INTRODUCTION: The evolution and preservation of venous gas emboli (VGE), as markers of decompression stress, were investigated during alternating high- and moderate altitude exposures, thus, simulating a fighter aircraft high-altitude flight, interrupted by refueling excursions to lower altitudes. METHODS: Eight men served as subjects during three normoxic simulated altitude exposures: High = 90 min at 24,000 ft; High-Low = three x 30 min at 24,000 ft, interspersed by two 30-min intervals at 15,000 ft; Low = 90 min at 15,000 ft. VGE scores were assessed by cardiac ultrasound, using a 5-grade scale. Respiratory nitrogen exchange was measured continuously using a modified closed-circuit electronic rebreather. RESULTS: Both High and High-Low induced persistent VGE, with no inter-condition difference either at rest [median (range): High: 1 (0-3), High-Low: 2 (0-3)] or during unloaded knee-bends [High: 3 (1-4), High-Low: 3 (0-4)], whereas VGE was considerably less in Low, both at rest [0 (0-1)] and during knee-bends [0 (0-2)]. In High-Low, VGE decreased temporarily during the 15,000-ft excursions, but resumed pre-excursion values upon return to 24,000 ft. During the final descent to ground level, VGE were more persistent following High-Low than High. In both High and Low, nitrogen was continuously washed out at altitude, whereas in High-Low, the washout at 24,000 ft was interrupted by nitrogen uptake at 15,000 ft. DISCUSSION: In normoxic conditions, long-duration flying at a cabin altitude of 24,000 ft is associated with substantial VGE occurrence, which is not abolished by intermittent excursions to a cabin altitude of 15,000 ft.

The purpose was to evaluate whether a cold-water immersion test could be used to identify individuals susceptible to local cold injuries (LCI). Sixty-five healthy non-injured (N-I) subjects, and fifteen subjects, who were tested either prior to or after a LCI, sequentially immersed one hand and one foot, in 8 degrees C water for 30 min (CWI phase); this was followed by 15 min of spontaneous rewarming (RW phase). The LCI group showed a lower toe temperature during the CWI phase, and a lower maximum RW temperature of the fingers than the N-I group. However, digit temperatures during the CWI and RW phases exhibited low predictive values for LCI, e.g. results implied that to identify 80% of the LCI subjects, 34-78% of the N-I subjects would also be excluded. Thus, the results suggest that, in practice, hand or foot cold-water immersion tests cannot be used to identify individuals at high risk of LCI.

What is the central question of this study? Controlled-hyperthermia heat acclimation protocols induce an array of thermoregulatory and cardiovascular adaptations that facilitate exercise in hot conditions. We investigated whether this ergogenic potential can be transferred to thermoneutral normoxic or hypoxic exercising conditions. What is the main finding and its importance? We show that heat acclimation did not affect maximal cardiac output or maximal aerobic power in thermoneutral normoxic/hypoxic conditions. Heat acclimation augmented the sweating response in thermoneutral normoxic conditions. The cross-adaptation theory according to which heat acclimation could facilitate hypoxic exercise capacity is not supported by our data. ABSTRACT: Heat acclimation (HA) mitigates heat-induced decrements in maximal aerobic power (V̇O_2peak ) and augments exercise thermoregulatory responses in the heat. Whether this beneficial effect of HA is observed in hypoxic or thermoneutral conditions remains unresolved. We explored the effects of HA on exercise cardiorespiratory and thermoregulatory responses in normoxic, hypoxic, and hot conditions. Twelve males (V̇O_2peak 54.7(5.7) mL·kg^-1 ·min^-1 ) participated in a HA protocol comprising 10 daily 90-min controlled-hyperthermia (target rectal temperature, T_re  = 38.5 °C) exercise sessions. Before and after HA, we determined V̇O_2peak in thermoneutral normoxic (NOR), thermoneutral hypoxic (13.5% F_i O₂ ; HYP) and hot (35 °C, 50% RH; HE) conditions in a randomized and counterbalanced order. Preceding each maximal cycling test, a 30-min steady-state exercise at 40% of the NOR peak power output (W_peak ) was employed to evaluate thermoregulatory responses. HA induced the expected adaptations in HE: reduced T_re and submaximal heart rate (HR), enhanced sweating response and expanded plasma volume. However, HA did not affect V̇O_2peak or maximal cardiac output (CO_max ) (P = 0.61). W_peak was increased post-HA in NOR (P < 0.001) and HE (P < 0.001) by 41 ± 21 and 26 ± 22 W, respectively but not in HYP (P = 0.14). Gross mechanical efficiency was higher (P = 0.004) whereas resting T_re and sweating thresholds were lower (P < 0.01) post-HA across environments. Nevertheless, the gain of the sweating response decreased (P = 0.05) in HYP. In conclusion, our data do not support a beneficial cross-over effect of HA on V̇O_2peak in normoxic or hypoxic conditions. This article is protected by copyright.

We examined the interactive effects of mild hypothermia and hypoxia on finger vasoreactivity to local cold stress. Eight male lowlanders performed, in a counterbalanced order, a normoxic and a hypoxic (partial pressure of oxygen: similar to 12 kPa) hand cold provocation (consisting of a 30-min immersion in 8 degrees C water), while immersed to the chest either in 21 degrees C [cold trials; 0.5 degrees C fall in rectal temperature (T-rec) from individual preimmersion values], or in 35.5 degrees C water, or while exposed to 27 degrees C air. The duration of the trials was kept constant in each breathing condition. Physiological (T-rec, skin temperature, cutaneous vascular conductance, oxygen uptake) and perceptual (thermal sensation and comfort, local pain, affective valence) reactions were monitored continually. Hypoxia accelerated the drop in T-rec by similar to 14 min (P = 0.06, d = 0.67). In the air-exposure trials, hypoxia did not alter finger perfusion during the local cooling. whereas it impaired the finger rewarming response following the cooling (P < 0.01). During the 35.5 degrees C immersion, the finger vasomotor tone was enhanced, especially in hypoxia (P = 0.01). Mild hypothermia aggravated finger vasoconstriction instigated by local cooling (P < 0.01), but the response did not differ between the two breathing conditions (P > 0.05). Hypoxia tended to attenuate the sensation of coldness (P = 0.10, r = 0.40) and thermal discomfort (P = 0.09, r = 0.46) in the immersed hand. Both in normoxia and hypoxia, the whole body thermal state dictates the cutaneous vasomotor reactivity to localized cold stimulus.

INTRODUCTION: The frequency of long-duration, high-altitude missions with fighter aircraft is increasing, which may increase the incidence of decompression sickness (DCS).The aim of the present study was to compare decompression stress during simulated sustained high-altitude flying vs. high-altitude flying interrupted by periods of moderate or marked cabin pressure increase. METHODS: The level of venous gas emboli (VGE) was assessed from cardiac ultrasound images using the 5-degree Eftedal-Brubakk scale. Nitrogen washout/uptake was measured using a closed circuit rebreather. Eight men were investigated in three conditions: one 80-min continuous exposure to a simulated cabin altitude of A) 24,000 ft, or four 20-min exposures to 24,000 ft interspersed by three 20-min intervals at 8) 20,000 ft or C) 900 ft. RESULTS: A and B induced marked and persistent VGE, With peak bubble scores of [median (range)]: A 2.5 (1-3); B: 3.5 (2-4). Peak VGE score was less in C [1.0(1-2),P < 0.01]. Condition A exhibitedan initially high and exponentially decaying rate of nitrogen washout. In C the washout rate was similar in each period at 24,000 ft, and the nitrogen uptake rate was similar during each 900-ft exposure. B exhibited nitrogen washout during each period at 24,000 ft and the initial period at 20,000 ft, but on average no washout or uptake during the last period at 20,000 ft. DISCUSSION: Intermittent reductions of cabin altitude from 24,000 to 20,000 ft do not appear to alleviate the DCS risk, presumably because the pressure increase is not sufficient to eliminate VGE. The nitrogen washout/uptake rate did not reflect DCS risk in the present exposures.

NEW FINDINGS: What is the central question of this study? It is well established that muscle and bone atrophy in conditions of inactivity or unloading, but there is little information regarding the effect of a hypoxic environment on the time course of these deconditioning physiological systems. What is the main finding and its importance? The main finding is that a horizontal 10 day bed rest in normoxia results in typical muscle atrophy, which is not aggravated by hypoxia. Changes in bone mineral content or in metabolism were not detected after either normoxic or hypoxic bed rest.

ABSTRACT: Musculoskeletal atrophy constitutes a typical adaptation to inactivity and unloading of weightbearing bones. The reduced-gravity environment in future Moon and Mars habitats is likely to be hypobaric hypoxic, and there is an urgent need to understand the effect of hypoxia on the process of inactivity-induced musculoskeletal atrophy. This was the principal aim of the present study. Eleven males participated in three 10 day interventions: (i) hypoxic ambulatory confinement; (ii) hypoxic bed rest; and (iii) normoxic bed rest. Before and after the interventions, the muscle strength (isometric maximal voluntary contraction), mass (lean mass, by dual-energy X-ray absorptiometry), cross-sectional area and total bone mineral content (determined with peripheral quantitative computed tomography) of the participants were measured. Blood and urine samples were collected before and on the 1st, 4th and 10th day of the intervention and analysed for biomarkers of bone resorption and formation. There was a significant reduction in thigh and lower leg muscle mass and volume after both normoxic and hypoxic bed rests. Muscle strength loss was proportionately greater than the loss in muscle mass for both thigh and lower leg. There was no indication of bone loss. Furthermore, the biomarkers of resorption and formation were not affected by any of the interventions. There was no significant effect of hypoxia on the musculoskeletal variables. Short-term normoxic (10 day) bed rest resulted in muscular deconditioning, but not in the loss of bone mineral content or changes in bone metabolism. Hypoxia did not modify these results.

The purpose of the study was to evaluate the recuperative efficacy of pre-exercise napping on physical capacity after military sustained operations (SUSOPS) with partial sleep deprivation. Before and after a 2-day SUSOPS, 61 cadets completed a battery of questionnaires, and performed a 2-min lunges trial and a 3,000-m running time-trial. After the completion of SUSOPS, subjects were randomized to either a control [without pre-exercise nap (CON); n = 32] or a nap [with a 30-min pre-exercise nap (NAP); n = 29] group. SUSOPS enhanced perceived sleepiness and degraded mood in both groups. Following SUSOPS, the repetitions of lunges, in the CON group, were reduced by similar to 2.3%, albeit the difference was not statistically significant (p = 0.62). In the NAP group, however, the repetitions of lunges were increased by similar to 7.1% (p = 0.01). SUSOPS impaired the 3,000-m running performance in the CON group (similar to 2.3%; p = 0.02), but not in the NAP group (0.3%; p = 0.71). Present results indicate, therefore, that a relatively brief pre-exercise nap may mitigate physical performance impairments ensued by short-term SUSOPS.

Background: Echocardiography is usually performed with the subject/patient lying in the left lateral position (LLP), because the acoustic window is better in this than in the supine position (SP). The aim was to investigate cardiac responses to rotational changes of position in the transversal plane, from SP to LLP while horizontal, and from leaning on the back (HUT-LB) to leaning on the left side (HUT-LL) while tilted 60° head-up from the horizontal. Methods: Healthy men (n = 12) underwent 10-min HUT provocations. Cardiac variables were measured using two-dimensional echocardiography, Doppler, tissue Doppler imaging and arterial pressures using a volume-clamp method. Results: In horizontal posture, cardiac volumes were smaller in SP than in LLP: end-diastolic volume (EDV) by 14%, end-systolic volume (ESV) by 13%, stroke volume (SV) by 14%, and cardiac output (CO) by 16% (P<0·03). In addition, the mitral annular plane systolic excursion (MAPSE) was 11% smaller (P = 0·001) and the left ventricle isovolumic relaxation time (IVRT) 27% longer in SP than in LLP. The ejection fraction, heart rate, arterial pressure and pulmonary ventilation were similar in SP and LLP. During HUT, EDV, SV, CO and MAPSE were smaller, and IVRT was longer, in HUT-LB than in HUT-LL, by −19%, −20%, −17%, −18% and +35%, respectively (P<0·04). Conclusions: Cardiac performance is enhanced in LLP versus SP and in HUT-LL versus HUT-LB, which can be attributed to improved venous return, conceivably, wholly or in part, due to increased hydrostatic pressure gradients between the caval veins and the heart in the LLP and HUT-LL positions.

BACKGROUND: +Gz tolerance is traditionally determined in centrifuges with open-loop G control, i.e., the centrifuge is under operator control (open loop), and thus the test subject is unable to influence the Gz load. In modern centrifuges, however, the subject is commonly able to continuously control the Gz load (closed loop). It is a widespread opinion among fighter pilots that +Gz tolerance is higher under closed- than open-loop G control. The aims were to investigate whether +Gz tolerance is higher in closed- than open-loop G control, and whether it is possible to use closed-loop G control during precise determination of +Gz tolerance.

METHODS: Relaxed +Gz tolerance was determined in eight men during rapid Gz-onset rate (ROR) under three conditions: 1) OL-VFB, open loop with visual feedback; 2) OL-NFB, open loop with no visual feedback; and 3) CL, closed loop. Straining +Gz tolerance was determined in 10 men during ROR in OL and CL conditions.

RESULTS: Relaxed +Gz tolerance did not differ between CL (3.66 Gz), OL-VFB (3.70 Gz) and OL-NFB (3.64 Gz). Straining +Gz tolerance was similar in the CL (8.5 Gz) and OL (8.6 Gz) conditions. In the CL condition, the Gz load varied substantially and was on average lower than in the OL conditions, at any stipulated G-time profile.

DISCUSSION: There is no systematic difference in relaxed or straining +Gz tolerance as determined in closed- vs. open-loop G-controlled systems. During closed-loop control, precision and reproducibility are too low to recommend it for accurate determination of relaxed G tolerance.Grönkvist M, Levin B, Eiken O. G tolerance during open- vs. closed-loop G-time control. Aerosp Med Hum Perform. 2018; 89(9):798-804.