Abstract
In recent studies, oxidative stress after scuba diving has been explored by measuring urinary biomarkers in volunteers under controlled conditions. Dive depth and duration, water temperature, and workload are all variables that can elicit metabolic responses. A controlled diving experiment was performed in an indoor pool at 20, 30, and 40 m depths at a water temperature of 32 °C, on three different days. Samples of urine from five male scuba divers were taken before diving and at four time points after diving, and then tested for their concentration of five different oxidative stress biomarkers by means of liquid chromatography tandem mass spectrometry and by 1H nuclear magnetic resonance metabolomics analysis. The results showed no variation in the five biomarkers after diving, but a decreasing trend was observed over the three days, with no differences among the three depths. The lack of effect on oxidative stress biomarkers has been attributed to the comfortable water temperature and to the absence of exercise in the divers during the experiment. Instead, an increase in hypoxanthine excretion, which can be considered a biomarker sensitive to hyperbaric exposure, was found after diving. Finally, the results suggest a physiological mechanism of metabolic adaptation to a new condition.
Highlights
Oxidative stress in self-contained underwater breathing apparatus divers has been hypothesized because of their exposure to an increased pressure of inhaled air that causes an increased partial pressure of oxygen in the lungs [1]
Conditions and time points, and that the group was always composed of the same subjects
The objective of the present study was to investigate the effect of the water depth on the excretion of oxidative stress biomarkers and other metabolites in scuba divers
Summary
Oxidative stress in self-contained underwater breathing apparatus (scuba) divers has been hypothesized because of their exposure to an increased pressure of inhaled air that causes an increased partial pressure of oxygen in the lungs [1]. The fraction of inspired oxygen will have pressure values higher than in normobaric condition: at a depth of 30 m 4 bar), oxygen has a partial pressure of 851 millibar. This does not create any problem in the alveolar-capillary exchange in the pulmonary alveoli, as this is the typical condition applied to patients with severe respiratory incapacity to satisfy the body’s demands. These responses could lead to physical drawbacks because of the consequent free radical production. In this regard, oxygen becomes toxic if breathed at a partial pressure of about 1.6 bar, which would correspond to 66 m of depth. Oxygen toxicity most commonly affects the lungs, central nervous system (CNS), and eyes [2]
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