Previous studies have suggested that, during prolonged cold exposure, shivering thermogenesis may gradually be attenuated, supposedly reflecting a state of central fatigue (aka ‘thermoregulatory fatigue’) provoked by extended shivering activity, that precipitates hypothermia. The purpose of this study was to revisit the validity of this notion. Twelve noncold-acclimatized men participated in three ∼10-h sessions, during which they performed repeatedly three 120-min cold-water immersions. To induce discrete amounts of heat-producing thermoeffector output, presumptively leading to distinct levels of fatigue during each session, subjects were submersed, within each session, in either severely (15°C), moderately (20°C), or slightly (28°C) cold water. The cold-induced elevation in thermogenic rate was similar across the three repeated immersions performed within the 15°C (∼130 W·m2) and 20°C (∼100 W·m2) sessions (P ≥ 0.43). In the 28°C-session, the metabolic heat production was augmented by ∼7% in the second and third immersions compared with the first immersion (P = 0.01). No intrasession differences were noted with regards to the body-core cooling rate, the cold-induced drop in skin temperature and forearm cutaneous vascular conductance, or the stress-hormone (salivary α-amylase and cortisol concentrations) and thermoperceptual responses (P > 0.05). The present findings, therefore, demonstrate that the ability to generate heat remains intact during prolonged iterative exposure to a high-heat loss environment in a single day, regardless of the severity of cold stressor. The intermittent application of slight cold stress (i.e., 28°C water) appears to mediate metabolic sensitization, reflecting either the circadian rhythmicity of heat-producing thermoeffector activity, or perhaps the rapid induction of metabolic adaptation.

Purpose: There is a scarcity of information regarding the effect of upper-body eccentric exercise on biomarkers of muscle damage. This study sought to investigate the effect of eccentric arm cycling on muscle damage [exercise-induced muscle damage (EIMD)].

Method: Ten subjects performed a 15 min eccentric arm cycling protocol (cadence 49 ± 7 rpm, power absorbed 248 ± 34 W). Maximal voluntary contraction (MVC) of the elbow flexors was evaluated at rest and at 5 min, 24 h, and 48 h post-exercise. In addition, blood samples were drawn at rest and thereafter at 30 min, 24 h, and 48 h intervals after exercise for quantification of creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH) and endothelin (ET-1) concentrations. Delayed onset muscle soreness (DOMS) was assessed using a category ratio scale (0-10).

Results: Myoglobin was increased from baseline at 30 min post-exercise (+114%, 46.08 ± 22.17 µg/L, p = 0.018). Individual peak values were higher than baseline values for CK (+72.8%, 204 ± 138 U/L, p = 0.046) and LDH (+17%, 3.3 ± 0.88 nmole/min/mL, p = 0.017), but not for ET-1 (+9%, 1.4 ± 0.48 pg/mL, p = 0.45). DOMS was reported at 24 h (median 4) and 48 h (median 4) post-exercise and MVC of the elbow flexors were reduced from baseline (216 ± 44 N) at 5 min (-34%, 147 ± 61 N, p < 0.001), 24 h (-17%, 181 ± 56 N, p = 0.005) and 48 h (-9%, 191 ± 54 N, p = 0.003).

Conclusion: Eccentric arm cycling incites EIMD with reduced MVC and elevation of myoglobin, CK and LDH.

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.

This study aimed to investigate the effect of eccentric exercise on exercise-induced muscle damage (EIMD) and inflammation on high-altitude-induced venous gas emboli (VGE). Subjects were exposed to an altitude of 24,000 ft. for 90 min, with either prior eccentric exercise (ECC) or no exercise (Control) 24 h before. Blood samples were collected at baseline (T0), before (T1), and after (T2) altitude exposures. VGE load was evaluated using the Eftedal-Brubakk (ΕΒ) scale. Creatine kinase (CK) and myoglobin were used to assess muscle damage, while interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), C-reactive protein (CRP), and fibrinogen were used to evaluate inflammation. ECC showed higher EB-scores during altitude exposures [median(range), 3(0–5)] than Control [1(0–4), p = 0.019]. Increases in myoglobin (+35%, p = 0.012), CK (+130%, p < 0.001), IL-6 (+72%, p = 0.02), and CRP (+63%, p = 0.004) were observed from T0 to T1 in ECC, but not Control. Significantly higher levels of myoglobin (p = 0.033), CK (p < 0.001), IL-6 (p = 0.016), and CRP (p = 0.002) were noted in the ECC compared to Control at T1. IL-6 increased from T1 to T2 in ECC (p = 0.005), with higher levels than Control at T2 (p = 0.046). A correlation was found between EB-scores and T1 myoglobin levels (rs = 0.450; p = 0.004), and to T1-T2 IL-6 changes (rs = 0.396; p = 0.037). Eccentric EIMD followed by inflammation is associated with a higher decompression strain, with VGE load aggravating systemic inflammation.

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.

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.

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.

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.

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.