Katsuyoshi Kubo

Assessment of autonomic nervous function by power spectral analysis of heart rate variability in the horse

We studied power spectral analysis of heart rate (HR) variability in the horse, with the hypothesis that the quantitative information provided by the spectral analysis of HR variability reflects the interaction between sympathetic and parasympathetic regulatory activities. For this purpose, electrocardiogram, blood pressure (BP) and respiratory (Resp) waveform were simultaneously recorded from Thoroughbred horses (3-5 years old) and analyzed by power spectrum. There were two major spectral components at low-frequency (LF) and high-frequency (HF) bands for HR variability. The peak of Resp variability clearly occurred at the HF range. In contrast to Resp variability, the power spectra of BP variability occurred at lower frequencies. The maximum coherence between HR and Resp variabilities and HR and BP variabilities occurred at approximately 0.15 and approximately 0.03 Hz, respectively. These relationships were similar to the ensemble spectra. On the basis of these data, we have defined two frequency bands of interest: LF (0.01-0.07 Hz) and HF (0.07-0.6 Hz). Therefore, we believe that power spectral analysis of HR variability provides a very powerful technique for assessing autonomic nervous activity in the horse.

Effects of altered FiO2 on maximum V̇O2 in the horse

Although the horse is considered an elite athlete with a specific VO2max some 2-4 times higher than man, maximal O2 transport is compromised both by moderately severe arterial desaturation and by failure to extract all O2 from blood perfusing exercising muscle. This prompted the present study to ascertain whether correction of arterial desaturation would proportionally augment VO2max and, if so, would O2 extraction behave in a manner predicted by diffusional transport limitation. Six two year old thoroughbreds were exercised to VO2max on a treadmill each on three separate occasions breathing gases of FIO2 = 0.15, 0.21 and 0.35, each used once in balanced order. VO2, ventilation, arterial and pulmonary arterial blood gases, pressures and lactate levels were measured both submaximally and maximally at each FIO2 and cardiac output was computed by mass balance for O2. At FIO2 = 0.21, VO2max = 143.9 +/- 4.8 ml kg-1 min-1, arterial saturation (SaO2) was 81.6 +/- 3.3% while venous PO2 (PvO2) was 15.3 +/- 1.4 Torr. At FIO2 = 0.35, VO2max was 172.6 +/- 8.2 ml kg-1 min-1, SaO2 reached 97.4 +/- 0.4% and PvO2 was 23.4 +/- 0.7 Torr. VO2max at FIO2 = 0.15 was 109.8 +/- 4.1 ml kg-1 min-1, SaO2 fell to 68.1 +/- 2.5% and PvO2 was 10.6 +/- 1.0 Torr, all changes being significant, p < 0.01. As FIO2 was varied, VO2max changed proportionally to calculated mean capillary Po2 as well as to total O2 delivery. These data confirm substantial O2 supply dependence of VO2max in the horse, and in such a manner as to be consistent with the hypothesis of combined diffusive and convective transport limitation within muscle.

Hypoxic helium breathing does not reduce alveolar-arterial PO2 difference in the horse

In a previous study we evaluated the mechanism of alveolar-arterial PO2 (AaPO2) reduction when nitrogen is replaced with helium in normoxia (FIO2 = 0.21). The reduction in AaPO2 was not due to changes in VA/Q inequality, pulmonary O2 diffusing capacity, or cardiac output, but to more complete diffusion equilibration as a consequence of the higher ventilation and thus PAO2 (which reduced the average slope of the hemoglobin O2 dissociation curve (ODC), and thus enhanced diffusive equilibration). We hypothesized that hypoxic He/O2 breathing in contrast would not reduce the AaPO2 because PAO2 and PaO2, although higher with He than N2, would remain constrained to the linear region of the ODC. Breathing hypoxic gas mixtures did constrain the PAO2 to the linear region of the ODC, even when PAO2 was increased by He/O2 breathing. Thus, the average slope of the ODC did not change when He replaced N2 and this explains the lack of change in AaPO2, as hypothesized.