Differential influence of vitamin C on the peripheral and cerebral circulation after diving and exposure to hyperoxia

Abstract

We examined if the diving-induced vascular changes in the peripheral and cerebral circulation could be prevented by oral antioxidant supplementation. Fourteen divers performed a single scuba dive to eighteen meter sea water for 47 min. Twelve of the divers participated in a follow-up study involving breathing 60% of oxygen at ambient pressure for 47 min. Before both studies, participants ingested vitamin C (2 g/day) or a placebo capsule for 6 days. After a 2-wk washout, the study was repeated with the different condition. Endothelium-dependent vasodilator function of the brachial artery was assessed pre- and postintervention using the flow-mediated dilation (FMD) technique. Transcranial Doppler ultrasound was used to measure intracranial blood velocities pre- and 90 min postintervention. FMD was reduced by ∼32.8% and ∼21.2% postdive in the placebo and vitamin C trial and posthyperoxic condition in the placebo trial by ∼28.2% ( P < 0.05). This reduction in FMD was attenuated by ∼10% following vitamin C supplementation in the hyperoxic study ( P > 0.05). Elevations in intracranial blood velocities 30 min after surfacing from diving were reduced in the vitamin C study compared with the placebo trial ( P < 0.05). O breathing had no postintervention effects on intracranial velocities ( P > 0.05). Prophylactic ingestion of vitamin C effectively abrogated peripheral vascular dysfunction following exposure to 60% O but did not abolish the postdive decrease in FMD. Transient elevations of intracranial velocities postdive were reduced by vitamin C. These findings highlight the differential influence of vitamin C on peripheral and cerebral circulations following scuba diving, which are only partly mediated via hyperoxia.

Alterations in resting cerebrovascular regulation do not affect reactivity to hypoxia, hyperoxia or neurovascular coupling following a SCUBA dive

“…The approximately 10% increase in PCAv observed in the current study is consistent with the 8-10% elevation in PCAv reported in two separate studies by Barak et al (2016Barak et al ( , 2018 following a single SCUBA dive with the same dive profile; that is, 18 m sea water with a 47 min bottom time. Further, our data extend these findings and reveal subtle alterations in changes in extra-cranial blood flow patterns, including vasodilatation and reductions in shear rate.…”

“…The increases in intra-cranial CBV are perhaps explained by hyperoxiainduced cerebral vasoconstriction due to (1) compensatory increases in respiration and resultant reductions in P CO 2 (Eldridge & Kiley, 1987); and/or (2) increased reactive oxygen species (ROS) (Modun et al, 2012;Obad et al, 2010) and related reductions in nitric oxide bioavailability (Theunissen et al, 2013) and cerebral metabolism (Mattos et al, 2019); and such changes are reflected in additional stresses of diving (e.g. high hydrostatic pressure, water temperature, exercise) independent of hyperoxia per se (Barak et al, 2018). Indeed, the previously reported transient elevations in CBV observed 30 min following a single SCUBA dive were acutely restored by 60 min post-dive (Barak et al, 2016(Barak et al, , 2018; such increases in CBV were suppressed with antioxidant administration and were not apparent during exposure to matched duration 60% O 2 breathing experienced during the dive (Barak et al, 2018).…”

“…18-30 m sea water with 30-47 min bottom time). Emerging data indicate that adverse changes in vascular function may also extend to cerebrovascular changes post-SCUBA dive (Barak et al, 2016(Barak et al, , 2018.…”

“…Recent studies indicate intra-cranial cerebral blood velocity (CBV) is increased following 47 min exposure to hyperoxia during a SCUBA dive (Barak et al, 2016(Barak et al, , 2018. This transient increase in CBV is perhaps attributable to free radical-mediated reductions in downstream resistance (i.e.…”

“…This transient increase in CBV is perhaps attributable to free radical-mediated reductions in downstream resistance (i.e. vasodilatation of pial arteries) provoked via elevations in oxidative stress (Leffler et al, 1990;Rosenblum, 1983;Wei, Christman, Kontos, & Povlishock, 1985) as antioxidant treatment abolishes the temporary elevation in CBV following a SCUBA dive (Barak et al, 2018). Conversely, lower nitric oxide bioavailability following a SCUBA dive (Theunissen et al, 2013) may contribute to reductions in resting CBF regulation (Mashour & Boock, 1999) via cerebral vasoconstriction (Kety & Schmidt, 1948;Lambertsen et al, 1953;Omae et al, 1997;Visser, Van Hulst, Wieneke, & Van Huffelen, 1996;Watson, Beards, Altaf, Kassner, & Jackson, 2000).…”