Effects of hyperventilation on repeated breath-holding while in a fasting state: do risks outweigh the benefits?

Breath-holding preceded by either an overnight fast or hyperventilation has been shown to potentiate the risk of a hypoxic blackout. However, no study has explored the combined effects of fasting and hyperventilation on apneic performance and associated physiological responses. Nine nondivers (8 males) attended the laboratory on two separate occasions (≥48 h apart), both after a 12-h overnight fast. During each visit, a hyperoxic rebreathing trial was performed followed by three repeated maximal static apneas preceded by either normal breathing (NORM) or a 30-s hyperventilation (HYPER). Splenic volume, hematology, cardiovascular, and respiratory variables were monitored. There were no interprotocol differences at rest or during hyperoxic rebreathing for any variable (P ≥ 0.09). On nine occasions (8 in HYPER), the subjects reached our safety threshold (oxygen saturation 65%) and were asked to abort their apneas, with the preponderance of these incidents (6 of 9) occurring during the third repetition. Across the sequential attempts, longer apneas were recorded in HYPER [median(range), 220(123-324) s vs. 185(78-296) s, P ≤ 0.001], with involuntary breathing movements occurring later [134(65-234) s vs. 97(42-200) s, P ≤ 0.001] and end-apneic partial end-tidal pressures of oxygen (PETO2) being lower (P ≤ 0.02). During the final repetition, partial end-tidal pressure of carbon dioxide [(PETCO2), 6.53 ± 0.46 kPa vs. 6.01 ± 0.45 kPa, P = 0.005] was lower in HYPER. Over the serial attempts, preapneic tidal volume was gradually elevated [from apnea 1 to 3, by 0.26 ± 0.24 L (HYPER) and 0.28 ± 0.30 L (NORM), P ≤ 0.025], with a correlation noted with preapneic PETCO2 (r = -0.57, P < 0.001) and PETO2 (r = 0.76, P < 0.001), respectively. In a fasted state, preapnea hyperventilation compared with normal breathing leads to longer apneas but may increase the susceptibility to a hypoxic blackout.NEW & NOTEWORTHY This study shows that breath-holds (apneas) preceded by a 12-h overnight fast coupled with a 30-s hyperventilation as opposed to normal breathing may increase the likelihood of a hypoxic blackout through delaying the excitation of hypercapnic ventilatory sensory chemoreflexes. Evidently, this risk is exacerbated over a series of repeated maximal attempts, possibly due to a shift in preapneic gas tensions facilitated by an unintentional increase in tidal volume breathing.

Eccentric exercise before a 90 min exposure at 24,000 ft increases decompression strain depending on body region but not total muscle mass recruited.

Eccentric upper-body exercise performed 24 h prior to high-altitude decompression has previously been shown to aggravate venous gas emboli (VGE) load. Yet, it is unclear whether increasing the muscle mass recruited (i.e., upper vs. whole-body) during eccentric exercise would exacerbate the decompression strain. Accordingly, this study aimed to investigate whether the total muscle mass recruited during eccentric exercise influences the decompression strain. Eleven male participants were exposed to a simulated altitude of 24,000 ft for 90 min on three separate occasions. Twenty-four hours before each exposure, participants performed one of the following protocols: (i) eccentric whole-body exercise (ECCw; squats and arm-cycling exercise), (ii) eccentric upper-body exercise (ECCu; arm-cycling), or (iii) no exercise (control). Delayed onset muscle soreness (DOMS) and isometric strength were evaluated before and after each exercise intervention. VGE load was evaluated at rest and after knee- and arm-flex provocations using the 6-graded Eftedal-Brubakk scale. Knee extensor (-20 ± 14%, P = 0.001) but not elbow flexor (-12 ± 18%, P = 0.152) isometric strength was reduced 24 h after ECCw. ECCu reduced elbow flexor isometric strength at 24 h post-exercise (-18 ± 10%, P < 0.001). Elbow flexor DOMS was higher in the ECCu (median 6) compared with ECCw (5, P = 0.035). VGE scores were higher following arm-flex provocations in the ECCu (median (range), 3 (0-4)) compared with ECCw (2 (0-3), P = 0.039) and control (0 (0-2), P = 0.011), and in ECCw compared with control (P = 0.023). VGE were detected earlier in ECCu (13 ± 20 min) compared with control (60 ± 38 min, P = 0.021), while no differences were noted between ECCw (18 ± 30 min) and control or ECCu. Eccentric exercise increased the decompression strain compared with control. The VGE load varied depending on the body region but not the total muscle mass recruited. HIGHLIGHTS: What is the central question of this study? Does exercise-induced muscle damage (EIMD) resulting from eccentric exercise influence the presence of venous gas emboli (VGE) during a 90 min continuous exposure at 24,000 ft? What is the main finding and its importance? EIMD led to an earlier manifestation and greater VGE load compared with control. However, the decompression strain was dependent on the body region but not the total muscle mass recruited.

Factors of significance for the ability of fighter pilots to visually indicate the magnitude of roll tilt during simulated turns in a centrifuge.

During coordinated flight and centrifugation, pilots show interindividual variability in perceived roll tilt. The study explored how this variability is related to perceptual and cognitive functions. Twelve pilots underwent three 6-min centrifugations on two occasions (G levels: 1.1G, 1.8G, and 2.5G; gondola tilts: 25°, 56°, and 66°). The subjective visual horizontal (SVH) was measured with an adjustable luminous line and the pilots gave estimates of experienced G level. Afterward, they were interrogated regarding the relationship between G level and roll tilt and adjusted the line to numerically mentioned angles. Generally, the roll tilt during centrifugation was underestimated, and there was a large interindividual variability. Both knowledge on the relationship between G level and bank angle, and ability to adjust the line according to given angles contributed to the prediction of SVH in a multiple regression model. However, in most cases, SVH was substantial smaller than predictions based on specific abilities.

Repetitive high-sustained gravitoinertial stress does not modulate pressure responsiveness to peripheral sympathetic stimulation.

PURPOSE: We evaluated the hypothesis that repetitive gravitoinertial stress would augment the arterial-pressure response to peripheral sympathetic stimulation. METHODS: Before and after a 5-weeks G-training regimen conducted in a human-use centrifuge, twenty healthy men performed a hand cold-pressor test, and nine of them also a foot cold-pressor test (4 min; 4 °C water). Arterial pressures and total peripheral resistance were monitored. RESULTS: The cold-induced elevation (P ≤ 0.002) in arterial pressures and total peripheral resistance did not vary between testing periods, either in the hand [mean arterial pressure: Before = + 16% vs. After = + 17% and total peripheral resistance: Before = + 13% vs. After = + 15%], or in the foot [mean arterial pressure: Before = + 19% vs. After = + 21% and total peripheral resistance: Before = + 16% vs. After = + 16%] cold-pressor tests (P > 0.05). CONCLUSION: Present results demonstrate that 5 weeks of prolonged iterative exposure to hypergravity does not alter the responsiveness of sympathetically mediated circulatory reflexes.

In vivo pressure-flow relation of human cutaneous vessels following prolonged iterative exposures to hypergravity.

The study examined intra- and interlimb variations in cutaneous vessel responsiveness to acute and repeated transmural pressure elevations. In 11 healthy men, red blood cell flux was assessed via laser-Doppler flowmetry on both glabrous and nonglabrous skin regions of an arm (finger and forearm) and leg (toe and lower leg), across a wide range of stepwise increasing distending pressures imposed in the vessels of each limb separately. The pressure-flux cutaneous responses were evaluated before and after 5 wk of intermittent (40 min, 3 sessions per week) exposures to hypergravity (∼2.6-3.3 G; G training). Before and after G training, forearm and lower leg blood flux were relatively stable up to ∼210 and ∼240 mmHg distending pressures, respectively; and then they increased two- to threefold (P < 0.001). Finger blood flux dropped promptly (P < 0.001), regardless of the G training (P = 0.64). At ≤120-mmHg distending pressures, toe blood flux enhanced by ∼40% (P ≤ 0.05); the increase was augmented after the G training (P = 0.01). At high distending pressures, toe blood flux dropped by ∼70% in both trials (P < 0.001). The present results demonstrate that circulatory autoregulation is more pronounced in glabrous skin than in nonglabrous skin, and in nonglabrous sites of the leg than in those of the arm. Repetitive high-sustained gravitoinertial stress does not modify the pressure-flow relationship in the dependent skin vessels of the arm nor in the nonglabrous sites of the lower leg. Yet it may partly inhibit the myogenic responsiveness of the toe's glabrous skin.

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.

Lumbar Loads and Muscle Activity During Flywheel and Barbell Leg Exercises.

ABSTRACT: Sjöberg, M, Eiken, O, Norrbrand, L, Berg, HE, and Gutierrez-Farewik, EM. Lumbar loads and muscle activity during flywheel and barbell leg exercises. J Strength Cond Res 37(1): 27-34, 2023-It is anticipated that flywheel-based leg resistance exercise will be implemented in future long-duration space missions, to counter deconditioning of weight-bearing bones and postural muscles. The aim was to examine low back loads and muscle engagements during flywheel leg press (FWLP) and flywheel squat (FWS) and, for comparisons, free-weight barbell back squat (BBS). Eight resistance-trained subjects performed 8 repetition maximums of FWLP, FWS, and BBS. Motion analysis and inverse dynamics-based musculoskeletal modeling were used to compute joint loads and muscle forces. Muscle activities were measured with electromyography (EMG). At the L4-L5 level, peak vertebral compression force was similarly high in all exercise modes, whereas peak vertebral posteroanterior shear force was greater ( p < 0.05) in FWLP and BBS than in FWS. Among the back-extensor muscles, the erector spinae longissimus exerted the greatest peak force, with no difference between exercises. Peak force in the lumbar multifidus was lower ( p < 0.05) during FWLP than during FWS and BBS. Peak EMG activity in the lumbar extensor muscles ranged between 31 and 122% of maximal voluntary isometric contraction across muscles and exercise modes, with the greatest levels in the lumbar multifidus. The vertebral compression forces and muscle activations during the flywheel exercises were sufficiently high to presume that when implementing such exercise in space countermeasure regimens, they may be capable of preventing muscle atrophy and vertebral demineralization in the lumbar region.

Acral skin vasoreactivity and thermosensitivity to hand cooling following 5 days of intermittent whole body cold exposure.

We sought to examine whether short-term, whole body cold acclimation would modulate finger vasoreactivity and thermosensitivity to localized cooling. Fourteen men were equally assigned to either the experimental (CA) or the control (CON) group. The CA group was immersed to the chest in 14°C water for ≤120 min daily over a 5-day period while the skin temperature of the right-hand fingers was clamped at ∼35.5°C. The CON group was instructed to avoid any cold exposure during this period. Before and after the intervention, both groups performed, on two different consecutive days, a local cold provocation trial consisting of a 30-min hand immersion in 8°C water while immersed to the chest once in 21°C (mild-hypothermic trial; 0.5°C fall in rectal temperature from individual preimmersion values) and on the other occasion in 35.5°C (normothermic trial). In the CA group, the cold-induced reduction in finger temperature was less (mild-hypothermic trial: P = 0.05; normothermic trial: P = 0.02), and the incidence of the cold-induced vasodilation episodes was greater (in normothermic trials: P = 0.04) in the post- than in the preacclimation trials. The right-hand thermal discomfort was also attenuated (mild-hypothermic trial: P = 0.04; normothermic trial: P = 0.01). The finger temperature responses of the CON group did not vary between testing periods. Our findings suggest that repetitive whole body exposure to severe cold within a week may attenuate finger vasoreactivity and thermosensitivity to localized cooling. These regional thermo-adaptions were ascribed to central neural habituation produced by the iterative, generalized cold stimulation.

Human cardiovascular adaptation to hypergravity.

Despite decades of experience from high-gravitoinertial (G) exposures in aircraft and centrifuges, information is scarce regarding primary cardiovascular adaptations to +Gz loads in relaxed humans. Thus, effects of G-training are typically evaluated after regimens that are confounded by concomitant use of anti-G straining maneuvers, anti-G suits, and pressure breathing. Accordingly, the aim was to evaluate cardiovascular adaptations to repeated +Gz exposures in the relaxed state. Eleven men underwent 5 wk of centrifuge G training, consisting of 15 × 40 min +Gz exposures at G levels close to their individual relaxed G-level tolerance. Before and after the training regimen, relaxed G-level tolerance was investigated during rapid onset-rate (ROR) and gradual onset-rate (GOR) G exposures, and cardiovascular responses were investigated during orthostatic provocation and vascular pressure-distension tests. The G training resulted in: 1) a 13% increase in relaxed ROR G tolerance (P < 0.001), but no change in GOR G tolerance, 2) increased pressure resistance in the arteries and arterioles of the legs (P < 0.001), but not the arms, and 3) a reduced initial drop in arterial pressure upon ROR high G, but no change in arterial pressure under basal resting conditions or during GOR G loading, or orthostatic provocation. The results suggest +Gz adaptation via enhanced pressure resistance in dependent arteries/arterioles. Presumably, this reflects local adaptations to high transmural pressures, resulting from the +Gz-induced exaggeration of the intravascular hydrostatic pressure gradients.

Effects of vision on energy expenditure and kinematics during level walking.

PURPOSE: We have previously observed substantially higher oxygen uptake in soldiers walking on terrain at night than when performing the same walk in bright daylight. The aims of the present study were to investigate the influence of vision on mechanical efficiency during slow, horizontal, constant-speed walking, and to determine whether any vision influence is modified by load carriage. METHODS: Each subject (n = 15) walked (3.3 km/h) for 10 min on a treadmill in four different conditions: (1) full vision, no carried load, (2) no vision, no carried load, (3) full vision with a 25.5-kg rucksack, (4) no vision with a 25.5-kg rucksack. RESULTS: Oxygen uptake was 0.94 ± 0.12 l/min in condition (1), 1.15 ± 0.20 l/min in (2), 1.15 ± 0.12 l/min in (3) and 1.35 ± 0.19 l/min in (4). Thus, lack of vision increased oxygen uptake by about 19%. Analyses of movement pattern, by use of optical markers attached to the limbs and torso, revealed considerably shorter step length (12 and 10%) in the no vision (2 and 4) than full vision conditions (1 and 3). No vision conditions (2 and 4) increased step width by 6 and 6%, and increased vertical foot clearance by 20 and 16% compared to full vision conditions (1 and 3). CONCLUSION: The results suggest that vision has a marked influence on mechanical efficiency even during entrained, repetitive movements performed on an obstacle-free horizontal surface under highly predictable conditions.

Differential responsiveness of glabrous and nonglabrous skin to local transmural pressure elevations: impact of 5 weeks of iterative local pressure loading.

We examined the in vivo pressure-flow relationship in human cutaneous vessels during acute and repeated elevations of local transmural pressure. In 10 healthy men, red blood cell flux was monitored simultaneously on the nonglabrous skin of the forearm and the glabrous skin of a finger during a vascular pressure provocation, wherein the blood vessels of an arm were exposed to a wide range of stepwise increasing distending pressures. Forearm skin blood flux was relatively stable at slight and moderate elevations of distending pressure, whereas it increased approximately three- to fourfold at the highest levels (P = 0.004). Finger blood flux, on the contrary, dropped promptly and consistently throughout the provocation (P < 0.001). Eight of the subjects repeated the provocation trial after a 5-wk pressure-training regimen, during which the vasculature in one arm was exposed intermittently (40 min, 3 times/wk) to increased transmural pressure (from +65 mmHg week 1 to +105 mmHg week 5). The training regimen diminished the pressure-induced increase in forearm blood flux by ∼34% (P = 0.02), whereas it inhibited the reduction in finger blood flux (P < 0.001) in response to slight and moderate distending pressure elevations. The present findings demonstrate that during local pressure perturbations, the cutaneous autoregulatory function is accentuated in glabrous compared with in the nonglabrous skin regions. Prolonged intermittent regional exposures to augmented intravascular pressure blunt the responsiveness of the glabrous skin but enhance arteriolar pressure resistance in the nonglabrous skin.

Heterogeneity of human adaptations to bed rest and hypoxia: a retrospective analysis within the skeletal muscle oxidative function.

This retrospective study was designed to analyze the interindividual variability in the responses of different variables characterizing the skeletal muscle oxidative function to normoxic (N-BR) and hypoxic (H-BR) bed rests and to a hypoxic ambulatory confinement (H-AMB) of 10 and 21 days. We also assessed whether and how the addition of hypoxia to bed rest might influence the heterogeneity of the responses. In vivo measurements of O2 uptake and muscle fractional O2 extraction were carried out during an incremental one-leg knee-extension exercise. Mitochondrial respiration was assessed in permeabilized muscle fibers. A total of 17 subjects were included in this analysis. This analysis revealed a similar variability among subjects in the alterations induced by N-BR and H-BR both in peak O2 uptake (SD: 4.1% and 3.3% after 10 days; 4.5% and 8.1% after 21 days, respectively) and peak muscle fractional O2 extraction (SD: 5.9% and 7.3% after 10 days; 6.5% and 7.3% after 21 days), independently from the duration of the exposure. The individual changes measured in these variables were significantly related (r = 0.66, P = 0.004 after N-BR; r = 0.61, P = 0.009 after H-BR). Mitochondrial respiration showed a large variability of response after both N-BR (SD: 25.0% and 15.7% after 10 and 21 days) and H-BR (SD: 13.0% and 19.8% after 10 and 21 days); no correlation was found between N-BR and H-BR changes. When added to bed rest, hypoxia altered the individual adaptations within the mitochondria but not those intrinsic to the muscle oxidative function in vivo, both after the short- and medium-term exposures.

Finger constrictor and thermoperceptual responsiveness to localised cooling following 5 weeks of intermittent regional exposures to moderately augmented transmural vascular pressure.

PURPOSE: To examine the effects of prolonged intermittent exposures to moderately increased transmural pressure on finger vasoreactivity and thermoperception to localised cooling. METHODS: Eleven men completed a 5-week regimen (3 sessions·week-1; 55 min·session-1), during which the vasculature in one arm (EXP) was exposed intermittently (10-min exposure: 5-min pause) to increased transmural pressure (from +65 mmHg week-1 to +105 mmHg week-5). Before and after the regimen, finger cutaneous vascular conductance (CVC), temperature (Tavg), and thermoperception (thermal sensation, discomfort and pain) were monitored during a 30-min hand cold (8 °C water) provocation trial. The responses of the non-trained hand were examined during an additional cold trial. RESULTS: After the regimen, baseline finger CVC and Tavg were higher in both hands (p ≤ 0.01). During cooling, neither finger CVC nor Tavg were modified (p > 0.05). Yet the magnitude of the cold-induced drop of CVC was augmented in both hands, and to a similar extent (p ≤ 0.02). The regimen alleviated thermal pain in both hands (p ≤ 0.02); the sensation of coldness and thermal discomfort were attenuated mainly in the EXP hand (p = 0.02). CONCLUSIONS: Present findings indicate that iterative local exposures to augmented intravascular pressure do not alter finger vasoreactivity to localised cooling. The pressure training, however, might impair finger basal vasomotor tone, and aggravate the magnitude of constrictor responsiveness to cooling. The pressure training also elicits thermoperceptual desensitisation to noxious thermal stimulus. To large extent, these vascular and perceptual adjustments seem to be transferred to the cutaneous vasculature of the non-trained limb.

Whole-body vibration preconditioning reduces the formation and delays the manifestation of high-altitude-induced venous gas emboli.

NEW FINDINGS: What is the central question of this study? Is performing a 30-min whole-body vibration (WBV) prior to a continuous 90-min exposure at 24,000 ft sufficient to prevent venous gas emboli (VGE) formation? What is the main finding and its importance? WBV preconditioning significantly reduces the formation and delays the manifestation of high-altitude-induced VGE. This study suggests that WBV is an effective strategy in lowering decompression stress. ABSTRACT: Rapid decompression may give rise to formation of venous gas emboli (VGE) and resultantly, increase the risk of sustaining decompression sickness. Preconditioning aims at lowering the prevalence of VGE during decompression. The purpose of this study was to investigate the efficacy of whole-body vibration (WBV) preconditioning on high-altitude-induced VGE. Eight male subjects performed, on separate days in a randomised order, three preconditioning strategies: 40-min seated-rest (control), 30-min seated-rest followed by 150 knee-squats performed over a 10-min period (exercise) and 30-min WBV proceeded by a 10-min seated-rest. Thereafter, subjects were exposed to an altitude of 24,000 ft (7315 m) for 90 min whilst laying in a supine position and breathing 100% oxygen. VGE were assessed ultrasonically both during supine rest (5-min intervals) and after three fast, unloaded knee-bends (15-min intervals) and were scored using a 5-grade scale and evaluated using the Kisman Integrated Severity Score (KISS). There was a significant difference in VGE grade (P < 0.001), time to VGE manifestation (P = 0.014) and KISS score following knee-bends (P = 0.002) across protocols, with a trend in KISS score during supine rest (P = 0.070). WBV resulted in lower VGE grades (median (range), 1 (0-3)) and KISS score (2.69 ± 4.56 a.u.) compared with control (2 (1-3), P = 0.002; 12.86 ± 8.40 a.u., P = 0.011) and exercise (3 (2-4) , P < 0.001; 22.04 ± 13.45 a.u., P = 0.002). VGE were detected earlier during control (15 ± 14 min, P = 0.024) and exercise (17 ± 24 min, P = 0.032) than WBV (54 ± 38 min). Performing a 30-min WBV prior to a 90-min continuous exposure at 24,000 ft both delays the manifestation and reduces the formation of VGE compared with control and exercise preconditioning.

Exercise temperature regulation following a 35-day horizontal bedrest.

NEW FINDINGS: What is the central question of this study? Does a 35-day horizontal bedrest impair thermoeffector responses during whole-body submaximal exercise performed in temperate conditions? What is the main finding and its importance? Cardiovascular and muscular deconditioning ensuing from prolonged recumbency seems to augment, at least to a degree, exercise-induced increase in body core temperature, most likely due to an impairment in non-evaporative heat loss. The response is a function of the absolute exercise intensity imposed. ABSTRACT: We examined the effects of a 35-day horizontal bedrest on thermoregulation during whole-body exercise. Fifteen healthy men were randomly assigned to either a bedrest (BR; n = 10) or a control (CON; n = 5) group. Prior to bedrest, both groups performed 40-min constant-load upright cycling at 30% of their peak workload (Wpeak ; PRE). One and 2 days after bedrest, the BR group performed, in a randomised counterbalanced order, two 40-min trials at 30% of (i) the pre-bedrest Wpeak (i.e., at a fixed absolute intensity; POST-A) and (ii) the post-bedrest Wpeak (i.e., at a fixed relative intensity; POST-R). The CON group conducted only the POST-A trial, at the same time intervals. During the trials, rectal (Trec ) and skin ( T¯sk ) temperatures, and the forehead sweating rate (SwR) were monitored. In the CON group, no differences were observed between the trials. Bedrest potentiated moderately the Trec elevation during the latter part of POST-A (∼0.10°C; P ≤ 0.05), but not of POST-R (∼0.04°C; P = 0.11). In both post-bedrest trials, T¯sk was attenuated by ∼1.5-2.0°C throughout (P < 0.01), whereas the forehead SwR was not modulated. Trec and T¯sk were similar in POST-A and POST-R, yet the forehead SwR was more dependent on the relative workload imposed (P = 0.04). The present findings therefore suggest that the cardiovascular and muscular deconditioning ensuing from a 35-day bedrest may aggravate the exercise-induced increase in body core temperature when working at a given absolute intensity, most likely due to an impairment in non-evaporative heat loss.

Do females and males exhibit a similar sarcopenic response as a consequence of normoxic and hypoxic bed rest?

NEW FINDINGS: What is the central question of this study? Do females and males exhibit a similar sarcopenic response as a consequence of normoxic and hypoxic bed rest? What is the main finding and its importance? During 10-day bed rest, exposure to a simulated (normobaric hypoxia) altitude of ∼4000 m does not exert additional significant structural or functional effect on the weight-bearing muscles in females compared to those noted under normoxic conditions. Whereas males and females exhibit decrements in muscle cross-sectional area and mass during normoxic and hypoxic bed rest, a concomitant strength decrement was only observed in males. ABSTRACT: This study investigated the effects of hypoxia on the known processes of adaptation of body composition and muscle function to normoxic inactivity. Females (n = 12) and males (n = 11) took part in the following interventions: hypoxic ambulation (HAMB; ∼4000 m); hypoxic bed rest (HBR; ∼4000 m) and normoxic bed rest (NBR). Prior to and immediately following each intervention, body composition, thigh and lower leg cross-sectional area (CSA) and isometric muscular strength were recorded. Participants lost body mass (HAMB: male -1.5 ± 0.9 kg, female -1.9 ± 0.7 kg; HBR: male -2.0 ± 1.8 kg, female -2.4 ± 0.8 kg; NBR: male -1.4 ± 1.3 kg, female -1.4 ± 0.9 kg) and lean mass (HAMB: male -3.9 ± 3.0%, female -3.4 ± 2.0%; HBR: male -4.0 ± 4.4%, female -4.1 ± 2.0%; NBR: male -4.0 ± 3.4%, female -2.2 ± 2.7%) with no between-condition or sex differences. Knee extension decreased for males in NBR compared to HAMB (HAMB: male -0.2 ± 9.1%, female 1.3 ± 4.9%; HBR: male -7.8 ± 10.3%, female -3.3 ± 10.9%; NBR: male -14.5 ± 11%, female -3.4 ± 6.9%). Loss of force during maximal voluntary contraction (MVC) in the knee extensors was significantly different between males and females following NBR. There were no other significant changes noted following the experimental interventions. There were no differences recorded between sexes in maximal MVC for elbow or ankle joints. Female lower leg CSA decreased following bed rest (HAMB: -4.5 ± 2.0%; HBR: -9.9 ± 2.6%; NBR: -8.0 ± 1.6%). These findings indicate that a 10-day hypoxic bed rest does not exert any significant additional effect on muscle atrophy when compared to NBR, except for female thigh CSA. In contrast to males, who exhibited a significant loss of muscle strength, no such decrement in strength was observed in the female participants.

High-altitude decompression strain can be reduced by an early excursion to moderate altitude while breathing oxygen.

Recent observations suggest that development of venous gas emboli (VGE) during high-altitude flying whilst breathing hyperoxic gas will be reduced by intermittent excursions to moderate altitude. The present study aimed to investigate if an early, single excursion from high to moderate altitude can be used as an in-flight means to reduce high-altitude decompression strain. Ten healthy men were investigated whilst breathing oxygen in a hypobaric chamber under two conditions, once during a 90-min continuous exposure to a simulated cabin altitude of 24,000 ft (High; H) and once during 10 min at 24,000 ft, followed by 30 min at 15,000 ft and by 80 min at 24,000 ft (high-low-high; H-L-H). VGE scores were assessed by cardiac ultrasound, using a 6-graded scale. In H, VGE increased throughout the course of the sojourn at 24,000 ft to attain peak value [median (range)] of 3 (2-4) at min 90, just prior to descent. In H-L-H, median VGE scores were 0 throughout the trial, except for at min 10, just prior to the excursion to 15,000 ft, whence the VGE score was 1.5 (0-3). Thus, an early, single excursion from high to moderate cabin altitude holds promise as an in-flight means to reduce the risk of altitude decompression sickness during long-duration high-altitude flying in aircraft with limited cabin pressurization. Presumably, such excursion acts by facilitating the gas exchange in decompression bubbles from a predomination of nitrogen to that of oxygen.

Heat acclimation enhances the cold-induced vasodilation response.

PURPOSE: It has been reported that the cold-induced vasodilation (CIVD) response can be trained using either regular local cold stimulation or exercise training. The present study investigated whether repeated exposure to environmental stressors, known to improve aerobic performance (heat and/or hypoxia), could also provide benefit to the CIVD response. METHODS: Forty male participants undertook three 10-day acclimation protocols including daily exercise training: heat acclimation (HeA; daily exercise training at an ambient temperature, Ta = 35 °C), combined heat and hypoxic acclimation (HeA/HypA; daily exercise training at Ta = 35 °C, while confined to a simulated altitude of ~ 4000 m) and exercise training in normoxic thermoneutral conditions (NorEx; no environmental stressors). To observe potential effects of the local acclimation on the CIVD response, participants additionally immersed their hand in warm water (35 °C) daily during the HeA/HypA and NorEx. Before and after the acclimation protocols, participants completed hand immersions in cold water (8 °C) for 30 min, followed by 15-min recovery phases. The temperature was measured in each finger. RESULTS: Following the HeA protocol, the average temperature of all five fingers was higher during immersion (from 13.9 ± 2.4 to 15.5 ± 2.5 °C; p = 0.04) and recovery (from 22.2 ± 4.0 to 25.9 ± 4.9 °C; p = 0.02). The HeA/HypA and NorEx protocols did not enhance the CIVD response. CONCLUSION: Whole-body heat acclimation increased the finger vasodilatory response during cold-water immersion, and enhanced the rewarming rate of the hand, thus potentially contributing to improved local cold tolerance. Daily hand immersion in warm water for 10 days during HeA/Hyp and NorEx, did not contribute to any changes in the CIVD response.

Hypoxia gradually augments metabolic and thermoperceptual responsiveness to repeated whole-body cold stress in humans.

NEW FINDINGS: What is the central question of this study? In male lowlanders, does hypoxia modulate thermoregulatory effector responses during repeated whole-body cold stress encountered in a single day? What is the main finding and its importance? A ∼10 h sustained exposure to hypoxia appears to mediate a gradual upregulation of endogenous heat production, preventing the progressive hypothermic response prompted by serial cold stimuli. Also, hypoxia progressively degrades mood, and compounds the perceived thermal discomfort, and sensations of fatigue and coldness. ABSTRACT: We examined whether hypoxia would modulate thermoeffector responses during repeated cold stress encountered in a single day. Eleven men completed two ∼10 h sessions, while breathing, in normobaria, either normoxia or hypoxia ( PO2 : 12 kPa). During each session, subjects underwent sequentially three 120 min immersions to the chest in 20°C water (CWI), interspersed by 120 min rewarming. In normoxia, the final drop in rectal temperature (Trec ) was greater in the third (∼1.2°C) than in the first and second (∼0.9°C) CWIs (P < 0.05). The first hypoxic CWI augmented the Trec fall (∼1.2°C; P = 0.002), but the drop in Trec did not vary between the three hypoxic CWIs (P = 0.99). In normoxia, the metabolic heat production ( Ṁ ) was greater during the first half of the third CWI than during the corresponding part of the first CWI (P = 0.02); yet the difference was blunted during the second half of the CWIs (P = 0.89). In hypoxia, by contrast, the increase in Ṁ was augmented by ∼25% throughout the third CWI (P < 0.01). Regardless of the breathing condition, the cold-induced elevation in mean arterial pressure was blunted in the second and third CWI (P < 0.05). Hypoxia aggravated the sensation of coldness (P = 0.05) and thermal discomfort (P = 0.04) during the second half of the third CWI. The present findings therefore demonstrate that prolonged hypoxia mediates, in a gradual manner, metabolic and thermoperceptual sensitization to repeated cold stress.