Respiratory modulation of human autonomic rhythms

We studied the influence of three types of breathing [spontaneous, frequency controlled (0.25 Hz), and hyperventilation with 100% oxygen] and apnea on R-R interval, photoplethysmographic arterial pressure, and muscle sympathetic rhythms in nine healthy young adults. We integrated fast Fourier transform power spectra over low (0.05-0.15 Hz) and respiratory (0.15-0.3 Hz) frequencies; estimated vagal baroreceptor-cardiac reflex gain at low frequencies with cross-spectral techniques; and used partial coherence analysis to remove the influence of breathing from the R-R interval, systolic pressure, and muscle sympathetic nerve spectra. Coherence among signals varied as functions of both frequency and time. Partialization abolished the coherence among these signals at respiratory but not at low frequencies. The mode of breathing did not influence low-frequency oscillations, and they persisted during apnea. Our study documents the independence of low-frequency rhythms from respiratory activity and suggests that the close correlations that may exist among arterial pressures, R-R intervals, and muscle sympathetic nerve activity at respiratory frequencies result from the influence of respiration on these measures rather than from arterial baroreflex physiology. Most importantly, our results indicate that correlations among autonomic and hemodynamic rhythms vary over time and frequency, and, thus, are facultative rather than fixed.     

The investigation of the synchronization between rhythms in the human cardiovascular system from time series of R-R-intervals

We demonstrated that, from the sequence of R-R intervals, it is possible to calculate the instantaneous phases and instantaneous frequencies of the main rhythmic processes governing the cardiovascular dynamics in humans, namely, the main heart rhythm, respiration, and the process of slow regulation of blood pressure with basic frequency close to 0.1 Hz. For the cases of spontaneous respiration and paced respiration with a fixed frequency, the synchronization between the rhythms of the cardiovascular system was investigated based on the analysis of only the time series of R-R intervals. It is shown that the main heart rhythm and the rhythm of low-frequency regulation of blood pressure can be synchronized with respiration.     

Spectral analysis of muscle sympathetic nerve activity in heat-stressed humans

Whole body heating increases muscle sympathetic nerve activity (MSNA); however, the effect of heat stress on spectral characteristics of MSNA is unknown. Such information may provide insight into mechanisms of heat stress-induced MSNA activation. The purpose of the present study was to test the hypothesis that heat stress-induced changes in systolic blood pressure variability parallel changes in MSNA variability. In 13 healthy subjects, MSNA, electrocardiogram, arterial blood pressure (via Finapres), and respiratory activity were recorded under both normothermic and heat stress conditions. Spectral characteristics of integrated MSNA, R-R interval, systolic blood pressure, and respiratory excursions were assessed in the low (LF; 0.03-0.15 Hz) and high (HF; 0.15-0.45 Hz) frequency components. Whole body heating significantly increased skin and core body temperature, MSNA burst rate, and heart rate, but not mean arterial blood pressure. Systolic blood pressure and R-R interval variability were significantly reduced in both the LF and HF ranges. Compared with normothermic conditions, heat stress significantly increased the HF component of MSNA, while the LF component of MSNA was not altered. Thus the LF-to-HF ratio of MSNA oscillatory components was significantly reduced. These data indicate that the spectral characteristics of MSNA are altered by whole body heating; however, heat stress-induced changes in MSNA do not parallel changes in systolic blood pressure variability. Moreover, the reduction in LF component of systolic blood pressure during heat stress is unlikely related to spectral changes in MSNA.     

Phase and frequency locking of 0.1-Hz oscillations in heart rate and baroreflex control of blood pressure by breathing of linearly varying frequency as determined in healthy subjects

Functional interaction was studied between the subsystems that ensure autonomic control of the heart rate (HR) and blood pressure (BP) and give rise to 0.1-Hz oscillations in R-R intervals (RRI) and photoplethysmogram (PPG). Twenty-five recordings were obtained from 18- to 32-year-old healthy persons (six women and nineteen men). The RRI and PPG were recorded simultaneously while the respiration rate of a subject in the sitting position increased linearly from 0.05 Hz to 0.25 Hz within 25 min. Phase and frequency locking of 0.1-Hz oscillations by breathing proved to be possible in both RRI and PPG. The intervals of phase and frequency locking of oscillations by respiration differed in duration and relative position. These distinctions suggest that the mechanisms of autonomic 0.1-Hz control of HR and BP are functionally independent.     

Heart rate and arterial pressure variability in humans during different orthostatic load.

The influence of posture on the rhythms in blood pressure, heart rate and respiration was tested by means of spectral analysis in 14 healthy subjects. During squatting, standing and sitting, the finger blood pressure was recorded by the non-invasive Penáz technique together with cardiac intervals and respiratory movements. The power spectra obtained from five-minute samples showed that the respiratory components of cardiac interval and pulse pressure were reduced significantly in standing. Compared to squatting, a significant increase of total power in the medium frequency band (0.05-0.15 Hz) for cardiac interval, diastolic and mean pressure could be detected.     

The relationship between respiratory sinus arrhythmia and heart rate during anesthesia in rat.

During inspiration the heart rate (HR) increases and during expiration it decreases. Contribution of respiratory sinus arrhythmia (RSA) to spontaneous heart rate variability (HRV) can be measured as the high frequency (HF) component of variation in consecutive R-R intervals on ECG. In conscious rats, slowing of HR is associated with an increase in HF. The aim of this study was to investigate whether this relationship between HF and HR is preserved during anesthesia in rat. A 15 minutes long ECG signal was recorded from rats (N=15) under moderate chloral hydrate (CHL) anesthesia. Recordings were extended with 45 minutes to investigate the effect of atropine (N=3), against controls (N=3). Short term HRV was investigated in 30 seconds long epochs. HF was considered the frequency band between 0.8 and 1.6 Hz. RSA was quantified as the relative spectral power of the HF. Respiratory frequency (RF) was quantified as the mean spectral frequency within the HF band. One minute estimates of HR, RSA and HF were calculated by averaging 3 epochs of 30 seconds overlapped 50%. The average HR was 427 +/- 3 bpm. The magnitude of RSA was 45 +/- 1% at a RF of 71 +/- 1 rpm. We found that: (1) the decrease in HR that occurs during CHL anesthesia in rat correlates with an increase in RSA; (2) atropine reduces RSA and the time-dependent decrease in HR; (3) the time-dependent increase in RSA is preserved after atropine. We conclude that the correlation between RSA and HR reflects the cardio-pulmonary coupling under parasympathetic control.     

Detection of low- and high-frequency rhythms in the variability of skin sympathetic nerve activity

Spectral analysis of skin blood flow has demonstrated low-frequency (LF, 0.03-0.15 Hz) and high-frequency (HF, 0.15-0.40 Hz) oscillations, similar to oscillations in R-R interval, systolic pressure, and muscle sympathetic nerve activity (MSNA). It is not known whether the oscillatory profile of skin blood flow is secondary to oscillations in arterial pressure or to oscillations in skin sympathetic nerve activity (SSNA). MSNA and SSNA differ markedly with regard to control mechanisms and morphology. MSNA contains vasoconstrictor fibers directed to muscle vasculature, closely regulated by baroreceptors. SSNA contains both vasomotor and sudomotor fibers, differentially responding to arousals and thermal stimuli. Nevertheless, MSNA and SSNA share certain common characteristics. We tested the hypothesis that LF and HF oscillatory components are evident in SSNA, similar to the oscillatory components present in MSNA. We studied 18 healthy normal subjects and obtained sequential measurements of MSNA and SSNA from the peroneal nerve during supine rest. Measurements were also obtained of the electrocardiogram, beat-by-beat blood pressure (Finapres), and respiration. Spectral analysis showed LF and HF oscillations in MSNA, coherent with similar oscillations in both R-R interval and systolic pressure. The HF oscillation of MSNA was coherent with respiration. Similarly, LF and HF spectral components were evident in SSNA variability, coherent with corresponding variability components of R-R interval and systolic pressure. HF oscillations of SSNA were coherent with respiration. Thus our data suggest that these oscillations may be fundamental characteristics shared by MSNA and SSNA, possibly reflecting common central mechanisms regulating sympathetic outflows subserving different regions and functions.     

Influence of Cheyne-Stokes respiration on ventricular response to atrial fibrillation in heart failure.

In subjects with sinus rhythm, respiration has a profound effect on heart rate variability (HRV) at high frequencies (HF). Because this HF respiratory arrhythmia is lost in atrial fibrillation (AF), it has been assumed that respiration does not influence the ventricular response. However, previous investigations have not considered the possibility that respiration might influence HRV at lower frequencies. We hypothesized that Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) would entrain HRV at very low frequency (VLF) in AF by modulating atrioventricular (AV) nodal refractory period and concealed conduction. Power spectral analysis of R-wave-to-R-wave (R-R) intervals and respiration during sleep were performed in 13 subjects with AF and CSR-CSA. As anticipated, no modulation of HRV was detected at HF during regular breathing. In contrast, VLF HRV was entrained by CSR-CSA [coherence between respiration and HRV of 0.69 (SD 0.22) at VLF during CSR-CSA vs. 0.20 (SD 0.19) at HF during regular breathing, P < 0.001]. Comparison of R-R intervals during CSR-CSA demonstrated a shorter AV node refractory period during hyperpnea than apnea [minimum R-R of 684 (SD 126) vs. 735 ms (SD 147), P < 0.001] and a lesser degree of concealed conduction [scatter of 178 (SD 56) vs. 246 ms (SD 72), P = 0.001]. We conclude that CSR-CSA entrains the ventricular response to AF, even in the absence of HF respiratory arrhythmia, by inducing rhythmic oscillations in AV node refractoriness and the degree of concealed conduction that may be a function of autonomic modulation of the AV node.     

Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans

Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified (R(2) = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% (P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% (P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.     

Head-down bed rest impairs vagal baroreflex responses and provokes orthostatic hypotension

We studied vagally mediated carotid baroreceptor-cardiac reflexes in 11 healthy men before, during, and after 30 days of 6 degrees head-down bed rest to test the hypothesis that baroreflex malfunction contributes to orthostatic hypotension in this model of simulated microgravity. Sigmoidal baroreflex response relationships were provoked with ramped neck pressure-suction sequences comprising pressure elevations to 40 mmHg followed by serial R-wave-triggered 15-mmHg reductions to -65 mmHg. Each R-R interval was plotted as a function of systolic pressure minus the neck chamber pressure applied during the interval. Compared with control measurements, base-line R-R intervals and the minimum, maximum, range, and maximum slope of the R-R interval-carotid pressure relationships were reduced (P less than 0.05) from bed rest day 12 through recovery day 5. Baroreflex slopes were reduced more in four subjects who fainted during standing after bed rest than in six subjects who did not faint (-1.8 +/- 0.7 vs. -0.3 +/- 0.3 ms/mmHg, P less than 0.05). There was a significant linear correlation (r = 0.70, P less than 0.05) between changes of baroreflex slopes from before bed rest to bed rest day 25 and changes of systolic blood pressure during standing after bed rest. Although plasma volume declined by approximately 15% (P less than 0.05), there was no significant correlation between reductions of plasma volume and changes of baroreflex responses. There were no significant changes of before and after plasma norepinephrine or epinephrine levels before and after bed rest during supine rest or sitting.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blunted respiratory responses to hypoxia in mutant mice deficient in nitric oxide synthase-3.

In the present study, the role of nitric oxide (NO) generated by endothelial nitric oxide synthase (NOS-3) in the control of respiration during hypoxia and hypercapnia was assessed using mutant mice deficient in NOS-3. Experiments were performed on awake and anesthetized mutant and wild-type (WT) control mice. Respiratory responses to 100, 21, and 12% O(2) and 3 and 5% CO(2)-balance O(2) were analyzed. In awake animals, respiration was monitored by body plethysmography along with O(2) consumption (VO(2)) and CO(2) production (VCO(2)). In anesthetized, spontaneously breathing mice, integrated efferent phrenic nerve activity was monitored as an index of neural respiration along with arterial blood pressure and blood gases. Under both experimental conditions, WT mice responded with greater increases in respiration during 12% O(2) than mutant mice. Respiratory responses to hyperoxic hypercapnia were comparable between both groups of mice. Arterial blood gases, changes in blood pressure, VO(2), and VCO(2) during hypoxia were comparable between both groups of mice. Respiratory responses to cyanide and brief hyperoxia were attenuated in mutant compared with WT mice, indicating reduced peripheral chemoreceptor sensitivity. cGMP levels in the brain stem during 12% O(2), taken as an index of NO production, were greater in mutant compared with WT mice. These observations demonstrate that NOS-3 mutant mice exhibit selective blunting of the respiratory responses to hypoxia but not to hypercapnia, which in part is due to reduced peripheral chemosensitivity. These results support the idea that NO generated by NOS-3 is an important physiological modulator of respiration during hypoxia.     

Respiratory input impedance in anesthetized paralyzed patients

Respiratory impedance (Zrs) was measured between 0.25 and 32 Hz in seven anesthetized and paralyzed patients by applying forced oscillation of low amplitude at the inlet of the endotracheal tube. Effective respiratory resistance (Rrs; in cmH2O.l-1.s) fell sharply from 6.2 +/- 2.1 (SD) at 0.25 Hz to 2.3 +/- 0.6 at 2 Hz. From then on, Rrs decreased slightly with frequency down to 1.5 +/- 0.5 at 32 Hz. Respiratory reactance (Xrs; in cmH2O.l-1.s) was -22.2 +/- 5.9 at 0.25 Hz and reached zero at approximately 14 Hz and 2.3 +/- 0.8 at 32 Hz. Effective respiratory elastance (Ers = -2pi x frequency x Xrs; in cmH2O/1) was 34.8 +/- 9.2 at 0.25 Hz and increased markedly with frequency up to 44.2 +/- 8.6 at 2 Hz. We interpreted Zrs data in terms of a T network mechanical model. We represented the proximal branch by central airway resistance and inertance. The shunt pathway accounted for bronchial distensibility and alveolar gas compressibility. The distal branch included a Newtonian resistance component for tissues and peripheral airways and a viscoelastic component for tissues. When the viscoelastic component was represented by a Kelvin body as in the model of Bates et al. (J. Appl. Physiol. 61: 873-880, 1986), a good fit was obtained over the entire frequency range, and reasonable values of parameters were estimated. The strong frequency dependence of Rrs and Ers observed below 2 Hz in our anesthetized paralyzed patients could be mainly interpreted in terms of tissue viscoelasticity. Nevertheless, the high Ers we found with low volume excursions suggests that tissues also exhibit plasticlike properties.     

New approach to the statistical analysis of cardiovascular data.

Fourier-based approaches to analysis of variability of R-R intervals or blood pressure typically compute power in a given frequency band (e.g., 0.01-0.07 Hz) by aggregating the power at each constituent frequency within that band. This paper describes a new approach to the analysis of these data. We propose to partition the blood pressure variability spectrum into more narrow components by computing power in 0.01-Hz-wide bands. Therefore, instead of a single measure of variability in a specific frequency interval, we obtain several measurements. The approach generates a more complex data structure that requires a careful account of the nested repeated measures. We briefly describe a statistical methodology based on generalized estimating equations that suitably handles this more complex data structure. To illustrate the methods, we consider systolic blood pressure data collected during psychological and orthostatic challenge. We compare the results with those obtained using the conventional methods to compute blood pressure variability, and we show that our approach yields more efficient results and more powerful statistical tests. We conclude that this approach may allow a more thorough analysis of cardiovascular parameters that are measured under different experimental conditions, such as blood pressure or heart rate variability.     

Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low-frequency (0.03-0.15 Hz), high-frequency (0.15-0.45 Hz), and very-high-frequency (0.45-2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities.     

The effects of morphine on the relationship between fetal EEG, breathing and blood pressure signals using fast wavelet transform

In this study, we introduce the fast wavelet transform (WT) as a method for investigating the effects of morphine on the electroencephalogram (EEG), respiratory activity and blood pressure in fetal lambs. Morphine was infused intravenously at 25 mg/h. The EEG, respiratory activity and blood pressure signals were analyzed using WT. We performed wavelet decomposition for five sets of parameters D _2j where -1 < j 5. The five series WTs represent the detail signal bandwidths: 1, 16–32 Hz; 2, 8–16 Hz; 3, 4–8 Hz; 4, 2–4 Hz; 5, 1–2 Hz. Before injection of the high-dose morphine, power in the EEG was high in all six frequency bandwidths. The respiratory and blood pressure signals showed common frequency components with respect to time and were coincident with the low-voltage fast activity (LVFA) EEG signal. Respiratory activity was observed during only some of the LVFA periods, and was completely absent during high-voltage slow activity (HVSA) EEG. The respiratory signal showed dominant power in the fourth wavelet band, and less power in the third and fifth bands. The blood pressure signal was also characterized by dominant power in the fourth wavelet band. This power was significantly increased during periods of respiratory activity. There was a strong relationship between fetal EEG, blood pressure and breathing movements. However, the injection of high-dose morphine resulted in a disruption of the normal cyclic pattern between the two EEG states and a significant increase in power in the first wavelet band. In addition, the high-dose drug resulted in a significant increase in the power of respiratory signal in the fourth and fifth wavelet bands, while power was reduced in the third wavelet band. Breathing activity was also continuous after the drug. The high-dose morphine also caused a temporary power shift from the third wavelet band to the fourth wavelet band for the 30-min period after injection of drug. Finally, high-dose morphine completely destroyed the correlation between EEG, breathing and blood pressure signals.     

Respiratory sinus arrhythmia in the denervated human heart

We performed this study to test whether the denervated human heart has the ability to manifest respiratory sinus arrhythmia (RSA). With the use of a highly sensitive spectral analysis technique (cross correlation) to define beat-to-beat coupling between respiratory frequency and heart rate period (R-R) and hence RSA, we compared the effects of patterned breathing at defined respiratory frequency and tidal volumes (VT), Valsalva and Mueller maneuvers, single deep breaths, and unpatterned spontaneous breathing on RSA in 12 normal volunteers and 8 cardiac allograft transplant recipients. In normal subjects R-R changes closely followed changes in respiratory frequency (P less than 0.001) but were little affected by changes in VT. On the R-R spectrum, an oscillation peak synchronous with respiration was found in heart transplant patients. However, the average magnitude of the respiration-related oscillations was 1.7-7.9% that seen in normal subjects and was proportionally more influenced by changes in VT. Changes in R-R induced by Valsalva and Mueller maneuvers were 3.8 and 4.9% of those seen in normal subjects, respectively, whereas changes in R-R induced by single deep breaths were 14.3% of those seen in normal subjects. The magnitude of RSA was not related to time since the heart transplantation, neither was it related to patient age or sex. Thus the heart has the intrinsic ability to vary heart rate in synchrony with ventilation, consistent with the hypothesis that changes, or rate of changes, in myocardial wall stretch might alter intrinsic heart rate independent of autonomic tone.     

Nine months in space: effects on human autonomic cardiovascular regulation.

We studied three Russian cosmonauts to better understand how long-term exposure to microgravity affects autonomic cardiovascular control. We recorded the electrocardiogram, finger photoplethysmographic pressure, and respiratory flow before, during, and after two 9-mo missions to the Russian space station Mir. Measurements were made during four modes of breathing: 1) uncontrolled spontaneous breathing; 2) stepwise breathing at six different frequencies; 3) fixed-frequency breathing; and 4) random-frequency breathing. R wave-to-R wave (R-R) interval standard deviations decreased in all and respiratory frequency R-R interval spectral power decreased in two cosmonauts in space. Two weeks after the cosmonauts returned to Earth, R-R interval spectral power was decreased, and systolic pressure spectral power was increased in all. The transfer function between systolic pressures and R-R intervals was reduced in-flight, was reduced further the day after landing, and had not returned to preflight levels by 14 days after landing. Our results suggest that long-duration spaceflight reduces vagal-cardiac nerve traffic and decreases vagal baroreflex gain and that these changes may persist as long as 2 wk after return to Earth.     

Spectral analysis of R-R interval variability in inspiratory breath holding in man at rest and during emotional strain

30 young males performed inspiratory breath holdings during expectation of an aversive stimulus and at relative rest. The consecutive R-R intervals of the ECG from breath-hold trial were analysed via spectral analysis of time series. Following parameters were ascertained for each breath holding: mean R-R interval, total R-R interval variability, breath-hold time and relative variability in three spectral bands 3-8 s, 8-12 s and 12-18 s. Neither of these variables was influenced by expectation of an aversive stimulus. The data were subsequently analysed by means of multivariate analysis. Three distinct frequency components were selected according to both histogram data and multivariate analysis. Their modal periods were 5-6 s, 12 s and 16 s respectively. The 8-12 s component of R-R interval variability dominated during breath holdings. The 3-8 s band bore a negative relationship to breath-hold time.     

The influence of exercise intensity on the power spectrum of heart rate variability

The power spectral analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in seven sedentary males at rest, during steady-state cycle exercise at 21 percent maximal oxygen uptake (%VO2max), SEM 2%, 49% VO2max, SEM 2% and 70% VO2max, SEM 2% and during recovery. The RRV, i.e. the absolute power of the spectrum, decreased 10, 100 and 500 times in the three exercise intensities, returning to resting value during recovery. In the RRV power spectrum three components have been identified: (1) high frequency peak (HF), central frequency about 0.24 Hz at rest and recovery, and 0.28 Hz, SEM 0.02, 0.37 Hz, SEM 0.03 and 0.48 Hz, SEM 0.06 during the three exercise intensities, respectively; (2) low frequency peak (LF), central frequency about 0.1 Hz independent of the metabolic state; (3) very low frequency component (VLF), less than 0.05 Hz, no peak observed. The HF peak power, as a percentage of the total power (HF%), averaged 16%, SEM 5% at rest and did not change during exercise, whereas during recovery it decreased to 5%-10%. The LF% and VLF% were about 50% and 35% at rest and during low exercise intensity, respectively. At higher intensities, LF% decreased to 16% and VLF% increased to 70%. During recovery a return to resting values occurred. The HF component may reflect the increased respiratory rate and the LF peak changes the resetting of the baroreceptor reflex with exercise. The hypothesis is made that VLF fluctuations in heart rate might be partially mediated by the sympathetic system.     

Respiratory water loss during rest and flight in European Starlings (Sturnus vulgaris)

Respiratory water loss in Starlings (Sturnus vulgaris) at rest and during flight at ambient temperatures (T(amb)) between 6 and 25 degrees C was calculated from respiratory airflow and exhaled air temperature. At rest, breathing frequency f (1.4+/-0.3 Hz) and tidal volume Vt (1.9+/-0.4 ml) were independent of T(amb), but negatively correlated with each other. Mean ventilation at rest was 156+/-28 ml min(-1) at all T(amb). Exhaled air temperature (T(exh)) at rest increased with T(amb) (T(exh) = 0.92.T(amb)+12.45). Respiratory water loss at rest averaged 0.18+/-0.09 ml h(-1) irrespective of T(amb). In flying Starlings f was 4.0+/-0.4 Hz and independent of T(amb). Vt during flight averaged 3.6+/-0.4 ml and increased with T(amb) (Vt = 0.06.T(amb)+2.83) as, correspondingly, did ventilation. T(exh) during flight increased with T(amb) (T(exh) = 0.85.T(amb)+17.29). Respiratory water loss during flight (average REWL(f) = 0.74+/-0.22 ml h(-1)) was significantly higher than at rest and increased with T(amb). Our measurements suggest that respiratory evaporation accounts for most water loss in flying Starlings and increases more than cutaneous evaporation with rising ambient temperature.