The impact of predive exercise on repetitive <scp>SCUBA</scp> diving

Madden, Dennis; Barak, Otto; Thom, Stephen R.; Yang, Ming; Bhopale, Veena M.; Ljubković, Marko; Dujić, Željko

doi:10.1111/cpf.12213

Cited by 8 publications

(7 citation statements)

References 32 publications

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“…The variability within our pre-dive data is comparable to that observed in human populations studied for reasons other than diving, and similar to results observed in divers without DCS 22,28–30 . However, it is greater than we have observed in several prior investigations 6,7,10,31,32 . A recent study reported that the blood transcriptome indicative of apoptotic, inflammatory, and innate immune responses in non-divers differed from experienced divers, even though they had abstained from diving for over 2 weeks 33 .…”

Section: Discussioncontrasting

confidence: 67%

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Microparticle and interleukin-1β production with human simulated compressed air diving

Brett

Nugent

Fraser

et al. 2019

Sci Rep

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Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.

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Section: Discussioncontrasting

confidence: 67%

“…MPs may serve as a nidus for the vascular gas emboli that are routinely seen in divers 12–14 . Some have reported a close association between MPs and bubbles, while others have not 7–10,31 . Whether MPs are the nucleation site for bubbles, or these are parallel events, remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Microparticle and interleukin-1β production with human simulated compressed air diving

Brett

Nugent

Fraser

et al. 2019

Sci Rep

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“…In addition to venous and arterial gas emboli, the aforementioned diving-related stress factors can lead to pathophysiological consequences such as hyperoxia-induced oxidative stress (182), impaired endothelial function (202), damaged endothelial integrity with shedding of microparticles (272), and platelet and neutrophil activation promoting inflammation (273)(274)(275)320). Depending on the severity of the diving stress, these alterations can last from hours to days (169,202,273). Other than peripheral endothelial damage, markers of blood-brain barrier damage and elevations in intracranial blood flow velocities have also been demonstrated following SCUBA diving, suggesting that oxidative stress and gas emboli can harm the cerebral circulation as well (17,31).…”

Section: Diving (Decompression Sickness)mentioning

confidence: 99%

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Brugniaux

Coombs

Barak

et al. 2018

American Journal of Physiology-Regulatory, Integrative and Comp

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105

108

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Molecular oxygen (O) is a vital element in human survival and plays a major role in a diverse range of biological and physiological processes. Although normobaric hyperoxia can increase arterial oxygen content ([Formula: see text]), it also causes vasoconstriction and hence reduces O delivery in various vascular beds, including the heart, skeletal muscle, and brain. Thus, a seemingly paradoxical situation exists in which the administration of oxygen may place tissues at increased risk of hypoxic stress. Nevertheless, with various degrees of effectiveness, and not without consequences, supplemental oxygen is used clinically in an attempt to correct tissue hypoxia (e.g., brain ischemia, traumatic brain injury, carbon monoxide poisoning, etc.) and chronic hypoxemia (e.g., severe COPD, etc.) and to help with wound healing, necrosis, or reperfusion injuries (e.g., compromised grafts). Hyperoxia has also been used liberally by athletes in a belief that it offers performance-enhancing benefits; such benefits also extend to hypoxemic patients both at rest and during rehabilitation. This review aims to provide a comprehensive overview of the effects of hyperoxia in humans from the "bench to bedside." The first section will focus on the basic physiological principles of partial pressure of arterial O, [Formula: see text], and barometric pressure and how these changes lead to variation in regional O delivery. This review provides an overview of the evidence for and against the use of hyperoxia as an aid to enhance physical performance. The final section addresses pathophysiological concepts, clinical studies, and implications for therapy. The potential of O toxicity and future research directions are also considered.

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“…For example, the impact of temperature, pressure, increased work of breathing, hyperoxia and psychological stress all have detrimental physiological consequences [22,25,35,42]. Following single or repetitive dives, impairment has been reported in systemic endothelial function [8,26,31], as well as cardiac and autonomic function [5,10,15]. Depending on the severity of the diving stress these alterations can last from hours up to even a few days [35] and are brought about by a range of factors like hyperoxia induced oxidative stress, venous (VGE) and arterial gas emboli (AGE) and impaired endothelial integrity with shedding of microparticles [44].…”

mentioning

confidence: 99%

Elevations in Intra-cranial blood flow velocities following a SCUBA Dive and the Influence of Post-dive Exercise

et al. 2016

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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.

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The impact of predive exercise on repetitive SCUBA diving

Abstract: Both groups experienced a significant decrease in MPs at all measurements in the second series of dives compared to the first, regardless of the placement of exercise. Whether this is related to an effect of suppression of MPs or exercise timing is not clear.

Cited by 8 publications

References 32 publications

Microparticle and interleukin-1β production with human simulated compressed air diving

Microparticle and interleukin-1β production with human simulated compressed air diving

Highs and lows of hyperoxia: physiological, performance, and clinical aspects

Elevations in Intra-cranial blood flow velocities following a SCUBA Dive and the Influence of Post-dive Exercise

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