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Heart rate and respiratory rhythm dynamics on ascent to high altitude.

OBJECTIVE: To investigate the alterations in autonomic control of heart rate at high altitude and to test the hypothesis that hypoxaemic stress during exposure to high altitude induces non-linear, periodic heart rate oscillations, similar to those seen in heart failure and the sleep apnoea syndrome. SUBJECTS: 11 healthy subjects aged 24-64. MAIN OUTCOME MEASURES: 24 hour ambulatory electrocardiogram records obtained at baseline (1524 m) and at 4700 m. Simultaneous heart rate and respiratory dynamics during 2.5 hours of sleep by fast Fourier transform analysis of beat to beat heart rate and of an electrocardiographically derived respiration signal. RESULTS: All subjects had resting hypoxaemia at high altitude, with an average oxyhaemoglobin saturation of 81% (5%). There was no significant change in mean heart rate, but low frequency (0.01-0.05 Hz) spectral power was increased (P < 0.01) at high altitude. Time series analysis showed a complex range of non-linear sinus rhythm dynamics. Striking low frequency (0.04-0.06 Hz) heart rate oscillations were observed during sleep in eight subjects at high altitude. Analysis of the electrocardiographically derived respiration signal indicated that these heart rate oscillations correlated with low frequency respiratory oscillations. CONCLUSIONS: These data suggest (a) that increased low frequency power during high altitude exposure is not simply attributable to increased sympathetic modulation of heart rate, but relates to distinctive cardiopulmonary oscillations at approximately 0.05 Hz and (b) that the emergence of periodic heart rate oscillations at high altitude is consistent with an unstable cardiopulmonary control system that may develop on acute exposure to hypoxaemic stress.

Adult↗

Peak expiratory flow at altitude.

The mini Wright peak flow meter is a useful, portable instrument for field studies but being sensitive to air density will under-read at altitude. True peak expiratory flow will increase at altitude, however, because of the decreased air density, given that dynamic resistance is unchanged. The effect of simulated altitude on peak expiratory flow (PEF) was determined in six subjects with both the mini Wright meter and a volumetric spirometer (which is unaffected by air density). With increasing altitude PEF as measured by the spirometer increased linearly with decreasing pressure, so that at a barometric pressure of 380 mm Hg* (half an atmosphere, corresponding to an altitude of 5455 m) there was a 20% increase over sea level values. The mini Wright flow meter gave readings 6% below sea level values for this altitude--that is, under-reading by 26%. Measurements of PEF made at altitude with the mini Wright meter should be corrected by adding 6.6% per 100 mm Hg drop in barometric pressure.

Altitude↗

Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude.

We evaluated the hypotheses that on acute exposure to hypobaric hypoxia, sympathetic stimulation leads to augmented muscle lactate production and circulating [lactate] through a beta-adrenergic mechanism and that beta-adrenergic adaptation to chronic hypoxia is responsible for the blunted exercise lactate response after acclimatization to altitude. Five control and 6 beta-blocked men were studied during rest and exercise at sea level (SL), on acute exposure to 4,300 m (A1), and after a 3-wk sojourn at altitude (A2). Exercise was by leg cycling at 49% of SL peak O2 consumption (VO2 peak) (65% of altitude VO2 peak or 87 +/- 2.6 W); beta-blockade was by propranolol (80 mg 3x daily), femoral arterial and venous blood was sampled; leg blood flow (Q) was measured by thermodilution, leg lactate net release [ = (2) (1-leg Q) venous-arterial concentrationL] was calculated, and vastus lateralis needle biopsies were obtained. Muscle [lactate] increased with exercise and acute altitude exposure but regressed to SL values with acclimatization; beta-blockade had no effect on muscle [lactate]. Arterial [lactate] rose during exercise at SL (0.9 +/- 0.1 to 1.5 +/- 0.3 mM); exercise at A1 produced the greatest arterial [lactate] (4.4 +/- 0.8 mM), and exercise at A2 an intermediate response (2.1 +/- 0.6 mM). beta-Blockade reduced circulating [lactate] approximately 45% during exercise under all altitude conditions. increased transiently at exercise onset but then declined over time under all conditions. Blood and muscle "lactate paradoxes" occurred independent of beta-adrenergic influences, and the hypotheses relating the blood lactate response at altitude to beta-adrenergic mechanisms are rejected. During exercise at altitude, arterial [lactate] is determined by factors in addition to hypoxemia, circulating epinephrine, and net lactate release from active muscle beds.

Acclimatization↗

Mechanical properties of the lungs during acclimatization to altitude.

Mechanical properties of the lung were studied in nine healthy lowlanders during a 6-day sojourn at an altitude of 3,457 m. In comparison to sea-level values, it was found at altitude that 1) lung volumes measured by plethysmography including total lung capacity, vital capacity, and functional residual capacity (FRC) presented small changes not exceeding 300 ml; 2) static and dynamic lung compliances were not modified but static pressure-volume curves of lungs were shifted progressively to the left (the decrease in lung elastic recoil averaged about 2 cmH2O on days 4-6); and 3) maximal midexpiratory flow, forced expiratory volume in 1 s, and maximal expiratory and inspiratory flows were increased and, conversely, airways and pulmonary flow resistances were decreased on most days at altitude. The unchanged FRC in the face of a decreased lung recoil may be explained by an increase in thoracic blood volume at altitude, but other possible mechanisms are discussed. The decrease in resistances and increase in maximal flows may be partly explained by the decreased air density at altitude, but another contributing factor such as a bronchodilatation is also suggested. It is proposed that changes in lung mechanics at altitude may account for some of the changes in the pattern of breathing and mouth occlusion pressure (P0.1) observed during acclimatization of lowlanders to altitude.

Acclimatization↗

Altitude acclimatization: influence on periodic breathing and chemoresponsiveness during sleep.

Although the influence of altitude acclimatization on respiration has been carefully studied, the associated changes in hypoxic and hypercapnic ventilatory responses are the subject of controversy with neither response being previously evaluated during sleep at altitude. Therefore, six healthy males were studied at sea level and on nights 1, 4, and 7 after arrival at altitude (14,110 ft). During wakefulness, ventilation and the ventilatory responses to hypoxia and hypercapnia were determined on each occasion. During both non-rapid-eye-movement and rapid-eye-movement sleep, ventilation, ventilatory pattern, and the hypercapnic ventilatory response (measured at ambient arterial O2 saturation) were determined. There were four primary observations from this study: 1) the hypoxic ventilatory response, although similar to sea level values on arrival at altitude, increased steadily with acclimatization up to 7 days; 2) the slope of the hypercapnic ventilatory response increased on initial exposure to a hypoxic environment (altitude) but did not increase further with acclimatization, although the position of this response shifted steadily to the left (lower PCO2 values); 3) the sleep-induced decrements in both ventilation and hypercapnic responsiveness at altitude were equivalent to those observed at sea level with similar acclimatization occurring during wakefulness and sleep; and 4) the quantity of periodic breathing during sleep at altitude was highly variable and tended to occur more frequently in individuals with higher ventilatory responses to both hypoxia and hypercapnia.

Acclimatization↗

Pulmonary hypertension and pulmonary vascular reactivity in beagles at high altitude.

It is unclear whether dogs develop pulmonary hypertension (PH) at high altitude. Beagles from sea level were exposed to an altitude of 3,100 m (PB 525 Torr) for 12-19 mo and compared with age-matched controls remaining at low altitude of 130 m (PB 750 Torr). In beagles taken to high altitude as adults, pulmonary arterial pressures (PAP) at 3,100 m were 21.6 +/- 2.6 vs. 13.2 +/- 1.2 Torr in controls. Likewise, in beagles taken to 3,100 m as puppies 2.5 mo old, PAP was 23.2 +/- 2.1 vs. 13.8 +/- 0.4 Torr in controls. This PH reflected a doubling of pulmonary vascular resistance and showed no progression with time at altitude. Pulmonary vascular reactivity to acute hypoxia was also enhanced at 3,100 m. Inhibition of prostaglandin synthesis did not attenuate the PH or the enhanced reactivity. Once established, the PH was only partially reversed by acute relief of chronic hypoxia, but reversal was virtually complete after return to low altitude. Hence, beagles do develop PH at 3,100 m of a severity comparable to that observed in humans at the same or even higher altitudes.

Altitude↗

A theoretical analysis of the effect of altitude on running performance.

A theoretical analysis of the effect of altitude on running performance is presented using a mathematical model we have recently described and validated (J. Appl. Physiol. 67: 453-465, 1989). This model relates the average power output available over a given running time for a given combination of anaerobic capacity, maximal aerobic power, and endurance capability. For short sprinting distances, the contribution of aerobic metabolism to the energy requirement is small and the speed sustained is high. The reduction of maximal aerobic power with altitude is, thus, negligible, whereas the reduction of aerodynamic resistance is beneficial. Accordingly the performance steadily increases with altitude (e.g., average speed for 100 m at Mexico City is 101.9% of the average speed at sea level). On the other hand, the reduction in maximal aerobic power with altitude is associated with a reduction in performance over middle and long distances (800 m to marathon). For 400 m an improvement in performance is observed up to an altitude of approximately 2,400-2,500 m (average speed approximately 101.4% of sea level speed). Beyond this altitude the reduction in air density cannot compensate for the reduction in maximal aerobic power, and the performance deteriorates. Tables of performances equivalent to the current world records for selected altitudes ranging from 0 to 4,000 m are proposed.

Aerobiosis↗

Increased energy intake minimizes weight loss in men at high altitude.

The hypothesis that high-altitude weight loss can be prevented by increasing energy intake to meet energy requirement was tested in seven men, 23.7 +/- 4.3 (SD) yr, taken to 4,300 m for 21 days. Energy intake required to maintain body weight at sea level was found to be 3,118 +/- 300 kcal/day, as confirmed by nitrogen balance. Basal metabolic rate (BMR), determined by indirect calorimetry, increased 27% on day 2 at altitude and then decreased and reached a plateau at 17% above the sea level BMR by day 10. Energy expended during strenuous activities was 37% lower at altitude than at sea level. Fecal excretion of energy, nitrogen, total fiber, and total volatile fatty acids was not significantly affected by altitude. Energy intake at altitude was adjusted after 1 wk, on the basis of the increased BMR, to 3,452 +/- 452 kcal/day. Mean nitrogen balance at altitude was negative (-0.25 +/- 0.71 g/day) before energy intake was adjusted but rose significantly thereafter (0.20 +/- 0.71 and 0.44 +/- 0.66 g/day during weeks 2 and 3). Mean body weight decreased 2.1 +/- 1.0 kg over the 3 wk of the study, but the rate of weight loss was significantly diminished after the increase in energy intake (201 +/- 75 vs. 72 +/- 48 g/day). Individual regression lines drawn through 7-day segments of body weight showed that in four of seven subjects the slopes of body weight were not significantly different from zero after the 2nd wk. Thus weight loss ceased in four of seven men in whom increased BMR at altitude was compensated with increased energy intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Sympathetic and parasympathetic indicators of heart rate control at altitude studied by spectral analysis.

The adaptive responses of the cardiovascular system to altitude appear to be dominated by increased sympathetic neural activity. We investigated the combined roles of the sympathetic and parasympathetic nervous systems (SNS and PNS, respectively) in the early (days 4-5) and subsequent (days 11-12) phases of acclimatization on Pike's Peak, CO (4,300 m), by spectral analysis of heart rate variability. Male subjects were randomly assigned to groups receiving oral propranolol (240 mg/day; n = 6) or a matched placebo (n = 3). On ascent to altitude, the high-frequency, fractal, and total spectral powers were reduced in the placebo group during days 4-5 and 11-12. At altitude during days 4-5, all three placebo group subjects increased SNS and decreased PNS activities compared with at sea level, and during days 11-12 SNS decreased and PNS increased compared with days 4-5. Relative to the placebo group, propranolol caused lengthening of the R-R interval; increases in high-frequency power, total spectral power, and the PNS indicator; and a decrease in the SNS indicator. Total spectral power tended to decrease at altitude, but there were no effects of altitude on PNS and SNS indicators in the propranolol group. The data from the placebo and propranolol groups suggest that both the PNS and SNS are involved in the elevated heart rate during the early phase of altitude acclimatization. Changes in heart rate variability during days 11-12 at altitude must be considered in light of the possible reductions in sympathetic receptor number noted in previous studies.

Acclimatization↗

Exercise performance of Tibetan and Han adolescents at altitudes of 3,417 and 4,300 m.

The difference was studied between O2 transport in lifelong Tibetan adolescents and in newcomer Han adolescents acclimatized to high altitude. We measured minute ventilation, maximal O2 uptake, maximal cardiac output, and arterial O2 saturation during maximal exercise, using the incremental exercise technique, at altitudes of 3,417 and 4,300 m. The groups were well matched for age, height, and nutritional status. The Tibetans had been living at the altitudes for a longer period than the Hans (14.5 +/- 0.2 vs. 7.8 +/- 0.8 yr at 3,417 m, P < 0.01; and 14.7 +/- 0.3 vs. 5.3 +/- 0.7 yr at 4,300 m, P < 0.01, respectively). At rest, Tibetans had significantly greater vital capacity and maximal voluntary ventilation than the Hans at both altitudes. At maximal exercise, Tibetans compared with Hans had higher maximal O2 uptake (42.2 +/- 1.7 vs. 36.7 +/- 1.2 ml . min-1 . kg-1 at 3,417 m, P < 0.01; and 36.8 +/- 1.9 vs. 30.0 +/- 1. 4 ml . min-1 . kg-1 at 4,300 m, P < 0.01, respectively) and greater maximal cardiac output (12.8 +/- 0.3 vs. 11.4 +/- 0.2 l/min at 3,417 m, P < 0.01; 11.5 +/- 0.5 vs. 10.0 +/- 0.5 l/min at 4,300 m, P < 0. 05, respectively). Although the differences in arterial O2 saturation between Tibetans and Hans were not significant at rest and during mild exercise, the differences became greater with increases in exercise workload at both altitudes. We concluded that exposure to high altitude from birth to adolescence resulted in an efficient O2 transport and a greater aerobic exercise performance that may reflect a successful adaptation to life at high altitude.

Acclimatization↗

"Living high-training low" altitude training improves sea level performance in male and female elite runners.

Acclimatization to moderate high altitude accompanied by training at low altitude (living high-training low) has been shown to improve sea level endurance performance in accomplished, but not elite, runners. Whether elite athletes, who may be closer to the maximal structural and functional adaptive capacity of the respiratory (i.e., oxygen transport from environment to mitochondria) system, may achieve similar performance gains is unclear. To answer this question, we studied 14 elite men and 8 elite women before and after 27 days of living at 2,500 m while performing high-intensity training at 1,250 m. The altitude sojourn began 1 wk after the USA Track and Field National Championships, when the athletes were close to their season's fitness peak. Sea level 3,000-m time trial performance was significantly improved by 1.1% (95% confidence limits 0.3-1.9%). One-third of the athletes achieved personal best times for the distance after the altitude training camp. The improvement in running performance was accompanied by a 3% improvement in maximal oxygen uptake (72.1 +/- 1.5 to 74.4 +/- 1.5 ml x kg(-1) x min(-1)). Circulating erythropoietin levels were near double initial sea level values 20 h after ascent (8.5 +/- 0.5 to 16.2 +/- 1.0 IU/ml). Soluble transferrin receptor levels were significantly elevated on the 19th day at altitude, confirming a stimulation of erythropoiesis (2.1 +/- 0.7 to 2.5 +/- 0.6 microg/ml). Hb concentration measured at sea level increased 1 g/dl over the course of the camp (13.3 +/- 0.2 to 14.3 +/- 0.2 g/dl). We conclude that 4 wk of acclimatization to moderate altitude, accompanied by high-intensity training at low altitude, improves sea level endurance performance even in elite runners. Both the mechanism and magnitude of the effect appear similar to that observed in less accomplished runners, even for athletes who may have achieved near maximal oxygen transport capacity for humans.

Acclimatization↗

Respiratory events and periodic breathing in cyclists sleeping at 2,650-m simulated altitude.

We examined the initial effect of sleeping at a simulated moderate altitude of 2,650 m on the frequency of apneas and hypopneas, as well as on the heart rate and blood oxygen saturation from pulse oximetry (SpO2) during rapid eye movement (REM) and non-rapid eye movement (NREM) sleep of 17 trained cyclists. Pulse oximetry revealed that sleeping at simulated altitude significantly increased heart rate (3 +/- 1 beats/min; means +/- SE) and decreased SpO2 (-6 +/- 1%) compared with baseline data collected near sea level. In response to simulated altitude, 15 of the 17 subjects increased the combined frequency of apneas plus hypopneas from baseline levels. On exposure to simulated altitude, the increase in apnea was significant from baseline for both sleep states (2.0 +/- 1.3 events/h for REM, 9.9 +/- 6.2 events/h for NREM), but the difference between the two states was not significantly different. Hypopnea frequency was significantly elevated from baseline to simulated altitude exposure in both sleep states, and under hypoxic conditions it was greater in REM than in NREM sleep (7.9 +/- 1.8 vs. 4.2 +/- 1.3 events/h, respectively). Periodic breathing episodes during sleep were identified in four subjects, making this the first study to show periodic breathing in healthy adults at a level of hypoxia equivalent to 2,650-m altitude. These results indicate that simulated moderate hypoxia of a level typically chosen by coaches and elite athletes for simulated altitude programs can cause substantial respiratory events during sleep.

Adult↗

Multifocal electroretinography changes in the macula at high altitude: a report of three cases.

BACKGROUND: To evaluate the short- and long-term effects of high-altitude hypobaric hypoxia on macula morphology and function during ascents, acclimatizations, and descents between 500 m and 5,650 m, macula function was evaluated in three healthy climbers of a trekking expedition. METHODS: Macula physiology was tested with multifocal electroretinography (MF ERG), near and farvisual acuity, and Amsler grid tests. Macula morphology was tested with optical coherence tomography (OCT) and with stereoscopic fundoscopy obtained 1 week before ascent, as well as 1 week and 2 weeks after high-altitude exposure. The following physiological parameters indicative of acclimatization were compared daily during the expedition at altitudes between 500 m and 5,050 m: hemoglobin, oxygen saturation, resting heart rate, retinal findings, and the Lake Louise score of acclimatization. RESULTS: The central macula MF ERG responses were significantly reduced 1 week after high-altitude exposure, and had recovered by the follow-up examination performed during the following week. Near visual acuity and Amsler grid tests remained unaffected at both follow-up examinations. No significant changes were found in the follow-up OCT and daily fundoscopy examinations in all three well-acclimatized climbers. CONCLUSIONS: High-altitude hypobaric hypoxia affects the function of the highly sensitive macula region. This suggests that the exposure of persons with macula diseases such as age-related macula degeneration, tapetoretinal degeneration, or diabetic retinopathy to high altitudes may influence the disease progression. For this reason, this population should avoid prolonged and unnecessary high-altitude exposure without proper acclimatization.

Acclimatization↗

Hypoxic pressor responses in lungs from rats acutely exposed to simulated high altitude.

Male Sprague-Dawley rats were exposed to 6, 3 or 1 h of simulated high altitude (380 Torr). The isolated perfused lung of each animal was challenged with 4 sequential periods of hypoxia, angiotensin II (AII), and 5-hydroxytryptamine (5-HT) following altitude exposure. Isolated perfused lungs of low altitude control rats were similarly challenged. The acute hypoxic vasoconstrictor response was significantly reduced in animals exposed to 3 and 6 h of high altitude compared to low altitude control animals. The hypoxic pressor response was not significantly different from control in animals exposed to 1 h of simulated altitude. Pressor responses to AII and 5-HT following altitude exposure were not significantly different from controls.

Altitude↗

Human llamas: adaptation to altitude in subjects with high hemoglobin oxygen affinity.

To assess the adaptive value of the right-shift of the oxyhemoglobin dissociation curve (decreased affinity for oxygen) observed in humans upon altitude exposure, the short-term physiologic responses to altitude-induced hypoxia were evaluated in two subjects with a high oxygen affinity hemoglobin (Hb Andrew-Minneapolis) and in two of their normal siblings. In striking contrast to normal subjects, at moderately high altitude (3,100 m) the high affinity subjects manifested: (a) lesser increments in resting heart rate; (b) minimal increases in plasma and urinary erythropoietin; (c) no decrement in maximal oxygen consumption; and (d) no thrombocytopenia. There was no difference between subject pairs in 2,3-diphosphoglycerate response to altitude exposure. These results tend to contradict the belief that a decrease in hemoglobin oxygen affinity is of adaptive value to humans at moderate altitudes. Rather, they support the hypothesis that, despite disadvantages at low altitude, a left-shifted oxyhemoglobin dissociation curve may confer a degree of preadaptation to altitude.

Adaptation, Physiological↗

Low serum estradiol and high serum progesterone concentrations characterize hypertensive pregnancies at high altitude.

OBJECTIVE: Intrauterine growth retardation and preeclampsia are more common at high than at low altitude. Because altered hormonal profiles have been linked with these disorders, we asked whether placental steroid hormone concentrations were altered during pregnancy at high altitude. METHODS: We measured progesterone, unconjugated estradiol, and estriol (by radioimmunoassay) at weeks 20, 30, and 36 of pregnancy in 18 women at low altitude (1600 m) and 40 women at high altitude (3100 m). RESULTS: Women at 3100 m compared with 1600 m had lower serum estradiol concentrations at week 36 of pregnancy, and lower estriol and higher progesterone concentrations throughout pregnancy. As a result, the progesterone/estradiol ratio was greater in the high- versus the low-altitude women. Estradiol fell between weeks 30 and 36 in women who developed transient hypertension or preeclampsia. The fall in estradiol was accompanied by a marked increase in progesterone concentrations among the preeclamptic women. At 3100 m, estradiol correlated negatively (r = -0.37, P < .05) and progesterone positively (r = 0.46, P < .05) with mean arterial pressure at week 36 of pregnancy. CONCLUSIONS: We speculate that reduced placental oxygen pressure (PO2) at high altitude may decrease placental aromatase activity and thereby lower estradiol and estriol concentrations. The factor(s) responsible for the rise in progesterone is unknown. Possibly, high progesterone relative to estradiol concentrations contributes to the development of preeclampsia at high altitude.

Adult↗

High-altitude pulmonary hypertension: a pathophysiological entity to different diseases.

Pulmonary hypertension is a hallmark of high-altitude pulmonary oedema (HAPE) and of congestive right heart failure in subacute mountain sickness (SMS) and chronic mountain sickness (CMS) in the Himalayas and in the end-stage of CMS (Monge's disease) in the Andes. There are studies to suggest that transmission of excessively elevated pulmonary artery pressure and/or flow to the pulmonary capillaries leading to alveolar haemorrhage is the pathophysiological mechanism of HAPE. In the Himalayas, HAPE was successfully prevented by extending the acclimatisation period from a few days to 5 weeks, however, this did not prevent the occurrence of congestive right heart failure after several weeks of stay at 6,000 m. This leads to the concept that rapid remodelling of the small precapillary arteries prevents HAPE but not the development of right heart failure in SMS and CMS. Unresponsiveness of pulmonary hypertension to oxygen at high altitude and its complete resolution only after weeks of stay at low altitude suggest that structural rather than functional changes are its pathophysiological mechanism. Since pulmonary hypertension at high altitude is the driving force leading to high-altitude pulmonary oedema and "high-altitude right heart failure" in newcomers and residents of high altitude, the authors propose to adjust current terminology accordingly.

Altitude Sickness↗

Effects of altitude versus economic status on birth weight and body shape at birth.

The compelling evidence linking small size at birth with later cardiovascular disease has renewed and amplified a clinical and scientific interest in the determinants of fetal growth. Although the effects of maternal nutrition on fetal growth have been extensively studied, comparatively little is known about the effects of maternofetal hypoxia. This study tested the hypothesis that in highland regions, high altitude rather than maternal economic status is associated with reduced and altered fetal growth by investigating the effects of high altitude versus economic status on birth weight and body shape at birth in Bolivia. Bolivia is geographically and socioeconomically unique. It contains several highland (>3500 m above sea level) and lowland (<500 m) cities that are inhabited by very economically divergent populations. Birth weight, body length, and head circumference were compared between a high- (n = 100) and low- (n = 100) income region of La Paz (3649 m; largest high-altitude city) and a high- (n = 100) and low- (n = 100) income region of Santa Cruz (437 m; largest low-altitude city). In addition, the frequency distribution across the continuum of birth weights was plotted for babies born from high- and low-income families in La Paz and Santa Cruz. Mean birth weights were lower in babies from La Paz than in babies from Santa Cruz in both high- and low-income groups. The cumulative frequency curve across all compiled birth weights was shifted to the left in babies from La Paz compared with those from Santa Cruz, regardless of economic status. The frequency of low birth weight (<2500 g) was higher in babies from La Paz than from Santa Cruz in both high- and low-income groups. In addition, at high altitude but not at low altitude, high income was associated with an increase in the head circumference:birth weight ratio. These findings suggest that high altitude rather than economic status is associated with low birth weight and altered body shape at birth in babies from Bolivia.

Altitude↗