determined by laser Doppler velocimetry. LBNP of –50 mmHg (cardiopulmonary + arterial baroreceptors) had no effect on skin sympathetic nerve activity or skin vascular resistance. In contrast, an upright posture with the arms dependent (baroreceptor+vestibular+exercise+veno-arteriolar reflexes) caused a two- to threefold increase in skin vascular resistance. In the supine position, passive movement of the arm into a dependent position to activate veno-arteriolar reflexes alone evoked an increase in skin vascular resistance which approximated the response to normal upright posture. Blocking central sympathetic nerve impulses by application of an axillary blockade did not influence the cutaneous vasoconstrictor response to an upright posture or changes in limb position. In contrast, application of a distal nerve block by local cutaneous surface anaesthesia completely blocked vasoconstrictor responses evoked by these manoeuvres. In conclusion, these experiments in human subjects identify a primary role for veno-arteriolar reflexes in triggering vasoconstriction in the cutaneous circulation during upright posture.     

Excitotoxic injury to thoracolumbar gray matter alters sympathetic activation and thermal pain sensitivity

Studies of humans, monkeys and rodents have implicated combined gray and white matter damage as important for development of chronic pain following spinal cord injury (SCI). Below-level chronic pain and hyperalgesia following injury to the spinal white matter, including the spinothalamic tract (STT), can be enhanced by excitotoxic influences within the gray matter at the site of SCI. Also, excitotoxic injury of thoracic gray matter without interruption of the STT results in below-level heat hyperalgesia. The present study evaluates the possibility that thoracolumbar gray matter injury increases sensitivity to nociceptive heat stimulation by altering spinal sympathetic outflow. Thermal preferences of rats for heat (45 °C) versus cold (15 °C) were evaluated before and after thoracolumbar injections of quisqualic acid (QUIS). A pre-injury preference for heat changed to a post-injury preference for cold. Systemic activation of the sympathetic nervous system by restraint stress decreased the heat preference pre-injury and increased the cold preference post-injury. The heat aversive effect of stress was magnified and prolonged post-injury, compared to pre-injury. Also, peripheral sympathetic activation by nociceptive stimulation was evaluated pre- and post-injury by measuring thermal transfer through a hindpaw during stimulation with 44.5 °C. Skin temperature recordings revealed enhanced sympathetic activation by nociceptive heat stimulation following spinal QUIS injury. However, increased sympathetic activation with peripheral vasoconstriction should enhance cold aversion, in contrast to the observed increase in heat aversion. Thus, peripheral sympathetic vasoconstriction can be ruled out as a mechanism for heat hyperalgesia following excitotoxic gray matter injury.     

Cardiovascular responses to cold-water immersions of the forearm and face, and their relationship to apnoea

Apnoea as well as cold stimulation of the face or the extremities elicits marked cardiovascular reflexes in humans. The purpose of this study was to investigate whether forearm immersion in cold water has any effect on the cardiovascular responses to face immersion and apnoea. We recorded cardiovascular responses to cold-water immersions of the forearm and face in 19 (part I) and 23 subjects (part II). The experimental protocol was divided in two parts, each part containing four tests: I₁, forearm immersion during eupnoea; I₂, face immersion during eupnoea; I₃, forearm and face immersion during eupnoea; I₄, face immersion during apnoea; II₁, apnoea without immersion; II₂, forearm immersion during apnoea; II₃, face immersion during apnoea; and II₄, forearm and face immersion during apnoea. The water temperature was 9–11 °C. Cold-water immersion of either the forearm or face was enough to elicit the most pronounced thermoregulatory vasoconstriction during both eupnoea and apnoea. During eupnoea, heart rate responses to forearm immersion (3% increase) and face immersion (9% decrease) were additive during concurrent stimulation (3% decrease). During apnoea, the heart rate responses were not affected by the forearm immersion. The oxygen-conserving diving response seems to dominate over thermoregulatory responses in the threat of asphyxia. During breathing, however, the diving response serves no purpose and does not set thermoregulatory adjustments aside. Accepted: 18 July 2000     

Hematological response and diving response during apnea and apnea with face immersion

Increased hematocrit (Hct) attributable to splenic contraction accompanies human apneic diving or apnea with face immersion. Apnea also causes heart rate reduction and peripheral vasoconstriction, i.e., a cardiovascular diving response, which is augmented by face immersion. The aim was to study the role of apnea and facial immersion in the initiation of the hematological response and to relate this to the cardiovascular diving response and its oxygen conservation during repeated apneas. Seven male volunteers performed two series of five apneas of fixed near-maximal duration: one series in air (A) and the other with facial immersion in 10°C water (FIA). Apneas were spaced by 2 min and series by 20 min of rest. Venous blood samples, taken before and after each apnea, were analysed for Hct, hemoglobin concentration (Hb), lactic acid, blood gases and pH. Heart rate, skin capillary blood flow and arterial oxygen saturation were continuously measured non-invasively. A transient increase of Hct and Hb by approximately 4% developed progressively across both series. As no increase of the response resulted with face immersion, we concluded that the apnea, or its consequences, is the major stimulus evoking splenic contraction. An augmented cardiovascular diving response occurred during FIA compared to A. Arterial oxygen saturation remained higher, venous oxygen stores were more depleted and lactic acid accumulation was higher across the FIA series, indicating oxygen conservation with the more powerful diving response. This study shows that the hematological response is not involved in causing the difference in oxygen saturation between apnea and apnea with face immersion.     

Changes in muscle sympathetic nerve activity and calf blood flow during static handgrip exercise

Summary To test the function of sympathetic vascoconstrictor nerves on blood flow in resting limbs during static muscle contraction, muscle sympathetic nerve activity (MSNA) to the leg muscle was recorded from the tibial nerve microneurographically before, during and after 2 min of static handgrip (SHG). Simultaneously, calf blood flow (CBF) was measured by strain gauge plethysmography. An increase in MSNA, a decrease in CBF and an increase in calf vascular resistance (CVR) in the same resting limb occurred concomitantly during SHG. However, the increase in CVR was blunted in the second minute of handgrip when MSNA was still increasing. The results indicated that the decrease of CBF during SHG reflects the increase in MSNA, while the dissociation between MSNA and CVR at the later period of SHG may be related to metabolic change produced by the vasoconstriction.     

The cold pressor test: effects on sympathetic nerve activity in human muscle and skin nerve fascicles

Micro-electrode multi-unit recordings of muscle nerve sympathetic activity (MSA) involved in cardiovascular homeostasis or skin nerve sympathetic activity (SSA) involved in thermoregulation were made in the right peroneal nerve of 48 healthy volunteers during performance of the cold pressor test, i.e. immersion of one hand in ice water (2 +/- 0.5 degrees C) for 1 min. Eleven subjects underwent the same procedure on a second MSA recording occasion. As a rule, immersion evoked an increase in MSA, with a gradual decrease on emersion. The response showed a wide range of variation between and within subjects; the intra-individual difference between first and second immersion on the same recording occasion was up to sevenfold, and from first to second recording up to fivefold. The increase in MSA correlated with the degree of discomfort from the ice water. In nine subjects with a large increase in MSA on ice water immersion, intracutaneous painful electrical stimulation to a level equalling the discomfort from the ice water was added, but it was not accompanied by any change in MSA. The increase in MSA was accompanied by and correlated quite well with an increase in blood pressure. Intra-arterial blood pressure recordings showed that MSA occurred at pressure levels normally associated with total inhibition of MSA, and that an inverse linear relationship between diastolic blood pressure and MSA at rest was abolished during the ice water immersion. SSA showed no consistent change with ice water immersion. It is concluded that the cold pressor test is a powerful activator of MSA, i.e. baroreceptor-governed vasoconstrictor outflow; that MSA contributes to the blood pressure elevation with this manoeuvre; that MSA operates at another blood pressure level during the manoeuvre and that the baroreflex inhibitory level consequently is changed; and that the response is not a reaction to pain only.     

Biphasic effects of tonic stimulation of muscle nociceptors on skin sympathetic nerve activity in human subjects

Skin sympathetic nerve activity (SSNA) controls skin blood flow and sweat release, and acute noxious stimulation of skin has been shown to cause a decrease in SSNA in the anaesthetised or spinal cat. In awake human subjects, acute muscle pain causes a transient rise in SSNA, but the impact of long-lasting (tonic) stimulation of muscle nociceptors on skin sympathetic outflow, blood flow and sweat release is unknown. We tested the hypothesis that tonic stimulation of muscle nociceptors causes a sustained increase in sympathetic outflow to the skin. SSNA was recorded from the common peroneal nerve of 10 awake human subjects. Tonic muscle pain was induced by infusing hypertonic saline (7 %) into the tibialis anterior muscle over ~40 min, titrated to achieve a constant level of muscle pain. SSNA initially increased following the onset of the infusion, reaching a peak of 164 % of baseline within 5 min, but then showed a prolonged and sustained decrease, reaching a nadir of 77 % in 20 min. Conversely, skin blood flow (and vascular conductance) initially decreased, followed by a progressive increase; there were no consistent changes in sweat release. In 9 of 10 subjects, SSNA and skin blood flow were inversely related. We conclude that sympathetic outflow to the skin exhibits a biphasic response to long-lasting stimulation of muscle nociceptors: an initial increase presumably related to the ‘arousal’ or ‘alerting’ component of pain, characterised by increased SSNA and decreased skin blood flow, followed by a prolonged decrease in SSNA and increased skin blood flow. The latter may be a purposeful response that contributes to wound healing.     

Effects of lung volume and involuntary breathing movements on the human diving response

The effects of lung volume and involuntary breathing movements on the human diving response were studied in 17 breath-hold divers. Each subject performed maximal effort apnoeas and simulated dives by apnoea and cold water face immersion, at lung volumes of 60%, 85%, and 100% of prone vital capacity (VC). Time of apnoea, blood pressure, heart rate, skin capillary blood flow, and fractions of end-expiratory CO₂ and O₂ were measured. The length of the simulated dives was the shortest at 60% of VC, probably because at this level the build up of alveolar CO₂ was fastest. Apnoeas with face immersion at 100% of VC gave a marked drop in arterial pressure during the initial 20?s, probably due to high intrathoracic pressure mechanically reducing venous return. The diving response was most pronounced at 60% of VC. We concluded that at the two larger lung volumes both mechanical factors and input from pulmonary stretch receptors influenced the bradycardia and vasoconstriction, resulting in a non-linear relationship between the breath-hold lung volume and magnitude of the diving response in the near-VC range. Furthermore, the involuntary breathing movements that appeared during the struggle phase of the apnoeas were too small to affect the diving response.     

Manoeuvres Affecting Sympathetic Outflow in Human Muscle Nerves

Multi-unit sympathetic activity was recorded in human muscle nerves, together with measurements of intra-arterial blood pressure and forearm or calf blood flow, during manoeuvres causing circulatory adjustments. Manoeuvres causing an increased vascular resistance in the forearm or calf were regularly associated with an increase in sympathetic outflow, proving that the neural activity was dominated by vasoconstrictor impulses. The inverse changes of blood pressure and sympathetic activity observed during Valsalva's manoeuvre and mental stress are explicable in terms of baroreflex control of the neural outflow. However, during muscle work and hyperventilation the relation between blood pressure and sympathetic activity was more complex, indicating that the baroreflex influence was superimposed or modified by other regulatory mechanisms. Some manoeuvres known to affect sympathetic outflow in skin nerves caused no appreciable change in sympathetic muscle nerve activity.     

Exercise-induced myofibrillar disruption with sarcolemmal integrity prior to simulated diving has no effect on vascular bubble formation in rats

Decompression sickness is initiated by gas bubbles formed during decompression, and it has been generally accepted that exercise before decompression causes increased bubble formation. There are indications that exercise-induced muscle injury seems to be involved. Trauma-induced skeletal muscle injury and vigorous exercise that could theoretically injure muscle tissues before decompression have each been shown to result in profuse bubble formation. Based on these findings, we hypothesized that exercise-induced skeletal muscle injury prior to decompression from diving would cause increase of vascular bubbles and lower survival rates after decompression. In this study, we examined muscle injury caused by eccentric exercise in rats prior to simulated diving and we observed the resulting bubble formation. Female Sprague–Dawley rats (n = 42) ran downhill (?16º) for 100 min on a treadmill followed by 90 min rest before a 50-min simulated saturation dive (709 kPa) in a pressure chamber. Muscle injury was evaluated by immunohistochemistry and qPCR, and vascular bubbles after diving were detected by ultrasonic imaging. The exercise protocol resulted in increased mRNA expression of markers of muscle injury; αB-crystallin, NF-κB, and TNF-α, and myofibrillar disruption with preserved sarcolemmal integrity. Despite evident myofibrillar disruption after eccentric exercise, no differences in bubble amounts or survival rates were observed in the exercised animals as compared to non-exercised animals after diving, a novel finding that may be applicable to humans.     

Inhibition of nitric oxide synthase evokes central sympatho-excitation in healthy humans

Animal studies have indicated that nitric oxide is a key signalling molecule involved in the tonic restraint of central sympathetic outflow from the brainstem. Extension of these findings to humans has been difficult because systemic infusion of nitric oxide synthase (NOS) inhibitors increases blood pressure due to inhibition of endothelial NOS, resulting in activation of the arterial baroreflex and subsequent inhibition of central sympathetic outflow. To overcome this confounding inhibitory influence of the baroreflex, in the current study we directly measured skin sympathetic nerve activity (SNA), which is not under baroreceptor control. Healthy, normotensive humans were studied before, during a 60 min intravenous infusion of the NOS inhibitor N ^G-nitro- l -arginine methyl ester ( l -NAME; 4 mg kg⁻¹), and for 120 min following the infusion (i.e. 180 min total). Skin SNA and arterial blood pressure (BP) were continuously measured. BP was increased from baseline at the end of the l -NAME infusion (Δ14 ± 2 mmHg; P < 0.05) and remained significantly elevated for the remainder of the experiment (Δ18 ± 3 mmHg; P < 0.05). Similarly, systemic NOS inhibition produced time-dependent increases in skin SNA, such that skin SNA was elevated at the end of the l -NAME infusion (total activity, 200 ± 22% baseline; P = 0.08) and was further increased at the end of the study protocol (total activity, 350 ± 41% baseline; P < 0.05). Importantly, skin SNA remained unchanged during time and hypertensive (phenylephrine) control experiments. These findings indicate that pharmacological inhibition of NOS causes sympathetic activation and support a role of nitric oxide in central sympathetic control in humans.     

Absence of short-term vestibular modulation of muscle sympathetic outflow,assessed by brief galvanic vestibular stimulation in awake human subjects

There is evidence in experimental animals for a potent vestibulosympathetic reflex, but its existence in humans is controversial. Static head-down neck flexion and off-vertical axis rotation have been shown to increase muscle sympathetic nerve activity (MSNA), but not skin sympathetic nerve activity (SSNA), whereas horizontal linear acceleration decreases MSNA in humans. However, both forms of stimuli also activate other receptors. To examine the effects of a pure vestibular stimulus on MSNA and SSNA, and its potential interaction with the baroreceptors, we used galvanic vestibular stimulation (GVS) in 12 healthy seated subjects. MSNA was recorded in ten subjects via a percutaneous microelectrode in the peroneal nerve; ECG, blood pressure, respiration, skin blood flow and sweating were also recorded. GVS (2 mA, 1 s pulse) was delivered via surface electrodes over the mastoid processes at unexpected times, triggered from the R-wave with a delay of 0, 200, 400 or 600 ms. In addition to causing robust postural illusions, GVS caused cutaneous vasoconstriction and sweat release in all subjects (due to a short-latency increase in SSNA, three subjects), but no significant change in MSNA. The failure of GVS to elicit a change in muscle sympathetic nerve activity, as documented by averaging, suggests that the vestibular system is not engaged in short-term modulation of muscle sympathetic activity. Conversely, phasic vestibular inputs do excite cutaneous sympathetic neurones, consistent with the observation that motion sickness is accompanied by pallor and sweating.     

The effect of transcutaneous electrical nerve stimulation on sympathetic skin response

The aim of present study was to determine whether combination of transcutaneous electrical nerve stimulation (TENS) and acupuncture inhibits sympathetic nerve activity in healthy humans. Multiunit efferent postganglionic sympathetic activity was recorded with Toennies set. In this study, the aim was to obtain latency, amplitude and duration of sympathetic skin response (SSR) and skin temperature (ST) from both hands in 15 healthy subjects. Subjects randomly assigned and everybody participated in all the three groups [Control Group (CG), Acupuncture Group (AG) and Nerve Stimulation Group (NSG)]. TENS (2 Hz, 250 microsecond) was applied over the median nerve of the right elbow in NSG for 20 min, either, TENS was applied over (HE-7) point of the right hand in CG (TENS off) and AG (TENS on) for 20 min. SSR (lat, amp, dur) and ST data was recorded before TENS and for immediate, 5 min and 10 min post--TENS. ST was recorded in distal phalanx of index finger of both hands and SSR was recorded from both hands. TENS in CG did not affect ST and SSR following stimulation. TENS applied at AG and NSG caused a significant increase in ST (P = 0.001), significant increase in latency of SSR (P = 0.001), significant decrease in amplitude of SSR (P = 0.001) and no significant changes were observed in duration of SSR (P > 0.05). Then statistical analysis showed differences between both of groups (AG & NSG) for ST and SSR post--TENS. Transcutaneous electrical nerve stimulation inhibits sympathetic nerve activity in healthy humans.     

Pulmonary gas exchange is reduced by the cardiovascular diving response in resting humans

The diving response reduces the pulmonary O(2) uptake in exercising humans, but it has been debated whether this effect is present at rest. Therefore, respiratory and cardiovascular responses were recorded in 16 resting subjects, performing apnea in air and apnea with face immersion in cold water (10 degrees C). Duration of apneas were predetermined to be identical in both conditions (average: 145 s) and based on individual maximal capacity (average: 184 s). Compared to apnea in air, an augmented diving response was elicited by apnea with face immersion. The O(2) uptake from the lungs was reduced compared to the resting eupneic control (4.6 ml min(-1)kg(-1)), during apnea in air (3.6 ml min(-1)kg(-1)) and even more so during apnea with face immersion (3.4 ml min(-1)kg(-1)). We conclude that the cardiovascular adjustments of the diving response reduces pulmonary gas exchange in resting humans, allowing longer apneas by preserving the lungs' O(2) store for use by vital organs.     

Resting discharge of human muscle spindles is not modulated by increases in sympathetic drive

There is evidence in experimental animals that, in addition to receiving fusimotor drive, muscle spindles are subject to modulation by the sympathetic nervous system. We examined the validity of this idea in human subjects by recording from muscle spindles in the relaxed ankle and toe extensor muscles during a strong and sustained physiological activation of muscle sympathetic outflow. Unitary recordings were made from 20 primary and 17 secondary muscle spindle afferents via a tungsten microelectrode inserted percutaneously into the peroneal nerve in 10 awake, healthy subjects seated with the legs supported in the extended position. ECG, blood pressure, respiration and calf circumference were also recorded. The majority of the muscle spindles were spontaneously active at rest; a background discharge was induced in four silent spindles by vibrating the tendon. A sustained increase in muscle vasoconstrictor activity, an increase in calf volume and a fall in pulse pressure were produced by subjects performing a 30-40 s maximal inspiratory breath-hold. Despite this strong increase in muscle sympathetic outflow no significant changes occurred in the discharge of either primary or secondary muscle spindle afferents, measured as a change in mean frequency and variability over sequential 5 s epochs and compared with the preceding period of rest. Strong chemoreceptor-driven sympathetic bursts during sustained expiratory breath-holds also failed to modulate the firing of 14 spindle endings. We conclude that a sustained, physiological increase in muscle sympathetic activity causes no detectable change in muscle spindle firing, lending no support to the concept that the sympathetic nervous system can influence the sensitivity of human muscle spindles directly.     

Cardiovascular responses elicited by different simulated diving manoeuvres

It has been documented that placing an ice-bag on the forehead causes similar cardiac and vascular responses as face immersion. There has been disagreement concerning the contribution of separate cold stimulation on the face and breathholding in the diving response. This study set out to unravel the extent to which these two factors contribute individually to the observed cardiovascular changes during the combined manoeuvre. It further aimed to reveal whether peripheral vascular responses to these stimuli are different in forearm and calf. We observed a significant rapid increase in the RR-interval, which was maintained until the end of the 25-s observation period and a homogeneous vasoconstriction in forearm and calf, despite minor changes in arterial blood pressure, during breathholding, placing the icebag on the forehead and the combined stimuli. Cardiac and peripheral vascular responses to the combined manoeuvre did not differ significantly from the responses elicitated by the two stimuli separately. This test is another example that illustrates the heterogeneous cardiovascular response involving both parasympathetic and sympathetic activation. Moreover, since the icebag on the forehead test is technically easy to perform and does not require the active co-operation of the patient, it may be a valid method to replace a full face immersion test accompanied by breathholding.     

Cardiovascular responses to face immersion and apnea during steady state muscle exercise. A heart catheterization study on humans

The cardiovascular adjustments to face immersion and apnea (FIA) in human beings during steady-state muscle exercise (163 and 98 watt) have been investigated. Using a triple lumen flow directed catheter inserted into the pulmonary artery we were able to measure cardiac output (CO) by thermodilution technique, pulmonary arterial pressure (PPA) right atrial pressure (PRA) and left ventricular filling pressure (PAD). Phasic arterial blood pressure (BP) was measured via a cannula in the radial artery. A 12 lead ECG was recorded continuously. FIA caused an immediate rise in BP (median 61%), the highest level being 25.33 kPa. CO during the last half of FIA was reduced by 49% (range 46-59, n = 7) systemic vascular resistance increased by median 200% (range 111-280). Myocardial oxygen demand determined by the heart rate pressure double product fell from median 33.6 to 16.8 (163 W) and 28.5 to 19.1 (98 W) given as beats/min X kPa X 10(2). Mean reduction was by 42%. PPA and PRA immediately increased and remained constant until a further pronounced increase was seen towards the end of FIA when pulmonary vascular resistance (PVR) went up. PACO2 and PAO2 at the end of 30 sec FIA (163 W) was 10.0 and 5.6 kPa, respectively, values which expectedly would cause pulmonary vasoconstriction. Our findings demonstrate that humans are able to make principally the same cardiovascular adjustments to diving as aquatic mammals, although the response patterns are slower and less efficient.(ABSTRACT TRUNCATED AT 250 WORDS)