Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers

Fellows’ Journal Club

Fifteen male freedivers underwent repetitive 3T pseudocontinuous ASL and 31P-/1H-MR spectroscopy before, during, and after a 5-minute breath-hold (split into early and late phases) and gave temporally matching venous blood gas samples. The spatial coefficient of variation of CBF (by arterial spin-labeling) decreased during the early breath-hold phase whereas CBF remained almost stable during this phase and increased in the late phase. Cerebrovascular reactivity differed between the anterior and the posterior circulation during all phases. The cerebral energy metabolism of trained freedivers withstands severe hypoxic hypercarbia in prolonged breath-hold due to a complex cerebrovascular hemodynamic response.

Abstract

BACKGROUND AND PURPOSE

cerebrovascular hemodynamic response
Mean CBF during the breath-hold experiment. False color maps of cohort mean cerebral blood flow during 5-minute breath-hold. Selected transverse brain sections of the cohort mean CBF before, during, and after the 5-minute breath-hold challenge. The mean total GM CBF over all participants and over all phases was scaled to 60 mL/100 g/min. Likewise, the mean total WM CBF for all participants over all phases was scaled to 20 mL/100 g/min for WM.

Experienced freedivers can endure prolonged breath-holds despite severe hypoxemia and are therefore ideal subjects to study apnea-induced cerebrovascular reactivity. This multiparametric study investigated CBF, the spatial coefficient of variation as a correlate of arterial transit time and brain metabolism, dynamics during prolonged apnea.

MATERIALS AND METHODS

Fifteen male freedivers (age range, 20–64 years; cumulative previous prolonged breath-holds >2 minutes and 30 seconds: 4–79,200) underwent repetitive 3T pseudocontinuous arterial spin-labeling and 31P-/1H-MR spectroscopy before, during, and after a 5-minute breath-hold (split into early and late phases) and gave temporally matching venous blood gas samples. Correlation of temporal and regional cerebrovascular reactivity to blood gases and cumulative previous breath-holds of >2 minutes and 30 seconds in a lifetime was assessed.

RESULTS

The spatial coefficient of variation of CBF (by arterial spin-labeling) decreased during the early breath-hold phase (−30.0%, P = .002), whereas CBF remained almost stable during this phase and increased in the late phase (+51.8%, P = .001). CBF differed between the anterior and the posterior circulation during all phases (eg, during late breath-hold: MCA, 57.3 ± 14.2 versus posterior cerebral artery, 42.7 ± 10.8 mL/100 g/min; P = .001). There was an association between breath-hold experience and lower CBF (1000 previous breath-holds reduced WM CBF by 0.6 mL/100 g/min; 95% CI, 0.15–1.1 mL/100 g/min; P = .01). While breath-hold caused peripheral lactate rise (+18.5%) and hypoxemia (oxygen saturation, −24.0%), cerebral lactate and adenosine diphosphate remained within physiologic ranges despite early signs of oxidative stress [−6.4% phosphocreatine / (adenosine triphosphate + adenosine diphosphate); P = .02].

CONCLUSIONS

This study revealed that the cerebral energy metabolism of trained freedivers withstands severe hypoxic hypercarbia in prolonged breath-hold due to a complex cerebrovascular hemodynamic response.

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Cerebrovascular Reactivity during Prolonged Breath-Hold in Experienced Freedivers
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Jeffrey Ross
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