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

Introduction: We assessed metabolic and hormonal responses to high-load resistance exercise under varying normobaric hypoxia conditions with a saturation clamp. Methods: 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), 15 min after the exposures (Pre 2), and at 0-, 15-, and 30-min post-exercises (T0, T15, and T30, respectively). Results: 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 2 at 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). Discussion: Severe simulated hypoxia, achieved through a saturation clamp during barbell back squats, may enhance metabolic and hormonal responses, particularly 30 min post-session. Nevertheless, the acute effects of hypoxia exposure seem to be overridden by the impact of high-load resistance exercise.

Influence of Running Velocity and Hypoxic Exposure on Vastus Lateralis Muscle Oxygenation.

PURPOSE: We investigated the effects of manipulating running velocity and hypoxic exposure on vastus lateralis muscle oxygenation levels during treadmill running. METHODS: Eleven trained male distance runners performed 7 randomized runs at different velocities (8, 10, 12, 14, 16, 18, and 20 km·h-1), each lasting 45 seconds on an instrumented treadmill in normoxia (fraction of inspired oxygen [FiO2] = 20.9%), moderate hypoxia (FiO2 = 16.1%), high hypoxia (FiO2 = 14.1%), and severe hypoxia (FiO2 = 13.0%). Continuous assessment of Tissue Saturation Index (TSI) in the vastus lateralis muscle was conducted using near-infrared spectroscopy. Subsequently, changes in TSI (ΔTSI) data over the final 20 seconds of each run were compared between velocities and conditions. RESULTS: There was a significant velocity × condition interaction for ΔTSI% (P < .001, ηp2=.19), with a smaller ΔTSI% decline in normoxia compared with high hypoxia and severe hypoxia at 8 km·h-1 (g = 1.30 and 1.91, respectively), 10 km·h-1 (g = 0.75 and 1.43, respectively), and 12 km·h-1 (g = 1.47 and 1.95, respectively) (pooled values for all conditions: P < .037). The ΔTSI% decline increased with each subsequent velocity increment from 8 km·h-1 (-9.2% [3.7%]) to 20 km·h-1 (-22.5% [4.1%]) irrespective of hypoxia severity (pooled values for all conditions: P < .048). CONCLUSIONS: Running at slower velocities in conjunction with high and severe hypoxia reduces vastus lateralis muscle oxygenation levels. Muscle ΔTSI% proves to be a sensitive indicator, underscoring the potential use of near-infrared spectroscopy as a reference index of internal load during treadmill runs.

Inter-individual variability in peripheral oxygen saturation and repeated sprint performance in hypoxia: an observational study of highly-trained subjects.

Individual variations in peripheral oxygen saturation (SpO2) during repeated sprints in hypoxia and their impact on exercise performance remain unclear despite fixed external hypoxic stimuli (inspired oxygen fraction: FiO2). This study examined SpO2 individual variations during repeated sprints in hypoxia and their impact on exercise performance. Thirteen highly-trained sprint runners performed 10 × 10-s cycle sprints with 30-s passive recoveries in normobaric hypoxia (FiO2: 0.150). Mean power output (MPO), post-sprint SpO2, and heart rate for each sprint were assessed. Sprint decrement score (Sdec), evaluating fatigue development, was calculated using MPO variables. Participants were categorized into a high saturation group (HiSat, n = 7) or a low saturation group (LowSat, n = 6) based on their mean post-sprint SpO2 (measured 10-15 s after each sprint). Individual mean post-sprint SpO2 ranged from 91.6% to 82.2%. Mean post-sprint SpO2 was significantly higher (P < 0.001, d = 1.54) in HiSat (89.1% ± 1.5%) than LowSat (84.7% ± 1.6%). A significantly larger decrease in Sdec (P = 0.008, d = 1.68) occurred in LowSat (-22.3% ± 2.3%) compared to HiSat (-17.9% ± 2.5%). MPO (P = 0.342 d = 0.55) and heart rate (P = 0.225 d = 0.67) did not differ between groups. There was a significant correlation (r = 0.61; P = 0.028) between SpO2 and Sdec. In highly-trained sprint runners, individual responses to hypoxia varied widely and significantly affected repeated sprint ability, with greater decreases in SpO2 associated with larger performance alterations (i.e., larger decrease in Sdec).

Dose-response effects of caffeine during repeated cycling sprints in normobaric hypoxia to exhaustion.

PURPOSE: With limited studies exploring the dose-response of caffeine consumption on repeated sprint ability in hypoxia, this study aimed to determine the optimal caffeine dose (low, moderate or high) during repeated sprints in hypoxia to exhaustion. METHODS: On separate visits, twelve active males randomly performed four experimental trials in normobaric hypoxia (inspired oxygen fraction: 16.5 ± 0.2%). Participants ingested placebo (PLA) or caffeine capsules (3, 6 or 9 mg/kg or LOW, MOD and HIGH, respectively) 1 h before exercise and then underwent a repeated cycling sprint test (10 s sprint/20 s active recovery) to exhaustion. Total sprint number and work done, peak and mean power output, blood lactate concentration, cardiorespiratory and perceptual responses were recorded. RESULTS: Total sprint number was greater in MOD and HIGH compared to PLA (20 ± 7 and 18 ± 8 vs. 13 ± 4; all P < 0.05), with MOD also higher than LOW (15 ± 6; P = 0.02). Total work done was greater in MOD (111 ± 40 kJ) and HIGH (100 ± 35 kJ) compared to LOW (83 ± 29 kJ) and PLA (76 ± 25 kJ) (all P < 0.05). However, there were no significant differences in total sprint number or total work done between MOD and HIGH (all P > 0.05). Blood lactate concentration was higher in both MOD and HIGH compared to PLA (all P < 0.05). However, peak and mean power outputs, fatigue index, and ratings of perceived exertion did not differ across different caffeine dosages (all P > 0.05). CONCLUSION: A moderate dose of caffeine (6 mg/kg) is the optimal amount for enhancing repeated cycling sprint ability when compared to low and high doses in moderate normobaric hypoxia.

Cognitive performance during exposure to moderate normobaric hypoxia after sleep restriction: relationship to physiological and stress biomarkers.

INTRODUCTION: Exposure to moderate levels of simulated hypoxia has subtle cognitive effects relative to ground level, in healthy individuals. However, there are few data on the cognitive consequences of the combination of hypoxia and partial sleep deprivation, which is a classic military or civilian operational context. In this study, we tested the hypothesis that exposure to moderate hypoxia while sleep-restricted impairs several domains of cognition, and we also assessed physiological parameters and salivary concentrations of cortisol and alpha-amylase. METHOD: Seventeen healthy males completed two sessions of cognitive tests (sustained attention using the PVT psychomotor vigilance task and executive functions using the Go-NoGo inhibition task and N-Back working memory task) after 30 minutes (T+30') and 4 hours (T+240') of exposure in a normobaric hypoxic tent (FIO2 = 13.6%, ≃ 3,500 m) (HY). This was completed after one night of sleep restriction (3 a.m. to 6 a.m. bedtime, SRHY) and one night of habitual sleep (10 p.m. to 6 a.m. bedtime, HSHY) (with cross-over randomization). The two nights sleep architecture and physiological parameters (oxygen saturation (SpO2) and heart rate (HR) during T+30' and T+240'sessions were analyzed. Salivary cortisol and alpha-amylase (sAA) concentrations were analyzed before hypoxia, after the T+30' and T+240' cognitive sessions, and after leaving the hypoxic tent. RESULTS: Sustained attention (RT and number of lapses in the PVT) and executive functions (Go-NoGo and 1-Back and 2-Back parameters, as inhibition and working memory signatures) were impaired in the SRHY condition compared to HSHY. SpO2 and HR were higher after 4 hours compared with 30 minutes of hypoxia in the HSHY condition, while only HR was statistically higher in the SRHY condition. In SRHY, salivary AA concentration was lower and cortisol was higher than in HSHY. A significant increase in sAA concentration is observed after the cognitive session at 4 hours of hypoxia exposure compared to that at 30 minutes, only in the SRHY condition. There are significant positive correlations between reaction time and the corresponding heart rate (a non-invasive marker of physiological stress) for the executive tasks in the two sleep conditions. This was not observed for salivary levels of sAA and cortisol, respective reliable indicators of the sympathoadrenomedullary system and the hypothalamic-pituitary adrenocortical system. CONCLUSION: Exposure to moderate normobaric hypoxia (≃ 3,500 m / ≃ 11,500 ft simulated) after a single night of 3-hour sleep impairs cognitive performance after 30 minutes and 4 hours of exposure. The key determinants and/or mechanism(s) responsible for cognitive impairment when exposed to moderate hypoxia with sleep restriction, particularly on the executive function, have yet to be elucidated.

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.

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.

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 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.

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.

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.

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.

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.

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.

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.

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.

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.