The long-term conditioning effects of physical training on cardiorespiratory interaction in 11 young healthy males were studied. Significant increases in maximum oxygen uptake (VO2max) (P < 0.05) and decreases in heart rate (P < 0.05) were achieved in all subjects following a 6-week training programme consisting of cycling for 25 min each day at a work level that increased heart rate to 85% of maximum. Heart rate variability, measured as the differences between the maximum and minimum R-R interval in a respiratory cycle, increased in nine of the subjects and decreased in two. The respiratory-cycle-related high-frequency peak in the power spectral plot of R-R variability also showed significant increases in the same nine subjects and decreases in two. The latter result was similar after normalisation of the data for changes in heart rate by calculating the common coefficient of variance [symbol: see text], where HF is the high-frequency component of the power spectral plots, using a further measure of vagal tone it was shown that, for all subjects, the R-R interval change in response to isometric contractions of the arm flexors in one respiratory cycle were significantly greater after training. These data suggest that cardiac vagal tone is increased by aerobic training for all subjects and that this is accompanied by a respiratory sinus arrhythmia (RSA) in most, but may be associated with a decrease in RSA in subjects with a very low (< 50 beats.min-1 heart rate.

Angiotensin II (Ang II) exerts an inhibitory action on vagal activity in animals and may also facilitate sympathetic activity. The object of this study was to compare autonomic activity resulting from equivalent steady-state baroreflex activation during intravenous Ang II infusion with that resulting from a control infusion of phenylephrine. Eight healthy subjects aged 22 to 34 years were studied in a single-blind, randomized, prospective crossover study. Autonomic activity was determined by computer analysis of RR interval variability in the time and frequency domains. Despite equal experimental hypertension with Ang II and phenylephrine infusion, at peak infusion rates the mean RR interval was significantly shorter with Ang II (983 +/- 179 milliseconds; mean +/- SD) than with phenylephrine (1265 +/- 187 milliseconds, P < .01). The variability of RR intervals was not significantly different, but the variability (median interquartile difference) of RR interval successive differences was significantly lower with Ang II (66 milliseconds) than with phenylephrine (104 milliseconds, P < .02). Power spectral analysis revealed the power of the 0.25-Hz component in normalized units to be significantly smaller during Ang II infusion (20.5 +/- 12.7 U) than during phenylephrine (38.2 +/- 14.7 U, P < .05), whereas the power of the 0.1-Hz component was significantly greater during Ang II infusion (67.8 +/- 17.1 U) than phenylephrine (38.8 +/- 20.3 U, P < .05). Measures of vagal modulation of heart rate were significantly attenuated, and sympathetic modulation appeared to be increased during Ang II infusion compared with control phenylephrine infusions. These observations may underlie reports of increased vagal activity during angiotensin-converting enzyme inhibitor therapy.

1. In order to increase our understanding of the central regulation of human cardiac vagal motoneurones we studied the interaction between two opposing influences on cardiac vagal tone, one related to diving and the other to exercise. 2. The heart rate response to cooling the face (0°C, trigeminal cutaneous receptor stimulation, TGS) and to a brief isometric muscle contraction was studied in fourteen healthy young adults (8 males, 6 females) during controlled ventilation at supine rest. 3. Fluctuations in R-R interval were quantified by spectral analysis. In addition the absolute values of R-R intervals occurring in any one of ten arbitrary phases of a respiratory cycle were measured over thirty to sixty cycles to give a graph of the changes in R-R interval throughout a respiratory cycle.4. TGS produced a significant decrease in heart rate (-21 + 2 beats min-' in females, -19 + 2 beats min-' in males; means + S.E.M.). In addition the autospectral plots of R-R interval variability showed that during TGS there was a significant increase both in the high frequency peak and in the low frequency peak in all subjects. These data suggested that in these experiments the bradycardia of TGS was due to an increase in cardiac vagal tone.5. Voluntary isometric contractions at 40 and 60 % of maximum (40 % MVC, 60 % MVC) were timed to occur early in expiration or early in inspiration. Analysis of the changes in R-R interval produced by these contractions was confined to the respiratory cycle in which they were initiated. The early onset of these changes was interpreted as showing a decrease in cardiac vagal tone. 6. The 40% MVC and 60% MVC increased heart rate significantly within one respiratory cycle with maximum effects having a mean of 9 5 + 3 and 11 + 3 beats min-1, respectively. When isometric muscle contraction was initiated during TGS the 60% MVC but not the 40 % MVC was able to significantly decrease R-R interval and hence increase heart rate. 7. It is concluded that the TGS excitatory inputs and the muscle inhibitory inputs to cardiac vagal neurones do not interact by one input gating the other early in the pathway but more probably by a process of algebraic summation closer to the cardiac vagal neurone.

1. We have previously shown that brief voluntary isometric contractions of upper arm flexor muscles performed for one respiratory cycle elicit a significant decrease in the R-R interval. The present study was designed to determine if similar changes are produced by non-voluntary electrically evoked contractions and, if so, to establish the consistency and repeatability of the associated changes in the R-R interval. 2. The heart rate (R-R interval) response to voluntary or non-voluntary brief isometric contraction equivalent to 40% of the maximum voluntary contraction was studied in 10 healthy young male subjects during controlled ventilation at supine rest. 3. The absolute values of R-R intervals occurring in any one of 10 arbitrary phases of a respiratory cycle were measured and plotted by a computer. 4. Both voluntary and non-voluntary contractions elicited similar changes in heart rate and R-R interval, which were greater during expiration than during inspiration. 5. This confirms our previous finding that the magnitude of the R-R interval changes, with brief isometric contraction, is positively related to the degree of cardiac vagal tone. 6. Analysis of the variability between repeated tests initiated in either inspiration or expiration revealed that there was significantly less variability with the electrically induced contraction. 7. It was concluded that electrically induced contractions of 40% maximal voluntary contraction are a viable alternative to voluntary contractions and provide a more controllable means of measuring cardiac vagal withdrawal.

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1. The influence of central inspiratory drive on heart rate variability was investigated in young human subjects using power spectral analysis of R-R intervals. 2. The area of the high-frequency component occurring at the respiratory frequency (0.2-0.25 Hz) in the power spectral density curves was used as an index of respiratory sinus arrhythmia. 3. Central inspiratory drive was increased by breathing a CO2-enriched (5%) gas mixture and this condition was compared with a similar degree of ventilation produced voluntarily. 4. Tests were conducted on eight young subjects with and without low-dose scopolamine (scopoderm TTS) in a double-blind cross-over trial. 5. Scopolamine decreased heart rate and increased the high-frequency peak, suggesting that its main action on the cardiac vagal pathway was a peripheral one, possibly increasing the efficacy of vagal impulses on the cardiac pacemaker. 6. With scopolamine, CO2 breathing increased the area of the high-frequency component significantly more than a similar degree of ventilatory movements produced by voluntary hyperventilation. 7. It is concluded that respiratory sinus arrhythmia in humans is at least partly dependent on a central respiratory-cardiac coupling, most probably similar to that shown in animal studies.

Evidence from animal studies suggests that beta-blockers can act within the central nervous system to increase cardiac vagal motoneuron activity. We have attempted to determine whether such an effect is evident in healthy humans, by examining the effects of lipophilic and hydrophilic agents on heart rate variability and cardiac vagal reflexes. A total of 20 healthy volunteers took part in the study. Autonomic studies were performed after 72 h of treatment with placebo, atenolol or metoprolol in a blinded cross-over design. ECG recordings were taken at rest and during mental and orthostatic stress. Heart rate variability was measured in the time and frequency domains. The effects on heart rate of two opposing cardiac vagal reflexes were examined. Trigeminal stimulation causing vagal stimulation, and isometric forearm muscle contraction ('muscle heart reflex') causing vagal inhibition, were performed alone and simultaneously. At rest, during mental stress and during trigeminal stimulation, beta-blocker therapy was associated with significantly increased high-frequency beat-to-beat heart rate variability when compared with placebo. There were no significant differences in effects on heart rate or heart rate variability between atenolol and metoprolol. Analysis of the muscle heart reflex, alone and with simultaneous trigeminal stimulation, showed that the magnitude of the R-R interval response was significantly greater after beta-blocker therapy compared with placebo, but the effects of atenolol and metoprolol were equivalent. beta-Blocker therapy increased cardiac vagal activity, as shown by measures of high-frequency heart rate variability and reflex studies. Lipophilic and hydrophilic beta-blockers appeared to be equally efficacious in increasing the cardiac vagal modulation of heart rate.

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