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J Appl Physiol 87: 830-834, 1999;
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Vol. 87, Issue 2, 830-834, August 1999

Slowing and attenuation of baroreflex heart rate control with nitrous oxide in exercising men

A. Östlund and D. Linnarsson

Section of Environmental Physiology, Department of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden


    ABSTRACT
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The objective of the present study was to determine whether mild inert-gas narcosis impairs cardiovascular control mechanisms and contributes to the relative bradycardia that occurs in humans exercising in a hyperbaric environment. Eight healthy subjects were exposed to a normoxic 30% nitrous oxide (N2O) mixture and an air control during dynamic exercise of 100-W intensity. Beat-by-beat heart rate (HR) and invasive arterial blood pressure measurements were made. The sensitivity and the response latency of the arterial-cardiac-chronotropic baroreflex were determined from repeated blood pressure and HR transients induced by rapid tilts between the upright and supine posture. A significant increase (37%, P <=  0.02) of latency in baroreflex responses was found with 30% N2O, as well as a significant depression (16%, P <=  0.05) in baroreflex sensitivity. There were no differences between air and N2O in steady-state HR or arterial pressure. We conclude that mild inert-gas narcosis increases the latency and decreases the gain of HR responses to arterial baroreflex stimuli, but this cannot in itself account for the modest, relative bradycardia observed during moderately heavy exercise in a normoxic, hyperbaric environment.

inert-gas narcosis; sedation; orthostatis; blood pressure; chronotropic control


    INTRODUCTION
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INTRODUCTION
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THE COMBINATION OF EXERCISE and some degree of inert-gas narcosis always occurs in air-breathing divers who swim at depths >25 m. Also, in very deep diving, with the use of helium-oxygen gas mixtures, narcotic partial pressures of N2 are added in the breathing gas to alleviate manifestations of high-pressure nervous syndrome (3). The present study addresses the question of whether mild-to-moderate levels of inert-gas narcosis have potentially unfavorable effects on cardiovascular control in exercising humans. Ebert (5) found that moderate inert-gas narcosis with nitrous oxide (N2O) reduced the sensitivity of the carotid-cardiac-chronotropic baroreflex to hypotensive stimuli in resting men, and a recent study from our laboratory lends support to that finding (19). A reduced baroreflex sensitivity may be a disadvantage in many situations, where external stimuli, such as transition from water immersion to dry, or variations in, airway pressure, influence the distribution and pressures of blood in the systemic and pulmonary circulations.

Changes in arterial baroreflex function may also have an impact on the modest relative bradycardia with maintained arterial pressure that is consistently observed in exercising humans in hyperbaria (8, 13). We base this on the notion that the arterial baroreflex during exercise is reset to a higher target level for arterial pressure and that the arterial-cardiac baroreflex contributes to exercise tachycardia as one of the means of compensating for a centrally perceived hypotension relative to the increased target level (24). Fagraeus et al. (9) found that the relative bradycardia in men who exercised in hyperbaric air had at least two components: one that could be ascribed to hyperoxia, and another component that must be related to some other aspect of the hyperbaric environment, whether it be increased hydrostatic pressure, increased gas density, inert-gas narcosis, or perhaps all three. Studying exercising subjects breathing normoxic gas mixtures with different combinations of hydrostatic pressure and inert-gas composition, we (unpublished observations) found that combined inert-gas narcosis and increased gas density contributed to the hyperbaric bradycardia. In the present study, we have used N2O as a model of hyperbaric N2, with N2O being 25-40 times more narcotic per unit partial pressure than N2 (3, 17). We hypothesized that partial pressures of N2O that induce significant impairments of psychomotor performance (17) and temperature control (16) would also influence the control of heart rate (HR) by slowing and/or attenuating the information processing involved in the arterial-cardiac-chronotropic baroreflex.


    METHODS
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Subjects. Eight healthy male volunteers were studied on two occasions. Age, weight, and height ranges were 22-31 yr, 68-98 kg, and 177-194 cm, respectively. The experimental protocol utilized in the present study was approved by the Ethics Committee of Karolinska Institutet. The subjects were instructed to abstain from caffeine and nicotine on the day of the experiment.

Breathing mixture and gas analysis. The two gas mixtures used were air for control and a mildly narcotic gas mixture that was composed of 21% O2 + 30% N2O + 49% N2. This N2O level corresponds to 29% of minimum alveolar concentration for surgical anesthesia. In terms of impairment of psychomotor performance, 30% N2O is equivalent to the narcotic potency of compressed air at a seawater depth of ~45-90 m (2, 17).

Subjects breathed the gas mixtures from a low-resistance demand regulator system. Inspired and end-expired N2O and CO2 fractional concentrations were monitored with a quadrupole mass spectrometer (Balzer QMG 420 as modified for respiratory use by Innovision A/S, Odense, Denmark). Subjects breathed through a mouthpiece and wore a noseclip. A 5-min period of washin was allowed before measurements were initiated, enabling the subjects to reach a steady-state end-tidal N2O level.

Procedures and experimental design. The subjects performed dynamic leg exercise on a tilt board on which an ergometer (type 380B, Siemens-Elema) was mounted with the crank axis at the level of the heart when the subjects were supine. The tilt board could be rapidly tilted within 2 s between 80° upright and horizontal (0°) or the reverse.

The subjects exercised at a 100-W workload. They started with a warm-up and washin period of 5 min in the upright position, followed by a 5-min recording time, after which they were tilted from 80 to 0° (down tilt) without prior notice for a 7-min period in the supine position and then back from 0 to 80° (up tilt). During the next 14 min of exercise, the tilt board was changed between upright and supine every 2 min, making a total of four down tilts and four up tilts during the session.

Each subject performed the described procedure twice: one session breathing air and one session breathing the 30% N2O mixture. Four of the subjects started with the air control, whereas the other four started with the N2O-breathing condition. The two sessions were separated by a 70-min resting time.

Cardiovascular measurements. HR was obtained beat by beat from a precordial electrocardiogram (Gould Biotach Amplifier 13-4615-65A). Arterial blood pressure was continuously recorded by a catheter placed in the radial artery and connected to a pressure transducer (DPT6003, Pvb Medizintechnik) attached to the chest in the midaxillary line at the level of the fourth intercostal space and by a blood pressure monitor (Hellige Servomed SMK 154-9). To obtain the arterial blood pressure at the carotid sinus, we used a second pressure transducer attached to the same site to measure the difference in hydrostatic pressure between heart level and the level of the carotid sinus in a fluid-filled tube. The blood pressure transducer was calibrated against a saline-filled tube of known height, and the carotid-level transducer was calibrated against a known vertical distance.

Data recording and analysis. Calibrated data were stored and subsequently analyzed by using an Acknowledge 3.2 Biopac digital data-handling system (Goleta, CA). The following variables were recorded at a sampling frequency of 100 Hz per channel: electrocardiogram, beat-by-beat HR, continuous arterial pressure, inspiratory flow, and inspiratory and expiratory concentrations of O2, CO2, and N2O. Off-line, beat-by-beat mean arterial pressure (MAP) at heart level was computed as the mean value between two systolic peaks, and mean carotid distending pressure (CDP) was computed similarly from the arterial pressure signal minus the heart-carotid difference in hydrostatic pressure. Each recording period with air or N2O mixture lasted 31 min, and a 5-min warm-up and washin period was allowed before data were used for calculations.

Analysis of arterial baroreflex control of HR. The sensitivity of arterial-cardiac-chronotropic responses was computed as
&Dgr;HR<SUB>max</SUB>/&Dgr;CDP<SUB>max</SUB>
where Delta HRmax is the maximum HR change and Delta CDPmax is the maximum change in CDP in response to up or down tilts (Fig. 1) (15). Both carotid and aortic baroreceptors are stimulated during a tilt with pressure changes of the same direction and timing but with lower amplitudes at the aortic site. A modeling study under similar experimental conditions as this study suggests that arterial baroreflex responses can account for 90% of Delta HRmax (15). Changes in arterial pulse pressure and stimulation of cardiopulmonary baroreceptors may be additional inputs to HR control during the transients between upright and supine. CDP will be used here as a convenient index of arterial baroreflex stimulation. Mean values for baroreflex sensitivity during down tilt were based on four down tilts, and sensitivity during up tilt was based on four up tilts.


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  		Fig. 1.   Typical individual responses of mean carotid distending pressure (CDP; A) and heart rate (HR; B) to down tilt and up tilt during dynamic exercise. Baseline values were taken as mean during 15 s before tilt. Peak and nadir changes (Delta ) from baseline HR [maximum HR (HRmax)] and CDP [maximum CDP (CDPmax)] in response to tilt are indicated. bpm, Beats/min.

Baroreflex latency was computed as the time difference between the instants of Delta CDPmax and the corresponding Delta HRmax in the opposite direction.

Computer simulation. Curve forms resembling those of the present HR responses to tilt were synthesized by using Acknowledge software. These curve forms were then subjected to low-pass filtering by using LabVIEW software (National Instruments, Austin, TX).

Statistical analysis. Differences between air control and N2O inhalation were analyzed by using a paired Student's t-test for dependent variables (Statistica, Statsoft, Tulsa, OK) with a 5% significance level.


    RESULTS
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INTRODUCTION
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RESULTS
DISCUSSION
REFERENCES

Eight subjects completed the experiments. During N2O inhalation, they were all able to pedal at the required frequency with no apparent coordination difficulties. Typical individual CDP and HR responses to up and down tilt during exercise are shown in Fig. 1.

Steady-state HR and MAP at heart level during exercise are shown in Table 1. There were no significant differences between air control and 30% N2O inhalation in the upright or supine position.

                              
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  		Table 1.   Steady-state mean values during exercise

Both the drop in HR due to down tilt and the rise in HR due to up tilt were less marked during N2O inhalation compared with air control, leading to a significant 16% reduction in baroreflex sensitivity with N2O inhalation during down tilt (P = 0.047) and up tilt (P = 0.035) (Table 2).

                              
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  		Table 2.   Sensitivity and timing of the carotid-cardiac baroreflex during 100-W exercise

The amplitudes and times for the tilt-induced CDP deviations were not changed by N2O inhalation, but there was a significant slowing of the carotid-cardiac baroreflex during N2O inhalation. The latency between the peaks and nadirs of CDP and the associated peaks and nadirs of HR increased by 1.1 ± 0.35 s (37%; P = 0.013) during down tilt and by 2.4 ± 0.79 s (37%; P = 0.020) during up tilt (Table 2). After a tilt, all subjects reached new steady states of HR and blood pressure within 30 s (Fig. 1).


    DISCUSSION
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The distinctive features of this study were that arterial-cardiac-chronotropic baroreflexes were studied within a physiological range of arterial pressures in exercising men and that subjects inspired N2O at partial pressures that have been shown to impair central nervous processing involved in psychomotor performance and temperature control (16, 17). Also, steady-state data were collected in both the upright and supine posture, and arterial blood pressure was determined by an invasive technique for the highest possible accuracy and resolution. The principal finding of this study was that the carotid-cardiac-chronotropic responses had an increased latency and a reduced gain during mild-to-moderate inert-gas narcosis but with no concomitant change in steady-state HR and arterial blood pressure.

N2O as a model of N2 narcosis. The narcotic signs and symptoms caused by hyperbaric nitrogen are similar to those produced by subanesthetic doses of N2O (17). Although qualitatively similar, comparable impairments of psychomotor and mental performance require 25-40 times higher partial pressures for N2 than for N2O (3, 17). Recent studies on the mechanisms of narcosis have shown that many clinically used anesthetics enhance the activity of the inhibitory GABA receptors in the central nervous system. However, the gases xenon and N2O exert their narcotic effects mainly by inhibiting the excitatory N-methyl-D-aspartate receptors (11, 12). Similar investigations have not been performed with N2, but the physiochemical similarities between xenon and N2O on one hand and N2 on the other justify the assumption that N2 operates with a similar mechanism at the receptor level. However, certain well-known effects of N2O on the autonomic nervous system have never been studied with hyperbaric N2. This is true, for example, for the sympathoexcitatory effect of N2O resulting in increased muscle sympathetic nerve activity (5). Thus the present findings with N2O can suggest possible contributions of hyperbaric N2 to cardiovascular phenomena in hyperbaria, but actual measurements with hyperbaric N2 are required for more definite conclusions.

Baroreflex sensitivity. It is well established that deep levels of anesthesia decrease the sensitivity of the arterial baroreceptor reflex (4, 21). The effects on neural information processing involved in cardiovascular control mechanisms during mild gas narcosis, however, have been studied less and not during exercise. Ebert (5), studying resting humans, found a decrease of baroreflex-mediated tachycardia induced by sodium nitroprusside injection during exposure to 40% N2O in oxygen. Östlund et al. (19), studying the whole range of baroreflex stimuli from hypotensive to hypertensive using external neck pressure and suction, found no change in carotid-cardiac-chronotropic responses to hypertensive stimuli with 39% N2O but found, at the same time, that the sensitivity of tachycardic responses to hypotensive stimuli tended to be lower than with air breathing. This appears, in part, to be in contrast to the present findings during exercise (Table 2), where there was a significant reduction of carotid-cardiac baroreflex sensitivity in response to both hypotensive and hypertensive stimuli. It must be kept in mind, however, that carotid-cardiac baroreflex operates on different portions of the baroreflex response curve during rest and exercise. During rest, the prevailing (unstimulated) point of HR-CDP combinations lies on the optimum (mid) point of the sigmoid baroreflex response curve (23, 25). During dynamic exercise, however, the prevailing point moves upward and toward the threshold for hypotensive stimuli (7, 22). Previous findings of attenuated baroreflex responses to hypotensive stimuli (5, 19) and the present finding of a reduced arterial-cardiac baroreflex sensitivity during exercise, therefore, support the notion that the effects of N2O on the arterial-cardiac baroreflex primarily concern mechanisms operating at the hypotensive ("upper left") side of the arterial-cardiac baroreflex response curve, normally characterized by vagal withdrawal and increased sympathetic outflow to the heart.

Interrelations between speed and amplitude of arterial-cardiac baroreflexes. Because of the differences in response speed between vagally induced and sympathetically induced HR responses to alterations in autonomic outflow to the heart (27), responses to short-lasting baroreflex stimuli are primarily vagal. Thus baroreflex sensitivity, as computed from rapid sequences of CDP changes induced by neck suction/neck pressure (23) and rapid tilts (15), primarily reflects vagally induced HR responses. In contrast, steady-state HR responses to changes in CDP, such as those seen several minutes after a tilt or the onset of external neck-pressure changes, will also be influenced by readjustments of sympathetic outflow to the heart (20). Our observations of a reduced arterial-cardiac baroreflex sensitivity to short-lasting CDP stimuli, but at the same time unchanged steady-state HR responses to tilt, therefore indicate that N2O attenuates vagally induced HR modulations but not steady-state HR modulations, where both vagal and sympathetic cardiac efferents contribute.

During air control, the latency between a sudden increase in the CDP and the associated HR response was ~3.5 s, which is similar to the latency reported in previous studies of upright exercise (15, 22, 26) but longer than that in supine resting subjects (26). Two different autonomic mechanisms have been proposed to account for the increased carotid-cardiac baroreflex latency in exercise compared with supine rest (15), and similar mechanisms should be considered in the case of N2O-induced slowing. The first mechanism to be considered is one in which chronotropic responses are brought about to an increasing extent by sympathetic pathways rather than vagal, with sympathetically induced HR changes being much slower than vagally induced changes (27). The second mechanism is one of sympathovagal interaction at the level of the heart. Yang et al. (28) showed that chronotropic responses to external vagal stimulation in open-chest dogs became much slowed with antecedent sympathetic stimulation. N2O has an inherent sympathostimulatory effect; Ebert and Kampine (6) observed a 50-60% increase in muscle sympathetic nerve activity with 40% N2O, and at the same time HR was increased by 10%. Because the autonomic outflow to the heart cannot be determined in the intact human, neither of the two mechanisms for sympathovagal interaction can be excluded. However, our findings of unchanged steady-state HR and MAP with N2O inhalation in both upright and supine positions speak against major N2O-induced changes in sympathetic outflow under the present exercise conditions.

Slowed central processing of baroreflex responses is an alternative explanation, and in our view a more likely one, for the increased Delta HRmax latency with N2O. Fowler et al. (10) suggested that a slowed processing of information could explain the impairments of psychomotor performance during mild-to-moderate inert-gas narcosis. Such impairments are seen both with relatively complex tasks involving cognitive abilities and short-term memory and with simpler reaction-time tests (10, 18). Animal experiments have also shown that cortical responses to peripheral electrical stimulation are delayed during anesthesia (1).

It should be considered whether the increased latency of the chronotropic responses may be the primary impairment of the arterial-cardiac baroreflex and that changes in the amplitude of the responses might be a consequence thereof when baroreceptor inputs are brief. This possibility is schematically illustrated in Fig. 2. Here the waveform of the HR change during down tilt has been synthesized, based on characteristics of the present data during air breathing. Thus pretilt HR, the nadir of the HR response, supine steady-state HR, and the slopes of HR changes have been chosen to mimic present group mean values (Tables 1 and 2). In a second step, this synthetic curve has been subjected to low-pass filtering to simulate a more slowly operating reflex as in the present N2O experiments. A simple first-order filter function was chosen so that the nadir was delayed by 1.1 s. The filter function so obtained can be characterized by its response to a step change of the input signal. This step response was a monoexponential function with a time constant of 1.75 s. The more sluggish response was associated with a damping of the maximum HR response amplitude by ~25%. At the same time the final response amplitude 10-15 s later was not changed. The exact nature of the slowing is not necessarily modeled in the present simulation, and its resulting amplitude reduction was larger than that observed as an N2O effect in the present study. Nevertheless, this simplistic model suggests that it is possible that a primary slowing of the arterial-cardiac baroreflex could result in a secondary reduction of HR responses to brief baroreceptor stimuli.


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  		Fig. 2.   Schematic representation of possible relationship between response latency and response amplitude. Solid line, HR response to down tilt during air breathing. Curve parameters, such as initial and final HR levels, response latency, fall and rise times, and amplitude of HR response, are taken from group mean data. Dashed line, same response after low-pass filtering causing a 1.1-s increased response latency. Low-pass filter function would have resulted in a monoexponential function with time constant of 1.75 s if input had been a sudden step change. Low-pass filtering causes amplitude of initial HR transient to be reduced by ~25%, but final response is unchanged. Time 0 corresponds to the instant of 30° tilt angle (i.e., half- way through rapid tilt).

In conclusion, light-to-moderate inert-gas narcosis with 30% N2O inhalation was found to increase the latency and decrease the gain of HR responses to short-lasting arterial baroreflex stimuli. The slowing of the responses could be the primary effect of N2O, with reduced response amplitudes to brief arterial pressure stimuli as a consequence. There was no alteration of steady-state HR or arterial blood pressure; hence, influences of inert-gas narcosis alone cannot account for the modest relative bradycardia, which is observed in subjects breathing dense and narcotic gases in hyperbaria.


    ACKNOWLEDGEMENTS

This study was supported by Swedish Medical Research Council Grant 5020 and AGA Medical Research Fund.


    FOOTNOTES

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: A. Östlund, Section of Environmental Physiology, Dept. of Physiology and Pharmacology, Karolinska Institutet, SE-171 77 Stockholm, Sweden.

Received 11 December 1998; accepted in final form 22 April 1999.


    REFERENCES
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ABSTRACT
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METHODS
RESULTS
DISCUSSION
REFERENCES

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J APPL PHYSIOL 87(2):830-834
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