Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

Lucy, S. Deborah; Hughson, Richard L.; Kowalchuk, John M.; Paterson, Donald H.; Cunningham, David A.

doi:10.1017/s0958067000019321

Cited by 7 publications

(4 citation statements)

References 23 publications

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“…Anchisi et al (2001) found a linear relationship between SaO 2 and _ Q" vO 2 ; which we interpret as applying to a condition of predominant sympathetic activation. This postulate relies on the following notions: (1) a resting human in normoxia is characterised by elevated vagal stimulation that is withdrawn at exercise start (Robinson et al 1966;Fagraeus and Linnarsson 1976;Malliani et al 1991); (2) the _ Q" vO 2 values observed by Anchisi et al (2001) in resting humans in normoxia fall well below the described SaO 2 vs _ Q" vO 2 line, and are significantly lower than the invariant _ Q" vO 2 values observed at exercise in normoxia in the same study; (3) acute hypoxia depresses vagal activation (Yamamoto et al 1996;Lucy et al 2000;Halliwill and Minson 2002) and increases sympathetic activation (Xie et al 2001); and (4) the _ Q" vO 2 values observed by Anchisi et al (2001) in resting humans in hypoxia lie on the described _ Q" vO 2 vs SaO 2 line. A direct consequence of this postulate is the hypothesis that selective blockade of heart b1-adrenergic receptors would reduce _ QaO 2 and _ Q" vO 2 in humans at given submaximal steady state workloads, and thus change the relationship between _ Q" vO 2 and SaO 2 .…”

Section: Introductionmentioning

confidence: 86%

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

Ferretti¹,

Licker²,

Anchisi³

et al. 2005

Eur J Appl Physiol

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At exercise steady state, the lower the arterial oxygen saturation (SaO(2)), the lower the O(2) return (QvO(2)). A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective beta1-adrenergic blockade (BB) would reduce O(2) delivery (QaO(2)) and QvO(2). To test this hypothesis, we studied the effects of BB on QaO(2) and QvO(2) in exercising humans in normoxia and hypoxia. O(2) consumption VO(2), cardiac output Q, CO(2) rebreathing), heart rate, SaO(2) and haemoglobin concentration were measured on six subjects (age 25.5 +/- 2.4 years, mass 78.1 +/- 9.0 kg) in normoxia and hypoxia (inspired O(2) fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150 W without (C) and with BB with metoprolol. Arterial O(2) concentration (CaO(2)), QaO(2) and QvO(2) were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each VO(2), Q was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO(2) and CaO(2) were unaffected by BB. The QaO(2) changes under BB were parallel to those in Q.QvO(2) was unaffected by exercise in normoxia. In hypoxia the slope of the relationship between QaO(2) and VO(2) was lower than 1, indicating a reduction of QvO(2) with increasing workload. QvO(2) was a linear function of SaO(2) both in C and in BB. The line for BB was flatter than and below that for C. The resting QvO(2) in normoxia, lower than the corresponding exercise values, lied on the BB line. These results agree with the tested hypothesis. The two observed relationships between QvO(2) and SaO(2) apply to conditions of predominant sympathetic or vagal activation, respectively. Moving from one line to the other implies resetting of the cardiovascular regulation.

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Section: Introductionmentioning

confidence: 86%

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

Ferretti¹,

Licker²,

Anchisi³

et al. 2005

Eur J Appl Physiol

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“…Another approach was used by Lucy, Hughson, Kowalchuk, Paterson, and Cunningham (2000), who used HR variability analysis to identify autonomic changes during steady-state isocapnic hypoxia in humans and found decreased vagal tone during the exposure. However, it may be only hypothesized that vagal withdrawal is secondary to the stimulation of lung mechanoreceptors.…”

Section: Introductionmentioning

confidence: 99%

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Paleczny

Seredyński

Tubek

et al. 2019

Experimental Physiology

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New Findings What is the central question of this research?Does increased ventilation contribute to the increase in heart rate during transient exposure to hypoxia in humans? What is the main finding and its importance?Voluntary suppression of the ventilatory response to transient hypoxia does not affect the magnitude of the heart rate response to the stimulus. This indicates that hypoxic tachycardia is not secondary to hyperpnoea in humans. Better understanding of the physiology underlying the cardiovascular response to hypoxia might help in identification of new markers of elevated chemoreceptor activity, which has been proposed as a target in treatment of sympathetically mediated diseases. Abstract Animal data suggest that hypoxic tachycardia is secondary to hyperpnoea, and for years this observation has been extrapolated to humans, despite a lack of experimental evidence. We addressed this issue in 17 volunteers aged 29 ± 7 (SD) years. A transient hypoxia test, comprising several nitrogen‐breathing episodes, was performed twice in each subject. In the first test, the subject breathed spontaneously (spontaneous breathing). In the second test, the subject was repeatedly asked to adjust his or her depth and rate of breathing according to visual (real‐time inspiratory flow) and auditory (metronome sound) cues, respectively (controlled breathing), to maintain respiration at the resting level during nitrogen‐breathing episodes. Hypoxic responsiveness, including minute ventilation [Hyp‐VI; in liters per minute per percentage of blood oxygen saturation (SnormalpO2)], tidal volume [Hyp‐VT; in litres per SnormalpO2], heart rate [Hyp‐HR; in beats per minute per SnormalpO2], systolic [Hyp‐SBP; in millimetres of mercury per SnormalpO2] and mean blood pressure [Hyp‐MAP; in millimetres of mercury per SnormalpO2] and systemic vascular resistance [Hyp‐SVR; in dynes seconds (centimetres)−5 per SnormalpO2] was calculated as the slope of the regression line relating the variable to SnormalpO2, including pre‐ and post‐hypoxic values. The Hyp‐VI and Hyp‐VT were reduced by 69 ± 25 and 75 ± 10%, respectively, in controlled versus spontaneous breathing (Hyp‐VI, −0.30 ± 0.15 versus −0.11 ± 0.09; Hyp‐VT, −0.030 ± 0.024 versus −0.007 ± 0.004; both P < 0.001). However, the cardiovascular responses did not differ between spontaneous and controlled breathing (Hyp‐HR, −0.62 ± 0.24 versus −0.71 ± 0.33; Hyp‐MAP, −0.43 ± 0.19 versus −0.47 ± 0.21; Hyp‐SVR, 9.15 ± 5.22 versus 9.53 ± 5.57; all P ≥ 0.22), indicating that hypoxic tachycardia is not secondary to hyperpnoea. Hyp‐HR was correlated with Hyp‐SVR (r = −074 and −0.80 for spontaneous and controlled breathing, respectively; both P < 0.05) and resting barosensitivity assessed with the sequence technique (r = −0.60 for spontaneous breathing; P < 0.05). This might suggest that the baroreflex mechanism is involved.

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“…However, acute effects of hypoxia were not clear. Several studies have examined that in subjects staying at the hypoxic chamber [17][18][19] , where oxygen contents were low. However, these studies failed to detect the relation between hypoxia and RR-interval fluctuations.…”

Section: Hypoxia and Rr-interval Fluctuationsmentioning

confidence: 99%

Hypoxia-associated Component of RR-interval Fluctuations in Patients with Obstructive Sleep Apnea Syndrome

Yamaki¹,

Sato²,

Fujii³

2015

ijccd

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An RR-interval fluctuation has been used as an important clinical tool for identifying a patient at risk in cardiovascular disease. However, the role of hypoxia on RR-interval fluctuations has not been determined. Methods and Results. We performed ambulatory ECGs monitoring and measured overnight arterial oxygen saturation (SpO 2 ) in 26 patients with obstructive sleep apnea syndrome in whom sever hypoxia occurred during sleep. By means of maximal entropy method, time series of ECG-RR intervals were transformed into frequencies. The minimal SpO 2 during sleep were compared with spectrum powers of the following frequency ranges; 1) 0.0001 -0.05 Hz, 2) 0.05 -0.1 Hz, 3) 0.1 -0.15 Hz, 4) 0.15 -0.2 Hz, 5) 0.2 -0.25 Hz, 6) 0.25 -0.3 Hz, and 7) 0.3 -0.5 Hz. Among the seven analyzed frequencies, the increase in the 0.05 -0.1 Hz power of RR-interval fluctuations was linearly correlated with the minimal SpO 2 during sleep (r=.80, p<.001). Conclusion. This study revealed that hypoxia contributes to 0.05 -0.1 Hz RR-interval fluctuations in patients with obstructive sleep apnea syndrome. RR-interval fluctuations will provide important information about hypoxia.

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Body position and cardiac dynamic and chronotropic responses to steady-state isocapnic hypoxaemia in humans

Cited by 7 publications

References 23 publications

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

The effects of β1-adrenergic blockade on cardiovascular oxygen flow in normoxic and hypoxic humans at exercise

Hypoxic tachycardia is not a result of increased respiratory activity in healthy subjects

Hypoxia-associated Component of RR-interval Fluctuations in Patients with Obstructive Sleep Apnea Syndrome

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