Eccentric exercise 24 h prior to hypobaric decompression increases decompression strain.

PURPOSE: Animal studies have shown that recent musculoskeletal injuries increase the risk of decompression sickness (DCS). However, to date no similar experimental study has been performed in humans. The aim was to investigate if exercise-induced muscle damage (EIMD)-as provoked by eccentric work and characterized by reduced strength and delayed-onset muscle soreness (DOMS)-leads to increased formation of venous gas emboli (VGE) during subsequent hypobaric exposure. METHODS: Each subject (n = 13) was on two occasions exposed to a simulated altitude of 24,000 ft for 90 min, whilst breathing oxygen. Twenty-four hours prior to one of the altitude exposures, each subject performed 15 min of eccentric arm-crank exercise. Markers of EIMD were reduction in isometric m. biceps brachii strength and DOMS as assessed on the Borg CR10 pain scale. The presence of VGE was measured in the right cardiac ventricle using ultrasound, with measurements performed at rest and after three leg kicks and three arm flexions. The degree of VGE was evaluated using the six-graded Eftedal-Brubakk scale and the Kisman integrated severity score (KISS). RESULTS: Eccentric exercise induced DOMS (median 6.5), reduced the biceps brachii strength (from 230 ± 62 N to 151 ± 8.8 N) and increased the mean KISS at 24,000 ft, both at rest (from 1.2 ± 2.3 to 6.9 ± 9.2, p = 0.01) and after arm flexions (from 3.8 ± 6.2 to 15.5 ± 17.3, p = 0.029). CONCLUSION: EIMD, induced by eccentric work, provokes release of VGE in response to acute decompression.

Decompression strain in parachute jumpmasters during simulated high-altitude missions: a special reference to preoxygenation strategies.

PURPOSE: Military parachute operations are often executed at high altitude, from an unpressurized aircraft compartment. Parachute jumpmasters (JM) are thus regularly exposed to 29,500 ft for 60 min. The aim was to investigate the decompression strain during a simulated JM mission at high altitude and to compare two strategies of preoxygenation, conducted either at sea-level or below 10,000 ft, during ascent to mission altitude. METHODS: Ten JM completed, on separate occasions, a 45-min preoxygenation either at sea-level (normobaric: N) or 8200ft (hypobaric: H), followed by exposure to 28,000 ft for 60 min, whilst laying supine and breathing 100% oxygen. At min 45 of the exposure to 28,000 ft, the JM performed 10 weighted squats. Decompression strain was determined from ultrasound assessment of venous gas emboli (VGE) during supine rest (5-min intervals), after three unloaded knee-bends (15-min intervals) and immediately following the weighted squats. The VGE were scored using a six-graded scale (0-5). RESULTS: In condition H, two JM experienced decompression sickness (DCS), whereas no DCS incidents were reported in condition N. The prevalence of VGE was higher in the H than the N condition, at rest [median(range), 3(0-4) vs 0(0-3); p = 0.017], after unloaded knee-bends [3(0-4) vs 0(0-3); p = 0.014] and after the 10 weighted squats [3(0-4) vs 0(0-3); p = 0.014]. VGE were detected earlier in the H (28 ± 20 min, p = 0.018) than the N condition (50 ± 19 min). CONCLUSIONS: A preoxygenation/altitude procedure commonly used by JM, with a 60-min exposure to 28,000 ft after pre-oxygenation for 45 min at 8200 ft is associated with high risk of DCS. The decompression strain can be reduced by preoxygenating at sea level.

The effect of dietary intake on apneic performance, cardiovascular and splenic responses during repeated breath holds.

Static apneas performed after an overnight fast as opposed to postprandially have been evinced to improve apneic performance. However, no study has explored the effect of dietary intake on apneic performance, cardiovascular or splenic responses over a series of repeated apneas. Ten healthy adults attended the laboratory on three separate occasions (≥48-h apart): after a 14-h fast (F14), 1 h postconsumption of a high-calorie, high-carbohydrate (HCHC) meal, or 1 h postconsumption of a low-calorie, low-carbohydrate (LCLC)-based meal. During each visit, the subjects performed a hyperoxic rebreathing trial and a series of three repeated maximal static apneas. Heart rate, peripheral oxyhemoglobin saturation ([Formula: see text]), and gas exchange were monitored continuously, whereas splenic volume (SV) and hematology were assessed after the rebreathing and apneas. At rest, after HCHC, the respiratory exchange ratio (0.87 ± 0.17, P ≤ 0.043), expired minute volume of carbon dioxide (CO2; HCHC, 0.35 ± 0.09 L/min, P ≤ 0.014), and SV (227 ± 45 mL, P ≤ 0.031) were higher compared with F14 (0.71 ± 0.08; 0.23 ± 0.04 L/min; 204 ± 49 mL) and LCLC (0.72 ± 0.07; 0.25 ± 0.03 L/min; 199 ± 49 mL). A faster CO2 accumulation was recorded during the HCHC (96 ± 35 s) rebreathing trial (F14, 162 ± 42 s, P = 0.001; LCLC, 151 ± 23 s, P = 0.002). Longer apneas were reported in F14 compared with HCHC (apneas 1-3, P ≤ 0.046) and LCLC (apneas 2-3, P ≤ 0.006). After the first apnea, SV was lower in F14 (141 ± 43 mL, P = 0.015) compared with HCHC (180 ± 34 mL). Moreover, after the third apnea, end-tidal partial pressure of oxygen and nadir [Formula: see text] were lower in F14 (8.6 ± 2.2 kPa, P = 0.028; 77 ± 13%, P = 0.009) compared with HCHC (10.1 ± 1.7 kPa; 84 ± 9%). No differences were measured in end-apneic end-tidal partial pressure of CO2, heart rate nor hematology across diets. Fasting improved apneic performance with apneas being terminated at lower oxygen levels through altering the rate of CO2 accumulation but without affecting the cardiovascular responses.