Abstract

Exercise generates reactive oxygen species (ROS), creating a redox imbalance towards oxidation when inadequately intense. Normobaric and hyperbaric oxygen (HBO) breathed while not exercising induces antioxidant enzymes expression, but literature is still poor. Twenty-two athletes were assigned to five groups: controls; 30%, or 50% O2; 100% O2 (HBO) at 1.5 or 2.5 atmosphere absolute (ATA). Twenty treatments were administered on non-training days. Biological samples were collected at T0 (baseline), T1 (end of treatments), and T2 (1 month after) to assess ROS, antioxidant capacity (TAC), lipid peroxidation, redox (amino-thiols) and inflammatory (IL-6, 10, TNF-α) status, renal function (i.e., neopterin), miRNA, and hemoglobin. At T1, O2 mixtures and HBO induced an increase of ROS, lipid peroxidation and decreased TAC, counterbalanced at T2. Furthermore, 50% O2 and HBO treatments determined a reduced state in T2. Neopterin concentration increased at T1 breathing 50% O2 and HBO at 2.5 ATA. The results suggest that 50% O2 treatment determined a reduced state in T2; HBO at 1.5 and 2.5 ATA similarly induced protective mechanisms against ROS, despite the latter could expose the body to higher ROS levels and neopterin concentrations. HBO resulted in increased Hb levels and contributed to immunomodulation by regulating interleukin and miRNA expression.

Highlights

  • Oxygen is the fundamental component of cellular aerobic metabolism

  • We present the results of a preliminary experiment involving the administration of oxygen at different concentrations and pressures to primarily investigate effects on the oxidative stress panel, and secondarily the effects on inflammation, miRNA

  • Levels at follow up, suggesting the protective role of these treatments against oxidative stress (Figure 4G). These results seem to suggest that hyperbaric oxygen (HBO) at 1.5 and 2.5 atmosphere absolute (ATA) induce a similar response in protective mechanisms against reactive oxygen species (ROS), despite the latter could expose the body to higher ROS levels (Figure 1A) and renal damage predisposition (Figure 3B: higher neopterin levels at T1)

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Summary

Introduction

By evolving at 1 atmosphere absolute (ATA), human cells have developed the most efficient way to use oxygen and, at the same time, to protect themselves from its byproducts. Reactive oxygen species (ROS) represent an important family of molecules produced during mitochondrial respiration acting as signaling molecules with regulatory roles on cell activities [1]. It is estimated that 0.2% to 2% of oxygen consumed by mitochondria results in ROS production [2]. Skeletal muscle contraction is related to ROS production [3]. As well as the onset of skeletal muscle fatigue [4] and age-related pathological conditions in skeletal muscle. During exercise, ROS levels increase and create an imbalance in redox status towards oxidation, potentially leading to intracellular damage [5].

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