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).

Testing of full face snorkel masks to examine recreational snorkeler deaths.

A recent rise in snorkeling-related deaths in Hawaii has inspired several bans on full face snorkel masks (FFSMs). However, while there are theories to explain the deaths, little physiological data exists about the way the FFSMs provide gas to an exercising subject. To evaluate the safety of the FFSM concept, this study was designed to test how use of a full face snorkel mask (FFSM) may be physiologically different than use of a conventional snorkel, and to assess if any of those differences could lead to increased risk for the snorkeler. Ten (10) volunteer human subjects were tested using a variety of commercially available FFSMs, with real-time monitoring of blood oxygen saturation (SpO2), inspired airway pressure, and inspired and expired levels of carbon dioxide and oxygen. Two of the three FFSM design types were shown not to function as advertised, but none of the masks provided physiologically problematic gas supplies to the snorkelers. While this testing yielded no conclusive "smoking gun" to explain the snorkeler deaths, some of the mask models showed patterns of increasing breathing resistance with water intrusion because of a shared design characteristic, and this increased resistance could potentially create elevated levels of respiratory distress to snorkelers during real-world use.

The Dewey Monitor: Pulse Oximetry can Warn of Hypoxia in an Immersed Rebreather Diver in Multiple Scenarios.

Divers who wish to prolong their time underwater while carrying less equipment often use devices called rebreathers, which recycle the gas expired after each breath instead of discarding it as bubbles. However, rebreathers' need to replace oxygen used by breathing creates a failure mechanism that can and frequently does lead to hypoxia, loss of consciousness, and death. The purpose of this study was to determine whether a pulse oximeter could provide a useful amount of warning time to a diver with a rebreather after failure of the oxygen addition mechanism. Twenty-eight volunteer human subjects breathed on a mixed-gas rebreather in which the oxygen addition system had been disabled. The subjects were immersed in water in four separate environmental scenarios, including cold and warm water, and monitored using pulse oximeters placed at multiple locations. Pulse oximeters placed on the forehead and clipped on the nasal ala provided a mean of 32 s (±10 s SD) of warning time to divers with falling oxygen levels, prior to risk of loss of consciousness. These devices, if configured for underwater use, could provide a practical and inexpensive alarm system to warn of impending loss of consciousness in a manner that is redundant to the rebreather.

Safety and Ergogenic Properties of Combined Aminophylline and Ambrisentan in Hypoxia.

We hypothesized that concomitant pharmacological inhibition of the endothelin and adenosine pathway is safe and improves exercise performance in hypoxic humans, via a mechanism that does not involve augmentation of blood oxygenation. To test this hypothesis, we established safety and drug interactions for aminophylline (500 mg) plus ambrisentan (5 mg) in normoxic volunteers. Subsequently, a placebo-controlled study was employed to test the combination in healthy resting and exercising volunteers at simulated altitude (4,267 m). No serious adverse events occurred. Drug interaction was minimal or absent. Aminophylline alleviated hypoxia-induced headaches. Aminophylline, ambrisentan, and their combination all significantly (P < 0.05 vs. placebo) improved submaximal hypoxic exercise performance (19.5, 20.6, and 19.1% >placebo). Single-dose ambrisentan increased blood oxygenation in resting, hypoxic subjects. We conclude that combined aminophylline and ambrisentan offer promise to safely increase exercise capacity in hypoxemic humans without relying on increasing blood oxygen availability.

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.

Venous Gas Emboli and Ambulation at 4.3 psia.

INTRODUCTION: Ambulation during extravehicular activity on Mars may increase the risk of decompression sickness through enhanced bubble formation in the lower body. HYPOTHESES: walking effort (ambulation) before an exercise-enhanced denitrogenation (prebreathe) protocol at 14.7 psia does not increase the incidence of venous gas emboli (VGE) at 4.3 psia, but does increase incidence if performed after tissues become supersaturated with nitrogen at 4.3 psia. METHODS: VGE results from 45 control subjects who performed exercise prebreathe without ambulation before or during a 4-h exposure to 4.3 psia were compared to 21 subjects who performed the same prebreathe but ambulated before and during the hypobaric exposure (Group I) and to 41 subjects who only ambulated before the hypobaric exposure (Group II). Monitoring for VGE in the pulmonary artery was for 4 min at about 12-min intervals using precordial Doppler ultrasound (2.5 mHz). Detected VGE were assigned a categorical grade from I to IV. The detection of Grade III or IV was classified as "high VGE grade." RESULTS: The incidence of high VGE grade for Group I (57%) was greater than the control (17%) and Group II (15%). The incidence of pain-only decompression sickness was greater for Group I (20%) than the control (0%) and Group II (5%). CONCLUSIONS: High-grade VGE are increased by mild ambulation conducted under a supersaturated state (Group I vs. II); however, no increase was observed with mild ambulation during the saturated state alone (control vs. Group II).Conkin J, Pollock NW, Natoli MJ, Martina SD, Wessell JH III, Gernhardt ML. Venous gas emboli and ambulation at 4.3 psia. Aerosp Med Hum Perform. 2017; 88(4):370-376.

Sildenafil: Possible Prophylaxis against Swimming-induced Pulmonary Edema.

Swimming-induced pulmonary edema (SIPE) occurs during swimming and scuba diving, usually in cold water, in susceptible healthy individuals, especially military recruits and triathletes. We have previously demonstrated that pulmonary artery (PA) pressure and PA wedge pressure are higher during immersed exercise in SIPE-susceptible individuals versus controls, confirming that SIPE is a form of hemodynamic pulmonary edema. Oral sildenafil 50 mg 1 h before immersed exercise reduced PA pressure and PA wedge pressure, suggesting that sildenafil may prevent SIPE. We present a case of a 46-yr-old female ultratriathlete with a history of at least five SIPE episodes. During a study of an exercise submerged in 20°C water, physiological parameters before and after sildenafil 50 mg orally were as follows: O2 consumption 1.75, 1.76 L·min; HR 129, 135 bpm; arterial pressure 189/88 (mean 121.5), 172/85 (mean 114.3) mm Hg; mean PA pressure 35.3, 28.8 mm Hg; and PA wedge pressure 25.3, 19.7 mm Hg. She has had no recurrences during 20 subsequent triathlons while taking 50 mg sildenafil before each swim. This case supports sildenafil as an effective prophylactic agent against SIPE during competitive surface swimming.

A randomized controlled pilot study of VO2 max testing: a potential model for measuring relative in vivo efficacy of different red blood cell products.

BACKGROUND: Randomized trials, for example, RECESS, comparing "young" (median, 7-day) versus "middle-aged" (median, 28-day) red blood cells (RBCs), showed no difference in outcome. These data are important; however, they do not inform us about the safety and effectiveness of the oldest RBCs, which some patients receive. It may not be feasible to conduct a clinical trial randomizing patients to receive the oldest blood. Therefore, we propose strenuous exercise (VO2 max testing) as a model to study the relative efficacy to increase oxygen delivery to tissue of different RBC products, for example, extremes of storage duration. STUDY DESIGN AND METHODS: In this pilot study, eight healthy subjects had 2 units of leukoreduced RBCs collected by apheresis in AS-3 using standard methods. Subjects were randomized to receive both (2) units of their autologous RBCs at either 7 or 42 days after blood collection. VO2 max testing on a cycle ergometer was performed 2 days before (Monday) and 2 days after (Friday) the transfusion visit (Wednesday). This design avoids confounding effects on intravascular volume from the 2-unit blood transfusion. The primary outcome was the difference in VO2 max between Friday and Monday (delta VO2 max). RESULTS: VO2 max increased more in the 7-day RBC arm (8.7 ± 6.9% vs. 1.9 ± 6.5%, p = 0.202 for comparison between arms). Exercise duration (seconds) increased in the 7-day RBC arm (8.4 ± 1.7%) but actually decreased in the 42-day arm (-2.6 ± 3.6%, p = 0.002). CONCLUSIONS: This pilot study suggests that VO2 max testing has potential as a rigorous and quantitative in vivo functional assay of RBC function. Our preliminary results suggest that 42-day RBCs are inferior to 7-day RBCs at delivering oxygen to tissues.

Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil.

BACKGROUND: Swimming-induced pulmonary edema (SIPE) occurs during swimming or scuba diving, often in young individuals with no predisposing conditions, and its pathophysiology is poorly understood. This study tested the hypothesis that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise than in the general population and are reduced by sildenafil. METHODS AND RESULTS: Ten study subjects with a history of SIPE (mean age, 41.6 years) and 20 control subjects (mean age, 36.2 years) were instrumented with radial artery and pulmonary artery catheters and performed moderate cycle ergometer exercise for 6 to 7 minutes while submersed in 20°C water. SIPE-susceptible subjects repeated the exercise 150 minutes after oral administration of 50 mg sildenafil. Work rate and mean arterial pressure during exercise were similar in controls and SIPE-susceptible subjects. Average o2 and cardiac output in controls and SIPE-susceptible subjects were: o2 2.42 L·min(-1) versus 1.95 L·min(-1), P=0.2; and cardiac output 17.9 L·min(-1) versus 13.8 L·min(-1), P=0.01. Accounting for differences in cardiac output between groups, mean pulmonary artery pressure at cardiac output=13.8 L·min(-1) was 22.5 mm Hg in controls versus 34.0 mm Hg in SIPE-susceptible subjects (P=0.004), and the corresponding pulmonary artery wedge pressure was 11.0 mm Hg versus 18.8 mm Hg (P=0.028). After sildenafil, there were no statistically significant differences in mean pulmonary artery pressure or pulmonary artery wedge pressure between SIPE-susceptible subjects and controls. CONCLUSIONS: These observations confirm that SIPE is a form of hemodynamic pulmonary edema. The reduction in pulmonary vascular pressures after sildenafil with no adverse effect on exercise hemodynamics suggests that it may be useful in SIPE prevention. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00815646.

Effects of elevated oxygen and carbon dioxide partial pressures on respiratory function and cognitive performance.

Hyperoxia during diving has been suggested to exacerbate hypercapnic narcosis and promote unconsciousness. We tested this hypothesis in male volunteers (12 at rest, 10 at 75 W cycle ergometer exercise) breathing each of four gases in a hyperbaric chamber. Inspired Po2 (PiO2 ) was 0.21 and 1.3 atmospheres (atm) without or with an individual subject's maximum tolerable inspired CO2 (PiO2 = 0.055-0.085 atm). Measurements included end-tidal CO2 partial pressure (PetCO2 ), rating of perceived discomfort (RPD), expired minute ventilation (V̇e), and cognitive function assessed by auditory n-back test. The most prominent finding was, irrespective of PetCO2 , that minute ventilation was 8-9 l/min greater for rest or exercise with a PiO2 of 1.3 atm compared with 0.21 atm (P < 0.0001). For hyperoxic gases, PetCO2 was consistently less than for normoxic gases (P < 0.01). For hyperoxic hypercapnic gases, n-back scores were higher than for normoxic gases (P < 0.01), and RPD was lower for exercise but not rest (P < 0.02). Subjects completed 66 hyperoxic hypercapnic trials without incident, but five stopped prematurely because of serious symptoms (tunnel vision, vision loss, dizziness, panic, exhaustion, or near syncope) during 69 normoxic hypercapnic trials (P = 0.0582). Serious symptoms during hypercapnic trials occurred only during normoxia. We conclude serious symptoms with hyperoxic hypercapnia were absent because of decreased PetCO2 consequent to increased ventilation.

Chemical oxygen generation: Evaluation of the Green Dot Systems, Inc portable, nonpressurized emOx device.

OBJECTIVE: To evaluate the performance of the emOx emergency powdered oxygen portable nonpressurized delivery system. This device produces oxygen through chemical reaction and is marketed for emergency first aid use until professional medical assistance is available. METHODS: Seven unmanned trials were conducted under standard laboratory conditions. Measures included oxygen flow, reaction canister external wall temperature, delivered gas temperature, and delivered gas relative humidity. RESULTS: The mean oxygen flow was 1.75 ± 1.58 L x min(-1) (mean ± SD) with a total yield of 40.4 ± 2.6 L. Oxygen flow increased slowly and with substantial variability between reactant groups, exceeding 2.0 L x min(-1) after 15.7 ± 6.4 minutes of operation. Oxygen flow briefly peaked at 5.93 ± 0.56 L x min(-1) at 17.8 ± 7.9 minutes before rapidly falling to zero. The mean oxygen fraction was 0.81 ± 0.28, exceeding 0.96 in 10.7 ± 2.9 minutes. The reaction canister external wall temperature reached 54.7 ± 7.4 °C. Delivered gas temperature varied little from ambient. Delivered gas relative humidity surpassed 75% in 8 ± 3 minutes and 90% in 15 ± 5 minutes of operation. CONCLUSIONS: A readily available, high concentration oxygen supply could have utility to manage many conditions in advance of the arrival of professional emergency medical services (EMS). Unfortunately, the highly variable activation time and low average oxygen flow rate make the rapid deployment value of the emOx equivocal. The limited total oxygen yield makes it inappropriate for conditions demanding significant oxygen resources. Advancement in oxygen concentrator systems likely holds far more promise than powdered chemical oxygen generation for first aid and emergency medical applications.

Effects of hyperoxia on ventilation and pulmonary hemodynamics during immersed prone exercise at 4.7 ATA: possible implications for immersion pulmonary edema.

Immersion pulmonary edema (IPE) can occur in otherwise healthy swimmers and divers, likely because of stress failure of pulmonary capillaries secondary to increased pulmonary vascular pressures. Prior studies have revealed progressive increase in ventilation [minute ventilation (Ve)] during prolonged immersed exercise. We hypothesized that this increase occurs because of development of metabolic acidosis with concomitant rise in mean pulmonary artery pressure (MPAP) and that hyperoxia attenuates this increase. Ten subjects were studied at rest and during 16 min of exercise submersed at 1 atm absolute (ATA) breathing air and at 4.7 ATA in normoxia and hyperoxia [inspired P(O(2)) (Pi(O(2))) 1.75 ATA]. Ve increased from early (E, 6th minute) to late (L, 16th minute) exercise at 1 ATA (64.1 +/- 8.6 to 71.7 +/- 10.9 l/min BTPS; P < 0.001), with no change in arterial pH or Pco(2). MPAP decreased from E to L at 1 ATA (26.7 +/- 5.8 to 22.7 +/- 5.2 mmHg; P = 0.003). Ve and MPAP did not change from E to L at 4.7 ATA. Hyperoxia reduced Ve (62.6 +/- 10.5 to 53.1 +/- 6.1 l/min BTPS; P < 0.0001) and MPAP (29.7 +/- 7.4 to 25.1 +/- 5.7 mmHg, P = 0.002). Variability in MPAP among subjects was wide (range 14.1-42.1 mmHg during surface and depth exercise). Alveolar-arterial Po(2) difference increased from E to L in normoxia, consistent with increased lung water. We conclude that increased Ve at 1 ATA is not due to acidosis and is more consistent with respiratory muscle fatigue and that progressive pulmonary vascular hypertension does not occur during prolonged immersed exercise. Wide variation in MPAP among healthy subjects is consistent with variable individual susceptibility to IPE.

Carbon monoxide, skeletal muscle oxidative stress, and mitochondrial biogenesis in humans.

Given that the physiology of heme oxygenase-1 (HO-1) encompasses mitochondrial biogenesis, we tested the hypothesis that the HO-1 product, carbon monoxide (CO), activates mitochondrial biogenesis in skeletal muscle and enhances maximal oxygen uptake (Vo(2max)) in humans. In 10 healthy subjects, we biopsied the vastus lateralis and performed Vo(2max) tests followed by blinded randomization to air or CO breathing (1 h/day at 100 parts/million for 5 days), a contralateral muscle biopsy on day 5, and repeat Vo(2max) testing on day 8. Six independent subjects underwent CO breathing and two muscle biopsies without exercise testing. Molecular studies were performed by real-time RT-PCR, Western blot analysis, and immunochemistry. After Vo(2max) testing plus CO breathing, significant increases were found in mRNA levels for nuclear respiratory factor-1, peroxisome proliferator-activated receptor-gamma coactivator-1alpha, mitochondrial transcription factor-A (Tfam), and DNA polymerase gamma (Polgamma) with no change in mitochondrial DNA (mtDNA) copy number or Vo(2max). Levels of myosin heavy chain I and nuclear-encoded HO-1, superoxide dismutase-2, citrate synthase, mitofusin-1 and -2, and mitochondrial-encoded cytochrome oxidase subunit-I (COX-I) and ATPase-6 proteins increased significantly. None of these responses were reproduced by Vo(2max) testing alone, whereas CO alone increased Tfam and Polgamma mRNA, and COX-I, ATPase-6, mitofusin-2, HO-1, and superoxide dismutase protein. These findings provide evidence linking the HO/CO response involved in mitochondrial biogenesis in rodents to skeletal muscle in humans through a set of responses involving regulation of the mtDNA transcriptosome and mitochondrial fusion proteins autonomously of changes in exercise capacity.

Performance characteristics of the second-generation remote emergency medical oxygen closed-circuit rebreather.

OBJECTIVE: Closed-circuit oxygen rebreathers may provide high concentrations of oxygen at extremely low flow rates appropriate for field use with limited oxygen supplies. The performance of the preproduction, second-generation remote emergency medical oxygen (REMO(2)) system developed for Divers Alert Network was evaluated. METHODS: The unidirectional circuit was made up of a solid, prepackaged CO(2) scrubber canister (984 +/- 14 [SD] g scrubber mass), standard 22-mm-inside-diameter anesthesia circuit hoses, 5-L breathing bag, 5-cm H(2)O positive end-expiratory pressure valve, and oronasal mask. Oxygen flow, inspired oxygen, expired CO(2), peak inspired and expired mask pressures, time to reach scrubber canister saturation or "breakthrough" (postscrubber CO(2) concentration reaching 3.8 mm Hg), and subject tolerance were measured under standard laboratory conditions. RESULTS: Six trials were completed using healthy volunteers (94.7 +/- 19.6 kg). Five of the 6 completed trials did not reach breakthrough at the planned trial limit of 8 hours. Mean average oxygen flow rate was 1.00 +/- 0.17 L x min(-1). Mean peak inspired and expired mask pressures were -5.0 +/- 1.9 and 6.5 +/- 1.9 cm H(2)O, respectively. Subjects generally reported good tolerance to circuit breathing. CONCLUSIONS: The second-generation REMO(2) was well tolerated by healthy subjects during 8-hour laboratory evaluation trials. The device provided high mean inspired oxygen fractions at low mean oxygen flow rates, relatively modest mean maximal inspired and expired pressures, and excellent scrubber canister duration. Further evaluation of field performance with a patient population is warranted.

Statistical models of acute mountain sickness.

Acute mountain sickness (AMS) is caused by exposure to altitudes exceeding 2500 m and often resolves by acclimatization without further ascent. Statistical models of AMS score and the probability of an AMS diagnosis were developed to allow the combination of dissimilar exposures for simultaneous analysis. The study population was 302 trekkers from a previous investigation who provided self-reported symptoms upon arrival at 3840 m during hikes through altitudes of 1500 to 6200 m. AMS score (Hackett scale) was estimated by linear regression and the probability of an AMS diagnosis (Lake Louise criteria) by logistic regression. AMS score or probability was significantly associated with exposure day and altitude. Increased altitude over the prior 3 days resulted in higher estimated AMS score or probability and decreased altitude in lower score or probability. The odds ratio (OR) of AMS was 3.6 if not on acetazolamide. Females appeared slightly more susceptible than males (1.5 OR). The approach offers the advantages of (1) improved statistical power by combining exposures, (2) insight into the dose-response relationship of altitude exposure and AMS risk, (3) quantitative tests for the significance of factors that might affect AMS susceptibility, and (4) practical tools to track individual climbers and plan operational ascents.

Risk of decompression sickness during exposure to high cabin altitude after diving.

BACKGROUND: Postdive altitude exposure increases the risk of decompression sickness (DCS). Certain training and operational situations may require U.S. Special Operations Forces (SOF) personnel to conduct high altitude parachute operations after diving. Problematically, the minimum safe preflight surface intervals (PFSI) between diving and high altitude flying are not known. METHODS: There were 102 healthy, male volunteers (34 +/- 10 [mean +/- SD] yr of age, 84.5 +/- 13.8 kg weight, 26.2 +/- 4.2 kg x m(-2) BMI) who completed simulated 60 fsw (feet of seawater)/60 min air dives preceding simulated 3-h flights at 25,000 ft to study DCS risk as a function of PFSI. Subjects were dry and at rest throughout. Oxygen was breathed for 30 min before and during flight in accordance with SOF protocols. Subjects were monitored for clinical signs of DCS and for venous gas emboli (VGE) using precordial Doppler ultrasound. DCS incidence was compared with Chi-squared; VGE onset time and time to maximum grade with one-way ANOVA (significance at p < 0.05). RESULTS: Three cases of DCS occurred in 155 subject-exposures: 1/35 and 0/24 in 2 and 3 h flight-only controls, respectively; 0/23, 1/37, and 1/36 for 24, 18, and 12 h dive-PFSI-flight profiles, respectively. DCS risk did not differ between profiles (chi2 [4] = 1.33; crit = 9.49). VGE were observed in 19% of flights. Neither VGE onset time nor time to max grade differed between profiles (82 +/- 38 min [p = 0.88] and 100 +/- 40 min [p = 0.68], respectively). CONCLUSION: Increased DCS risk was not detected as a result of dry, resting 60 fsw/60 min air dives conducted 24-12 h before a resting, 3-h oxygen-breathing 25,000 ft flight (following 30 min oxygen prebreathe). The current SOF-prescribed minimum PFSI of 24 h may be unnecessarily conservative.