Exercise In Normobaric Hypoxia Research Articles

Repeated Short Cold-water Immersions Are Sufficient To Habituate To The Cold, But Do Not Lead To Adaptations During Exercise In Normobaric Hypoxia

Repeated Short Cold-water Immersions Are Sufficient To Habituate To The Cold, But Do Not Lead To Adaptations During Exercise In Normobaric Hypoxia

Impact of the Menstrual Cycle on the Cardiovascular and Ventilatory Responses During Exercise in Normoxia and Hypoxia.

Citherlet, Tom, Antoine Raberin, Giorgio Manferdelli, Nicolas Bourdillon, and Grégoire P Millet. Impact of the menstrual cycle (MC) on the cardiovascular and ventilatory responses during exercise in normoxia and hypoxia. High Alt Med Biol. 00:00-00, 2024. Introduction: Ovarian hormones influence several physiological functions in women. This study investigated how the hormonal variations across the menstrual cycle (MC) impact cardiovascular and ventilatory responses during rest and moderate exercise in normobaric hypoxia. Methods: Thirteen eumenorrheic women were tested during the early follicular (Fol1), late follicular (Fol2), and mid-luteal (Lut3) phases with measurement of hormonal levels. Heart rate (HR) variability, blood pressure, and baroreflex sensitivity (BRS) were evaluated at rest in normoxia. Ventilation (VE), peripheral oxygen saturation, and HR were monitored at rest and during moderate-intensity cycling exercise in hypoxia (FiO2 = 14%). Results: Despite expected hormone level variations, no significant changes were observed across the MC in HR variability (root mean square of successive differences; 64 (95% confidence interval [47, 81]) at Fol1, 54 [42, 66] at Fol2, 60 [44, 77] ms at Lut3), blood pressure (mean blood pressure; 85 [79, 90]), 87 [81, 93]), 84 [77, 92] mmHg), BRS (26 [17, 36], 28 [20, 35], 23 [17, 29] ms/mmHg), VE (rest: 8.9 [7.9, 9.8], 9.5 [9.0, 9.9], 9.0 [8.1, 9.9]; exercise: 53 [41, 66], 51.1 [36.4, 65.7], 54.4 [34.0, 74.8] l/min), peripheral oxygen saturation (rest: 89.8 [87.4, 92.1], 91.9 [88.7, 95.0], 90.2 [87.8, 92.6]; exercise: 80.5 [77.4, 83.5], 84.4 [80.4, 88.3], 81.9 [78.3, 85.4] %) HR (rest: 69.7 [60.2, 79.1], 70.8 [63.2, 78.3], 70.5 [64.0, 77.0]; exercise: 148 [136, 160], 146 [132, 161], 146 [132, 160] bpm), and cycling efficiency (0.17 [0.16, 0.18], 0.17 [0.13, 0.21], 0.16 [0.15, 0.18] %) (all p > 0.05). Discussion: From a practical point of view, there is no strong evidence of any usefulness of monitoring hormonal variations and the MC phases for women exercising in hypoxia.

Metabolic and hormonal responses to acute high-load resistance exercise in normobaric hypoxia using a saturation clamp.

We assessed metabolic and hormonal responses to high-load resistance exercise under varying normobaric hypoxia conditions with a saturation clamp. Employing a counterbalanced, crossover test design, ten well-trained men participated in three exercise trials with normoxic or hypoxic gas mixtures to maintain arterial oxygen saturation at -90% and 80% [moderate (MH) and severe (SH) hypoxia, respectively]. The resistance exercise regimen comprised five sets of 10 repetitions of barbell back squats at 70% of one repetition maximum, with 1-min rest between sets. Metabolic and hormonal responses were measured before normoxia or hypoxia exposures (Pre 1), 15min after the exposures (Pre 2), and at 0-, 15-, and 30-min post-exercises (T0, T15, and T30, respectively). Compared to Pre 2, blood lactate concentrations and growth hormone values were elevated at T0, T15, and T30 (p ≤ 0.001), while testosterone values increased at T0 in all conditions (p ≤ 0.009). Epinephrine values increased significantly from Pre 2 to T0 in SH only (p < 0.001). SH had significantly higher blood lactate concentrations (p = 0.023), growth hormone (p = 0.050), and epinephrine (p = 0.020) values at T30 compared to NM. Cortisol values were elevated above Pre 2at T15 in MH and SH, while lower testosterone values were noted at T0 and T15 for SH compared to NM and MH (all p ≤ 0.05). Severe simulated hypoxia, achieved through a saturation clamp during barbell back squats, may enhance metabolic and hormonal responses, particularly 30min post-session. Nevertheless, the acute effects of hypoxia exposure seem to be overridden by the impact of high-load resistance exercise.

Repeated short cold-water immersions are sufficient to habituate to the cold, but do not lead to adaptations during exercise in normobaric hypoxia.

We sought to assess the effects of repeated cold-water immersions (CWI) on respiratory, metabolic, and sympathoadrenal responses to graded exercise in hypoxia. Sixteen (2 female) participants (age: 21.2 ± 1.3 years; body fat: 12.3±7.7%; body surface area 1.87±0.16m2, VO2peak: 48.7±7.9mL/kg/min) underwent 6 CWI in 12.0±1.2°C. Each CWI was 5 min, twice daily, separated by≥4 h, for three consecutive days, during which metabolic data were collected. The day before and after the repeated CWI intervention, participants ran in normobaric hypoxia (FIO2=0.135) for 4 min at 25%, 40%, 60%, and 75% of their sea level peak oxygen consumption (VO2peak). CWI had no effect on VO2 (p>0.05), but reduced the VE (CWI #1: 27.1±17.8versus CWI #6: 19.9±12.1L/min) (p<0.01), VT (CWI #1: 1.3±0.4vs CWI #6: 1.1±0.4L) (p<0.01), and VE:VO2 (CWI #1: 53.5±24.1vs CWI #6: 41.6±20.5) (p<0.01) during subsequent CWI. Further, post exercise plasma epinephrine was lower after CWI compared to before (103.3±43.1; 73.4±34.6 pg/mL) (p=0.03), with no change in pre-exercising values (75.4±30.7; 72.5±25.9 pg/mL). While these changes were noteworthy, it is important to acknowledge there were no changes in pulmonary (VE, VT, and VE:VO2) or metabolic (VO2, SmO2, and SpO2) variables across multiple hypoxic exercise workloads following repeated CWI. CWI habituated participants to cold water, but this did not lead to adaptations during exercise in normobaric hypoxia.

Cardio-Respiratory and Muscle Oxygenation Responses to Submaximal and Maximal Exercise in Normobaric Hypoxia: Comparison between Children and Adults.

As differential physiological responses to hypoxic exercise between adults and children remain poorly understood, we aimed to comprehensively characterise cardiorespiratory and muscle oxygenation responses to submaximal and maximal exercise in normobaric hypoxia between the two groups. Following familiarisation, fifteen children (Age = 9 ± 1 years) and fifteen adults (Age = 22 ± 2 years) completed two graded cycling exercise sessions to exhaustion in a randomized and single-blind manner in normoxia (NOR; FiO2 = 20.9) and normobaric hypoxia (HYP; FiO2 = 13.0) exercises conditions. Age-specific workload increments were 25 W·3 min-1 for children and 40 W·3 min-1 for adults. Gas exchange and vastus lateralis oxygenation parameters were measured continuously via metabolic cart and near-infrared spectroscopy, respectively. Hypoxia provoked significant decreases in maximal power output PMAX (children = 29%; adults 16% (F = 39.3; p < 0.01)) and power output at the gas exchange threshold (children = 10%; adults:18% (F = 8.08; p = 0.01)) in both groups. Comparable changes were noted in most respiratory and gas exchange parameters at similar power outputs between groups. Children, however, demonstrated, lower PETCO2 throughout the test at similar power outputs and during the maintenance of V˙CO2 at the maximal power output. These data indicate that, while most cardiorespiratory responses to acute hypoxic exercise are comparable between children and adults, there exist age-related differential responses in select respiratory and muscle oxygenation parameters.

The effects of normobaric hypoxia on the leukocyte responses to resistance exercise

There is growing interest in the use of systemic hypoxia to improve the training adaptations to resistance exercise. Hypoxia is a well-known stimulator of the immune system, yet the leukocyte responses to this training modality remain uncharacterised. The current study characterised the acute leukocyte responses to resistance exercise in normobaric hypoxia. The single-blinded, randomised trial recruited 13 healthy males aged 18-35 years to perform a bout of resistance exercise in normobaric hypoxia (14.4% O2; n = 7) or normoxia (20.9% O2; n = 6). Participants completed 4 × 10 repetitions of lower and upper body exercises at 70% 1-repetition maximum. Oxygen saturation, rating of perceived exertion and heart rate were measured during the session. Venous blood was sampled before and up to 24 hours post-exercise to quantify blood lactate, glucose and leukocytes including neutrophils, lymphocytes, monocytes, eosinophils and basophils. Neutrophils were higher at 120 and 180 minutes post-exercise in hypoxia compared to normoxia (p<0.01), however lymphocytes, monocytes, eosinophils and basophils were unaffected by hypoxia. Oxygen saturation was significantly lower during the four exercises in hypoxia compared to normoxia (p < 0.001). However, there were no differences in blood lactate, heart rate, perceived exertion or blood glucose between groups. Hypoxia amplified neutrophils following resistance exercise, though all other leukocyte subsets were unaffected. Therefore, hypoxia does not appear to detrimentally affect the lymphocyte, monocyte, eosinophil or basophil responses to exercise.

The acute leukocyte and cytokine response of older adults to resistance exercise in normobaric hypoxia.

Ageing causes a decline in leukocyte function and blunted leukocyte responses to resistance exercise. Systemic hypoxia exposure augments the leukocyte response to resistance exercise in young adults, yet this response remains uncharacterised in older adults. This study characterised the effects of normobaric hypoxia on the acute leukocyte and inflammatory cytokine responses to resistance exercise in older adults. We recruited 20 adults aged 60-70 years to perform an acute bout of resistance exercise in normobaric hypoxia (FiO2 14.4%; n = 10) or normoxia (FiO2 20.93%; n = 10). Participants completed 4 × 10 repetitions of lower and upper body exercises at 70% of their predicted 1-repetition maximum. Venous blood was sampled before and up to 24 hours post-exercise to quantify neutrophils, lymphocytes, monocytes, eosinophils, basophils and cytokines (IL-1β, IL-4, IL-6, IL-8, IL-10, TNFα). Flow cytometry was used to classify lymphocytes as T (CD4+ helper and CD8+ cytotoxic), B and NK cells, in addition to the expression of the senescence marker CD45RA on T cells. The hypoxic group showed a larger lymphocyte response over the 24 hours post-exercise compared to the normoxic group (p = 0.035). Specifically, there were greater concentrations of CD4+ T helper cells following hypoxic exercise compared to normoxia (p = 0.046). There was also a greater proportion of CD45RA+ CD4+ T helper cells, suggesting that the cells were more senescent (p = 0.044). Hypoxia did not impact any other leukocyte population or cytokine following exercise. Normobaric hypoxia increases the lymphocyte response to an acute bout of resistance exercise in older adults.

Cardiorespiratory Response and Power Output During Submaximal Exercise in Normobaric Versus Hypobaric Hypoxia: A Pilot Study Using a Specific Chamber that Controls Environmental Factors

2021.—Many previous studies have examined hypoxia-induced physiological responses using various conditions, e.g., artificially reduced atmospheric oxygen concentration [normobaric hypoxia (NH) condition] or low barometric pressure at a mountain [hypobaric hypoxia (HH) condition]. However, when comparing the results from these previous studies conducted in artificial NH and HH including real high altitude, we must consider the possibility that environmental factors, such as temperature, humidity, and fraction of inspired carbon dioxide, might affect the physiological responses. Therefore, we examined cardiorespiratory responses and exercise performances during low- to high-intensity exercise at a fixed heart rate (HR) in both NH and HH using a specific chamber where atmospheric oxygen concentration and barometric pressure as well as the abovementioned environmental factors were precisely controlled. Ten well-trained university students (eight males and two females) performed the exercise test consisting of two 20-minute submaximal pedaling at the intensity corresponding to 50% (low) and 70% (high) of their HR reserve, under three conditions [NH (fraction of inspired oxygen, 0.135; barometric pressure, 754 mmHg), HH (fraction of inspired oxygen, 0.209; barometric pressure, 504 mmHg), and normobaric normoxia (NN; fraction of inspired oxygen, 0.209; barometric pressure, 754 mmHg)]. Peripheral oxygen saturation (SpO2) to estimate arterial oxygen saturation and partial pressure of end-tidal carbon dioxide (PETCO2) were monitored throughout the experiment. SpO2, PETCO2, and power output at fixed HRs (i.e., pedaling efficiency) in NH and HH were all significantly lower than those in NN. Moreover, high-intensity exercise in HH induced greater decreases in SpO2 and power output than did high-intensity exercise in NH (NH vs. HH; SpO2, 78.2% - 5.0% vs. 75.1% - 7.1%; power output, 120.7 - 24.9 W vs. 112.4 - 23.2 W, both p &lt; 0.05). However, high-intensity exercise in HH induced greater increases in PETCO2 than did high-intensity exercise in NH (NH vs. HH; 54.2 - 5.9mmHg vs. 57.2 - 3.4 mmHg, p &lt; 0.01). These results suggest that physiological responses and power output at a fixed HR during hypoxic exposure might depend on the method used to generate the hypoxic condition.

Normobaric Hypoxia Exposure During Treadmill Aerobic Exercise After Stroke: A Safety and Feasibility Study.

ObjectiveTo evaluate the safety and feasibility of performing treadmill aerobic exercise in moderate normobaric hypoxia among chronic hemiparetic stroke survivors.DesignObservational study using convenience sampling.SettingResearch laboratory in a tertiary rehabilitation hospital.ParticipantsChronic hemiparetic stroke survivors who could walk at least 10-m with or without assistance and had no absolute contraindications to exercise testing.InterventionParticipants (three male and four female) were asked to complete three normobaric hypoxia exposure protocols within a single session. First, they were passively exposed to normobaric hypoxia through gradual reductions in the fraction of inspired oxygen (FIO2 = 20.9, 17.0, and 15.0%) while seated (5-min at each level of FIO2). Participants were then exposed to the same reductions in FIO2 during constant-load exercise performed on a treadmill at 40% of heart rate reserve. Finally, participants completed 20-min of exercise while intermittently exposed to moderate normobaric hypoxia (5 × 2-min at FIO2 = 15.0%) interspaced with 2-min normoxia intervals (FIO2 = 20.9%).Outcome MeasuresThe primary outcome was occurrence of adverse events, which included standardized criteria for terminating exercise testing, blood oxygen saturation (SpO2) <80%, or acute mountain sickness score >2. The increased cardiovascular strain imposed by normobaric hypoxia exposure at rest and during exercise was evaluated by changes in SpO2, heart rate (HR), blood pressure, and rating of perceived exertion (RPE).ResultsOne participant reported mild symptoms of nausea during exercise in normobaric hypoxia and discontinued participation. No other adverse events were recorded. Intermittent normobaric hypoxia exposure was associated with reduced SpO2 (MD = −7.4%, CI: −9.8 to −5.0) and increased HR (MD = 8.2, CI: 4.6 to 11.7) compared to intervals while breathing typical room air throughout the 20-min constant-load exercise period. The increase in HR was associated with a 10% increase in relative effort. However, reducing FIO2 had little effect on blood pressure and RPE measurements.ConclusionModerate normobaric hypoxia appeared to be a safe and feasible method to increase the cardiovascular strain of submaximal exercise in chronic hemiparetic stroke survivors. Future studies evaluating the effects of pairing normobaric hypoxia exposure with existing therapies on secondary prevention and functional recovery are warranted.

Systolic and Diastolic Functions After a Brief Acute Bout of Mild Exercise in Normobaric Hypoxia.

Acute hypoxia (AH) is a challenge to the homeostasis of the cardiovascular system, especially during exercise. Research in this area is scarce. We aimed to ascertain whether echocardiographic, Doppler, and tissue Doppler measures were able to detect changes in systolic and diastolic functions during the recovery after mild exercise in AH. Twelve healthy males (age 33.5 ± 4.8 years) completed a cardiopulmonary test on an electromagnetically braked cycle-ergometer to determine their maximum workload (Wmax). On separate days, participants performed randomly assigned two exercise sessions consisting in 3 min pedalling at 30% of Wmax: (1) one test was conducted in normoxia (NORMO) and (2) one in normobaric hypoxia with FiO2 set to 13.5% (HYPO). Hemodynamics were assessed with an echocardiographic system. The main result was that the HYPO session increased parameters related to myocardial contractility such as pre-ejection period and systolic myocardial velocity with respect to the NORMO test. Moreover, the HYPO test enhanced early transmitral filling peak velocities. No effects were detected for left ventricular volumes, as end-diastolic, end-systolic, and stroke volume were similar between the NORMO and the HYPO test. Results of the present investigation support the hypothesis that a brief, mild exercise bout in acute normobaric hypoxia does not impair systolic or diastolic functions. Rather, it appears that stroke volume is well preserved and that systolic and early diastolic functions are enhanced by exercise in hypoxia.

Cardiorespiratory Response and Power Output During Submaximal Exercise in Normobaric Versus Hypobaric Hypoxia: A Pilot Study Using a Specific Chamber that Controls Environmental Factors.

Takezawa, Toshihiro, Shohei Dobashi, and Katsuhiro Koyama. Cardiorespiratory response and power output during submaximal exercise in normobaric versus hypobaric hypoxia: a pilot study using a specific chamber that controls environmental factors. High Alt Med Biol. 22: 201-208, 2021. Background: Many previous studies have examined hypoxia-induced physiological responses using various conditions, e.g., artificially reduced atmospheric oxygen concentration [normobaric hypoxia (NH) condition] or low barometric pressure at a mountain [hypobaric hypoxia (HH) condition]. However, when comparing the results from these previous studies conducted in artificial NH and HH including real high altitude, we must consider the possibility that environmental factors, such as temperature, humidity, and fraction of inspired carbon dioxide, might affect the physiological responses. Therefore, we examined cardiorespiratory responses and exercise performances during low- to high-intensity exercise at a fixed heart rate (HR) in both NH and HH using a specific chamber where atmospheric oxygen concentration and barometric pressure as well as the abovementioned environmental factors were precisely controlled. Methods: Ten well-trained university students (eight males and two females) performed the exercise test consisting of two 20-minute submaximal pedaling at the intensity corresponding to 50% (low) and 70% (high) of their HR reserve, under three conditions [NH (fraction of inspired oxygen, 0.135; barometric pressure, 754 mmHg), HH (fraction of inspired oxygen, 0.209; barometric pressure, 504 mmHg), and normobaric normoxia (NN; fraction of inspired oxygen, 0.209; barometric pressure, 754 mmHg)]. Peripheral oxygen saturation (SpO2) to estimate arterial oxygen saturation and partial pressure of end-tidal carbon dioxide (PETCO2) were monitored throughout the experiment. Results: SpO2, PETCO2, and power output at fixed HRs (i.e., pedaling efficiency) in NH and HH were all significantly lower than those in NN. Moreover, high-intensity exercise in HH induced greater decreases in SpO2 and power output than did high-intensity exercise in NH (NH vs. HH; SpO2, 78.2% ± 5.0% vs. 75.1% ± 7.1%; power output, 120.7 ± 24.9 W vs. 112.4 ± 23.2 W, both p < 0.05). However, high-intensity exercise in HH induced greater increases in PETCO2 than did high-intensity exercise in NH (NH vs. HH; 54.2 ± 5.9 mmHg vs. 57.2 ± 3.4 mmHg, p < 0.01). Conclusions: These results suggest that physiological responses and power output at a fixed HR during hypoxic exposure might depend on the method used to generate the hypoxic condition.

Effect of normobaric hypoxic exercise on blood pressure in old individuals

PurposeTo test the hypothesis that the combination of endurance training and hypoxia leads to greater improvements in resting and exercise blood pressure in old sedentary individuals compared to endurance training only.MethodsWe randomly assigned 29 old overweight participants (age: 62 ± 6 years, body mass index (BMI): 28.5 ± 0.5 kg/m2, 52% men) to single blind 8-week bicycle exercise in hypoxia (fraction of inspired oxygen (FIO2) = 0.15) or normoxia (FIO2 = 0.21). Brachial blood pressure was measured at rest, during maximal incremental exercise testing, and during a 30 min constant work rate test, at baseline and after the training period.ResultsWork rate, heart rate and perceived exertion during training were similar in both groups, with lower oxygen saturation for participants exercising under hypoxia (88.7 ± 1.5 vs. 96.2 ± 1.2%, t(27) = − 13.04, p < 0.001, |g|= 4.85). Office blood pressure and blood pressure during incremental exercise tests did not change significantly in either group after the training program. Systolic blood pressure during the constant work rate test was reduced after training in hypoxia (160 ± 18 vs. 151 ± 14 mmHg, t(13) = 2.44 p < 0.05, |d|= 0.55) but not normoxia (154 ± 22 vs. 150 ± 16 mmHg, t(14) = 0.75, p = 0.46, |d|= 0.18) with no difference between groups over time (F = 0.08, p = 0.77, η2 = 0.01).ConclusionIn old individuals hypoxia in addition to exercise does not have superior effects on office or exercise blood pressure compared to training in normoxia.Trial registration numberClinicalTrials.gov No. NCT02196623 (registered 22 July 2014).

Changes in prefrontal cerebral oxygenation and microvascular blood volume in hypoxia and possible association with acute mountain sickness.

What is the central question of this study? The role of the cerebral haemodynamic response to either normobaric or hypobaric hypoxia in people susceptible to acute mountain sickness (AMS) is still under debate. Prefrontal cortex near-infrared spectroscopy-derived parameters were monitored in normobaric hypoxia at rest and during moderate-intensity exercise in AMS-prone and non-AMS individuals. What is the main finding and its importance? The AMS-prone individuals did not increase microvascular blood volume and showed lower prefrontal cerebral oxygenation in normobaric hypoxia both at rest and during exercise compared with non-AMS subjects, suggesting that these changes might underpin later development of AMS at altitude. The aim of this study was to evaluate changes in prefrontal cerebral oxygenation and microvascular blood volume during exercise in normobaric hypoxia and to investigate possible associations with the occurrence of acute mountain sickness (AMS) at altitude. Twenty-two healthy individuals (age, 26±4years; peak oxygen uptake, 42±4mlkg-1 min-1 ) were tested in two different conditions: normoxia (NORM) and normobaric hypoxia (fraction of inspired O2 =0.13; HYPO). Data were collected at rest and during submaximal constant-speed exercise. The peripheral oxyhaemoglobin saturation was measured by finger pulse oximeter. Changes in prefrontal cerebral oxygenation (ΔHbO2 ), deoxygenation (ΔHHb) and microvascular blood volume (ΔHbtot ) were obtained by near-infrared spectroscopy. Within 2weeks after laboratory testing, subjects rapidly ascended to 3647m a.s.l., and AMS was evaluated using the Lake Louise scale. Eight subjects were AMS+ , whereas 14 were AMS- . During NORM, near-infrared spectroscopy variables did not change from baseline values both at rest and during exercise, with similar results in AMS+ and AMS- subjects. During HYPO, ΔHHb increased to a similar extent in both groups, both at rest and during exercise. The ΔHbO2 was significantly less in AMS+ compared with AMS- subjects, both at rest [-3.23±5.90 versus 1.44±2.14μm, P=0.04, effect size (ES)=1.1, respectively] and during exercise (-6.56±5.51versus 0.37±4.36μm,P<0.01,ES=1.2, respectively). Total haemoglobin did not change from baseline, both at rest (-1.67±9.53μm) and during exercise (-0.96±9.12μm) in AMS+ subjects, which was significantly different from the AMS- group (5.49±3.99μm, P=0.03, ES=1.0 and 8.17±7.34μm, P=0.02, ES=1.0, respectively). Individuals prone to AMS seem to be unable to increase microvascular blood volume and to maintain oxygenation at the cerebral level during exercise in acute normobaric hypoxia, suggesting that these changes might underpin later development of AMS.

Reduced inflammatory and phagocytotic responses following normobaric hypoxia exercise despite evidence supporting greater immune challenge.

This study examined changes in immune markers following sustained treadmill exercise in normobaric hypoxia. Ten subjects performed 1 h of treadmill exercise (65% maximal oxygen uptake) under normoxic (NORM: fraction of inspired oxygen (FIO2) = 20.9%) and normobaric hypoxic (HYP: FIO2 = 13.5%) conditions. Blood samples, collected before, after (Post), 1 h after (1-Post), and 4 h after (4-Post) exercise, were assayed for plasma cytokines (interleukin (IL)-1RA/IL-1β/IL-8/tumor necrosis factor alpha (TNF-α)) and markers of leukocyte activation (macrophage inflammatory protein-1β (MIP-1β)/myeloperoxidase (MPO)/soluble intercellular adhesion molecule-1 (sICAM-1)) using ELISA. Pro- to anti-inflammatory cytokine ratios (TNF-α/IL-1RA; IL-1β/IL-1RA) were calculated. Peripheral blood mononuclear cells (PBMC) were analyzed for changes in inflammatory status (phosphorylated nuclear factor kappa B/nuclear factor kappa B) using Western Blot. Data were analyzed with 2-way (condition × time) repeated-measure ANOVAs with Newman-Keuls post hoc tests. MIP-1β was elevated at 1-Post HYP exercise (+11%; p < 0.01) but did not increase following exercise in NORM. TNF-α/IL-1RA and IL-1β/IL-1RA ratios were both reduced (p < 0.05) following HYP exercise (-16% and -52%, respectively, at 1-Post and -7% and -32%, respectively, at 4-Post). IL-8 increased (p < 0.05) at Post and 1-Post NORM (+33% and +57%, respectively) and HYP (+60% and +83%, respectively) exercise, but was not different between conditions (p > 0.05). Interestingly, plasma sICAM-1 did not increase (p > 0.05) following NORM exercise but was increased (p < 0.05) at Post (+17%), 1-Post (+16%), and 4-Post (+14%) HYP exercise. There was also a delayed peak in plasma MPO concentrations following HYP exercise and PBMC exhibited a reduced (p < 0.05) inflammatory capacity at Post (-38%) and 1-Post (-49%). Novelty Following HYP exercise, participants exhibited (i) circulatory bias towards anti-inflammation; (ii) elevated sICAM; (iii) delayed peak in plasma MPO; and (iv) diminished inflammatory response in PBMC. Collectively, these data suggest immunosuppression. This is undesirable, given that elevated MIP-1β (reported here) and elevated intestinal fatty acid binding protein (reported previously) both suggest higher lipopolysaccharide concentrations following HYP exercise.

5-Hydroxymethylfurfural and α-ketoglutaric acid supplementation increases oxygen saturation during prolonged exercise in normobaric hypoxia

This double-blinded, randomized and placebo-controlled, crossover study investigated whether α-ketoglutaric-acid (α-KG) and 5-hydroxymethylfurfural (5-HMF) supplementation improves exercise performance in hypoxia and affects physiological responses during the exercise task. Eight moderately trained male participants (age: 25.3±2.0 y, VO2max: 48.0±8.3ml/min/kg) performed an incremental exercise test to exhaustion in normoxia and two 2-hour cycle time trial (TT) tests in hypoxia (3,500m) each separated by 1-week. Prior to the TT, participants supplemented with either α-KG and 5-HMF or placebo (random order). Supplementation did not improve TT performance at altitude and did not affect heart rate, effort perception and oxidative stress levels (p>0.05). Oxygen saturation (SpO2) was enhanced during the α-KG and 5-HMF supplementation trial (79.5±3.3 vs. 78.2±3.7%, p=0.026). Even though TT performance was unaffected, the enhanced SpO2 - possibly originated from changed O2-affinity - deserves further consideration as the exercise performance decline at altitude is strongly linked to the SpO2 decline. The inclusion of moderately fit participants, not specifically cycle trained, might have prevented any visible performance enhancement.

Muscle Oxygenation During Repeated Double-Poling Sprint Exercise in Normobaric Hypoxia and Normoxia.

We compared upper limb muscle oxygenation responses during repeated double-poling sprint exercise in normobaric hypoxia and normoxia. Eight male kayakers completed a repeated double-poling sprint exercise (3 × 3 × 20-s maximal sprints, 40-s passive recovery, 5-min rest) in either hypoxia (HYP, FiO2 = 14.5%) or normoxia (NOR, FiO2 = 20.9%). Power output, muscle oxygenation of triceps brachii muscle (using near infrared spectroscopy), arterial oxygen saturation, and cardiorespiratory variables were monitored. Mean power output tended to be lower (-5.2%; P = 0.06) in HYP compared with NOR, while arterial oxygen saturation (82.9 ± 0.9% vs. 90.5 ± 0.8%) and systemic oxygen uptake (1936 ± 140 vs. 2408 ± 83 mL⋅min-1) values were lower (P < 0.05). Exercise-induced increases in deoxygenated hemoglobin (241.7 ± 46.9% vs. 175.8 ± 27.2%) and total hemoglobin (138.0 ± 18.1% vs. 112.1 ± 6.7%) were greater in HYP in reference to NOR (P < 0.05). Despite moderate hypoxia exacerbating exercise-induced elevation in blood perfusion of active upper limb musculature, power output during repeated double-poling exercise only tended to be lower.

Influences of Hypoxia Exercise on Whole-Body Insulin Sensitivity and Oxidative Metabolism in Older Individuals.

Aging is a primary risk factor for most chronic diseases, including type 2 diabetes. Both exercise and hypoxia regulate pathways that ameliorate age-associated metabolic muscle dysfunction. We hypothesized that the combination of hypoxia and exercise would be more effective in improving glucose metabolism than normoxia exercise. We randomized 29 older sedentary individuals (62 ± 6 years; 14 women, 15 men) to bicycle exercise under normobaric hypoxia (fraction of inspired oxygen = 15%) or normoxia (fraction of inspired oxygen = 21%). Participants trained thrice weekly for 30 to 40 minutes over 8 weeks at a heart rate corresponding to 60% to 70% of peak oxygen update. Insulin sensitivity measured by hyperinsulinemic-euglycemic glucose clamp and muscle protein expression before and after hyperinsulinemic-euglycemic glucose clamp. Heart rate and perceived exertion during training were similar between groups, with lower oxygen saturation when exercising under hypoxia (88.7 ± 1.5 vs 96.2 ± 1.2%, P < 0.01). Glucose infusion rate after 8 weeks increased in both the hypoxia (5.7 ± 1.1 to 6.7 ± 1.3 mg/min/kg; P < 0.01) and the normoxia group (6.2 ± 2.1 to 6.8 ± 2.1 mg/min/kg; P = 0.04), with a mean difference between groups of -0.44 mg/min/kg; 95% CI, -1.22 to 0.34; (P = 0.25). Markers of mitochondrial content and oxidative capacity in skeletal muscle were similar after training in both groups. Changes in Akt phosphorylation and glucose transporter 4 under fasting and insulin-stimulated conditions were not different between groups over time. Eight weeks of hypoxia endurance training led to similar changes in insulin sensitivity and markers of oxidative metabolism compared with normoxia training. Normobaric hypoxia exercise did not enhance metabolic effects in sedentary older women and men beyond exercise alone.

Effects of exercise in normobaric hypoxia on hemodynamics during muscle metaboreflex activation in normoxia.

Little is known about the cardiovascular effects of the transition from exercise in hypoxia (EH) to normoxia. This investigation aimed to assess hemodynamics during the metaboreflex elicited in normoxia after EH. Ten trained athletes (four females and six males, age 35.6 ± 8.4years) completed a cardiopulmonary test to determine the workload at anaerobic threshold (AT). On separate days, participants performed three randomly assigned exercise sessions (10min pedalling at 80% of AT): (1) one in normoxia (EN); (2) one in normobaric hypoxia with FiO2 15.5% (EH15.5%); and (3) one in normobaric hypoxia with FiO2 13.5% (EH13.5%). After each session, the following protocol was randomly assigned: either (1) post-exercise muscle ischemia after cycling for 3min, to study the metaboreflex, or (2) a control exercise recovery (CER) session, without any metaboreflex stimulation. The main result were that both EH15.5% and EH13.5% impaired (p < 0.05) the ventricular filling rate response during the metaboreflex (- 18 ± 32 and - 20 ± 27mls-1), when compared to EN (+ 29 ± 32mls-1), thereby causing a reduction in stroke volume response (- 9.1 ± 3.2, - 10.6 ± 8.7, and + 5 ± 5.7ml for EH15.5%, EH13.5% and EN test, respectively, p < 0.05). Moreover, systemic vascular resistance was increased after the EH15.5% and the EH13.5% in comparison with the EN test. These data demonstrate that moderate exercise in hypoxia impairs the capacity to enhance venous return during the metaboreflex stimulated in normoxia. Overall, there is a functional shift from a flow to vasoconstriction-mediated mechanism for maintaining the target blood pressure during the metaboreflex.

One-week cocoa flavanol intake increases prefrontal cortex oxygenation at rest and during moderate-intensity exercise in normoxia and hypoxia.

During exercise in hypoxia, O2 delivery to brain and muscle is compromised, and oxidative stress is elicited. Cocoa flavanols (CF) have antioxidant capacities and can increase blood flow by stimulating endothelial function. We aimed to examine the effects of 7-day CF intake on oxidative stress, nitric oxide production, and tissue oxygenation in response to exercise in normobaric hypoxia (14.3% O2). In a randomized, double-blind, cross-over study, 14 well-trained male cyclists completed four trials: exercise in normoxia or hypoxia, after 7-day CF or placebo intake. Flow-mediated dilation (FMD) was measured before intake of the last dose CF or placebo. One hundred minutes later, 20-min steady-state (SS; 45% V̇o2max) and 20-min time trial (TT) (cycling) were performed. Blood samples were taken. Prefrontal and muscular oxygenation was assessed by near-infrared spectroscopy. At baseline, FMD was increased by CF. Hypoxia increased exercise-induced elevations in lipid peroxidation and antioxidant capacity. CF suppressed exercise-induced lipid peroxidation but did not influence antioxidant capacity. At rest and during SS, prefrontal and muscular oxygenation was decreased by hypoxia. CF elevated prefrontal oxygenation but did not impact muscular oxygenation. During TT, hypoxia accelerated the exercise-induced decrease in prefrontal oxygenation, but not in muscular oxygenation. During TT, CF did not alter prefrontal and muscular oxygenation. CF did not change plasma nitrite, nitrate, and arginine:citrulline. During high-intensity exercise, CF improved neither tissue oxygenation nor performance in well-trained athletes. At rest and during moderate-intensity exercise, CF reduced exercise-induced lipid peroxidation and partially restored the hypoxia-induced decline in prefrontal oxygenation. NEW & NOTEWORTHY For the first time, we showed that CF had beneficial effects on endothelial function at rest, as well as on prefrontal oxygenation at rest and during moderate-intensity exercise, both in normoxia and hypoxia. Moreover, we showed that CF intake inhibited oxidative stress during exhaustive exercise in hypoxia.

High adventure shunts old notions of pulmonary vascular control during hypoxic exercise: contrasting views that might just burst your bubble!

High adventure shunts old notions of pulmonary vascular control during hypoxic exercise: contrasting views that might just burst your bubble!