Effects of high-intensity interval training with hyperbaric oxygen.

Hyperbaric Oxygen (HBO2) has been proposed as a pre-conditioning method to enhance exercise performance. Most prior studies testing this effect have been limited by inadequate methodologies. Its potential efficacy and mechanism of action remain unknown. We hypothesized that HBO2 could enhance aerobic capacity by inducing mitochondrial biogenesis via redox signaling in skeletal muscle. HBO2 was administered in combination with high-intensity interval training (HIIT), a potent redox stimulus known to induce mitochondrial biogenesis. Aerobic capacity was tested during acute hypobaric hypoxia seeking to shift the limiting site of whole body V̇O2 from convection to diffusion, more closely isolating any effect of improved oxidative capacity. Healthy volunteers were screened with sea-level (SL) V̇O2peak testing. Seventeen subjects were enrolled (10 men, 7 women, ages 26.5±1.3 years, BMI 24.6±0.6 kg m-2, V̇O2peak SL = 43.4±2.1). Each completed 6 HIIT sessions over 2 weeks randomized to breathing normobaric air, "HIIT+Air" (PiO2 = 0.21 ATM) or HBO2 (PiO2 = 1.4 ATM) during training, "HIIT+HBO2" group. Training workloads were individualized based on V̇O2peak SL test. Vastus Lateralis (VL) muscle biopsies were performed before and after HIIT in both groups. Baseline and post-training V̇O2peak tests were conducted in a hypobaric chamber at PiO2 = 0.12 ATM. HIIT significantly increased V̇O2peak in both groups: HIIT+HBO2 31.4±1.5 to 35.2±1.2 ml kg-1·min-1 and HIIT+Air 29.0±3.1 to 33.2±2.5 ml kg-1·min-1 (p = 0.005) without an additional effect of HBO2 (p = 0.9 for interaction of HIIT x HBO2). Subjects randomized to HIIT+HBO2 displayed higher skeletal muscle mRNA levels of PPARGC1A, a regulator of mitochondrial biogenesis, and HK2 and SLC2A4, regulators of glucose utilization and storage. All other tested markers of mitochondrial biogenesis showed no additional effect of HBO2 to HIIT. When combined with HIIT, short-term modest HBO2 (1.4 ATA) has does not increase whole-body V̇O2peak during acute hypobaric hypoxia. (ClinicalTrials.gov Identifier: NCT02356900; https://clinicaltrials.gov/ct2/show/NCT02356900).

The Dewey monitor: Pulse oximetry can independently detect hypoxia in a rebreather diver.

Rebreather diving has one of the highest fatality rates per man hour of any diving activity in the world. The leading cause of death is hypoxia, typically from equipment or procedural failures. Hypoxia causes very few symptoms prior to causing loss of consciousness. Additionally, since the electronics responsible for controlling oxygen levels in rebreathers often control their alarm systems, frequently divers do not receive any external warnings. This study investigated the use of a forehead pulse oximeter as an independent warning device in the event of rebreather failure. Ten test subjects (seven male, three female, median age 29, range 26-35) exercised at a targeted rate of 2 L/minute oxygen consumption while on a non-functional rebreather breathing loop (mean consumption achieved 2.09 ± 0.36 L/minute). Each subject was tested both at the surface and at pressurized depth of 77 fsw (starting pO2=0.7 atm). The data show that a pulse oximeter could be used to provide an Mk 16 rebreather diver with a minimum mean of 49 seconds (± 17 seconds SD) of warning time after a noticeable change in blood oxygen saturation (SpO2 ≤ 95%) but before any risk of loss of consciousness (calculated SpO2 ≤ 80%), so that the diver may take mitigating actions. No statistical difference in warning time was found between the tests at surface and at 77 fsw (P=0.46).

Hypercapnia in diving: a review of CO2 retention in submersed exercise at depth.

Carbon dioxide (CO2) retention, or hypercapnia, is a known risk of diving that can cause mental and physical impairments leading to life-threatening accidents. Often, such accidents occur due to elevated inspired carbon dioxide. For instance, in cases of CO2 elimination system failures during rebreather dives, elevated inspired partial pressure of carbon dioxide (PCO2) can rapidly lead to dangerous levels of hypercapnia. Elevations in PaCO2 (arterial pressure of PCO2) can also occur in divers without a change in inspired PCO2. In such cases, hypercapnia occurs due to alveolar hypoventilation. Several factors of the dive environment contribute to this effect through changes in minute ventilation and dead space. Predominantly, minute ventilation is reduced in diving due to changes in respiratory load and associated changes in respiratory control. Minute ventilation is further reduced by hyperoxic attenuation of chemosensitivity. Physiologic dead space is also increased due to elevated breathing gas density and to hyperoxia. The Haldane effect, a reduction in CO2 solubility in blood due to hyperoxia, may contribute indirectly to hypercapnia through an increase in mixed venous PCO2. In some individuals, low ventilatory response to hypercapnia may also contribute to carbon dioxide retention. This review outlines what is currently known about hypercapnia in diving, including its measurement, cause, mental and physical effects, and areas for future study.