The effect of normobaric hypoxia on acute exercise-induced changes in blood sphingoid base-1-phosphates metabolism in cyclists.

Extracellular sphingosine-1-phosphate (S1P) emerged as an important regulator of muscle function. We previously found that plasma S1P concentration is elevated in response to acute exercise and training. Interestingly, hypoxia, which is commonly utilized in training programs, induces a similar effect. Therefore, the aim of the current study was to determine the effect of normobaric hypoxia on exercise-induced changes in blood sphingolipid metabolism. Fifteen male competitive cyclists performed a graded cycling exercise until exhaustion (GE) and a simulated 30 km individual time trial (TT) in either normoxic or hypoxic (FiO2 = 16.5%) conditions. Blood samples were taken before the exercise, following its cessation, and after 30 min of recovery. We found that TT increased dihydrosphingosine-1-phosphate (dhS1P) concentration in plasma (both HDL- and albumin-bound) and blood cells, as well as the rate of dhS1P release from erythrocytes, regardless of oxygen availability. Plasma concentration of S1P was, however, reduced during the recovery phase, and this trend was augmented by hypoxia. On the other hand, GE in normoxia induced a selective increase in HDL-bound S1P. This effect disappeared when the exercise was performed in hypoxia, and it was associated with reduced S1P level in platelets and erythrocytes. We conclude that submaximal exercise elevates total plasma dhS1P concentration via increased availability of dihydrosphingosine resulting in enhanced dhS1P synthesis and release by blood cells. Maximal exercise, on the other hand, induces a selective increase in HDL-bound S1P, which is a consequence of mechanisms not related to blood cells. We also conclude that hypoxia reduces post-exercise plasma S1P concentration.

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-1ß, 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.

Hormonal and metabolic responses of older adults to resistance training in normobaric hypoxia.

PURPOSE: In young adults, the hormonal responses to resistance exercise are amplified by normobaric hypoxia. Hormone concentrations and metabolism are typically dysregulated with age, yet the impact of hypoxia on these responses to resistance exercise are uncharacterised. Therefore, this study aimed to characterise the acute and chronic hormonal and metabolic responses of older adults to resistance training in normobaric hypoxia. METHODS: Adults aged 60-75 years completed 8 weeks of resistance training in either normoxia (20.9% O2; n = 10) or normobaric hypoxia (14.4% O2, n = 10) twice weekly at 70% of their predicted 1-repetition maximum. Growth hormone, glucose, lactate, insulin, homeostatic model assessment of insulin resistance (HOMA-IR), cortisol, total testosterone, adrenaline, noradrenaline and dopamine were quantified at pre- and post-training, and in the 60 min following the first training session (untrained state) and the last training session (trained state). RESULTS: Eight weeks of training in hypoxia did not affect the resting levels of the hormones or physiological factors measured. However, hypoxia significantly blunted the acute growth hormone response in the 15 min following the last training session at week eight (43.87% lower in the hypoxic group; p = 0.017). This novel and unexpected finding requires further investigation. All other hormones were unaffected acutely by hypoxia in the 60 min following the first and the last training session. CONCLUSION: Chronic resistance training in normobaric hypoxia supresses the growth hormone response to exercise in older adults. All other hormones and metabolic markers were unaffected both acutely and chronically by hypoxia.

Acute physiological response to a normobaric hypoxic exposure: sex differences.

Although preliminary studies suggested sex-related differences in physiological responses to altitude/hypoxia, controlled studies from standardised exposures to normobaric hypoxia are largely lacking. Hence, the goals of this study were to provide information on cardiorespiratory responses to a 7-h normobaric hypoxia exposure and to explore potential differences between men and women. In this crossover study, a total of 15 men and 14 women were subjected to a 7-h exposure in normoxia (FiO2: 21%) and normobaric hypoxia (FiO2: 15%). Values of peripheral oxygen saturation, heart rate, systolic and diastolic blood pressure and respiratory gases were recorded every hour (8 time points), and oxygen saturation every 30 min (15 time points). Compared to normoxia, exposure to hypoxia significantly increased minute ventilation from baseline to hour 7 in males (+ 71%) and females (+ 40%), significantly greater in men (p < 0.05). A steeper decrease in peripheral oxygen saturation until 2.5 h in hypoxia was seen in females compared to males (p < 0.05). In conclusion, the ventilatory response to hypoxia was more pronounced in men compared to women. Moreover, during the first hours in hypoxia, peripheral oxygen saturation dropped more markedly in women than in men, likely due an initially lower and/or less efficient ventilatory response to moderate hypoxia. Those findings should be considered when performing interventions for therapy or prevention in normobaric hypoxia. Nevertheless, further large-scaled and well-controlled studies are needed.

Hypoxic training improves blood pressure, nitric oxide and hypoxia-inducible factor-1 alpha in hypertensive patients.

PURPOSE: To examine the effects of intermittent hypoxic breathing at rest (IHR) or during exercise (IHT) on blood pressure and nitric oxide metabolites (NOx) and hypoxia-inducible factor-1 alpha levels (HIF-1α) over a 6-week period. METHODS: 47 hypertensive patients were randomly allocated to three groups: hypertensive control (CON: n = 17; IHR: n = 15 and IHT: n = 15. The CON received no intervention; whereas, IH groups received eight events of hypoxia (FIO2 0.14), and normoxia (FIO2 0.21), 24-min hypoxia and 24-min normoxia, for 6 weeks. The baseline data were collected 2 days before the intervention; while, the post-test data were collected at days 2 and 28 after the 6-week intervention. RESULTS: We observed a significant decrease of the SBP in both IH groups: IHR (- 12.0 ± 8.0 mmHg, p = 0.004 and - 9.9 ± 8.8 mmHg, p = 0.028, mean ± 95% CI) and IHT (- 13.0 ± 7.8 mmHg, p = 0.002 and - 10.0 ± 8.4 mmHg, p = 0.016) at days 2 and 28 post-intervention, respectively. Compared to CON, IHR and IHT had increased of NOx (IHR; 8.5 ± 7.6 µmol/L, p = 0.031 and IHT; 20.0 ± 9.1 µmol/L, p < 0.001) and HIF-1α (IHR; 170.0 ± 100.0 pg/mL, p = 0.002 and IHT; 340.5 ± 160.0 pg/mL, p < 0.001). At 2 days post-intervention, NOx and HIF-1α were negatively correlated with SBP in IHT. CONCLUSION: IH programs may act as an alternative therapeutic strategy for hypertension patients probably through elevation of NOx and HIF-1α production.

Sessional work-rate does not affect the magnitude to which simulated hypoxia can augment acute physiological responses during resistance exercise.

PURPOSE: To investigate whether performing resistance exercise in hypoxia augments physiological and perceptual responses, and if altering work-rate by performing repetitions to failure compared to sub-maximally increases the magnitude of these responses. METHODS: Twenty male university students (minimum of 2 year resistance training experience) completed four sessions, two in hypoxia (fraction of inspired oxygen [FiO2] = 0.13), and two in normoxia (FiO2 = 0.21). For each condition, session one comprised three sets to failure of shoulder press and bench press (high work-rate session), while session two involved the same volume load, distributed over six sets (low work-rate session). Muscle oxygenation (triceps brachii), surface electromyographic activity (anterior deltoid, pectoralis major, and triceps brachii), heart rate (HR), and arterial blood oxygen saturation were recorded. Blood lactate concentration ([Bla-]) was recorded pre-exercise and 2 min after each exercise. Muscle thickness was measured pre- and post-exercise via ultrasound. RESULTS: Muscle oxygenation values during sets and inter-set rest periods were lower in hypoxia vs normoxia (p = 0.001). Hypoxia caused greater [Bla-] during the shoulder press of failure sessions (p = 0.003) and both shoulder press (p = 0.048) and bench press (p = 0.005) of non-failure sessions. Hypoxia increased HR during non-failure sessions (p < 0.001). There was no effect of hypoxia on muscular swelling, surface electromyographic activity, perceived exertion, or number of repetitions performed. CONCLUSIONS: Hypoxia augmented metabolite accumulation, but had no impact on any other physiological or perceptual response compared to the equivalent exercise in normoxia. Furthermore, the magnitude to which hypoxia increased the measured physiological responses was not influenced by sessional work-rate.

Cognitive performance is associated with cerebral oxygenation and peripheral oxygen saturation, but not plasma catecholamines, during graded normobaric hypoxia.

NEW FINDINGS: What is the central question of this study? What are the mechanisms responsible for the decline in cognitive performance following exposure to acute normobaric hypoxia? What are the main findings and their importance? We found that (1) performance of a complex central executive task (n-back) was reduced at FIO2 0.12; (2) there was a strong correlation between performance of the n-back task and reductions in SpO2 and cerebral oxygenation; and (3) plasma adrenaline, noradrenaline, cortisol and copeptin were not correlated with cognitive performance. ABSTRACT: It is well established that hypoxia impairs cognitive function; however, the physiological mechanisms responsible for these effects have received relatively little attention. This study examined the effects of graded reductions in fraction of inspired oxygen ( FIO2 ) on oxygen saturation ( SpO2 ), cerebral oxygenation, cardiorespiratory variables, activity of the sympathoadrenal system (adrenaline, noradrenaline) and hypothalamic-pituitary-adrenal axis (cortisol, copeptin), and cognitive performance. Twelve healthy males [mean (SD), age: 22 (4) years, height: 178 (5) cm, mass: 75 (9) kg, FEV1 /FVC ratio: 85 (5)%] completed a four-task battery of cognitive tests to examine inhibition, selective attention (Eriksen flanker), executive function (n-back) and simple and choice reaction time (Deary-Liewald). Tests were completed before and following 60 min of exposure to FIO2 0.2093, 0.17, 0.145 and 0.12. Following 60 min of exposure, response accuracy in the n-back task was significantly reduced in FIO2 0.12 compared to baseline [82 (9) vs. 93 (5)%; P < 0.001] and compared to all other conditions at the same time point [ FIO2 0.2093: 92 (3)%; FIO2 0.17: 91 (6)%; FIO2 0.145: 85 (10)%; FIO2 12: 82 (9)%; all P < 0.05]. The performance of the other tasks was maintained. Δaccuracy and Δreaction time of the n-back task was correlated with both Δ SpO2 [r(9) = 0.66, P < 0.001 and r(9) = -0.36, P = 0.037, respectively] and Δcerebral oxygenation [r(7) = 0.55, P < 0.001 and r(7) = -0.38, P = 0.045, respectively]. Plasma adrenaline, noradrenaline, cortisol and copeptin were not significantly elevated in any condition or correlated with any of the tests of cognitive performance. These findings suggest that reductions in peripheral oxygen saturation and cerebral oxygenation, and not increased activity of the sympathoadrenal system and hypothalamic-pituitary-adrenal axis, as previously speculated, are responsible for a decrease in cognitive performance during normobaric hypoxia.

Physiological and performance effects of nitrate supplementation during roller-skiing in normoxia and normobaric hypoxia.

The present study examined the effects of acute nitrate (NO3-) supplementation ingested in the form of concentrated beetroot juice on cross-country roller-ski performance in normoxia (N) and normobaric hypoxia (H). Eight competitive cross-country skiers (five males: age 22 ± 3 years, V·O2max 71.5 ± 4.7 mL kg-1·min-1; three females: age 21 ± 1 years, V·O2max 58.4 ± 2.5 mL kg-1·min-1) were supplemented with a single dose of NO3--rich beetroot juice (BRJ, ∼13 mmol NO3-) or a NO3--depleted placebo (PL, ∼0 mmol NO3-) and performed 2 x 6-min submaximal exercise bouts and a 1000-m time-trial (TT) on a treadmill in N (20.9% O2) or H (16.8% O2). The four experimental trials were presented in a randomised, counter-balanced order. Plasma NO3- and nitrite concentrations were significantly higher following BRJ compared to PL (both p < 0.001). However, respiratory variables, heart rate, blood lactate concentration, ratings of perceived exertion, and near-infrared spectroscopy-derived measures of muscle tissue oxygenation during submaximal exercise were not significantly different between BRJ and PL (all p > 0.05). Likewise, time to complete the TT was unaffected by supplementation in both N and H (p > 0.05). In conclusion, an acute dose of ∼13 mmol NO3- does not affect physiological or performance responses to submaximal or maximal treadmill roller-skiing in competitive cross-country skiers exercising in N and H.

No Additional Benefit of Repeat-Sprint Training in Hypoxia than in Normoxia on Sea-Level Repeat-Sprint Ability.

To assess the impact of 'top-up' normoxic or hypoxic repeat-sprint training on sea-level repeat-sprint ability, thirty team sport athletes were randomly split into three groups, which were matched in running repeat-sprint ability (RSA), cycling RSA and 20 m shuttle run performance. Two groups then performed 15 maximal cycling repeat-sprint training sessions over 5 weeks, in either normoxia (NORM) or hypoxia (HYP), while a third group acted as a control (CON). In the post-training cycling RSA test, both NORM (13.6%; p = 0.0001, and 8.6%; p = 0.001) and HYP (10.3%; p = 0.007, and 4.7%; p = 0.046) significantly improved overall mean and peak power output, respectively, whereas CON did not change (1.4%; p = 0.528, and -1.1%; p = 0.571, respectively); with only NORM demonstrating a moderate effect for improved mean and peak power output compared to CON. Running RSA demonstrated no significant between group differences; however, the mean sprint times improved significantly from pre- to post-training for CON (1.1%), NORM (1.8%), and HYP (2.3%). Finally, there were no group differences in 20 m shuttle run performance. In conclusion, 'top-up' training improved performance in a task-specific activity (i.e. cycling); however, there was no additional benefit of conducting this 'top-up' training in hypoxia, since cycle RSA improved similarly in both HYP and NORM conditions. Regardless, the 'top-up' training had no significant impact on running RSA, therefore the use of cycle repeat-sprint training should be discouraged for team sport athletes due to limitations in specificity. Key points'Top-up' repeat-sprint training performed on a cycle ergometer enhances cycle repeat-sprint ability compared to team sport training only in football players.The addition of moderate hypoxia to repeat-sprint training provides no additional performance benefits to sea-level repeat-sprint ability or endurance performance than normoxic repeat-sprint training.'Top-up' cycling repeat-sprint training provides no significant additional benefit to running RSA or endurance performance than team sport training only, and therefore running based repeat-sprint interventions are recommended for team sport athletes.

Hypoxia Does Not Impair Resistance Exercise Performance or Amplify Post-Exercise Fatigue.

Purpose: To determine whether performing resistance exercise in hypoxia acutely reduces performance and increases markers of fatigue, and whether these responses are exaggerated if exercising at high versus low work rates (i.e., exercising to failure or volume matched non-failure). Methods: Following a within-subject design, 20 men completed two trials in hypoxia (13% oxygen) and two in normoxia (21% oxygen). The first session for hypoxic and normoxic conditions comprised six sets of bench press and shoulder press to failure (high work rate), while subsequent sessions involved the same volume distributed over 12 sets (low work rate). Physical performance (concentric velocity) and perceptual responses were measured during exercise and for 72 hr post-exercise. Neuromuscular performance (bench throw velocity) was assessed pre- and post-session. Results: Hypoxia did not affect physical performance, neuromuscular performance, and perceptual recovery when exercising at high or low work rates. Higher work rate exercise caused greater acute decrements in physical performance and post-exercise neuromuscular performance and increased perceived exertion and muscle soreness (p ≤ 0.006), irrespective of hypoxia. Conclusions: Hypoxia does not impact on resistance exercise performance or increase markers of physical and perceptual fatigue. Higher exercise work rates may impair physical performance, and exaggerate fatigue compared to low work rate exercise, irrespective of environmental condition. Practitioners can prescribe hypoxic resistance exercise without compromising physical performance or inducing greater levels of fatigue. For athletes who are required to train with high frequency, decreasing exercise work rate may reduce post-exercise markers of fatigue for the same training volume.

The chronic leukocyte and inflammatory cytokine responses of older adults to resistance training in normobaric hypoxia; a randomized controlled trial.

TRIAL DESIGN: Older adults experience chronic dysregulation of leukocytes and inflammatory cytokines, both at rest and in response to resistance training. Systemic hypoxia modulates leukocytes and cytokines, therefore this study characterized the effects of normobaric hypoxia on the leukocyte and cytokine responses of older adults to resistance training. METHODS: 20 adults aged 60-70 years performed eight weeks of moderate-intensity resistance training in either normoxia or normobaric hypoxia (14.4% O2), consisting of two lower body and two upper body exercises. Venous blood was drawn before and after the training intervention and flow cytometry was used to quantify resting neutrophils, lymphocytes, monocytes, eosinophils and basophils, in addition to the subsets of lymphocytes (T, B and natural killer (NK) cells). Inflammatory cytokines were also quantified; interleukin 1 beta (IL-1ß), IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor alpha (TNF-α). Acute changes in leukocytes and cytokines were also measured in the 24 h following the last training session. RESULTS: After the intervention there was a greater concentration of resting white blood cells (p = 0.03; 20.3% higher) T cells (p = 0.008; 25.4% higher), B cells (p = 0.004; 32.6% higher), NK cells (p = 0.012; 43.9% higher) and eosinophils (p = 0.025; 30.8% higher) in hypoxia compared to normoxia, though the cytokines were unchanged. No acute effect of hypoxia was detected in the 24 h following the last training session for any leukocyte population or inflammatory cytokine (p < 0.05). CONCLUSIONS: Hypoxic training caused higher concentrations of resting lymphocytes and eosinophils, when compared to normoxic training. Hypoxia may have an additional beneficial effect on the immunological status of older adults. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry (ANZCTR). TRIAL NUMBER: ACTRN12623001046695. Registered 27/9/2023. Retrospectively registered. All protocols adhere to the COSORT guidelines.

How does multi-set high-load resistance exercise impact neuromuscular function in normoxia and hypoxia?

This study examined whether hypoxia during multi-set, high-load resistance exercise alters neuromuscular responses. Using a single-blinded (participants), randomised crossover design, eight resistance-trained males completed five sets of five repetitions of bench press at 80% of one repetition maximum in moderate normobaric hypoxia (inspiratory oxygen fraction = 0.145) and normoxia. Maximal isometric bench press trials were performed following the warm-up, after 10 min of altitude priming and 5 min post-session (outside, inside and outside the chamber, respectively). Force during pre-/post-session maximal voluntary isometric contractions and bar velocity during exercise sets were measured along with surface electromyographic (EMG) activity of the pectoralis major, anterior deltoid and lateral and medial triceps muscles. Two-way repeated measures ANOVA (condition×time) were used. A significant time effect (p = 0.048) was found for mean bar velocity, independent of condition (p = 0.423). During sets of the bench press exercise, surface EMG amplitude of all studied muscles remained unchanged (p > 0.187). During maximal isometric trials, there were no main effects of condition (p > 0.666) or time (p > 0.119), nor were there any significant condition×time interactions for peak or mean forces and surface EMG amplitudes (p > 0.297). Lower end-exercise blood oxygen saturation (90.9 ± 1.8 vs. 98.6 ± 0.6%; p < 0.001) and higher blood lactate concentration (5.8 ± 1.4 vs. 4.4 ± 1.6 mmol/L; p = 0.007) values occurred in hypoxia. Acute delivery of systemic normobaric hypoxia during multi-set, high-load resistance exercise increased metabolic stress. However, only subtle neuromuscular function adjustments occurred with and without hypoxic exposure either during maximal isometric bench press trials before versus after the session or during actual exercise sets.HighlightsPerforming multi-set, high-load bench press resistance exercise in hypoxia accentuates metabolic stress, as evidenced by lower arterial oxygen saturation and higher blood lactate concentration, compared to normoxia.Acute hypoxic exposure doesn't alter neuromuscular responses during the execution of the sets since mean bar velocity dropped similarly in both conditions from set 2 to set 5 with no difference in peak velocity and surface EMG amplitude of the prime movers during the bench press.Only subtle adjustments in peak or mean force and accompanying surface EMG activity occur with and without hypoxic exposure during maximal isometric bench press trials after a 10-min hypoxic priming period and 5 min after the session in reference to post-warm-up.

Influence of exercise intensity and hypoxic exposure on physiological, perceptual and biomechanical responses to treadmill running.

Acute physiological, perceptual and biomechanical consequences of manipulating both exercise intensity and hypoxic exposure during treadmill running were determined. On separate days, eleven trained individuals ran for 45 s (separated by 135 s of rest) on an instrumented treadmill at seven running speeds (8, 10, 12, 14, 16, 18 and 20 km.h-1) in normoxia (NM, FiO2 = 20.9%), moderate hypoxia (MH, FiO2 = 16.1%), high hypoxia (HH, FiO2 = 14.1%) and severe hypoxia (SH, FiO2 = 13.0%). Running mechanics were collected over 20 consecutive steps (i.e. after running ∼25 s), with concurrent assessment of physiological (heart rate and arterial oxygen saturation) and perceptual (overall perceived discomfort, difficulty breathing and leg discomfort) responses. Two-way repeated-measures ANOVA (seven speeds × four conditions) were used. There was a speed × condition interaction for heart rate (p = 0.045, ηp2 = 0.22), with lower values in NM, MH and HH compared to SH at 8 km.h-1 (125 ± 12, 125 ± 11, 128 ± 12 vs 132 ± 10 b.min-1). Overall perceived discomfort (8 and 16 km.h-1; p = 0.019 and p = 0.007, ηp2 = 0.21, respectively) and perceived difficulty breathing (all speeds; p = 0.023, ηp2 = 0.37) were greater in SH compared to MH, whereas leg discomfort was not influenced by hypoxic exposure. Minimal difference was observed in the twelve kinetics/kinematics variables with hypoxia (p > 0.122; ηp2 = 0.19). Running at slower speeds in combination with severe hypoxia elevates physiological and perceptual responses without a corresponding increase in ground reaction forces.Highlights The extent to which manipulating hypoxia severity (between normoxia and severe hypoxia) and running speed (from 8 to 20 km.h-1) influence acute physiological and perceptual responses, as well as kinetic and kinematic adjustments during treadmill running was determined.Running at slower speeds in combination with severe hypoxia elevates heart rate, while this effect was not apparent at faster speeds.Arterial oxygen saturation was increasingly lower as running speed and hypoxic severity increased.Overall perceived discomfort (8 and 16 km.h-1) and perceived difficulty breathing (all speeds) were lower in moderate hypoxia than in severe hypoxia, whereas leg discomfort remained unchanged with hypoxic exposure.

Vagal Threshold Determination during Incremental Stepwise Exercise in Normoxia and Normobaric Hypoxia.

This study focuses on the determination of the vagal threshold (Tva) during exercise with increasing intensity in normoxia and normobaric hypoxia. The experimental protocol was performed by 28 healthy men aged 20 to 30 years. It included three stages of exercise on a bicycle ergometer with a fraction of inspired oxygen (FiO2) 20.9% (normoxia), 17.3% (simulated altitude ~1500 m), and 15.3% (~2500 m) at intensity associated with 20% to 70% of the maximal heart rate reserve (MHRR) set in normoxia. Tva level in normoxia was determined at exercise intensity corresponding with (M ± SD) 45.0 ± 5.6% of MHRR. Power output at Tva (POth), representing threshold exercise intensity, decreased with increasing degree of hypoxia (normoxia: 114 ± 29 W; FiO2 = 17.3%: 110 ± 27 W; FiO2 = 15.3%: 96 ± 32 W). Significant changes in POth were observed with FiO2 = 15.3% compared to normoxia (p = 0.007) and FiO2 = 17.3% (p = 0.001). Consequentially, normoxic %MHRR adjusted for hypoxia with FiO2 = 15.3% was reduced to 39.9 ± 5.5%. Considering the convenient altitude for exercise in hypoxia, POth did not differ excessively between normoxic conditions and the simulated altitude of ~1500 m, while more substantial decline of POth occurred at the simulated altitude of ~2500 m compared to the other two conditions.

An Updated Panorama of "Living Low-Training High" Altitude/Hypoxic Methods.

With minimal costs and travel constraints for athletes, the "living low-training high" (LLTH) approach is becoming an important intervention for modern sport. The popularity of the LLTH model of altitude training is also associated with the fact that it only causes a slight disturbance to athletes' usual daily routine, allowing them to maintain their regular lifestyle in their home environment. In this perspective article, we discuss the evolving boundaries of the LLTH paradigm and its practical applications for athletes. Passive modalities include intermittent hypoxic exposure at rest (IHE) and Ischemic preconditioning (IPC). Active modalities use either local [blood flow restricted (BFR) exercise] and/or systemic hypoxia [continuous low-intensity training in hypoxia (CHT), interval hypoxic training (IHT), repeated-sprint training in hypoxia (RSH), sprint interval training in hypoxia (SIH) and resistance training in hypoxia (RTH)]. A combination of hypoxic methods targeting different attributes also represents an attractive solution. In conclusion, a growing number of LLTH altitude training methods exists that include the application of systemic and local hypoxia stimuli, or a combination of both, for performance enhancement in many disciplines.

Effects of an Alkalizing or Acidizing Diet on High-Intensity Exercise Performance under Normoxic and Hypoxic Conditions in Physically Active Adults: A Randomized, Crossover Trial.

Pre-alkalization caused by dietary supplements such as sodium bicarbonate improves anaerobic exercise performance. However, the influence of a base-forming nutrition on anaerobic performance in hypoxia remains unknown. Herein, we investigated the effects of an alkalizing or acidizing diet on high-intensity performance and associated metabolic parameters in normoxia and hypoxia. In a randomized crossover design, 15 participants (24.5 ± 3.9 years old) performed two trials following four days of either an alkalizing (BASE) or an acidizing (ACID) diet in normoxia. Subsequently, participants performed two trials (BASE; ACID) after 12 h of normobaric hypoxic exposure. Anaerobic exercise performance was assessed using the portable tethered sprint running (PTSR) test. PTSR assessed overall peak force, mean force, and fatigue index. Blood lactate levels, blood gas parameters, heart rate, and rate of perceived exertion were assessed post-PTSR. Urinary pH was analyzed daily. There were no differences between BASE and ACID conditions for any of the PTSR-related parameters. However, urinary pH, blood pH, blood bicarbonate concentration, and base excess were significantly higher in BASE compared with ACID (p < 0.001). These findings show a diet-induced increase in blood buffer capacity, represented by blood bicarbonate concentration and base excess. However, diet-induced metabolic changes did not improve PTSR-related anaerobic performance.

Is Maximal Heart Rate Decrease Similar Between Normobaric Versus Hypobaric Hypoxia in Trained and Untrained Subjects?

We compared the decrease in maximal heart rate (HRmax) from normoxia to normobaric (NH) and hypobaric (HH) hypoxia, respectively, in trained and untrained subjects (n = 187). HRmax data in normoxia and NH (n = 55) or HH (n = 26) were collected from 81 publications. No study directly compared HRmax in NH and HH. Concomitant arterial oxygen saturation (SaO2) and HRmax data were found in 60 studies. Overall, the results showed that the higher the desaturation, the greater the decrease in HRmax. Since desaturation appeared to be slightly higher during HH versus NH and was higher in trained than in untrained subjects, the decrease in HRmax tended (p = 0.07) to be higher in trained subjects in HH than in NH (e.g., -12.7 bpm vs. -8.6 bpm at 4000 m), whereas in untrained subjects the difference was negligible (-9.9 bpm vs. -8.3 bpm). To conclude, when compared with normoxia, the decrease in HRmax was slightly higher in HH than in NH in trained subjects. However, this result has to be confirmed and from a practical point of view, one may question the significance of this difference as well as the relevance of using different HR values for prescribing training intensity during exercise performed in NH or in HH.

Intermittent Hypoxia-Hyperoxia Conditioning Improves Cardiorespiratory Fitness in Older Comorbid Cardiac Outpatients Without Hematological Changes: A Randomized Controlled Trial.

AIM: To compare a program based on intermittent hypoxia-hyperoxia training (IHHT) consisting of breathing hypoxic-hyperoxic gas mixtures while resting to a standard exercise-based rehabilitation program with respect to cardiorespiratory fitness (CRF) in older, comorbid cardiac outpatients. MATERIALS AND METHODS: Thirty-two cardiac patients with comorbidities were randomly allocated to IHHT and control (CTRL) groups. IHHT completed a 5-week program of exposure to hypoxia-hyperoxia while resting, CTRL completed an 8-week tailored exercise program, and participants in the CTRL were also exposed to sham hypoxia exposure. CRF and relevant hematological biomarkers were measured at baseline and after treatment in both groups. RESULTS: After intervention, CRF in the IHHT group was not significantly different (n = 15, 19.9 ± 6.1 mlO2 minutes-1 kg-1) compared with the CTRL group (n = 14, 20.6 ± 4.9 mlO2 minutes-1 kg-1). CRF in IHHT increased significantly from baseline (6.05 ± 1.6 mlO2 minutes-1 kg-1), while no difference was found in CTRL. Systolic and diastolic blood pressures were not significantly different between groups after treatment. Hemoglobin content was not significantly different between groups. Erythrocytes and reticulocytes did not change pre/post interventions in both experimental groups. CONCLUSIONS: IHHT is safe in patients with cardiac conditions and common comorbidities and it might be a suitable option for older patients who cannot exercise. A 5-week IHHT is as effective as an 8-week exercise program in improving CRF, without hematological changes. Further studies are needed to clarify the nonhematological adaptations to short, repeated exposure to normobaric hypoxia-hyperoxia.

Simulated Altitude via Re-Breathing Creates Arterial Hypoxemia but Fails to Improve Elements of Running Performance.

Acclimatization to altitude has been shown to improve elements of performance. Use of simulated altitude is popular among athletes across the sports spectrum. This work was on a handheld, re-breathing device touted to enhance performance. Seven recreationally-trained athletes used the device for 18 hours over the course of the 37-day intervention trial. The elevations simulated were progressively increased from 1,524m to 6,096m. To ascertain potential efficacy, four performance trials were included (familiarization, baseline, and 2 follow-ups). Hematological (hematocrit, hemoglobin, and lactate), physiological (respiratory exchange ratio, heart rate, and oxygen consumption), and perceptual (Borg's RPE) variables were monitored at rest, during two steady state running economy stages, and at maximal effort during each visit. The device is clearly capable of creating arterial hypoxemic conditions equating to high altitude. This fact is exemplified by average pulse oximetry values of approximately 78.5% in the final 6-day block of simulation. At the same time, there were no changes observed in any hematological (p>0.05), physiological (p>0.05), or perceptual (p>0.05) variable at either follow-up performance trial. Relative VO2 data was analyzed with a 15-breath moving average sampling frequency in accordance with our recent findings (Scheadler et al.) reported in Medicine and Science in Sports and Exercise. Effect sizes are reported within, but most were trivial (d=0.0-0.19). Overall, findings align with speculation that a more robust altitude stimulus than can be offered by short-term arterial hypoxemia is required for changes to be evidenced. The device has shown some promise in other work, but our data is not supportive.