Exercising in Hypoxia and Other Stimuli: Heart Rate Variability and Ventilatory Oscillations

Figures

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  Figure 1. Example of an IBI spectral density (logarithmic scale), including the different bands: Ultra-low, very low, low, and high frequencies (ULF, VLF, LF, and HF, respectively). Extracted from [7].

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  Figure 2. Breath-by-breath output of minute ventilation (V˙E), pulse O2 saturation (SpO2), and end tidal PCO2 (PETCO2) during a hypoxia exercise test. Lower panel: Subject with a high HVRe (0.93 L.min−1.kg−1). Upper panel: Subject with a low HVRe (0.60 L.min−1.kg−1). From [17].

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  Figure 3. Example of spectral analysis of minute ventilation by Fast Fourier Transform in the 4 phases of a hypoxia exercise test. RN: Rest in normoxia, RH: Rest in hypoxia, EH: Exercise in hypoxia, EN: Exercise in normoxia. PSD: Power Spectral Density. Note that the frequency of the main peak in hypoxic exercise conditions (EH) is around 0.08 Hz, which corresponds to a period of 12.5 s. From [17].

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  Figure 4. V˙E power of the main peak obtained from the spectral analysis of minute ventilation during the various phases of a hypoxia exercise test. RN: Rest in normoxia, RH: Rest in hypoxia, EH: Exercise in hypoxia, EN: Exercise in normoxia. Mean ± SD. Condition vs RN: ++, p < 0.01, +++, p < 0.001. High HVRe vs. low HVRe: *, p < 0.05; **, p < 0.01. From [17].

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  Figure 5. Power spectral density of the ventilation signal at exercise: Normoxia and hypercapnic hyperoxia. From [20].

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  Figure 6. Power spectral density of the ventilation signal at exercise: Normoxia and hyperoxia. From [24].

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  Figure 7. Example of breath-by-breath ventilation recordings under placebo (upper panel) and acetazolamide (lower panel) treatment. Inlets: Ventilatory response to CO2 (upper right: Placebo, lower right: Acetazolamide). From [24].

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  Figure 8. Left panel: Example of breath-by-breath ventilation recordings in hypoxia without and with added dead space (respectively upper and lower panels). Right panel: Power spectral densities of ventilation signal at exercise in 2 conditions: Hypoxia without added dead space (aDS) and hypoxia with aDS. From [48]. Copyright permission has been obtained from Elsevier.

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  Figure 9. Schematic diagram of potential mechanisms involved in the genesis of ventilatory oscillations in normal subjects at exercise. Breathing instability is directly related to the intensity of V˙E and Q˙c. Exercise, hypoxia, and hypercapnia increase V˙E and Q˙c, and therefore increase ventilatory oscillations. ACZ inhibits the effect of hypoxia and enhances the effect of hypercapnia on ventilation and blunts the relation between V˙E or Q˙c and ventilatory oscillations. From [24].

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  Figure 10. Diagrams of a central/peripheral interactive model of ventilation control system. The central respiratory command receives direct or indirect afferences from peripheral (through nucleus tractus solitaries, NTS) and central chemoreceptors (PCR and CCR, respectively), modulated by PaO2 and PaCO2. Hence, the level of hypoxia and hypercapnia acts on respiratory outputs via O2 gain (peripheral GO2, as a ventilatory response to a change of FIO2) and CO2 gain (peripheral GCO2P and central GCO2C, to a change of FICO2). From [56]. Copyright permission has been obtained from Elsevier.

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  Figure 11. Variation of V˙E for 2 levels of FIO2 in the additive model: Normoxia (FIO2 = 0.21) and hypoxia (FIO2 = 0.14). From [56]. Copyright permission has been obtained from Elsevier.

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  Figure 12. Period of ventilatory oscillations according to several cardiorespiratory variables from their nominal values: Peripheral O2 gain (GO2), central CO2 gain (GCO2C), inhaled fraction of O2 (FIO2), delay of blood convection from lung to carotid bodies (DeltaTp), arterial O2 partial pressure at SaO2 = 50% (P50), total lung capacity (TLC), and alveolar/total ventilation ratio (rVAVE). From [56]. Copyright permission has been obtained from Elsevier.