The relationship of respiratory sinus arrhythmia amplitude (RSA) to tidal volume and breathing frequency was quantified during voluntarily controlled tidal volume and breathing frequency and spontaneous quiet breathing. Seventeen seated subjects breathed via mouthpiece and nose-clip, maintaining constant tidal volumes at each of several breathing frequencies. Inspiratory breath hold was zero frequency. Log RSA was plotted vs. log frequency for each tidal volume. The large stable RSA for frequencies less than 6 cycles/min was called low-frequency intercept (LFI, 20 +/- 5 beats/min). Low-frequency intercept was inversely proportional to a subject's age only to 35 yr. At higher breathing frequencies above a characteristic corner frequency (fC, 7.2 +/- 1.5 cycles/min) RSA decreased with constant slope (roll-off; 21 +/- 3.4 dB/decade). The RSA-volume relationship was linear permitting normalization of RSA-frequency curves for tidal volume to yield one curve. Spontaneous breathing data points fell on this curve. Voluntarily coupling of heart rate to breathing frequency in integer ratios reduced breath-by-breath variability of RSA without changing mean RSA. In conclusion, low-frequency intercept, corner frequency, and roll-off characterize an individual's RSA-frequency relationship during both voluntarily controlled and spontaneous breathing.

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The hypothermic response of rats to only brief ( approximately 2 h) hypoxia has been described previously. The present study analyzes the hypothermic response in rats, as well as level of activity (L(a)), to prolonged (63 h) hypoxia at rat thermoneutral temperature (29 degrees C). Mini Mitter transmitters were implanted in the abdomens of 10 adult Sprague-Dawley rats to continuously record body temperature (T(b)) and L(a). After habituation for 7 days to 29 degrees C and 12:12-h dark-light cycles, 48 h of baseline data were acquired from six control and four experimental rats. The mean T(b) for the group oscillated from a nocturnal peak of 38.4 +/- 0.18 degrees C (SD) to a diurnal nadir of 36.7 +/- 0.15 degrees C. Then the experimental group was switched to 10% O(2) in N(2). The immediate T(b) response, phase I, was a disappearance of circadian rhythm and a fall in T(b) to 36.3 +/- 0.52 degrees C. In phase II, T(b) increased to a peak of 38.7 +/- 0.64 degrees C. In phase III, T(b) gradually decreased. At reoxygenation at the end of the hypoxic period, phase IV, T(b) increased 1.1 +/- 0.25 degrees C. Before hypoxia, L(a) decreased 70% from its nocturnal peak to its diurnal nadir and was entrained with T(b). With hypoxia L(a) decreased in phase I to essential quiescence by phase II. L(a) had returned, but only to a low level in phase III, and was devoid of any circadian rhythm. L(a) resumed its circadian rhythm on reoxygenation. We conclude that 63 h of sustained hypoxia 1) completely disrupts the circadian rhythms of both T(b) and L(a) throughout the hypoxic exposure, 2) the hypoxia-induced changes in T(b) and L(a) are independent of each other and of the circadian clock, and 3) the T(b) response to hypoxia at thermoneutrality has several phases and includes both hypothermic and hyperthermic components.

Steady-state breathing patterns on mouthpiece and noseclip (MP) and face mask (MASK) during air and chemostimulated breathing were obtained from pneumotachometer flow. On air, all 10 subjects decreased frequency (f) and increased tidal volume (VT) on MP relative to that on MASK without changing ventilation (VE), mean inspiratory flow (VT/TI), or mean expiratory flow (VT/TE). On elevated CO2 and low O2, MP exaggerated the increase in VE, f, and VT/TE due to profoundly shortened TE. On elevated CO2, MASK exaggerated VT increase with little change in f. Increased VE and VT/TI were thus due to increased VT. During low O2 on MASK, both VT and f increased. During isocapnia, shortened TE accounted for increased f; during hypocapnia, increased f was related primarily to shortened TI. Thus the choice of a mouthpiece or face mask differentially alters breathing pattern on air and all components of ventilatory responses to chemostimuli. In addition, breathing apparatus effects are not a simple consequence of a shift from oronasal to oral breathing, since a noseclip under the mask did not change breathing pattern from that on mask alone.