Severe steady state exercise at sea level and altitude in Olympic oarsmen.

Respiratory and metabolic functions were studied at rest and during exercise in 13 Olympic oarsmen at peak of training at sea level and after one month's residence at 2350 m. At sea level each subject completed two severe five minute treadmill runs at 5 mph on a 20% incline inspiring 21% O2 for one run and 16% O2 for the other. Two more runs at the same speed and incline were carried out at altitude with F102's of 21% and 28%. Pulmonary function tests were carried out at sea level and altitude and steady state diffusion capacity was determined during rest and exercise while breathing 21% O2. Heart rates were monitored by direct electrocardiography. At altitude significant increases were found in MVV (10%), FEV1 (6%), MMEF (15%) and PF (9%) but not in VC. A rise of the DLCO during exercise from 64.8 to 75.4 ml/min/mm Hg was largely the result of increased ventilation. The response to acute hypoxia (16% O2) and to chronic hypoxia were as follows: VE from 113 to 135/122 1/min; VE/O2 from 2.55 to 3.14/3.08 1/100ml; and PETCO2 from 40 to 36/34 mm Hg. The effect of chronic hypoxia could be abolished by acute normoxia (28%O2) within five minutes; VE returned to 99 l/min, VE/Vo2 to 2.46 1/100 ml, and PETCO2 to 40 mm Hg. Vo2 for the standard exercise (5 mph - 20% grade) for normoxic and acute hypoxic conditions were similar; 4421 and 4301 ml/min, but this variable decreased significantly upon chronic altitude exposure; 3966 ml/min. This decrement in Vo2 was attributed in part to a lower work of breathing.     

Increased plasma hypoxanthine values in humans during exposure to simulated altitude of 7,620 meters (25,000 feet).

In this study we have determined the effect of severe and moderate hypoxemia on plasma hypoxanthine and lactate values. Hypoxemia was induced in healthy humans in a low pressure chamber. The test subjects breathed atmospheric air at barometric pressures of 279 mm Hg and 385 mm Hg, representing a simulated altitude of about 7,620 and 5,334 m (25,000 and 17,500 ft), respectively. Exposure to 279 mm Hg represents a severe hypoxemia and all subjects exposed to this simulated altitude for 2 min showed symptoms related to hypoxia. After this exposure, plasma hypoxanthine increased by an average of 2.4 times compared to preexposure values. Exposure to 385 mm Hg represents a moderate hypoxemia and the persons tested at this simulated altitude for 45 min showed no or minor symptoms related to hypoxia and there was no change in plasma hypoxanthine values. In contrast to the unchanged plasma hypoxanthine values there was a 50% increase in plasma lactate values after 30 min exposure. We conclude that plasma hypoxanthine is a reliable marker for severe cellular hypoxia in humans and that enhanced plasma hypoxanthine levels are a rapid response to cellular hypoxia.     

Autonomic response to hypobaric hypoxia assessed by time-dependent frequency decomposition of heart rate.

BACKGROUND: Acute hypoxia tolerance varies substantially among healthy individuals. We hypothesized that this variability results from a difference in autonomic (ANS) response to hypoxic stress. METHODS: Peripheral oxygen saturation, respiration and ECG were recorded from 21 healthy subjects (age, 29 +/- 7 yr) in an altitude chamber during normoxia, severe hypoxia (282 mm Hg), and mild hypoxia (360 mm Hg). Cardiovascular control was assessed by time-frequency decomposition of the heart rate signal applying the Selective Discrete Transform Algorithm (SDA). This procedure uses a variable time window, thus providing reliable physiological data even during transient states. Autonomic activity was quantified by power spectral density integrals over a 3-dimensional time-dependent spectral distribution of heart rate fluctuations. RESULTS: Subjects who had slower peripheral oxygen desaturation during severe hypoxia onset (mean 92.9 vs. 58.4 s) were those who displayed higher ANS activity in all ambient states, namely normoxia and hypoxia. These same subjects withstood hypoxia for significantly longer time periods (mean 313 vs. 244 s). CONCLUSION: Improved hypoxia tolerance is linked to enhanced autonomic activity, involving a better management of peripheral blood flow.     

Circulatory response to acute hypobaric hypoxia in conscious dogs.

Hemodynamics were studied in seven conscious dogs during acute hypobaric stress at 14,000 ft simulated altitude. Silastic catheters were chronically implanted in the pulmonary artery, left atrium, and aorta. Pulmonary and central aortic pressures, cardiac output, and pulmonary blood volume were determined under conditions of normoxia and acute hypoxia in a hypobaric chamber maintained at 446 mm Hg pressure (14,000 ft). Altitude resulted in significant increases in heart rate, cardiac output, pulmonary blood volume, and pulmonary artery pressure. Left atrial pressure and calculated systemic vascular resistance decreased during hypobaric hypoxia while stroke volume, stroke work index, arterial pressure and pulmonary vascular resistance remained unchanged. Arterial blood PO2 decreased markedly at altitude, and all animals hyperventilated with resultant systemic hypocarbic alkalosis. The combination of elevated pulmonary arterial pressure and increased pulmonary blood volume may by an etiologic factor in the development of high-altitude pulmonary edema.     

Analyses of maximum cardiopulmonary performance during exposure to acute hypoxia at simulated altitude--sea level to 5000 meters (760-404 mm Hg)

The maximum cardiopulmonary performance of seven healthy male subjects was studied repeatedly in graded hypoxia at ambient pressures ranging from 760 to 404 mm Hg (sea level to 5000 m of simulated altitude). Using this approach it has been possible to not only establish a reproducible value for VO2max, but to determine an equation which may be used to predict the VO2 at altitude for healthy, unacclimatized males exercising to exhaustion. Moreover, we have attempted to explain the limits to pulmonary ventilation at decreasing levels of PO2 by comparing a given VO2max (STPD) to the corresponding VEmax (BTPS), showing that any further increase in the latter is impossible when a certain level of altitude has been reached. Finally, our series of experiments indicates that the HRmax falls at altitude. Although statistically significant, this decrement is not conspicuous. Thus, when used with the VO2max to calculate the number of ml of O2 consumed per beat of the heart, the "oxygen pulse" turns out to be more sensitive to the fall in VO2max at altitude than to the corresponding decrease in the HRmax.     

Aldosterone, cortisol, and electrolyte responses to hypobaric hypoxia in moderate-altitude natives

Serum aldosterone, cortisol, and electrolyte concentration, and urinary aldosterone and electrolyte excretion responses were examined in seven low-altitude natives (LAN) (373 m or less, aged 19-25 yr) and nine moderate-altitude natives (MAN) (1,830-2,200 m, aged 19-23 yr) for 2 d at their own residence (home) altitude (PB 740 or 585 mm Hg, respectively) and later for 2 d during decompression at a simulated altitude of 4,270 m (PB 447 mm Hg). The LAN group demonstrated higher (p less than 0.05) serum cortisol concentrations and respiration rates, and lower (p less than 0.05) serum aldosterone and potassium, and urinary aldosterone, sodium, and potassium concentrations at certain times during decompression compared to their home responses. Moderate-altitude native responses, on the other hand, were generally unchanged. Manifestations of acute mountain sickness at PB 447 mm Hg were also significantly greater in the LAN group. Thus, it appears that the MAN subjects were influenced less by the drop in ambient oxygen tension associated with PB 447 mm Hg.     

Effects of acute hypoxia on cardiopulmonary responses to head-down tilt

Six male subjects were exposed on two separate occasions to simulated microgravity with 28 degrees head-down tilt (HD) for 1 h with baseline followed by recovery at + 17 degrees head-up. Pulmonary ventilation, gas exchange, spirometry, and central and cerebral blood flow characteristics were compared while breathing ambient air (PIO2 = 122 mm Hg) and reduced FIO2 equivalent to 14,828 ft (PIO2 = 81 mm Hg). With hypoxia (HY), the increased tidal volume served to attenuate the drop in arterial saturation by reducing deadspace ventilation. Arterial and mixed venous PO2 values, estimated from peripheral venous samples and cardiac output (CO), were both maintained during HD in HY. Mixed venous PO2 was elevated by an increase in CO associated with a reduction in systemic resistance. Changes in spirometric indices during HD were not accentuated by HY, making the presence of interstitial edema unlikely. Cerebral flow and resistance showed minor reductions with HD. Tissue oxygenation and cardiopulmonary function were not notably effected by HD during HY, but a combination of these two stressors may predispose subjects to subsequent orthostatic intolerance during initial recovery.     

Effect of hypoxia on heart glycogen utilization during exercise

An investigation was made into the effects of physical exercise upon heart glycogen change in rats exposed to decreased barometric pressure in hypobaric chamber simulating the effects of 3,000 m and 5,000 m altitude. Blood and cardiac tissue samples were examined after 1 h and 5 h of treadmill running at sea level and at 3,000 m, and after 1 h at 5,000 m. At sea level, cardiac glycogen level showed a classic biphasic evolution which was not affected by running. At 3,000 m, 1 h of running promoted an initial increase of 16% from control values, while a secondary decrease of 15% was measured after 5 h of running. Running for 1 h at 5,000 m induced a total depletion in cardiac glycogen level, the latter being depressed by 90% from control values. Free fatty acid (FFA) plasma level was increased by physical exercise at all barometric pressures, but the response was gradually enhanced by hypoxia. These data indicate that heart glycogen utilization during prolonged physical exercise is stimulated by acute altitude exposure, which suppresses the sparing effect observed at sea level upon dependence of enhanced FFA availability. The great differences in cardiac glycogen utilization support the views that enhanced glycogenolysis during hypoxia is promoted by different parameters, thus affecting various pathways. The slight decrease at 3,000 m suggests a moderate increase in anaerobic metabolism while the exhaustion observed after 1 h of running at 5,000 m indicates a decrease in cellular respiration response and enhanced heart anaerobic metabolism.     

Altitude-related hypoxia: risk assessment and management for passengers on commerical aircraft

BACKGROUND: Individuals with pulmonary and cardiac disorders are particularly at risk of developing hypoxemia at altitude. Our objective is to describe the normal and maladaptive physiological responses to altitude-related hypoxia, to review existing methods and guidelines for preflight assessment of air travelers, and to provide recommendations for treatment of hypoxia at altitude. DATA SYNTHESIS: Falling partial pressure of oxygen with altitude results in a number of physiologic adaptations including hyperventilation, pulmonary vasoconstriction, altered ventilation/perfusion matching, and increased sympathetic tone. According to three guideline statements, the arterial pressure of oxygen (PaO2) should be maintained above 50 to 55 mm Hg at all altitudes. General indicators such as oxygen saturation and sea level blood gases may be useful in predicting altitude hypoxia. More specialized techniques for estimation of altitude PaO2, such as regression equations, hypoxia challenge testing, and hypobaric chamber exposure have also been examined. A regression equation using sea level PaO2 and spirometric parameters can be used to estimate PaO2 at altitude. Hypoxia challenge testing, performed by exposing subjects to lower inspired FIO2 at sea level may be more precise. Hypobaric chamber exposure, the gold standard, mimics lower barometric pressure, but is mainly used in research. CONCLUSION: Oxygen supplementation during air travel is needed for individuals with an estimated PaO2 (8000 ft) below 50 mmHg. There are a number of guidelines for the pre-flight assessment of patients with pulmonary and/or cardiac diseases. However, these data are based on small studies in patients with a limited group of diseases.     

Reduced tolerance of simulated altitude (4200 m) in young men with borderline hypertension

BACKGROUND: Primary hypertensives who are acutely exposed to hypoxic hypoxia show an enhanced reactivity of arterial chemoreceptors as well as an exaggerated response of the sympathetic nervous system. Since these phenomena could influence their ability to tolerate sustained hypoxic hypoxia, this study was performed to determine whether persons predisposed to hypertension have a normal tolerance of simulated high altitude. METHODS: Subjects were 18 young men with a family history of hypertension (sons of hypertensives, SOHT) whose BP values were in the upper normal or borderline hypertensive range. Controls were 15 young men without parental hypertension (sons of normotensives, SONT) who had normal BP values. Each subject underwent both a control and an altitude experiment. The latter consisted of an 8-h exposure to hypobaric hypoxia (equivalent to 4200 m) while resting supine in an altitude chamber. Fluids were administered by mouth and by intravenous line to produce sustained diuresis. Variables measured included heart rate, BP, respiratory rate, O2 saturation, urine flow rate, and sodium excretion. RESULTS: All subjects tolerated the control experiment and all SONT also completed altitude exposure. However, 8 of 18 SOHT developed antidiuresis and had to leave the chamber early due to symptoms of mild acute mountain sickness. Compared with SONT, SOHT exhibited more stable cardiorespiratory parameters at altitude. CONCLUSIONS: The data support the hypothesis that borderline hypertensives have stronger cardiorespiratory responses to altitude than controls, a response that is compatible with higher excitability of their arterial chemoreceptors. However, their altitude tolerance is reduced even at rest, probably because of the renal effects of an exaggerated response in the sympathetic nervous system.     

Effect of spironolactone on acute mountain sickness

This study examined the effectiveness of spironolactone as a prophylactic agent for the prevention of acute mountain sickness (AMS). Spironolactone, 25 mg PO QID, or placebo was administered to nine subjects in a double-blind, placebo-controlled, crossover design. Medication was given for 48 h prior to and during a 46-h exposure to 427 mm Hg (4570 m) in a hypobaric chamber. Six subjects demonstrated prevention of either the cerebral or respiratory symptoms of AMS during at least one segment of the altitude sojourn.     

Chronic intermittent hypoxia at high altitude exposure for over 12 years: assessment of hematological, cardiovascular, and renal effects

The aim of this cross-sectional study was to assess the health status of subjects weekly commuting between sea level and 3550-m altitude for at least 12 yr (average 22.1 +/- 5.8). We studied 50 healthy army men (aged 48.7 +/- 2.0) working 4 days in Putre at 3550-m altitude, with 3 days rest at sea level (SL) at Arica, Chile. Blood pressure, heart rate, Sa(O(2) ), and altitude symptoms (AMS score and sleep status) were measured at altitude (days 1, 2, and 4) and at SL (days 1, 2, and 3). Hematological parameters, lipid profile, renal function, and echocardiography were performed at SL on day 1. The results showed signs of acute exposure to hypoxia (tachycardia, high blood pressure, low Sa(O(2) )), AMS symptoms, and sleep disturbances on day 1, which rapidly decreased on day 2. In addition, echocardiographic findings showed pulmonary hypertension (PAPm > 25 mmHg, RV and RA enlargement) in 2 subjects (4%), a PAPm > 20 mmHg in 14%, and a right ventricle thickness >40 mm in 12%. Hematocrit (45 +/- 2.7) and hemoglobin (15 +/- 1.0) were elevated, but lower than in permanent residents. There was a remarkably high triglyceride level (238 +/- 162) and a mild decrease of glomerular filtration rate (34% under 90 mL/min and 8% under 80 mL/min of creatinine clearance). In conclusion, in these preliminary results, in chronic intermittent hypoxia exposure even over longer periods, most subjects still show symptoms of acute altitude illnesses, but a faster recovery. Findings in triglycerides, in the pulmonary circulation and in renal function, are also a matter of concern.     

1984 Armstrong lecture. Hypoxic man: lessons from extreme altitude

Physiological responses to extreme prolonged hypoxia were studied during the American Medical Research Expedition to Mount Everest in the fall of 1981. Measurements were carried out at four sites on the mountain, including the summit. The results show that man can tolerate the extreme hypoxia of these great altitudes only by an enormous increase in ventilation. Alveolar PCO2 on the summit was 7.5 mm Hg, the arterial pH and PO2 were calculated to be over 7.7 and less than 30 mm Hg, respectively, and maximum oxygen uptake was about 1 L X min-1. Our experimental program is now moving to Spacelab IV to study the effects of weightlessness on pulmonary function in 1985 or early 1986.     

高压氧干预对抗低氧效果的观察

目的探讨高压氧干预对初入高海拔地区青年的作用。方法将42名受试者随机分为A、B、C三组,每组14人。于进驻高原前2 d对A组在海拔1400 m进行高压氧干预,每天1次共2次;于第3天三组青年同时乘汽车历时2 d到达海拔3700 m地区休整2 d,同时对B组进行高压氧干预(方法同A组);C组为对照组。于第7天三组青年同时乘汽车历时1 d到达海拔5200 m某边防哨卡。对三组进驻哨卡第2、4、6天的急性高原反应症状分度评分,同时检测心率(HR)和血氧饱和度(SaO2)。结果A组及B组较C组分值降低、HR减慢、SaO2增高,差异均有统计学意义(P<0.05)。结论高压氧干预可改善高原低氧血症,降低急性高原反应的发病率。     

Conjunctival oxygen tension at high altitude

Transconjunctival oxygen tension (PcjO2) was studied using a hypobaric chamber and during mountaineering excursions. Measurements obtained during acute chamber exposures (15-20 min) at sea level, 1829 m (6,000 ft), 3048 m (10,000 ft), 4267 m (14,000 ft) and return to sea level were (means +/- SEM): 60.1 +/- 2.7, 49.1 +/- 1.8, 38.3 +/- 2.4, 27.4 +/- 1.5, and 61.1 +/- 2.8 mm Hg, respectively (n = 13). The ratio of PcjO2 to arterial blood oxygen tension (PaO2) did not change in a consistent manner between sea level and 4267 m; PcjO2 was 74 +/- 6.9% of PaO2. The 16 subjects participating in the mountaineering phase of the study revealed similar means at sea level and 1829 m (57.4 +/- 2.4 and 46.3 +/- 1.9 mm Hg respectively), but a smaller decrement was observed at 3048 m (43.0 +/- 1.6 mm Hg). The difference between mountain and chamber values may be accounted for by a partial acclimatization to altitude brought about by longer exposure on the mountain excursions. A comparison between PcjO2 and transcutaneous oxygen tension during the chamber study suggests that a greater precision and sensitivity is obtained with measurement of oxygen tension at the conjunctival site. PcjO2 measurement is a non-invasive reflection of PaO2 which is suitable for continuous monitoring during hypoxia studies.     

Effects of sildenafil on the human response to acute hypoxia and exercise

We examined the effects of the 5-phosphodiesterase (5-PDE) inhibitor sildenafil on pulmonary arterial pressure and some oxygen transport and cardiopulmonary parameters in humans during exposure to hypobaric hypoxia at rest and after exercise. In a double-blind study, 100 mg sildenafil or placebo was administered orally to 14 healthy volunteers 45 min before exposure to 5,000 m of simulated altitude. Arterial oxygen saturation (SaO2), heart rate (HR), tidal volume (VT), respiratory rate (RR), left ventricular ejection fraction (EF), and pulmonary arterial pressure (PAP) were measured first at rest in normoxia, at rest and immediately after exercise during hypoxia, and after exercise in normoxia. The increase in systolic PAP produced by hypoxia was significantly decreased by sildenafil at rest from 40.9 +/- 2.6 to 34.9 +/- 3.0 mmHg (-14.8%; p = 0.0046); after exercise, from 49.0 +/- 3.9 to 42.9 +/- 2.6 mmHg (-12.6%; p = 0.003). No significant changes were found in normoxia either at rest or after exercise. Measurements of the effect of sildenafil on exercise capacity during hypoxia did not provide conclusive data: a slight increase in SaO2 was observed with exercise during hypoxia, and sildenafil did not cause significant changes in ventilatory parameters under any condition. Sildenafil diminishes the pulmonary hypertension induced by acute exposure to hypobaric hypoxia at rest and after exercise. Further studies are needed to determine the benefit from this treatment and to further understand the effects of sildenafil on exercise capacity at altitude.     

A time-saving incremental cycle ergometer protocol to determine peak oxygen consumption.

Previously we have demonstrated that an accelerated arm ergometry testing protocol results in a higher peak oxygen consumption than continuous or discontinuous protocols reported in the literature (Brit. J. Sports Med. 20: 25-26, 1986). The purpose of this investigation was to determine if an accelerated protocol was superior to two commonly used protocols in cycle ergometry. Nine male subjects were tested on three different exercise protocols; a discontinuous test (DT), a continuous test (CT) and a new proposed "jump-max test" (JMT). The CT began at a work rate of 70 W with the power output (PO) being increased 35 W.min-1. The DT began at a work rate of 70 W; the work rate was increased by 35 W every 2 minutes with 2-minutes rest between stages. The JMT began with a 3-minute pretest to determine a PO which elicited a HR of 145 +/- 5 bpm. After a 2-minute rest, subjects began exercise at the predetermined work rate with the PO being increased 35 W.min-1. Testing sessions were terminated when subjects failed to maintain the desired PO. No significant difference (p greater than 0.05) existed in peak PO or peak oxygen consumption (VO2) between the three protocols. However, JMT protocol did result in a shorter time to exhaustion than the other protocols employed (P less than 0.05).     

High-altitude exposure reduces inspiratory muscle strength

It was the aim of the study to assess the maximal pressure generated by the inspiratory muscles (MIP) during exposure to different levels of altitude (i.e., hypobaric hypoxia). Eight lowlanders (2 females and 6 males), aged 27 - 46 years, participated in the study. After being evaluated at sea level, the subjects spent seven days at altitudes of more than 3000 metres. On the first day, they rode in a cable car from 1200 to 3200 metres and performed the first test after 45 - 60 minutes rest; they then walked for two hours to a mountain refuge at 3600 metres, where they spent three nights (days 2 - 3); on day 4, they walked for four hours over a glacier to reach Capanna Regina Margherita (4559 m), where they spent days 5 - 7. MIP, flow-volume curve and SpO (2) % were measured at each altitude, and acute mountain sickness (Lake Louise score) was recorded. Increasing altitude led to a significant decrease in resting SpO (2) % (from 98 % to 80 %) and MIP (from 134 to 111 cmH (2)O) (baseline to day 4: p < 0.05); there was an improvement in SpO (2) % and a slight increase in MIP during the subsequent days at the same altitude. Expiratory (but not inspiratory) flows increased, and forced vital capacity and FEF (75) decreased at higher altitudes. We conclude that exposure to high altitude hypoxia reduces the strength of the respiratory muscles, as demonstrated by the reduction in MIP and the lack of an increase in peak inspiratory flows. This reduction is more marked during the first days of exposure to the same altitude, and tends to recover during the acclimatisation process.     

Changes in running speed, blood lactic acid concentration and hormone balance during sprint training performed at an altitude of 1860 metres

The development of results of five national level sprinters (Group A) was followed up during a training period of two weeks at an altitude of 1860 m aiming at increase of strength and speed and after it. Changes in anaerobic capacity were monitored by making blood lactic acid determinations, and occurrence of any overstrain by serum testosterone, cortisol, growth hormone and SHBG (sex hormone binding globulin) determinations. A control group (Group B) trained simultaneously according to a similar programme at sea level. Maximal 150 m running speeds increased in Group A significantly during the two weeks at the altitude of 1860 m (p less than 0.001). No such increase was observable in Group B. Maximal 300 m running speeds and maximal lactic acid concentrations after running did not increase significantly in either group. Serum hormone levels did not change significantly either, in either group. Training at an altitude of 1860 m to increase strength and speed significantly improved results at the shorter distance of 150 m but had not significant effects on anaerobic capacity or on serum testosterone, cortisol, growth hormone or SHBG levels.     

Intermittent hypoxia research in the former soviet union and the commonwealth of independent States: history and review of the concept and selected applications

This review aims to summarize the basic research in the field of intermittent hypoxia in the Soviet Union and the Commonwealth of Independent States (CIS) that scientists in other Western countries may not be familiar with, since Soviet scientists were essentially cut off from the global scientific community for about 60 years. In the 1930s the concept of repeated hypoxic training was developed and the following induction methods were utilized: repeated stays at high-mountain camps for several weeks, regular high altitude flights by plane, training in altitude chambers, and training by inhalation of low-oxygen-gas mixtures. To the present day, intermittent hypoxic training (IHT) has been used extensively for altitude preacclimatization; for the treatment of a variety of clinical disorders, including chronic lung diseases, bronchial asthma, hypertension, diabetes mellitus, Parkinson's disease, emotional disorders, and radiation toxicity, in prophylaxis of certain occupational diseases; and in sports. The basic mechanisms underlying the beneficial effects of IHT are mainly in three areas: regulation of respiration, free-radical production, and mitochondrial respiration. It was found that IHT induces increased ventilatory sensitivity to hypoxia, as well as other hypoxia-related physiological changes, such as increased hematopoiesis, alveolar ventilation and lung diffusion capacity, and alterations in the autonomic nervous system. Due to IHT, antioxidant defense mechanisms are stimulated, cellular membranes become more stable, Ca(2+) elimination from the cytoplasm is increased, and O(2) transport in tissues is improved. IHT induces changes within mitochondria, involving NAD-dependent metabolism, that increase the efficiency of oxygen utilization in ATP production. These effects are mediated partly by NO-dependent reactions. The marked individual variability both in animals and humans in the response to, and tolerance of, hypoxia is described. Studies from the Soviet Union and the CIS significantly contributed to the understanding of intermittent hypoxia and its possible beneficial effects and should stimulate further research in this direction in other countries.