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This study compared the joint kinematics between the front squat (FS) conducted in the upright (natural gravity) position and in the supine position on a short arm human centrifuge (SAHC). Male participants (N = 12) with no prior experience exercising on a centrifuge completed a FS in the upright position before (PRE) and after (POST) a FS exercise conducted on the SAHC while exposed to artificial gravity (AG). Participants completed, in randomized order, three sets of six repetitions with a load equal to body weight or 1.25 × body weight for upright squats, and 1 g and 1.25 g at the center of gravity (COG) for AG. During the terrestrial squats, the load was applied with a barbell. Knee (left/right) and hip (left/right) flexion angles were recorded with a set of inertial measurement units. AG decreased the maximum flexion angle (MAX) of knees and hips as well as the range of motion (ROM), both at 1 and 1.25 g. Minor adaptation was observed between the first and the last repetition performed in AG. AG affects the ability to FS in naïve participants by reducing MAX, MIN and ROM of the knees and hip., (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

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, T a  = 35 °C), combined heat and hypoxic acclimation (HeA/HypA; daily exercise training at T a  = 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., (© 2021. The Author(s).)

Purpose: As part of our investigations of intraocular pressure (IOP) as a potential contributing factor to the spaceflight-associated neuro-ocular syndrome using the 6° head-down tilt (6°HDT) bed rest experimental model, we compared the effect of rest and isometric exercise in prone and supine 6°HDT positions on IOP with that observed in the seated position., Methods: Ten male volunteers (age = 22.5 ± 3.1 yrs) participated in six interventions. All trials comprised a 10-min rest period, a 3-min isometric handgrip exercise at 30% of participant's maximum, and a 10-min recovery period. The trials were conducted under normocapnic (NCAP) or hypercapnic (F I CO 2  = 0.01; HCAP) conditions, the latter mimicking the ambient conditions on the International Space Station. IOP, systolic and diastolic pressures, and heart rate (HR) were measured during the trials., Results: Isometric exercise-induced elevations in HR and mean arterial blood pressure. IOP in the prone 6°HDT position was significantly higher (p < 0.001) compared to IOP in supine 6°HDT position and seated trials at all time points. IOP increased with exercise only in a seated HCAP trial (p = 0.042). No difference was observed between trials in NCAP and HCAP. IOP in the prone 6°HDT position was constantly elevated above 21 mmHg, the lower limit for clinical ocular hypertension., Conclusions: IOP in the prone 6°HDT position was similar to IOP reported in astronauts upon entering microgravity, potentially indicating that prone, rather than supine 6°HDT position might be a more suitable experimental analog for investigating the acute ocular changes that occur in microgravity., (© 2021 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

New Findings: What is the central question of this study? Astronauts on-board the International Space Station (ISS) perform daily exercises designed to prevent muscle atrophy and bone demineralization: what is the effect of resistive exercise performed by subjects while exposed to the same level of hypercapnia as on the ISS on intraocular pressure (IOP)? What is the main finding and its importance? The static exercise-induced elevation in IOP during 6° prone head-down tilt (simulating the headward shift of body fluids in microgravity) is augmented by hypercapnia and exceeds the ocular hypertension threshold., Abstract: The present study assessed the effect of 6° head-down (establishing the cephalad fluid displacement noted in astronauts in microgravity) prone (simulating the effect on the eye) tilt during rest and exercise (simulating exercise performed by astronauts to mitigate the sarcopenia induced by unloading of weight-bearing limbs), in normocapnic and hypercapnic conditions (the latter simulating conditions on the International Space Station) on intraocular pressure (IOP). Volunteers (mean age = 57.8 ± 6 years, n = 10) participated in two experimental sessions, each comprising: (i) 10 min rest, (ii) 3 min static handgrip exercise (30% max), and (iii) 2 min recovery, inspiring either room air (NCAP) or a hypercapnic mixture (1% CO 2 , HCAP). We measured IOP in the right eye, cardiac output (CO), stroke volume (SV), heart rate (HR) and mean arterial pressure (MAP) at regular intervals. Baseline IOP in the upright seated position while breathing room air was 14.1 ± 2.9 mmHg. Prone 6° head-down tilt significantly (P < 0.01) elevated IOP in all three phases of the NCAP (rest: 27.0 ± 3.7 mmHg; exercise: 32.2 ± 4.8 mmHg; recovery: 27.4 ± 4.0 mmHg) and HCAP (rest: 27.3 ± 4.3 mmHg; exercise: 34.2 ± 6.0 mmHg; recovery: 29.1 ± 5.8 mmHg) trials, with hypercapnia augmenting the exercise-induced elevation in IOP (P < 0.01). CO, SV, HR and MAP were significantly increased during handgrip dynamometry, but there was no effect of hypercapnia. The observed IOP measured during prone 6° HDT in all phases of the NCAP and HCAP trials exceeded the threshold pressure defining ocular hypertension. The exercise-induced increase in IOP is exacerbated by hypercapnia., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Purpose: Hypoxic acclimation enhances convective oxygen delivery to the muscles. Heat acclimation-elicited thermoregulatory benefits have been suggested not to be negated by adding daily exposure to hypoxia. Whether concomitant acclimation to both heat and hypoxia offers a synergistic enhancement of aerobic performance in thermoneutral or hot conditions remains unresolved., Methods: Eight young males ([Formula: see text]: 51.6 ± 4.6 mL min -1  kg -1 ) underwent a 10-day normobaric hypoxic confinement (F i O 2  = 0.14) interspersed with daily 90-min normoxic controlled hyperthermia (target rectal temperature: 38.5 °C) exercise sessions. Prior to, and following the confinement, the participants conducted a 30-min steady-state exercise followed by incremental exercise to exhaustion on a cycle ergometer in thermoneutral normoxic (NOR), thermoneutral hypoxic (F i O 2  = 0.14; HYP) and hot (35 °C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. The steady-state exercise was performed at 40% NOR peak power output (W peak ) to evaluate thermoregulatory function. Blood samples were obtained from an antecubital vein before, on days 1 and 10, and the first day post-acclimation., Results: [Formula: see text] and ventilatory thresholds were not modified in any environment following acclimation. W peak increased by 6.3 ± 3.4% in NOR and 4.0 ± 4.9% in HE, respectively. The magnitude and gain of the forehead sweating response were augmented in HE post-acclimation. EPO increased from baseline (17.8 ± 7.0 mIU mL -1 ) by 10.7 ± 8.8 mIU mL -1 on day 1 but returned to baseline levels by day 10 (15.7 ± 5.9 mIU mL -1 )., Discussion: A 10-day combined heat and hypoxic acclimation conferred only minor benefits in aerobic performance and thermoregulation in thermoneutral or hot conditions. Thus, adoption of such a protocol does not seem warranted.

New Findings: 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 exercise conditions. What is the main finding and its importance? We showed that heat acclimation did not affect maximal cardiac output or maximal aerobic power in thermoneutral normoxic or 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 ( V ̇ O 2 peak ) 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 cardiorespiratory and thermoregulatory responses to exercise in normoxic, hypoxic and hot conditions. Twelve men [ V ̇ O 2 peak 54.7(standard deviation 5.7) ml kg -1 min -1 ] participated in a HA protocol consisting of 10 daily 90-min controlled-hyperthermia (target rectal temperature, T re  = 38.5°C) exercise sessions. Before and after HA, we determined V ̇ O 2 peak in thermoneutral normoxic (NOR), thermoneutral hypoxic (fractional inspired O 2  = 13.5%; HYP) and hot (35°C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. Preceding each maximal cycling test, a 30-min steady-state exercise bout at 40% of the NOR peak power output was used to evaluate thermoregulatory responses. Heat acclimation induced the expected adaptations in HE: reduced T re and submaximal heart rate, enhanced sweating response and expanded plasma volume. However, HA did not affect V ̇ O 2 peak or maximal cardiac output (P = 0.61). The peak power output 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 V ̇ O 2 peak in normoxic or hypoxic conditions., (© 2018 The Authors. Experimental Physiology © 2018 The Physiological Society.)

We aimed to elucidate potential differential effects of hypoxia on cardiorespiratory responses during submaximal cycling and simulated skiing exercise between adults and pre-pubertal children. Healthy, low-altitude residents (adults, N=13, Age=40±4yrs.; children, N=13, age=8±2yrs.) were tested in normoxia (Nor: P i O 2 =134±0.4 mmHg; 940 m) and normobaric hypoxia (Hyp: P i O 2 =105±0.6 mmHg; ~3 000 m) following an overnight hypoxic acclimation (≥12-hrs). On both days, the participants underwent a graded cycling test and a simulated skiing protocol. Minute ventilation (V E ), oxygen uptake (VO 2 ), heart rate (HR) and capillary-oxygen saturation (SpO 2 ) were measured throughout both tests. The cycling data were interpolated for 2 relative workload levels (1 W·kg -1 & 2 W·kg -1 ). Higher resting HR in hypoxia, compared to normoxia was only noted in children (Nor:78±17; Hyp:89±17 beats·min -1 ; p<0.05), while SpO 2 was significantly lower in hypoxia (Nor:97±1%; Hyp:91±2%; p<0.01) with no between-group differences. The V E , VO 2 and HR responses were higher during hypoxic compared to normoxic cycling test in both groups (p<0.05). Except for greater HR during hypoxic compared to normoxic skiing in children (Nor:155±19; Hyp:167±13 (beats·min -1 ); p<0.05), no other significant between-group differences were noted during the cycling and skiing protocols. In summary, these data suggest similar cardiorespiratory responses to submaximal hypoxic cycling and simulated skiing in adults and children., Competing Interests: Conflict of interest: The authors have no conflicts of interest to declare., (© Georg Thieme Verlag KG Stuttgart · New York.)

New Findings: What is the central question of this study? What are the distinct and interactive effects of a 10 day exposure to hypoxia and horizontal bedrest on the whole-body peak oxygen uptake and on the regional cerebral and skeletal muscle tissue oxygenation during upright cycle ergometry in male lowlanders? What is the main finding and its importance? A 10 day sustained exposure to hypoxia aggravates the bedrest-induced reduction in peak oxygen uptake during dynamic exercise engaging large muscle groups, but mitigates the skeletal muscle oxidative capacity impairment elicited by bedrest. The study examined the interactive effects of a 10 day exposure to hypoxia and bedrest on the whole-body peak oxygen uptake (V̇O2 peak ) during maximal exercise and on skeletal muscle and cerebral oxygenation during submaximal exercise. Nine males underwent three 10 day confinements, in a Latin-square order, as follows: (i) a normoxic bedrest [NBR; partial pressure of inspired O 2 (PI,O2) = 134.2 ± 0.7 mmHg]; (ii) a hypoxic bedrest (HBR; PI,O2 = 102.9 ± 0.1 mmHg at day 1, 91.5 ± 1.2 mmHg at days 3-10); and (iii) a hypoxic ambulation (HAMB; PI,O2 as in HBR). Before, 1 (R+1) and 3 days (R+3) after each confinement, subjects performed exhaustive, incremental-load and moderate-intensity constant-load (CLTs) cycle-ergometry trials, while breathing either room air or a hypoxic gas mixture. During the CLTs, changes in the regional oxygenation of the cerebral frontal cortex and the vastus lateralis and intercostal muscles were monitored with near-infrared spectroscopy. At R+1, the confinement-related impairment in V̇O2 peak was greater after HBR than after NBR or HAMB, regardless of whether the trial was performed in room air or hypoxia (HBR, -16.2%; NBR, -8.3%; HAMB, -4.1%; P = 0.001). During the CLTs, bedrest aggravated the exercise-induced reduction in locomotor and respiratory muscle oxygenation (P ≤ 0.05); an effect that was less after HBR than after NBR (P ≤ 0.05). The hypoxic exercise-induced cerebral vasodilatory response was blunted by HBR, probably because of the marked hyperventilation-dependent hypocapnia, attendant to the sustained hypoxic stimulus. Hence, short-term exposure to hypoxia potentiates the reduction in V̇O2 peak , but it mitigates the impairment in skeletal muscle oxidative capacity induced by bedrest., (© 2017 The Authors. Experimental Physiology © 2017 The Physiological Society.)

Purpose: Acute hypoxia alters the threshold for sensation of cutaneous thermal stimuli. We hypothesised that hypoxia-induced alterations in cutaneous temperature sensation may lead to modulation of the perception of temperature, ultimately influencing behavioural thermoregulation and that the magnitude of this effect could be influenced by daily physical training., Methods: Fourteen men were confined 10 days to a normobaric hypoxic environment (P I O 2  = 88.2 ± 0.6 mmHg, corresponding to 4175 m elevation). Subjects were randomly assigned to a non-exercising (Live-high, LH, N = 6), or exercising group (Live-high Train-high, LH-TH, N = 8) comprised of 1-h bouts of cycle ergometry, twice daily, at a work-rate equivalent to 50% hypoxic peak power output. A subset of subjects (N = 5) also completed a control trial under normoxic conditions. The thermal comfort zone (TCZ) was determined in normoxia, and during hypoxic confinement days 2 (HC2) and 10 (HC10) in both groups using a water-perfused suit in which water temperature was regulated by the subjects within a range, they deemed thermally comfortable. Mean skin temperature and proximal-distal temperature gradients (two sites: forearm-fingertip, calf-toe) were recorded each minute throughout the 60-min protocol., Results: The average width of the TCZ did not differ between the control group (9.0 ± 6.9 °C), and the LH and LH-TH groups on days HC2 (7.2 ± 4.2 °C) and HC10 (10.2 ± 7.5 °C) of the hypoxic exposure (p = 0.256). [Formula: see text] was marginally higher on HC2 (35.9 ± 1.0 °C) compared to control (34.9 ± 0.8 °C, p = 0.040), but not on HC10 (35.6 ± 1.0 °C), reflecting the responses of hand perfusion., Conclusion: There was a little systematic effect of hypoxia or exercise training on TCZ magnitude or boundary temperatures.

Background and Objective: Hypoxic exercise exacerbates periodic breathing in otherwise healthy, awake humans. Interactions between sleep, exercise and hypoxic exposure have not been fully elucidated., Methods: Fourteen men were confined 10 days to a simulated altitude of 4175 m (FIO2 = 0.139; PIO2 = 88 mm Hg). They were randomly assigned to an exercise intervention of 2 × 60-min cycle exercise/day at 50% of their hypoxia-specific peak power output (exercise, n = 8), or they completed no exercise (control, n = 6, random order). Sleep and breathing were objectively assessed via full polysomnography on night 1, after 14-h acute exposure (N1), and again on night 10 (N10)., Results: The exercise group spent more time in light sleep than control on N10 (95% confidence interval (CI): 8.5-15.0%; P = 0.013) and experienced more stage shifts (CI: 13-44; P = 0.023) on both nights compared with control. The exercise group experienced more apnoea-hypopnoea (AH) events per hour compared with control (CI: 1-110; P = 0.046); AH events that were associated with night desaturations were also higher on N1 (exercise: 397 ± 320, control: 124 ± 205, P = 0.047) and N10 (exercise: 375 ± 229, control: 110 ± 138, P = 0.028, CI: 49-489 total events; P = 0.020). The length of hyperpnoea was increased from 12.8 ± 2.2 s on N1 to 14.6 ± 2.7 s on N10 (P = 0.008), and thus, total cycle length also increased (P = 0.002) in both cohorts. Mean pooled duty ratios were 0.68 ± 0.02 on N1 and 0.69 ± 0.02 on N10 (group effect P = 0.617)., Conclusion: Daily, moderate-intensity exercise in normobaric hypoxia equivalent to 4175 m exacerbated AH events, and negatively affected sleep architecture in exercisers compared with matched controls., (© 2015 Asian Pacific Society of Respirology.)

Study Objectives: Exposure to hypoxia elevates chemosensitivity, which can lead to periodic breathing. Exercise impacts gas exchange, altering chemosensitivity; however, interactions between sleep, exercise and chronic hypoxic exposure have not been examined. This study investigated whether exercise exacerbates sleep-related periodic breathing in hypoxia., Methods: Two experimental phases. Short-Term Phase: a laboratory controlled, group-design study in which 16 active, healthy men (age: 25 ± 3 y, height: 1.79 ± 0.06 m, mass: 74 ± 8 kg) were confined to a normobaric hypoxic environment (FIO2 = 0.139 ± 0.003, 4,000 m) for 10 days, after random assignment to a sedentary (control, CON) or cycle-exercise group (EX). Long-Term Phase: conducted at the Concordia Antarctic Research Station (3,800 m equivalent at the Equator) where 14 men (age: 36 ± 9 y, height: 1.77 ± 0.09 m, mass: 75 ± 10 kg) lived for 12-14 months, continuously confined. Participants were stratified post hoc based on self-reported physical activity levels. We quantified apnea-hypopnea index (AHI) and physical activity variables., Results: Short-Term Phase: mean AHI scores were significantly elevated in the EX group compared to CON (Night1 = CON: 39 ± 51, EX: 91 ± 59; Night10 = CON: 32 ± 32, EX: 92 ± 48; P = 0.046). Long-Term Phase: AHI was correlated to mean exercise time (R(2) = 0.4857; P = 0.008) and the coefficient of variation in night oxyhemoglobin saturation (SpO2; R(2) = 0.3062; P = 0.049)., Conclusions: Data indicate that exercise (physical activity) per se affects night SpO2 concentrations and AHI after a minimum of two bouts of moderate-intensity hypoxic exercise, while habitual physical activity in hypobaric hypoxic confinement affects breathing during sleep, up to 13+ months' duration., (© 2016 Associated Professional Sleep Societies, LLC.)

The post-exercise emotional response is mainly dependent on the intensity of the exercise performed; moderate exercise causes positive feelings, whereas maximal exercise may prompt negative affects. Acute hypoxia impairs peak O2 uptake (V̇O2peak), resulting in a shift to a lower absolute intensity at the point of exhaustion. Hence, the purpose of the study was to examine whether a severe hypoxic stimulus would influence the post-exercise affective state in healthy lowlanders performing an incremental exercise to exhaustion. Thirty-six male lowlanders performed, in a counter-balanced order and separated by a 48-h interval, two incremental exercise trials to exhaustion to determine their V̇O2peak, while they were breathing either room air (AIR; FiO2: 0.21), or a hypoxic gas mixture (HYPO; FiO2: 0.12). Before and immediately after each trial, subjects were requested to complete two questionnaires, based on how they felt at that particular moment: (i) the Profile of Mood States-Short Form, and (ii) the Activation Deactivation Adjective Check List. During the post-exercise phase, they also completed the Multidimensional Fatigue Inventory. V̇O2peak was significantly lower in the HYPO than the AIR trial (~15%; p<0.001). Still, after the HYPO trial, energy, calmness and motivation were markedly impaired, whereas tension, confusion, and perception of physical and general fatigue were exaggerated (p≤0.05). Accordingly, present findings suggest that an incremental exercise to exhaustion performed in severe hypoxia provokes negative post-exercise emotions, induces higher levels of perceived fatigue and decreases motivation; the affective responses coincide with the comparatively lower V̇O2peak than that achieved in normoxic conditions., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The study examined the effects of two short-term, intermittent hypoxic training protocols, namely exercising in hypoxia and living in normoxia (LL-TH; n=8), and exercising in normoxia preceded by a series of brief intermittent hypoxic exposures at rest (IHE+NOR; n=8), on the finger temperature response during a sea-level local cold test. In addition, a normoxic group was assigned as a control group (NOR; n=8). All groups trained on a cycle-ergometer 1 h/day, 5 days/week for 4 weeks at 50% of peak power output. Pre, post, and 11 days after the last training session, subjects immersed their right hand for 30 min in 8°C water. In the NOR group, the average finger temperature was higher in the post (+2.1°C) and 11-day after (+2.6°C) tests than in the pre-test (p≤0.001). Conversely, the fingers were significantly colder immediately after both hypoxic protocols (LL-TH: -1.1°C, IHE+NOR: -1.8°C; p=0.01). The temperature responses returned to the pre-training level 11 days after the hypoxic interventions. Ergo, present findings suggest that short-term intermittent hypoxic training impairs sea-level local cold tolerance; yet, the hypoxic-induced adverse responses seem to be reversible within a period of 11 days.

Background: Both exposure to hypoxia and exercise training have the potential to modulate appetite and induce beneficial metabolic adaptations. The purpose of this study was to determine whether daily moderate exercise training performed during a 10-day exposure to normobaric hypoxia alters hormonal appetite regulation and augments metabolic health., Methods: Fourteen healthy, male participants underwent a 10-day hypoxic confinement at ∼ 4000 m simulated altitude (FIO2 = 0.139 ± 0.003%) either combined with daily moderate intensity exercise (Exercise group; N = 8, Age = 25.8 ± 2.4 yrs, BMI = 22.9 ± 1.2 kg · m(-2)) or without any exercise (Sedentary group; N = 6 Age = 24.8 ± 3.1 yrs, BMI = 22.3 ± 2.5 kg · m(-2)). A meal tolerance test was performed before (Pre) and after the confinement (Post) to quantify fasting and postp randial concentrations of selected appetite-related hormones and metabolic risk markers. 13C-Glucose was dissolved in the test meal and 13CO2 determined in breath samples. Perceived appetite ratings were obtained throughout the meal tolerance tests., Results: While body mass decreased in both groups (-1.4 kg; p = 0.01) following the confinement, whole body fat mass was only reduced in the Exercise group (-1.5 kg; p = 0.01). At Post, postprandial serum insulin was reduced in the Sedentary group (-49%; p = 0.01) and postprandial plasma glucose in the Exercise group (-19%; p = 0.03). Fasting serum total cholesterol levels were reduced (-12%; p = 0.01) at Post in the Exercise group only, secondary to low-density lipoprotein cholesterol reduction (-16%; p = 0.01). No differences between groups or testing periods were noted in fasting and/or postprandial concentrations of total ghrelin, peptide YY, and glucagon-like peptide-1, leptin, adiponectin, expired 13CO2 as well as perceived appetite ratings (p>0.05)., Conclusion: These findings suggest that performing daily moderate intensity exercise training during continuous hypoxic exposure does not alter hormonal appetite regulation but can improve the lipid profile in healthy young males.

Purpose: Both acute hypoxia and physical exercise are known to increase oxidative stress. This randomized prospective trial investigated whether the addition of moderate exercise can alter oxidative stress induced by continuous hypoxic exposure., Methods: Fourteen male participants were confined to 10-d continuous normobaric hypoxia (FIO2 = 0.139 ± 0.003, PIO2 = 88.2 ± 0.6 mm Hg, ∼4000-m simulated altitude) either with (HCE, n = 8, two training sessions per day at 50% of hypoxic maximal aerobic power) or without exercise (HCS, n = 6). Plasma levels of oxidative stress markers (advanced oxidation protein products [AOPP], nitrotyrosine, and malondialdehyde), antioxidant markers (ferric-reducing antioxidant power, superoxide dismutase, glutathione peroxidase, and catalase), nitric oxide end-products, and erythropoietin were measured before the exposure (Pre), after the first 24 h of exposure (D1), after the exposure (Post) and after the 24-h reoxygenation (Post + 1). In addition, graded exercise test in hypoxia was performed before and after the protocol., Results: Maximal aerobic power increased after the protocol in HCE only (+6.8%, P < 0.05). Compared with baseline, AOPP was higher at Post + 1 (+28%, P < 0.05) and nitrotyrosine at Post (+81%, P < 0.05) in HCS only. Superoxide dismutase (+30%, P < 0.05) and catalase (+53%, P < 0.05) increased at Post in HCE only. Higher levels of ferric-reducing antioxidant power (+41%, P < 0.05) at Post and lower levels of AOPP (-47%, P < 0.01) at Post + 1 were measured in HCE versus HCS. Glutathione peroxidase (+31%, P < 0.01) increased in both groups at Post + 1. Similar erythropoietin kinetics was noted in both groups with an increase at D1 (+143%, P < 0.01), a return to baseline at Post, and a decrease at Post + 1 (-56%, P < 0.05)., Conclusions: These data provide evidence that 2 h of moderate daily exercise training can attenuate the oxidative stress induced by continuous hypoxic exposure.

Fighter pilots are commonly recommended strength training as a means of improving the tolerance to withstand high gravitoinertial (G) loads. Previous studies on the effect of short-term strength-training regimens on G-endurance show equivocal results, with a majority of the studies suggesting improved G-endurance. The mechanisms underlying such improvement are unknown. Presumably, any change in G-tolerance induced by physical training habits should be manifest following long-term training. We also reasoned that during repeated straining maneuvers--as during certain G-endurance protocols--the relaxed G-tolerance and the exercise pressure response may play a significant role in maintaining adequate arterial pressure, and hence that different training modalities might alter G-endurance, by altering the exercise pressor response. Three groups of males were studied, long-term (>6 months) endurance-trained (E; n = 17), strength-trained (S; n = 16) and untrained (U; n = 17) individuals. The pressor response was studied during sustained (40 s) isometric knee extensions at 50 % of the maximal contraction level. Relaxed gradual onset-rate G-tolerance was determined. G-tolerance was similar in the E (4.6 ± 0.5 G), S (4.9 ± 0.8 G) and U (4.6 ± 0.8 G) groups. The mean arterial pressure increase during isometric exercise was higher in the S (36 ± 7 mmHg = mean ± SD) and U (35 ± 16 mmHg) groups than in the E group (28 ± 8 mmHg). The results suggest that relaxed G-tolerance is unaffected by physical training habits, and that the training modality affects the magnitude of the exercise pressor response. However, it seems that the response is blunted by endurance training rather than enhanced by strength training.

The purpose of this study was to examine whether the forearm-finger skin temperature gradient (T(forearm-finger)), an index of vasomotor tone during resting conditions, can also be used during steady-state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow (BFF ) was measured with a laser-Doppler flowmeter, and finger skin blood flow (PPG) was recorded from the left index fingertip using a pulse plethysmogram. T(forearm-finger) of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased (P<0.001), and T(forearm-finger) decreased (P<0.001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between T(forearm-finger) and both PPG (r = -0.68; P<0.001) and BFF (r = -0.50; P<0.001). It is concluded that T(forearm-finger) is a valid qualitative index of cutaneous vasomotor tone during steady-state exercise., (© 2013 Scandinavian Society of Clinical Physiology and Nuclear Medicine. Published by John Wiley & Sons Ltd.)

The potentiated exercise-sweating rate observed during acute hypoxia is diminished after a sleep-high train-low (SH-TL) regimen. We tested the hypothesis that this attenuation of the sweating response after SH-TL is compensated for by an increase in heat loss via vasodilatation. Nine male subjects participated in a 28-day SH-TL regimen. Before (pre-), and after (post-) the SH-TL protocol, they performed an VO2peak test under normoxia and hypoxia. Additionally, pre- and post-SH-TL they completed three 30-min constant-work rate trials on a cycle ergometer. In one trial, the subjects inspired room air while exercising at 50% of normoxic VO2peak (CT). In the remaining trials, subjects exercised in hypoxia (F(I)O2 12.5%), either at the same absolute (HAT) or relative (50% of hypoxic VO2peak work rate (HRT) as in CT. Despite similar exercise core temperature responses between pre- and post-SH-TL trials, sweating rate was potentiated in HAT pre-SH-TL [CT: 1.97 (0.42); HRT: 1.86 (0.31); HAT: 2.55 (0.53) mg cm(-2) min(-1); p < 0.05]. Post-SH-TL exercise sweating rate was increased for CT, and remained unchanged in HRT and HAT [CT: 2.42 (0.76); HRT: 2.01 (0.33); HAT: 2.59 (0.30) mg cm(-2) min(-1)]. Pre-SH-TL, the forearm-fingertip skin temperature difference (Tsk(f-f)) was higher in HAT than in CT and HRT by ~3.5 °C (p < 0.05). The inter-condition differences in Tsk(f-f) were diminished post-SH-TL. In conclusion, the decrease in sweating rate during hypoxic exercise, following a SH-TL regimen, was countered by an increase in vasodilatation (reduced Tsk(f-f)), whereas SH-TL enhanced the sweating response during normoxic exercise. The mechanisms underlying these SH-TL-induced alterations in thermoregulatory responses remain to be settled.

This study investigated the effects of four exposures to normobaric hypoxia (SIH group; FIO₂ = 0.120, N=10) or placebo-control normoxia (Control group; FIO₂ = 0.209, N=9) on cardio-respiratory responses to hypoxic exercise. Before and after the exposures all subjects performed a constant power test (CP) to exhaustion in hypoxia FIO₂ = 0.120 at a work load corresponding to 75% of previously determined normoxic VO₂ peak. Arterial oxygen saturation (SPO₂) and minute ventilation (V(E)) were measured continuously. NIRS was used to monitor regional changes in oxygenated, de-oxygenated and total hemoglobin concentrations of the frontal cortex, vastus lateralis and serratus anterior. Although neither group improved CP time, the SIH group exhibited increases in both V(E) (+15%; P<0.05) and SPO₂ (+4%; P<0.05) after intermittent hypoxia. No physiologically significant differences were observed during exercise in vastus lateralis, serratus anterior and cerebral oxygenation between groups and testing periods. These data suggest that normobaric SIH enhances hypoxic exercise V(E) and SPO₂ without affecting regional oxygenation or time to exhaustion., (Copyright © 2012 Elsevier B.V. All rights reserved.)

The present study evaluated the effect of a sleep high-train low regimen on the finger cold-induced vasodilation (CIVD) response. Seventeen healthy males were assigned to either a control (CON; n=9) or experimental (EXP; n=8) group. Each group participated in a 28-day aerobic training program of daily 1-h exercise (50% of peak power output). During the training period, the EXP group slept at a simulated altitude of 2800 meters (week 1) to 3400 m (week 4) above sea level. Normoxic (CIVD(NOR); CON and EXP groups) and hypoxic (CIVD(HYPO); F(I)O(2)=0.12; EXP group only) CIVD characteristics were assessed before and after the training period during a 30-min immersion of the hand in 8°C water. After the intervention, the EXP group had increased average finger skin temperature (CIVD(NOR): +0.5°C; CIVD(HYPO): +0.5°C), number of waves (CIVD(NOR): +0.5; CIVD(HYPO): +0.6), and CIVD amplitude (CIVD(NOR): +1.5°C; CIVD(HYPO): +3°C) in both CIVD tests (p<0.05). In contrast, the CON group had an increase in only the CIVD amplitude (+0.5°C; p<0.05). Thus, the enhancement of aerobic performance combined with altitude acclimatization achieved with the sleep high-train low regimen contributed to an improved finger CIVD response during cold-water hand immersion in both normoxic and hypoxic conditions.

The purpose of the study was to investigate the effect of 30-min voluntary hyperpnoea on cerebral, respiratory and leg muscle balance between O(2) delivery and utilization during a subsequent constant-power test. Eight males performed a V˙O(2max) test, and two exercise tests at 85% of peak power output: (a) a control constant-power test (CPT), and (b) a constant-power test after a respiratory maneuver (CPT(RM)). Oxygenated (Δ[O(2)Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) hemoglobin in cerebral, intercostal and vastus lateralis were monitored with near-infrared spectroscopy. The performance time dropped ∼15% in CPT(RM) (6:55±2:52min) compared to CPT (8:03±2:33min), but the difference was not statistically significant. The vastus lateralis and intercostal Δ[tHb] and Δ[HHb] were lower in CPT(RM) than in CPT (P≤0.05). There were no differences in cerebral oxygenation between the trials. Thus, respiratory work prior to an exercise test influences the oxygenation during exercise in the leg and respiratory muscles, but not in the frontal cortex., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Cold-induced vasodilatation (CIVD) has been proposed as a potential protective mechanism against cold injuries during exposure of extremities to a cold environment. The purpose of this study was to evaluate the effect of exercise and the associated elevation in core temperature on toe skin temperatures during immersion of the foot in cold (8 degrees C) water. Subjects (N = 8) participated in two trials. In one, they conducted an incremental exercise to exhaustion (exercise) on a cycle ergometer, which was followed by immersion of the right foot in 8 degrees C water. In the second trial (control), immersion of the foot in cold water was not preceded by exercise. Upon completion of the exercise in the exercise trial, and at the onset of the immersion of the foot in cold water, tympanic temperature was 0.6 degrees C (P < 0.01) higher than pre-exercise levels. There was a significant increase (P < 0.05) in the number of CIVD waves, but not their amplitudes, in the exercise trial compared to the control trial. A CIVD response occurred in 57.5% of all toes in the exercise trial, and in only 27.5% in the control trial. Additionally, 50% of subjects exhibited CIVD in at least one toe in the control trial, and 87.5% during the exercise trial. It is concluded that exercise, and particularly the associated elevation in core temperature, enhances the frequency of the toe CIVD responses, and can therefore potentially act as a protective mechanism against cold injury.

Introduction: It is generally accepted that the palmar (volar) and dorsal surfaces of human hands display different sudomotor responses to mental or thermal stimuli. We tested the hypothesis that, during thermal stimulation, secretion from the dorsal surfaces would always exceed that from the volar aspect of the hand., Methods: Sweat secretion from 10 hand sites and the forehead was examined (ventilated capsules) in 10 subjects during passive heating (climate chamber: 36 degrees C, 60% relative humidity, water-perfusion suit: 40 degrees C) immediately followed by incremental cycling to volitional fatigue., Results: This treatment significantly increased core temperature (39.3 degrees C), heart rate (178 bpm), and sweat rate at all sites. Mean sweat secretion during exercise was greater at the forehead (2.90 mg x cm(-2) x min(-1); +/- 0.19) than the hand (1.49 mg x cm(-2) min(-1); +/- 0.27). While no significant differences in sweating were observed among dorsal sites, a nonuniform secretion pattern was observed across the volar surface, with sweating at the palm being the lowest, and that from the volar aspect of the distal phalanges being equivalent to the dorsal hand. These differences became more evident as exercise progressed. Mean hand sweat rate during exercise was 41.7 ml x h(-1), with sweating from the palm accounting for only about 6% of sweat secretion., Conclusion: Sweat secretion from both the palmar and dorsal surfaces of the hand increases during exercise in the heat, although this occurs in a nonuniform fashion. It is possible that a greater sweat gland density on the fingers may account for variations across the volar surface. However, higher dorsal sweating with lower gland counts (high glandular flow) may be attributable to either larger sweat glands, or to a greater cholinergic sensitivity of these glands.

The importance of the head in dissipating body heat under hot conditions is well recognised, although very little is known about local differences in sweat secretion across the surface of the head. In this study, we focused on the intra-segmental distribution of head sweating. Ten healthy males were exposed to passive heating and exercise-induced hyperthermia (36 degrees C, 60% relative humidity, water-perfusion suit: 46 degrees C), with ventilated sweat capsules (3.16 cm(2)) used to measure sweat rates from the forehead and nine sites inside the hairline. Sweat secretion from both non-hairy (glabrous) and hairy areas of the head increased linearly with increments in work rate and core temperature, with heart rate and core temperature peaking at 175 b min(-1) (+/-6) b min(-1) and 39.2 degrees C (+/-0.1). The mean sweat rate during exercise for sites within the hairline was 1.95 mg cm(-2) min(-1). However, the evolution of this secretion pattern was not uniformly distributed within the head, with the average sweat rate for the top of the head being significantly lower than at the anterior lateral aspect of the head (P < 0.05), and representing only 30% of the forehead sweat rate (P < 0.05). It is hypothesised that these intra-segmental observations may reflect variations in the local adaptation of eccrine glands to differences in local evaporation associated either with bipedal locomotion, which will influence forehead sweating, or the hidromeiotic suppression of sweating, which impacts upon sweat glands within the hairline.

Thermal sweating from the human torso accounts for about half of the whole-body sweat secretion, yet its intra-segmental distribution has not been thoroughly examined. Therefore, the aim of the current study was to provide a detailed description of the distribution of eccrine sweating within the torso during passively-induced (water-perfusion garment: 40 degrees C) and progressively increasing, exercise-related thermal strain (36 degrees C, 60% relative humidity). Sudomotor function was measured in ten males using ventilated sweat capsules (3.16 cm(2)) attached to twelve sites on the ventral (four), lateral (three) and dorsal (four) torso, and upper shoulder surfaces. Sweating increased asymptotically in all sites, with the final core temperature averaging 39.7 degrees C (+/-0.1) and heart rates being 181 b min(-1) (+/-2). During exercise, the mean torso sweat rate averaged 1.35 mgcm(-2)min(-1), with sweating from the lateral torso surfaces generally being the lowest. Each of the between-site comparisons with the lateral torso differed significantly (P < 0.05), except for comparisons with the chest (P = 0.051) and shoulder (P > 0.05). The intra-segmental differences between the lateral torso and the chest, abdomen, upper- and lower-back areas were significantly accentuated during exercise. From these data, it is evident that the torso is another region that does not have a uniform distribution of thermally-induced sweating. Thus, it is no longer acceptable for researchers, modellers, sweating manikins engineers or clothing manufacturers to assume that the sweat rates for all local sites within any body segment are equivalent.

Heat-loss responses during steady-load exercise are affected by an increase in relative work rate induced by muscle ischaemia or hypoxaemia. The present study investigated whether progressive increases in perception of exertion and relative oxygen uptake %VO2peak which occur during prolonged steady-load exercise as a result of progressively increased peripheral fatigue, might also affect the regulation of heat loss responses and hence the exercise-induced increase in mean body temperature. Ten male subjects first performed a ramp-test to exhaustion on a cycle ergometer to evaluate their initial peak oxygen uptake (Control VO2peak). On a separate day, 120 min of cycling at constant power output corresponding to 60% of Control VO2peak was performed in thermoneutral environment (Ta = 23 degrees C, RH = 50%, wind speed = 5 m s(-1)). This was immediately followed by another maximal performance test (Fatigue VO2peak). During prolonged exercise, median (range) rating of perceived exertion for whole-body (RPEwb) increased (P < 0.01) from initial 3.5 (1-5) to 5.5 (5-9) at the end of exercise. Fatigue VO2peak and peak power output were 9 (5) and 10 (5)% lower (P < 0.01) when compared to control values. At the onset of exercise, heat production, mechanical efficiency, heat loss and mean body temperature increased towards asymptotic values, thereafter remained constant throughout the 120 min exercise, despite the concomitant progressive increase in relative work rate, as reflected in increased RPEwb and relative oxygen uptake. It is thus concluded that the increase in relative work rate induced predominantly by peripheral muscle fatigue affects neither the level of increase in mean body temperature nor the regulation of heat loss responses during prolonged steady-load exercise.

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high-train low regimen). Peak oxygen uptake (VO2(peak)) and peak work rate (WR(peak)) were determined under normoxic (20.9%O(2)) and hypoxic (13.5%O(2)) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WR(peak) attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WR(peak) attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease (P < 0.001) in (VO2(peak)) pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially (P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead (m(sw)f) was greater (P < 0.01) in the HAT (2.60 (0.80) mg cm(-2) min(-1)) compared to the other two trials (CT = 1.87 (1.09) mg cm(-2) min(-1); HRT = 1.57 (0.82) mg cm(-2) min(-1)) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented (P < 0.01) gain of the sweating response (m(sw)f/Delta T(re)). The augmented (m(sw)f) and m(sw)f/Delta T(re) during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures.

Introduction: Little is known regarding local differences in foot sweat secretion. Since such information is important to our understanding of sweat gland control for thermoregulatory modeling and for the design of footwear we explored this topic., Methods: Local sweat rates were investigated across core temperatures from 37-39 degrees C, achieved using endogenous (cycling) and exogenous heat (water-perfusion garment: 46 degrees C). Six healthy adults (three men, three women) performed one-legged, incremental cycling in a heated, climate-controlled chamber (36 degrees C, 60% relative humidity). Sweat rates were measured at the forehead and stationary (left) foot (capsules 3.16 cm2): three dorsal sites (base of toes, second metatarsal, and mid point), the lateral, and the central plantar surfaces., Results: Terminal core temperatures ranged between 38.3-39.1 oC, with peak heart rates of 155-187 bpm. Most foot sweat rates were < 50% of that observed at the forehead: dorsal 1 (38%); dorsal 2 (54%); dorsal 3 (37%); lateral (24%); and plantar surfaces (18%). When averaged across the trial, local sweat rates were: 2.61 (forehead); 0.98 (dorsal 1); 1.39 (dorsal 2); 0.95 (dorsal 3); 0.62 (lateral); and 0.47 mg cm2 2 min-1 (plantar)., Conclusion: Two key observations emerged. First, sweat secretion from the experimental foot averaged 30 ml x h(-1), peaking in the last 5 min at 50 ml x h(-1). Second, approximately 70% of the measured sweat flow emanated from the upper skin surfaces, with only 30% coming from the plantar surface.

In a series of three companion papers published in this Journal, we identify and validate the available thermal stress indicators (TSIs). In this first paper of the series, we conducted a systematic review (registration: INPLASY202090088) to identify all TSIs and provide reliable information regarding their use (funded by EU Horizon 2020; HEAT-SHIELD). Eight databases (PubMed, Agricultural and Environmental Science Collection, Web of Science, Scopus, Embase, Russian Science Citation Index, MEDLINE, and Google Scholar) were searched from database inception to 15 April 2020. No restrictions on language or study design were applied. Of the 879 publications identified, 232 records were considered for further analysis. This search identified 340 instruments and indicators developed between 200 BC and 2019 AD. Of these, 153 are nomograms, instruments, and/or require detailed non-meteorological information, while 187 can be mathematically calculated utilizing only meteorological data. Of these meteorology-based TSIs, 127 were developed for people who are physically active, and 61 of those are eligible for use in occupational settings. Information regarding the equation, operating range, interpretation categories, required input data, as well as a free software to calculate all 187 meteorology-based TSIs is provided. The information presented in this systematic review should be adopted by those interested in performing on-site monitoring and/or big data analytics for climate services to ensure appropriate use of the meteorology-based TSIs. Studies two and three in this series of companion papers present guidance on the application and validation of these TSIs, to guide end users of these indicators for more effective use. [ABSTRACT FROM AUTHOR]

Human extravehicular activity (EVA) is essential to space exploration and involves risk of decompression sickness (DCS). On Earth, the effect of microgravity on physiological systems is simulated in an experimental model where subjects are confined to a 6° head-down bed rest (HDBR). This model was used to investigate various resting and exercise regimen on the formation of venous gas emboli (VGE), an indicator of decompression stress, post-hyperbaric exposure. Eight healthy male subjects participating in a bed rest regimen also took part in this study, which incorporated five different hyperbaric exposure (HE) interventions made before, during and after the HDBR. Interventions i–iv were all made with the subjects lying in 6° HD position. They included (C1) resting control, (C2) knee-bend exercise immediately prior to HE, (T1) HE during the fifth week of the 35-day HDBR period, (C3) supine cycling exercise during the HE. In intervention (C4), subjects remained upright and ambulatory. The HE protocol followed the Royal Navy Table 11 with 100 min spent at 18 m (280 kPa), with decompression stops at 6 m for 5 min, and at 3 m for 15 min. Post-HE, regular precordial Doppler audio measurements were made to evaluate any VGE produced post-dive. VGE were graded according to the Kisman Masurel scale. The number of bubbles produced was low in comparison to previous studies using this profile [Kisman integrated severity score (KISS) ranging from 0–1], and may be because subjects were young, and lay supine during both the HE and the 2 h measurement period post-HE for interventions i–iv. However, the HE during the end of HDBR produced significantly higher maximum bubble grades and KISS score than the supine control conditions (p < 0.01). In contrast to the protective effect of pre-dive exercise on bubble production, a prolonged period of bed rest prior to a HE appears to promote the formation of post-decompression VGE. This is in contrast to the absence of DCS observed during EVA. Whether this is due to a difference between hypo- and hyperbaric decompression stress, or that the HDBR model is a not a good model for decompression sensitivity during microgravity conditions will have to be elucidated in future studies. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effect of respiratory muscle endurance training on endurance exercise performance in normoxic and hypoxic conditions. Eighteen healthy males were stratified for age and aerobic capacity; and randomly assigned either to the respiratory muscle endurance training (RMT = 9) or to the control training group (CON = 9). Both groups trained on a cycle-ergometer 1 h day(-1), 5 days per week for a period of 4 weeks at an intensity corresponding to 50% of peak power output. Additionally, the RMT group performed a 30-min specific endurance training of respiratory muscles (isocapnic hyperpnea) prior to the cycle ergometry. Pre, Mid, Post and 10 days after the end of training period, subjects conducted pulmonary function tests (PFTs), maximal aerobic tests in normoxia (VO(2max)NOR), and in hypoxia (VO(2max)HYPO; F(I)O(2) = 0.12); and constant-load tests at 80% of VO(2max)NOR in normoxia (CLT(NOR)), and in hypoxia (CLTHYPO). Both groups enhanced VO(2max)NOR (CON: +13.5%; RMT: +13.4%), but only the RMT group improved VO(2max)HYPO Post training (CON: -6.5%; RMT: +14.2%). Post training, the CON group increased peak power output, whereas the RMT group had higher values of maximum ventilation. Both groups increased CLT(NOR) duration (CON: +79.9%; RMT: +116.6%), but only the RMT group maintained a significantly higher CLT(NOR) 10 days after training (CON: +56.7%; RMT: +91.3%). CLT(HYPO) remained unchanged in both groups. Therefore, the respiratory muscle endurance training combined with cycle ergometer training enhanced aerobic capacity in hypoxia above the control values, but did not in normoxia. Moreover, no additional effect was obtained during constant-load exercise. [ABSTRACT FROM AUTHOR]

Cold-induced vasodilation (CIVD) is an acute increase in peripheral blood flow observed during cold exposures. It is hypothesized to protect against cold injuries, yet despite continuous research it remains an unexplained phenomenon. Contrary to the traditionally held view, we propose that CIVD is a thermoregulatory reflex mechanism contributing to heat loss. Ten adults (4 females; 23.8 +/- 2.0 years) randomly underwent three 130-min exposures to -20 degrees C incorporating a 10-min moderate exercise period at the 65th min, while wearing a liquid conditioning garment (LCG) and military arctic clothing. In the pre-warming condition, rectal temperature was increased by 0.5 degrees C via the LCG before the cold exposure. In the warming condition, participants regulated the LCG throughout the cold exposure to subjective comfort. In the control condition, the LCG was worn but was not operated either before or during the cold exposure. Results demonstrated that the majority of CIVD occurred during the warming condition when the thermometrically-estimated mean body temperature (T (b)) was at its highest. A thermoregulatory pattern was identified whereby CIVD occurred soon after T (b) increased past a threshold (approximately 36.65 degrees C in warming and pre-warming; approximately 36.4 degrees C in control). When CIVD occurred, T (b) was reduced and CIVD ceased when T (b) fell below the threshold. These findings were independent of extremity temperature since CIVD episodes occurred at a large range of finger temperatures (7.2-33.5 degrees C). These observations were statistically confirmed by auto-regressive integrated moving average analysis (t = 9.602, P < 0.001). We conclude that CIVD is triggered by increased T (b) supporting the hypothesis that CIVD is a thermoregulatory mechanism contributing to heat loss. [ABSTRACT FROM AUTHOR]

The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2)°C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3)°C) and Absolute (2.4 (0.7)°C) trials, but was substantially lower ( P<0.01) in the Relative trial (1.4 (0.8)°C). Ischaemia potentiated ( P<0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m−2 min−1) compared to the Control trial (13.4 (6.2) g m−2 min−1), concomitant with an attenuated ( P<0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex. [ABSTRACT FROM AUTHOR]

Environmental hypoxia and inactivity have both been shown to modulate appetite. To elucidate the independent and combined effects of hypoxia and bed rest-induced inactivity on appetite-related hormones and subjective appetite, eleven healthy, non-obese males underwent three experimental interventions in a cross-over and randomized fashion: 1) Hypoxic confinement combined with daily moderate-intensity exercise (HAMB, FiO2 = 0.141 ± 0.004; PiO2 = 90.0 ± 0.4 mmHg) 2) Bed rest in normoxia (NBR, FiO2 = 0.209; PiO2 = 133.1 ± 0.3 mmHg) and 3) Bed rest in hypoxia (HBR, FiO2 = 0.141 ± 0.004; PiO2 = 90.0 ± 0.4 mmHg). A mixed-meal tolerance test (MTT), followed by an ad libitum meal were performed before (Pre) and after 16-days (Post) of each intervention. Composite satiety scores (CSS) during the MTT were calculated from visual analogue scores, while fasting and postprandial concentrations of total ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1) and leptin were quantified from arterialized-venous samples. Postprandial CSS were significantly lower at Post compared to Pre in NBR only (P < 0.05) with no differences observed in ad libitum meal intakes. Postprandial concentrations and incremental area under the curve (AUC) for total ghrelin and PYY were unchanged following all interventions. Postprandial GLP-1 concentrations were only reduced at Post following HBR (P < 0.05) with resulting AUC changes being significantly lower compared to HAMB (P < 0.01). Fasting leptin was reduced following HAMB (P < 0.05) with no changes observed following NBR and HBR. These findings suggest that independently, 16-day of simulated altitude exposure (∼4000 m) and bed rest-induced inactivity do not significantly alter subjective appetite or ad libitum intakes. The measured appetite-related hormones following both HAMB and HBR point to a situation of hypoxia-induced appetite stimulation, although this did not reflect in higher ad libitum intakes.Clinical Trial Registration Number: NCT02293772. [ABSTRACT FROM AUTHOR]

Abstract: Immobilization-induced bone loss is usually greater in the epiphyses than in the diaphyses. The larger fraction of trabecular bone in the epiphyses than in the diaphyses offers an intuitive explanation to account for this phenomenon. However, recent evidence contradicts this notion and suggests that immobilization-induced bone loss from the distal tibia epiphysis is mainly from the cortical compartment. The aim of this study was to establish whether this pattern of bone loss was a general rule during immobilization. We monitored various skeletal sites with different tissue composition during 5 weeks of immobilization. Ten healthy male volunteers with mean age of 24.3 years (SD 2.6 years) underwent strict horizontal bed rest. Bone scans were obtained during baseline data collection, at the end of bed rest and after 14 days of recovery by peripheral Quantitative Computed Tomography (pQCT). Sectional images were obtained from the distal tibia epiphysis (at 4% of the tibia''s length), from the diaphysis (at 38%), from the proximal metaphysis (at 93%) and from the proximal epiphysis (at 98%), as well as from the distal femur epiphysis (at 4% of the femur''s length) and from the patella. Relative bone losses were largest at the patella, where they amounted to −3.2% (SD 1.8%, p <0.001) of the baseline values, and smallest at the tibia diaphysis, where they amounted to −0.7% (SD 1.0%, p =0.019). The relative losses were generally larger from cortical than from trabecular compartments (p =0.004), and whilst all skeletal sites depicted such cortical losses, substantial trabecular losses were found only from the proximal tibia epiphysis. Results confirm that the differential losses from the various skeletal sites cannot be explained on the basis of trabecular vs. cortical tissue composition differences, but that endocortical circumference can account for the different amounts of bone loss in the tibia. The present study therefore supports the suggestion of the subendocortical layer as a transitional zone, which can readily be transformed into trabecular bone in response to immobilization. The latter will lead to cortical thinning, a factor that has been associated with the risk of fracture and with osteoarthritis. [Copyright &y& Elsevier]