Intermittent Hypobaric Hypoxia Exposure Research Articles

Point: Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia

Point: Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia

Combined intermittent hypoxia and surface muscle electrostimulation as a method to increase peripheral blood progenitor cell concentration

BackgroundOur goal was to determine whether short-term intermittent hypoxia exposure, at a level well tolerated by healthy humans and previously shown by our group to increase EPO and erythropoiesis, could mobilize hematopoietic stem cells (HSC) and increase their presence in peripheral circulation.MethodsFour healthy male subjects were subjected to three different protocols: one with only a hypoxic stimulus (OH), another with a hypoxic stimulus plus muscle electrostimulation (HME) and the third with only muscle electrostimulation (OME). Intermittent hypobaric hypoxia exposure consisted of only three sessions of three hours at barometric pressure 540 hPa (equivalent to an altitude of 5000 m) for three consecutive days, whereas muscular electrostimulation was performed in two separate periods of 25 min in each session. Blood samples were obtained from an antecubital vein on three consecutive days immediately before the experiment and 24 h, 48 h, 4 days and 7 days after the last day of hypoxic exposure.ResultsThere was a clear increase in the number of circulating CD34+ cells after combined hypobaric hypoxia and muscular electrostimulation. This response was not observed after the isolated application of the same stimuli.ConclusionOur results open a new application field for hypobaric systems as a way to increase efficiency in peripheral HSC collection.

Enzyme activity and myoglobin concentration in rat myocardium and skeletal muscles after passive intermittent simulated altitude exposure

We studied the effect of intermittent hypobaric hypoxia exposure on lactate dehydrogenase and citrate synthase activities, together with myoglobin content, of rat myocardium, tibialis anterior, and diaphragm muscles. The intermittent hypoxia exposure programme consisted of daily 4-h sessions in a hypobaric chamber (5000 m) over a period of 22 days. Samples were taken at the end of the programme, and 20 and 40 days later, and compared with those of control animals. In myocardium, lactate dehydrogenase activity was significantly depressed in animals 20 days post-exposure (314.6 ± 15.3 IU · g−1) compared with control animals (400 ± 14.3 IU · g−1), while citrate synthase activity and myoglobin concentration showed a significant stepwise increase from control animals (88.2 ± 3.6 IU · g−1 and 4.38 ± 0.13 μm · mg−1) to animals 20 days (104.7 ± 3.7 IU · g−1 and 5.01 ± 0.17 μm · mg−1) and 40 days post-exposure (108.8 ± 6.5 IU · g−1 and 5.11 ± 0.22 μm · mg−1). In contrast, no differences were found in diaphragm and tibialis anterior muscles. Our results show that intermittent hypobaric hypoxia exposure increased the oxidative character of myocardium even 20 days after the hypoxic stimulus has ceased, and that this effect lasts for more than 40 days for citrate synthase activity and myoglobin concentration. These findings support our previous results on skeletal and cardiac muscle capillarization after passive intermittent simulated altitude exposure, thus providing morphofunctional and biochemical evidence for increased cardiac aerobic efficiency.

Intermittent hypobaric hypoxia exposure does not cause sustained alterations in autonomic control of blood pressure in young athletes

Intermittent hypoxia (IH), which refers to the discontinuous use of hypoxia to reproduce some key features of altitude acclimatization, is commonly used in athletes to improve their performance. However, variations of IH are also used as a model for sleep apnea, causing sustained sympathoexcitation and hypertension in animals and, thus, raising concerns over the safety of this model. We tested the hypothesis that chronic IH at rest alters autonomic control of arterial pressure in healthy trained individuals. Twenty-two young athletes (11 men and 11 women) were randomly assigned to hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normoxia (500 m) in a double-blind and placebo-controlled design. Both groups rested in a hypobaric chamber for 3 h/day, 5 days/wk for 4 wk. In the sitting position, resting hemodynamics, including heart rate (HR), blood pressure (BP), cardiac output (Q(c), C(2)H(2) rebreathing), stroke volume (SV = Q(c)/HR), and total peripheral resistance (TPR = mean BP/Q(c)), were measured, dynamic cardiovascular regulation was assessed by spectral and transfer function analysis of cardiovascular variability, and cardiac-vagal baroreflex function was evaluated by a Valsalva maneuver, twice before and 3 days after the last chamber exposure. We found no significant differences in HR, BP, Q(c), SV, TPR, cardiovascular variability, or cardiac-vagal baroreflex function between the groups at any time. These results suggest that exposure to intermittent hypobaric hypoxia for 4 wk does not cause sustained alterations in autonomic control of BP in young athletes. In contrast to animal studies, we found no secondary evidence for sustained physiologically significant sympathoexcitation in this model.

Increased serum erythropoietin but not red cell production after 4 wk of intermittent hypobaric hypoxia (4,000–5,500 m)

This study tested the hypothesis that athletes exposed to 4 wk of intermittent hypobaric hypoxia exposure (3 h/day, 5 days/wk at 4,000-5,500 m) or double-blind placebo increase their red blood cell volume (RCV) and hemoglobin mass (Hbmass) secondary to an increase in erythropoietin (EPO). Twenty-three collegiate level athletes were measured before (Pre) and after (Post) the intervention for RCV via Evans blue (EB) dye and in duplicate for Hbmass using CO rebreathing. Hematological indexes including EPO, soluble transferrin receptor, and reticulocyte parameters were measured on 8-10 occasions spanning the intervention. The subjects were randomly divided among hypobaric hypoxia (Hypo, n = 11) and normoxic (Norm, n = 12) groups. Apart from doubling EPO concentration 3 h after hypoxia there was no increase in any of the measures for either Hypo or Norm groups. The mean change in RCV from Pre to Post for the Hypo group was 2.3% (95% confidence limits = -4.8 to 9.5%) and for the Norm group was -0.2% (-5.7 to 5.3%). The corresponding changes in Hbmass were 1.0% (-1.3 to 3.3%) for Hypo and -0.3% (-2.6 to 3.1%) for Norm. There was good agreement between blood volume (BV) from EB and CO: EB BV = 1.03 x CO BV + 142, r2 = 0.85, P < 0.0001. Overall, evidence from four independent techniques (RCV, Hbmass, reticulocyte parameters, and soluble transferrin receptor) suggests that intermittent hypobaric hypoxia exposure did not accelerate erythropoiesis despite the increase in serum EPO.

Intermittent hypoxia impairs performance of adult mice in the two‐way shuttle box but not in the Morris water maze

We have previously found that neonatal intermittent hypobaric hypoxia exposure enhanced mouse spatial, but impaired associative, cognition. This study sought to investigate the effects of hypobaric hypoxia on adult mice cognition. Mice were exposed to 2, 5, 10, 15, or 25 days of intermittent hypoxia (IH; 4 hr/day) at 2 km (16.0% O2) or 5 km (10.8% O2) altitudes in a hypobaric chamber for the Morris water maze (MWM) test and exposed to IH for 2, 10, or 25 days for the shuttle-box test. Amino acid dynamics in vivo in the hippocampus and amygdala of mice exposed to 2 km hypoxia were analyzed by high-pressure liquid chromatography. The results in MWM task showed that IH-2d to -25d at 2 km or 5 km did not change the escape latencies of mice in the training test or the retention of platform in the probe test. In the shuttle-box task, however, IH-10d at 5 km significantly reduced mouse avoidances in the acquisition test on day 4, and IH-10d at 2 km reduced avoidances in the retention test; IH-25d at 5 km significantly reduced avoidances of mice throughout the acquisition days. Glutamate in the amygdala persisted in declining to 69% of baseline at 8 hr posthypoxia (P = 0.040 vs. GLU released during 30 min before hypoxia) during the posthypoxia stage. These results suggest that adult hypobaric IH impairs the hippocampal-independent, but not the hippocampal-dependent, task in mice. The different GLU releases in the hippocampus and amygdala in response to hypoxia are involved in the different behaviors.