Influence of high altitude on cerebral blood flow and fuel utilization during exercise and recovery

Smith, Kurt J.; MacLeod, David B.; Willie, Christopher K.; Lewis, Nia C. S.; Hoiland, Ryan L.; Ikeda, Keita; Tymko, Michael M.; Donnelly, Joseph E.; Day, Trevor A.; MacLeod, N.; Lucas, Samuel J. E.; Ainslie, Philip N.

doi:10.1113/jphysiol.2014.281212

Cited by 62 publications

(125 citation statements)

References 51 publications

(85 reference statements)

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“…A diffusion limitation, however, is not probable given that cerebral O 2 extraction is well maintained even during exercise under both normoxic and hypoxic conditions (Smith et al . ). A diffusion limitation is also not probable based on the mathematical cerebral blood flow/metabolism relationship described by Gjedde ().…”

Section: Discussionmentioning

confidence: 97%

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Bain

Ainslie

Hoiland

et al. 2016

The Journal of Physiology

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Key points The present study describes the cerebral oxidative and non‐oxidative metabolism in man during a prolonged apnoea (ranging from 3 min 36 s to 7 min 26 s) that generates extremely low levels of blood oxygen and high levels of carbon dioxide. The cerebral oxidative metabolism, measured from the product of cerebral blood flow and the radial artery‐jugular venous oxygen content difference, was reduced by ∼29% at the termination of apnoea, although there was no change in the non‐oxidative metabolism. A subset study with mild and severe hypercapnic breathing at the same level of hypoxia suggests that hypercapnia can partly explain the cerebral metabolic reduction near the apnoea breakpoint. A hypercapnia‐induced oxygen‐conserving response may protect the brain against severe oxygen deprivation associated with prolonged apnoea. Abstract Prolonged apnoea in humans is reflected in progressive hypoxaemia and hypercapnia. In the present study, we explore the cerebral metabolic responses under extreme hypoxia and hypercapnia associated with prolonged apnoea. We hypothesized that the cerebral metabolic rate for oxygen (CMRO2) will be reduced near the termination of apnoea, attributed in part to the hypercapnia. Fourteen elite apnoea‐divers performed a maximal apnoea (range 3 min 36 s to 7 min 26 s) under dry laboratory conditions. In a subset study with the same divers, the impact of hypercapnia on cerebral metabolism was determined using varying levels of hypercapnic breathing, against the background of similar hypoxia. In both studies, the CMRO2 was calculated from the product of cerebral blood flow (ultrasound) and the radial artery‐internal jugular venous oxygen content difference. Non‐oxidative cerebral metabolism was calculated from the ratio of oxygen and carbohydrate (lactate and glucose) metabolism. The CMRO2 was reduced by ∼29% (P < 0.01, Cohen's d = 1.18) near the termination of apnoea compared to baseline, although non‐oxidative metabolism remained unaltered. In the subset study, in similar backgrounds of hypoxia (arterial O2 tension: ∼38.4 mmHg), severe hypercapnia (arterial CO2 tension: ∼58.7 mmHg), but not mild‐hypercapnia (arterial CO2 tension: ∼46.3 mmHg), depressed the CMRO2 (∼17%, P = 0.04, Cohen's d = 0.87). Similarly to the apnoea, there was no change in the non‐oxidative metabolism. These data indicate that hypercapnia can partly explain the reduction in CMRO2 near the apnoea breakpoint. This hypercapnic‐induced oxygen conservation may protect the brain against severe hypoxaemia associated with prolonged apnoea.

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Section: Discussionmentioning

confidence: 97%

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Bain

Ainslie

Hoiland

et al. 2016

The Journal of Physiology

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show abstract

“…This study was part of a larger research expedition conducted in April-June 2012 Lewis et al 2014;Smirl et al 2014;Smith et al 2014;Willie et al 2014Willie et al , 2015Stembridge et al 2015). All participants provided written informed consent before participation in this study.…”

Section: Methodsmentioning

confidence: 99%

Reduced blood flow through intrapulmonary arteriovenous anastomoses during exercise in lowlanders acclimatizing to high altitude

Boulet

Lovering

Tymko

et al. 2017

Experimental Physiology

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What is the central question of this study? The aim was to determine, using the technique of agitated saline contrast echocardiography, whether exercise after 4-7 days at 5050 m would affect blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) compared with exercise at sea level. What is the main finding and its importance? Despite a significant increase in both cardiac output and pulmonary pressure during exercise at high altitude, there is very little Q̇IPAVA at rest or during exercise after 4-7 days of acclimatization. Mathematical modelling suggests that bubble instability at high altitude is an unlikely explanation for the reduced Q̇IPAVA. Blood flow through intrapulmonary arteriovenous anastomoses (Q̇IPAVA) is elevated during exercise at sea level (SL) and at rest in acute normobaric hypoxia. After high altitude (HA) acclimatization, resting Q̇IPAVA is similar to that at SL, but it is unknown whether this is true during exercise at HA. We reasoned that exercise at HA (5050 m) would exacerbate Q̇IPAVA as a result of heightened pulmonary arterial pressure. Using a supine cycle ergometer, seven healthy adults free from intracardiac shunts underwent an incremental exercise test at SL [25, 50 and 75% of SL peak oxygen consumption (V̇O2 peak )] and at HA (25 and 50% of SL V̇O2 peak ). Echocardiography was used to determine cardiac output (Q̇) and pulmonary artery systolic pressure (PASP), and agitated saline contrast was used to determine Q̇IPAVA (bubble score; 0-5). The principal findings were as follows: (i) Q̇ was similar at SL rest (3.9 ± 0.47 l min ) compared with HA rest (4.5 ± 0.49 l min ; P = 0.382), but increased from rest during both SL and HA exercise (P < 0.001); (ii) PASP increased from SL rest (19.2 ± 0.7 mmHg) to HA rest (33.7 ± 2.8 mmHg; P = 0.001) and, compared with SL, PASP was further elevated during HA exercise (P = 0.003); (iii) Q̇IPAVA was increased from SL rest (0) to HA rest (median = 1; P = 0.04) and increased from resting values during SL exercise (P < 0.05), but was unchanged during HA exercise (P = 0.91), despite significant increases in Q̇ and PASP. Theoretical modelling of microbubble dissolution suggests that the lack of Q̇IPAVA in response to exercise at HA is unlikely to be caused by saline contrast instability.

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“…)) suggest that

gC {normalD}_{O_{2}}

may be insufficient to match the 20% increase in cerebral metabolism (Smith et al . ). Thus, researchers have speculated, with little actual support, that altering CBF (reducing or enhancing) either at rest or during maximal exercise improves or impairs the matching of

gC {normalD}_{O_{2}}

to cerebral metabolism, making it difficult to identify the extent that CBF and

gC {normalD}_{O_{2}}

contribute to reductions in corticospinal excitability.…”

Section: Cerebral Oxygen Delivery During Normoxic Exercise?mentioning

confidence: 97%

Fuelling cortical excitability during exercise: what's the matter with delivery?

Smith

2016

The Journal of Physiology

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Influence of high altitude on cerebral blood flow and fuel utilization during exercise and recovery

Cited by 62 publications

References 51 publications

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Cerebral oxidative metabolism is decreased with extreme apnoea in humans; impact of hypercapnia

Reduced blood flow through intrapulmonary arteriovenous anastomoses during exercise in lowlanders acclimatizing to high altitude

Fuelling cortical excitability during exercise: what's the matter with delivery?

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