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.

The effect that a SCUBA dive has on cerebral blood flow (CBF) at rest and during exercise is poorly understood. We examined the hypothesis that the altered hemodynamic parameters following a SCUBA dive will lead to differential changes in CBF at rest and during exercise. 16 divers completed a field-based study with a single dive at a depth of 18 m sea water with a 47-min bottom time. A follow-up laboratory based study was conducted - 1 week later. Intra-cranial velocities were measured with transcranial Doppler ultrasound (TCD) pre-dive, post-dive at rest and throughout incremental exercise until exhaustion. Following the dive at rest, middle cerebral artery velocity (MCAv) was elevated 15 and 30 min after surfacing (by 3.3±5.8 and 4.0±6.9 cm/s, respectively; p<0.05); posterior cerebral artery velocity (PCAv) was increased at 30 min after surfacing (by 3.0±4.5 cm/s; p<0.05). During exercise following the dive, both MCAv and PCAv increased up to 150W followed by a decrease towards baseline at 180W (p<0.05). We found no difference in CBV during exercise between field and laboratory studies (p<0.05). The novel finding of this study is the transient elevation in resting intra-cranial velocities within 30 min following a SCUBA dive.

In addition to respiratory symptoms, COVID-19 often causes damage to many other organs, especially in severe forms of the disease. Long-term consequences after COVID-19 are common and often have neurological symptoms. Cerebral vasoreactivity may be impaired after acute COVID-19 and in our study, we wanted to show how constant and reversible are the changes in brain vasoreactivity after infection. This cross-sectional observational study included 49 patients diagnosed with COVID-19 and mild neurological symptoms 300 days after the onset of the disease. We used a transcranial color-coded Doppler (TCCD) and a breath-holding test (BHT) to examine cerebral vasoreactivity and brain endothelial function. We analyzed the parameters of the flow rate through the middle cerebral artery (MCA): peak systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MV), resistance index (RI) and pulsatility index (PI), and we calculated the breath-holding index (BHI). Subjects after COVID-19 infection had lower measured velocity parameters through MCA at rest period and after BHT, lower relative increases of flow velocities after BHT, and lower BHI. We showed that subjects, 300 days after COVID-19, still have impaired cerebral vasoreactivity measured by TCCD and they have chronic endothelial dysfunction.

Novel genetic predispositions reported here in PFO subjects should be investigated further in larger stroke and/or TIA patient datasets.

Walking limitation assessment in multiple sclerosis patients (MSPs) is a demanding task, especially in the clinical setting. The aim of this study is to correlate the visual analogue scale (VAS), a simple method for measuring subjective experience, with measures of walking ability used in clinical research of MS. The study included 82 ambulatory MSPs who have resided in the local community. The applied measures of walking ability were the following: the single-item and patient-rated Walking Ability Visual Analogue Scale (WA-VAS), the Expanded Disability Status Scale (EDSS), the 25-foot walk test (25FWT), the Six Spot Step Test (SSST), the 2 min timed walk (2 min TW), the Multiple Sclerosis Walking Scale-12 (MSWS-12), and step activity monitor accelerometer (SAM) during 7 day period. The SAM analysis included the average daily step count, the average steps/min of the highest 1 min of a day, and the average steps/min of the highest continuous 60 min of a day. The WA-VAS scores significantly and strongly correlated with EDSS (ρ = 0.679, P < 0.001), 25FWT (ρ = 0.606, P < 0.001), SSST (ρ = 0.729, P < 0.001), 2 min TW (ρ = -0.643, P < 0.001), MSWS-12 (ρ = 0.746, P < 0.001), average daily step count (ρ = -0.507, P < 0.001), average steps/min of the highest 1 min of a day (ρ = -0.544, P < 0.001), and average steps/min of the highest continuous 60 min of a day (ρ = -0.473, P < 0.001). Correlations between WA-VAS and measures of walking ability used in clinical research of MS were satisfactory. The results obtained in this research indicate that the WA-VAS could be an instrument for simple measurement of walking limitations in MSPs in the clinical setting.