DNA damage after long-term repetitive hyperbaric oxygen exposure.
MED 09-11 200919023023 NDN- 230-0919-4585-0
AUTHORS- Groeger, Michael; Oter, Soukrou; Simkova, Vladislava; Bolten, Markus; Koch, Andreas; Warninghoff, Volker; Georgieff, Michael; Muth, Claus-Martin; Speit, Gounter; Radermacher, Peter
JOURNAL NAME- J Appl Physiol
VOLUME 106
NUMBER 1
PUBLICATION DATE- 2009 Jan
PP 311-5
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 8502536
JOURNAL SUBSET- MEDJSIM
ISSN- 8750-7587
CORPORATE AUTHOR- Sektion Anoasthesiologische Pathopyhsiologie und Verfahrensentwicklung Universitoatsklinikum, Parkstrasse 11, D-89073 Ulm, Germany. peter.radermacher@uni-ulm.de).
PUBLICATION COUNTRY- United States
LANGUAGE- English
A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O(2)(*-)) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O(2)(*-) production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage.
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Gas bubbles may not be the underlying cause of decompression illness - The at-depth endothelial dysfunction hypothesis.
Madden LA, Laden G.
Postgraduate Medical Institute, University of Hull, Cottingham Road, Hull HU6 7RX, UK.
Med Hypotheses. 2009 Jan 5. [Epub ahead of print]
Gas formed in tissues and the circulating blood due to decompression is thought to be a significant factor in the progression of decompression illness (DCI). DCI is a potential problem for a growing population of professional and recreational divers. We hypothesise that these gas bubbles are not the causative agent in progression of DCI, rather an exacerbating factor. Endothelial dysfunction caused by a temporary loss of haemostasis due to increased total oxidant status is postulated to be the cause in this at-depth endothelial dysfunction hypothesis. Breathing oxygen at any pressure increases the oxidant status in the circulation causing vasoconstriction; this increase can be prevented by antioxidants, such as Vitamin C, maintaining haemostasis and preventing activation of endothelium, leukocyte recruitment and subsequent localised inflammation. Bubbles have the potential to exacerbate the situation on decompression by damaging the vascular endothelium either through ischemia/reperfusio n, physical contact with the endothelium or by an increase in shear stress. Furthermore, this damage may manifest itself in the release of endothelial membrane fragments (microparticles) .
PMID: 19128890 [PubMed - as supplied by publisher]
Editor’s comment: The chicken before the egg - or vice versa??
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Exerc Sport Sci Rev. 2008 Jan;36(1):38-42.
Beneficial role of exercise on scuba diving.
Department of Physiology, University of Split School of Medicine, Split, Croatia. zdujic@bsb.mefst.hr
Exercising before, during, or after diving is proscribed because of the assumption that it would increase incidence of decompression sickness. Our findings show that exercise performed in a timely fashion before diving or during decompression will reduce the number of venous gas bubbles formed. Exercise after diving did not increase the number of bubbles. Nitric oxide seems to play a protective role.
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Venous bubble count declines during strenuous exercise after an open sea dive to 30 m.
Dujić Z, Obad A, Palada I, Ivancev V, Valic Z.
Department of Physiology, University of Split School of Medicine, Croatia. zdujic@bsb.mefst.hr
INTRODUCTION: The effect of post-dive exercise on bubble formation remains controversial, although the current practice of divers and aviators is to avoid strenuous exercise after diving. Previously, we have shown that exercising 24 h before a dive, or during a decompression stop, significantly reduces bubble formation in man. The objective of this study was to determine whether a short period of strenuous post-dive exercise promotes venous bubble formation. METHODS: Seven male military divers performed an open-sea field dive to a maximum depth of 30 m for 30 min. At maximum depth, subjects performed mild underwater fin swimming, followed by standard decompression. Diving was followed by a post-dive exercise session consisting of short, strenuous incremental upright cycle ergometry, up to 85% of maximal oxygen uptake, for about 10 min. Subjects were monitored for venous gas bubbles in the right heart with an echo-imaging system starting 20 min post-dive while in the supine position, during cycle ergometry in the seated upright position, and immediately after exercise in a supine position. RESULTS: The average number of bubbles was 1.5 +/- 1.4 bubbles x cm(-2) 20 min after diving. Changes in posture from supine to seated upright resulted in significant reduction of bubbles to 0.6 +/- 1.3 bubbles x cm(-2) (p = 0.043), with further reduction to 0.2 +/- 0.3 bubbles x cm(-2) at the end of exercise (p = 0.02). No cases of DCS or intra-pulmonary shunt were observed during or following post-dive exercise. DISCUSSION: These results suggest that post-dive strenuous exercise after a single field dive reduces post-dive gas bubble formation in well-trained military divers. Additional findings are needed for normal sports divers.
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J Physiol. 2004 Mar 16;555(Pt 3):637-42. Epub 2004 Jan 30.
- Comment in:
- J Physiol. 2004 Mar 16;555(Pt 3):588.
Aerobic exercise before diving reduces venous gas bubble formation in humans.
Dujic Z, Duplancic D, Marinovic-Terzic I, Bakovic D, Ivancev V, Valic Z, Eterovic D, Petri NM, Wisløff U, Brubakk AO.
Department of Physiology and Biophysics, University of Split School of Medicine, Split, Croatia. zdujic@bsb.mefst.hr
We have previously shown in a rat model that a single bout of high-intensity aerobic exercise 20 h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate was 9 m min(-1) with a 7 min stop at 130 kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3 min, followed by exercise at 50% of maximum heart rate for 2 min; this was repeated eight times for a total exercise period of 40 min. Venous gas bubbles were monitored with an ultrasonic scanner every 20 min for 80 min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm(-2)(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre-dive exercise, thereby increasing safety. This is the first report to indicate that pre-dive exercise may form the basis for a new way of preventing serious decompression sickness.
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J Appl Physiol. 2005 Sep;99(3):944-9. Epub 2005 Apr 21.
Exercise-induced intrapulmonary shunting of venous gas emboli does not occur after open-sea diving.
Dujić Z, Palada I, Obad A, Duplancić D, Brubakk AO, Valic Z.
Dept. of Physiology and Biophysics, Univ. of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. zdujic@bsb.mefst.hr
Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 m breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at approximately 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.
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