Regulation of cardiac output in hypoxia

Siebenmann, Christoph; Lundby, Carsten

doi:10.1111/sms.12619

Cited by 72 publications

(77 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The influence of the baroreflex has been proposed as an alternative explanation for hypoxic tachycardia in humans, because arterial baroreceptor unloading owing to either hypoxia‐induced peripheral vasodilatation (Tamisier, Norman, Anand, Choi, & Weiss, ; Weisbrod, Minson, Joyner, & Halliwill, ) or the reset of baroreflex regulation of HR and vascular sympathetic outflow to higher blood pressures (Halliwill & Minson, ) may cause tachycardia (Siebenmann & Lundby, ).…”

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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…1) (38,56). The heart rate-mediated initial increase in cardiac output compensates for the decrease in arterial oxygen content, so that the product of both, the systemic oxygen delivery, remains unchanged at rest (38,56). With sojourns at altitude over several days, the resting cardiac output normalizes through a decrease in stroke volume, which is attributed to a hypoxia-induced reduction in plasma volume and thus lower left ventricular end-diastolic volume (55).…”

Section: Introductionmentioning

confidence: 99%

“…Acute exposure to high altitude induces an increase in ventilation and heart rate, mainly driven by hypoxemiainduced carotid chemoreceptor activation, sympathoexcitation, and vagal withdrawal ( Fig. 1) (38,56). The heart rate-mediated initial increase in cardiac output compensates for the decrease in arterial oxygen content, so that the product of both, the systemic oxygen delivery, remains unchanged at rest (38,56).…”

Section: Introductionmentioning

confidence: 99%

“…As resting cardiac output returns to baseline within 1-2 wk of acclimatization, even before the onset of polycythemia, an increased cellular oxygen extraction has been postulated (38,56), and this should be especially pronounced during exercise to match the heightened oxygen demand of exercising muscles. However, absolute oxygen extraction at rest and during peak exercise were decreased in five subjects after 5-6 days at an altitude of 4,559 m, with an unchanged oxygen extraction ratio (i.e., an unchanged ratio of arterial-venous oxygen content to arterial oxygen content) (35).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

Ulrich

Schneider

Bloch

2017

Journal of Applied Physiology

View full text Add to dashboard Cite

Exercise performance is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension, exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects as well as in patients with pulmonary hypertension (PH) maximal performance during progressive ramp exercise and endurance of submaximal constant load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH-patients these improvements were mediated by a better arterial, muscular and cerebral oxygenation along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with pulmonary hypertension, alterations in the inspiratory PO2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen delivery to the muscles and the brain, by effects on cardiovascular and respiratory control and by alterations in pulmonary gas exchange. The understanding of these physiologic mechanisms helps counselling individuals planning altitude or air travel and prescribing oxygen therapy to patients with pulmonary hypertension. is determined by oxygen supply to working muscles and vital organs. In healthy individuals, exercise performance is limited in the hypoxic environment at altitude, when oxygen delivery is diminished due to the reduced alveolar and arterial oxygen partial pressures. In patients with pulmonary hypertension (PH), exercise performance is already reduced near sea level due to impairments of the pulmonary circulation and gas exchange, and, presumably, these limitations are more pronounced at altitude. In studies performed near sea level in healthy subjects, as well as in patients with PH, maximal performance during progressive ramp exercise and endurance of submaximal constant-load exercise were substantially enhanced by breathing oxygen-enriched air. Both in healthy individuals and in PH patients, these improvements were mediated by a better arterial, muscular, and cerebral oxygenation, along with a reduced sympathetic excitation, as suggested by the reduced heart rate and alveolar ventilation at submaximal isoloads, and an improved pulmonary gas exchange efficiency, especially in patients with PH. In summary, in healthy individuals and in patients with PH, alterations in the inspiratory PO 2 by exposure to hypobaric hypoxia or normobaric hyperoxia reduce or enhance exercise performance, respectively, by modifying oxygen deliv...

show abstract

“…Hence, sufficient delivery and perfusion of oxygen to the brain tissue are critical for avoiding life‐threatening conditions . In acute hypoxia, cardiac output is increased to maintain systemic oxygen delivery and cerebral blood flow (CBF) also increases to maintain oxygen delivery to the brain . However, hypoxia may still have detrimental effects on the central nervous system and cause neurological deficits and structural damage to the brain tissue .…”

Section: Introductionmentioning

confidence: 99%

The interactive effects of acute exercise and hypoxia on cognitive performance: A narrative review

Andò

Komiyama

Sudo

et al. 2019

Scandinavian Med Sci Sports

View full text Add to dashboard Cite

Acute moderate intensity exercise has been shown to improve cognitive performance. In contrast, hypoxia is believed to impair cognitive performance. The detrimental effects of hypoxia on cognitive performance are primarily dependent on the severity and duration of exposure. In this review, we describe how acute exercise under hypoxia alters cognitive performance, and propose that the combined effects of acute exercise and hypoxia on cognitive performance are mainly determined by interaction among exercise intensity and duration, the severity of hypoxia, and duration of exposure to hypoxia. We discuss the physiological mechanism(s) of the interaction and suggest that alterations in neurotransmitter function, cerebral blood flow, and possibly cerebral metabolism are the primary candidates that determine cognitive performance when acute exercise is combined with hypoxia. Furthermore, acclimatization appears to counteract impaired cognitive performance during prolonged exposure to hypoxia although the precise physiological mechanism(s) responsible for this amelioration remain to be elucidated. This review has implications for sporting, occupational, and recreational activities at terrestrial high altitude where cognitive performance is essential. Further studies are required to understand physiological mechanisms that determine cognitive performance when acute exercise is performed in hypoxia.

show abstract

Regulation of cardiac output in hypoxia

Cited by 72 publications

References 58 publications

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

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

Effect of hypoxia and hyperoxia on exercise performance in healthy individuals and in patients with pulmonary hypertension: a systematic review

The interactive effects of acute exercise and hypoxia on cognitive performance: A narrative review

Contact Info

Product

Resources

About