Brain-muscle interplay during endurance self-paced exercise in normobaric and hypobaric hypoxia.

Purpose: Hypoxia is one major environmental factor, supposed to mediate central motor command as well as afferent feedbacks at rest and during exercise. By using a comparison of normobaric (NH) and hypobaric (HH) hypoxia with the same ambient pressure in oxygen, we examined the potential differences on the cerebrovascular and muscular regulation interplay during a self-paced aerobic exercise. Methods: Sixteen healthy subjects performed three cycling time-trials (250 kJ) in three conditions: HH, NH and normobaric normoxia (NN) after 24 h of exposure. Cerebral and muscular oxygenation were assessed by near-infrared spectroscopy, cerebral blood flow by Doppler ultrasound system. Gas exchanges, peripheral oxygen saturation, power output and associated pacing strategies were also continuously assessed. Results: The cerebral oxygen delivery was lower in hypoxia than in NN but decreased similarly in both hypoxic conditions. Overall performance and pacing were significantly more down-regulated in HH versus NH, in conjunction with more impaired systemic (e.g. saturation and cerebral blood flow) and prefrontal cortex oxygenation during exercise. Conclusions: The difference in pacing was likely the consequence of a complex interplay between systemic alterations and cerebral oxygenation observed in HH compared to NH, aiming to maintain an equivalent cerebral oxygen delivery despite higher adaptive cost (lower absolute power output for the same relative exercise intensity) in HH compared to NH

Vascular and oxygenation responses of local ischemia and systemic hypoxia during arm cycling repeated sprints.

The purpose of this study was to investigate the acute vascular and oxygenation responses to repeated sprint exercise during arm cycling with either blood flow restriction (BFR) or systemic hypoxia alone or in combination. The study design was a single-blinded repeated-measures assessment of four conditions with two levels of normobaric hypoxia (400 m and 3800 m) and two levels of BFR (0% and 45% of total occlusion). Sixteen active participants (eleven men and five women; mean ± SD; 26.4 ± 4.0 years old; 73.8 ± 9.8 kg; 1.79 ± 0.07 m) completed 5 sessions (1 familiarization, 4 conditions). During each test visit, participants performed a repeated sprint arm cycling test to exhaustion (10 s maximal sprints with 20 s recovery until exhaustion) to measure power output, metabolic equivalents, blood flow, as well as oxygenation (near-infrared spectroscopy) of the biceps brachii muscle tissue. Repeated sprint performance was decreased with both BFR and systemic hypoxia conditions. Greater changes between minimum-maximum of sprints in total hemoglobin concentration (Δ[tHb]) were demonstrated with BFR (400 m, 45% and 3800 m, 45%) than without (400 m, 0% and 3800 m, 0%) (p < 0.001 for both). Additionally, delta tissue saturation index (ΔTSI) decreased more with both BFR conditions than without (p < 0.001 for both). The absolute maximum TSI was progressively reduced with both BFR and systemic hypoxia (p < 0.001). By combining high-intensity, repeated sprint exercise with BFR and/or systemic hypoxia, there is a robust stimulus detected by increased changes in blood perfusion placed on specific vascular mechanisms, which were more prominent in BFR conditions

Positive expiratory pressure improves arterial and cerebral oxygenation in acute normobaric and hypobaric hypoxia.

Positive expiratory pressure (PEP) has been shown to limit hypoxia-induced reduction in arterial oxygen saturation, but its effectiveness on systemic and cerebral adaptations, depending on the type of hypoxic exposure [normobaric (NH) versus hypobaric (HH)], remains unknown. Thirteen healthy volunteers completed three randomized sessions consisting of 24-h exposure to either normobaric normoxia (NN), NH (inspiratory oxygen fraction, = 13.6%; barometric pressure, BP = 716 mmHg; inspired oxygen partial pressure, = 90.9 ± 1.0 mmHg), or HH (3,450 m, = 20.9%, BP = 482 mmHg, = 91.0 ± 0.6 mmHg). After the 6th and the 22nd hours, participants breathed quietly through a facemask with a 10-cmH <sub>2</sub> O PEP for 2 × 5 min interspaced with 5 min of free breathing. Arterial ( , pulse oximetry), quadriceps, and cerebral (near-infrared spectroscopy) oxygenation, middle cerebral artery blood velocity (MCAv; transcranial Doppler), ventilation, and cardiovascular responses were recorded continuously. without PEP was significantly lower in HH (87 ± 4% on average for both time points, P < 0.001) compared with NH (91 ± 3%) and NN (97 ± 1%). PEP breathing did not change in NN but increased it similarly in NH and HH (+4.3 ± 2.5 and +4.7 ± 4.1% after 6h; +3.5 ± 2.2 and +4.1 ± 2.9% after 22h, both P < 0.001). Although MCAv was reduced by PEP (in all sessions and at all time points, -6.0 ± 4.2 cm/s on average, P < 0.001), the cerebral oxygenation was significantly improved (P < 0.05) with PEP in both NH and HH, with no difference between conditions. These data indicate that PEP could be an attractive nonpharmacological means to improve arterial and cerebral oxygenation under both normobaric and hypobaric mild hypoxic conditions in healthy participants

Cycling Time Trial Is More Altered in Hypobaric than Normobaric Hypoxia

PURPOSE: Slight physiological differences between acute exposure in normobaric hypoxia (NH) and hypobaric hypoxia (HH) have been reported. Taken together, these differences suggest different physiological responses to hypoxic exposure to a simulated altitude (NH) versus a terrestrial altitude (HH). For this purpose, in the present study, we aimed to directly compare the time-trial performance after acute hypoxia exposure (26 h, 3450 min) by the same subjects under three different conditions: NH, HH, and normobaric normoxia (NN). Based on all of the preceding studies examining the differences among these hypoxic conditions, we hypothesized greater performance impairment in HH than in NH. METHODS: The experimental design consisted of three sessions: NN (Sion: FiO2, 20.93), NH (Sion, hypoxic room: FiO2, 13.6%; barometric pressure, 716 mm Hg), and HH (Jungfraujoch: FiO2, 20.93; barometric pressure, 481 mm Hg). The performance was evaluated at the end of each session with a cycle time trial of 250 kJ. RESULTS: The mean time trial duration in NN was significantly shorter than under the two hypoxic conditions (P < 0.001). In addition, the mean duration in NH was significantly shorter than that in HH (P < 0.01). The mean pulse oxygen saturation during the time trial was significantly lower for HH than for NH (P < 0.05), and it was significantly higher in NN than for the two other sessions (P < 0.001). CONCLUSION: As previously suggested, HH seems to be a more stressful stimulus, and NH and HH should not be used interchangeability when endurance performance is the main objective. The principal factor in this performance difference between hypoxic conditions seemed to be the lower peripheral oxygen saturation in HH at rest, as well as during exercise

Neuromuscular evaluation of arm-cycling repeated sprints under hypoxia and/or blood flow restriction.

This study aimed to determine the effects of hypoxia and/or blood flow restriction (BFR) on an arm-cycling repeated sprint ability test (aRSA) and its impact on elbow flexor neuromuscular function. Fourteen volunteers performed an aRSA (10 s sprint/20 s recovery) to exhaustion in four randomized conditions: normoxia (NOR), normoxia plus BFR (N <sub>BFR</sub> ), hypoxia (FiO <sub>2</sub> = 0.13, HYP) and hypoxia plus BFR (H <sub>BFR</sub> ). Maximal voluntary contraction (MVC), resting twitch force (Db10), and electromyographic responses from the elbow flexors [biceps brachii (BB)] to electrical and transcranial magnetic stimulation were obtained to assess neuromuscular function. Main effects of hypoxia, BFR, and interaction were analyzed on delta values from pre- to post-exercise. BFR and hypoxia decreased the number of sprints during aRSA with no significant cumulative effect (NOR 16 ± 8; N <sub>BFR</sub> 12 ± 4; HYP 10 ± 3 and H <sub>BFR</sub> 8 ± 3; P < 0.01). MVC decrease from pre- to post-exercise was comparable whatever the condition. M-wave amplitude (- 9.4 ± 1.9% vs. + 0.8 ± 2.0%, P < 0.01) and Db10 force (- 41.8 ± 4.7% vs. - 27.9 ± 4.5%, P < 0.01) were more altered after aRSA with BFR compared to without BFR. The exercise-induced increase in corticospinal excitability was significantly lower in hypoxic vs. normoxic conditions (e.g., BB motor evoked potential at 75% of MVC: - 2.4 ± 4.2% vs. + 16.0 ± 5.9%, respectively, P = 0.03). BFR and hypoxia led to comparable aRSA performance impairments but with distinct fatigue etiology. BFR impaired the muscle excitation-contraction coupling whereas hypoxia predominantly affected corticospinal excitability indicating incapacity of the corticospinal pathway to adapt to fatigue as in normoxia

Exposure to hypobaric hypoxia results in higher oxidative stress compared to normobaric hypoxia.

Sixteen healthy exercise trained participants underwent the following three, 10-h exposures in a randomized manner: (1) Hypobaric hypoxia (HH; 3450m terrestrial altitude) (2) Normobaric hypoxia (NH; 3450m simulated altitude) and (3) Normobaric normoxia (NN). Plasma oxidative stress (malondialdehyde, MDA; advanced oxidation protein products, AOPP) and antioxidant markers (superoxide dismutase, SOD; glutathione peroxidase, GPX; catalase; ferric reducing antioxidant power, FRAP) were measured before and after each exposure. MDA was significantly higher after HH compared to NN condition (+24%). SOD and GPX activities were increased (vs. before; +29% and +54%) while FRAP was decreased (vs. before; -34%) only after 10h of HH. AOPP significantly increased after 10h for NH (vs. before; +83%), and HH (vs. before; +99%) whereas it remained stable in NN. These results provide evidence that prooxidant/antioxidant balance was impaired to a greater degree following acute exposure to terrestrial (HH) vs. simulated altitude (NH) and that the chamber confinement (NN) did likely not explain these differences

Acute and chronic changes in baroreflex sensitivity in hypobaric vs. normobaric hypoxia.

Normobaric hypoxia (NH) is used as a surrogate for hypobaric hypoxia (HH). Recent studies reported physiological differences between NH and HH. Baroreflex sensitivity (BRS) decreases at altitude or following intense training. However, until now no study compared the acute and chronic changes of BRS in NH vs. HH. First, BRS was assessed in 13 healthy male subjects prior and after 20 h of exposure at 3450 m (study 1), and second in 15 well-trained athletes prior and after 18 days of "live-high train-low" (LHTL) at 2250 m (study 2) in NH vs. HH. BRS decreased (p < 0.05) to the same extent in NH and HH after 20 h of hypoxia and after LHTL. These results confirm that altitude decreases BRS but the decrease is similar between HH and NH. The persistence of this decrease after the cessation of a chronic exposure is new and does not differ between HH and NH. The previously reported physiological differences between NH and HH do not appear strong enough to induce different BRS responses

Comparison of Sleep Disorders between Real and Simulated 3,450-m Altitude.

Hypoxia is known to generate sleep-disordered breathing but there is a debate about the pathophysiological responses to two different types of hypoxic exposure: normobaric hypoxia (NH) and hypobaric hypoxia (HH), which have never been directly compared. Our aim was to compare sleep disorders induced by these two types of altitude. Subjects were exposed to 26 h of simulated (NH) or real altitude (HH) corresponding to 3,450 m and a control condition (NN) in a randomized order. The sleep assessments were performed with nocturnal polysomnography (PSG) and questionnaires. Thirteen healthy trained males subjects volunteered for this study (mean ± SD; age 34 ± 9 y, body weight 76.2 ± 6.8 kg, height 179.7 ± 4.2 cm). Mean nocturnal oxygen saturation was further decreased during HH than in NH (81.2 ± 3.1 versus 83.6 ± 1.9%; P < 0.01) when compared to NN (95.5 ± 0.9%; P < 0.001). Heart rate was higher in HH than in NH (61 ± 10 versus 55 ± 6 bpm; P < 0.05) and NN (48 ± 5 bpm; P < 0.001). Total sleep time was longer in HH than in NH (351 ± 63 versus 317 ± 65 min, P < 0.05), and both were shorter compared to NN (388 ± 50 min, P < 0.05). Breathing frequency did not differ between conditions. Apnea-hypopnea index was higher in HH than in NH (20.5 [15.8-57.4] versus 11.4 [5.0-65.4]; P < 0.01) and NN (8.2 [3.9-8.8]; P < 0.001). Subjective sleep quality was similar between hypoxic conditions but lower than in NN. Our results suggest that HH has a greater effect on nocturnal breathing and sleep structure than NH. In HH, we observed more periodic breathing, which might arise from the lower saturation due to hypobaria, but needs to be confirmed