Biomedical subjects

A Cymerman

Publications and source records attributed to A Cymerman.

At least 55 records · Page 3Linked to original sources

PubMed1993

Hypoxic ventilatory responsiveness in Tibetan compared with Han residents of 3,658 m.

Lifelong high-altitude residents of North and South America acquire blunted hypoxic ventilatory responses and exhibit decreased ventilation compared with acclimatized newcomers. The ventilatory characteristics of Himalayan high-altitude residents are of interest in the light of their reportedly lower hemoglobin levels and legendary exercise performance. Until recently, Sherpas have been the only Himalayan population available for study. To determine whether Tibetans exhibited levels of ventilation and hypoxic ventilatory drives that were as great as acclimatized newcomers, we compared 27 lifelong Tibetan residents of Lhasa, Tibet, China (3,658 m) with 30 acclimatized Han ("Chinese") newcomers matched for age, body size, and extent of exercise training. During room air breathing, minute ventilation was greater in the Tibetan than in the Han young men because of an increased respiratory frequency, but arterial O2 saturation and end-tidal PCO2 did not differ, indicating similar levels of effective alveolar ventilation. The Tibetan subjects had higher hypoxic ventilatory response shape parameter A values and hypercapnic ventilatory responsiveness than the Han subjects. Among the Han subjects, duration of high-altitude residence correlated with the degree of blunting of the hypoxic ventilatory drive. Paradoxically, hyperoxia (inspired O2 fraction 0.70) increased minute ventilation and decreased end-tidal PCO2 in the Tibetan but not in the Han men. We concluded that lifelong Tibetan residents of high altitude neither hypoventilated nor exhibited blunted hypoxic ventilatory responses compared with acclimatized Han newcomers, suggesting that the effects of lifelong high-altitude residence on ventilation and ventilatory response to hypoxia differ in Tibetan compared with other high-altitude populations.

Adult↗

PubMed1993

Sea-level PCO2 relates to ventilatory acclimatization at 4,300 m.

There is considerable variation among individuals in the extent of, and the time required for, ventilatory acclimatization to altitude. Factors related to this variation are unclear. The present study tested whether interindividual variation in preascent ventilation or magnitude of hypoxic ventilatory response related to ventilatory acclimatization to altitude. Measurements in 37 healthy resting male subjects at sea level indicated a wide range (34-48 Torr) of end-tidal PCO2 values. When these subjects were taken to Pikes Peak, CO (4,300 m, barometric pressure 462 mmHg), the end-tidal PCO2 values measured on arrival and repeatedly over 19 days were correlated with the sea-level end-tidal PCO2. At 4,300 m, subjects with high end-tidal PCO2 had low values of arterial oxygen saturation (SaO2). Also, sea-level end-tidal PCO2 related to SaO2 after 19 days at 4,300 m. Twenty-six of the subjects had measurements of isocapnic hypoxic ventilatory response (HVR) at sea level. The end-tidal PCO2 values on arrival and after 19 days residence at 4,300 m were inversely related to the sea-level HVR values. Thus both the PCO2 and the HVR as measured at sea level related to the extent of subsequent ventilatory acclimatization (decrease in end-tidal PCO2) and the level of oxygenation at altitude. The finding in our cohort of subjects that sea-level end-tidal PCO2 was inversely related to HVR raised the possibility that among individuals the magnitude of the hypoxic drive to breathe influenced the amount of ventilation at all altitudes, including sea level.

Acclimatization↗

PubMed1993

Effects of altitude acclimatization on fluid regulatory hormone response to submaximal exercise.

To determine the effect of altitude acclimatization on plasma levels of atrial natriuretic peptide (ANP) during submaximal exercise and its relationship with renin and aldosterone, seven male volunteers aged 17-23 yr exercised to exhaustion on a cycle ergometer at 80-85% of their maximum O2 uptake at sea level (SL; 50 m), during 1 h in a hypobaric chamber [acute altitude (AA); 4,300 m], and after 14 or 16 days of residence on the summit of Pikes Peak, CO [chronic altitude (CA); 4,300 m]. Plasma samples taken before exercise, 10 min after the start of exercise, and 5 min postexercise were analyzed for ANP, plasma renin activity (PRA), and aldosterone (ALDO). ANP showed a progressive increase from rest to postexercise [7.49 +/- 1.63 to 11.32 +/- 1.80 (SE) pmol/ml and 6.05 +/- 2.55 to 10.38 +/- 7.20 pmol/ml; P = 0.049, exercise] at SL and AA, respectively, but not at CA (P = 0.039, altitude). Similarly, PRA and ALDO rose from rest to postexercise (P < 0.001, exercise), but the rise in ALDO with exercise was less during AA than during SL and CA (P = 0.002, phase). The decreased ANP levels during exercise after altitude acclimatization, with no change in PRA and ALDO, suggest that ANP has little effect on PRA and ALDO under these conditions.

Acclimatization↗

PubMed1993

Effects of simulated high altitude exposure on long-latency event-related brain potentials and performance.

The N100, P200, N200 and P300 components of the auditory event-related potential were recorded from 10 male subjects at 0900, 1600, and 1830 hours at sea level and again following a rapid ascent to simulated 4300 m altitude. Amplitude and latency of components, ear oximetry, and concurrent performance measures (reaction time and counting errors) were assessed. Amplitude of P300 decreased, while P300 latency and reaction time increased, following ascent to altitude. However, the time course of altitude effects differed for amplitude versus latency. Components N100, P200, N200, and counting errors were unaffected by altitude. The results indicate that central measures of cognitive capacities are differentially sensitive to high altitude. The time course of altitude effects on P300 amplitude versus P300 latency suggests that the two measures reflect different aspects of a response to hypobaric hypoxia exposure.

Adult↗

PubMed1993

Operation Everest II: gas tensions in expired air and arterial blood at extreme altitude.

Measurements in alveolar gas have suggested extreme hypocapnia and alkalosis on the summit of Mt. Everest. However, tensions in both expired gas and arterial blood have not been reported for the summit of Mt. Everest (PIO2 = 43 mm Hg). To approach the problem, we examined alveolar (and end-tidal) and arterial gas tensions in 6 healthy men who completed a 40-d chamber study to the simulated "summit," with 20 d above 6,400 m and 9 d above 8,000 m. In 27 simultaneous samples of alveolar air and arterial blood for inspired oxygen tensions ranging from PIO2 of 55 mm Hg (7,380 m) to 43 mm Hg, the mean alveolar-arterial difference was negligible for PO2 (-0.8 +/- 2.4 (S.D.) mm Hg) and PCO2 (0.5 +/- 1.4 mm Hg). For all 6 subjects at the summit, PACO2 was 12.0 +/- 1.8 and PACO2 was 11.4 +/- 1.6 mm Hg, and for the two with the lowest values, alveolar and arterial PCO2, respectively, were 9.5 and 9.8 mm Hg. Arterial pH averaged 7.53 units. We conclude that while acclimatization to severe hypoxia results in extreme hypocapnia, alkalosis is more moderate than previously reported. Alveolar gas tensions reflect well the values obtained in arterial blood.

Acclimatization↗

PubMed1992

Oxygen transport and cardiovascular function at extreme altitude: lessons from Operation Everest II.

Operation Everest II was designed to examine the physiological responses to gradual decompression simulating an ascent of Mt Everest (8,848 m) to an inspired PO2 of 43 mmHg. The principal studies conducted were cardiovascular, respiratory, muscular-skeletal and metabolic responses to exercise. Eight healthy males aged 21-31 years began the "ascent" and six successfully reached the "summit", where their resting arterial blood gases were PO2 = 30 mmHg and PCO2 = 11 mmHg, pH = 7.56. Their maximal oxygen uptake decreased from 3.98 +/- 0.2 L/min at sea level to 1.17 +/- 0.08 L/min at PIO2 43 mmHg. The principal factors responsible for oxygen transport from the atmosphere to tissues were (1) Alveolar ventilation--a four fold increase. (2) Diffusion from the alveolus to end capillary blood--unchanged. (3) Cardiac function (assessed by hemodynamics, echocardiography and electrocardiography)--normal--although maximum cardiac output and heart rate were reduced. (4) Oxygen extraction--maximal with PvO2 14.8 +/- 1 mmHg. With increasing altitude maximal blood and muscle lactate progressively declined although at any submaximal intensity blood and muscle lactate was higher at higher altitudes.

Adult↗

PubMed1992

Use of bioelectrical impedance to assess body composition changes at high altitude.

This study determined the feasibility of using bioelectrical impedance analysis (BIA) to assess body composition alterations associated with body weight (BW) loss at high altitude. The BIA method was also evaluated relative to anthropometric assessments. Height, BW, BIA, skinfold (SF, 6 sites), and circumference (CIR, 5 sites) measurements were obtained from 16 males (23-35 yr) before, during, and after 16 days of residence at 3,700-4,300 m. Hydrostatic weighings (HW) were performed pre- and postaltitude. Results of 13 previously derived prediction equations using various combinations of height, BW, age, BIA, SF, or CIR measurements as independent variables to predict fat-free mass (FFM), fat mass (FM), and percent body fat (%Fat) were compared with HW. Mean BW decreased from 84.74 to 78.84 kg (P less than 0.01). As determined by HW, FFM decreased by 2.44 kg (P less than 0.01), FM by 3.46 kg (P less than 0.01), and %Fat by 3.02% (P less than 0.01). The BIA and SF methods overestimated the loss in FFM and underestimated the losses in FM and %Fat (P less than 0.01). Only the equations utilizing the CIR measurements did not differ from HW values for changes in FFM, FM, and %Fat. It was concluded that the BIA and SF methods were not acceptable for assessing body composition changes at altitude.

Adult↗

PubMed1992

Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m.

We hypothesized that the increased blood glucose disappearance (Rd) observed during exercise and after acclimatization to high altitude (4,300 m) could be attributed to net glucose uptake (G) by the legs and that the increased arterial lactate concentration and rate of appearance (Ra) on arrival at altitude and subsequent decrease with acclimatization were caused by changes in net muscle lactate release (L). To evaluate these hypotheses, seven healthy males [23 +/- 2 (SE) yr, 72.2 +/- 1.6 kg], on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-D2]glucose (Brooks et al., J. Appl. Physiol. 70: 919-927, 1991) and [3-13C]lactate (Brooks et al., J. Appl. Physiol. 71:333-341, 1991) and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 uptake (65 +/- 2% of both acute altitude and acclimatization peak O2 uptake). Glucose and lactate arteriovenous differences across the legs and arms and leg blood flow were measured. Leg G increased during exercise compared with rest, at altitude compared with sea level, and after acclimatization. Leg G accounted for 27-36% of Rd at rest and essentially all glucose Rd during exercise. A shunting of the blood glucose flux to active muscle during exercise at altitude is indicated. With acute altitude exposure, at 5 min of exercise L was elevated compared with sea level or after acclimatization, but from 15 to 45 min of exercise the pattern and magnitude of L from the legs varied and followed neither the pattern nor the magnitude of responses in arterial lactate concentration or Ra. Leg L accounted for 6-65% of lactate Ra at rest and 17-63% during exercise, but the percent Ra from L was not affected by altitude. Tracer-measured lactate extraction by legs accounted for 10-25% of lactate Rd at rest and 31-83% during exercise. Arms released lactate under all conditions except during exercise with acute exposure to high altitude, when the arms consumed lactate. Both active and inactive muscle beds demonstrated simultaneous lactate extraction and release. We conclude that active skeletal muscle is the predominant site of glucose disposal during exercise and at high altitude but not the sole source of blood lactate during exercise at sea level or high altitude.

Acclimatization↗

PubMed1992

Operation Everest II: metabolic and hormonal responses to incremental exercise to exhaustion.

The reasons for the reduced exercise capacities observed at high altitudes are not completely known. Substrate availability or accumulations of lactate and ammonium could have significant roles. As part of Operation Everest II, peak oxygen uptakes were determined in five normal male volunteers with use of progressively increasing cycling work loads at ambient barometric pressures of 760, 380, and 282 Torr. Decrements from sea level (SL) to 380 and 282 Torr occurred in peak power output (19 and 47%), time to exhaustion (19 and 48%), and oxygen uptake (41 and 61%), respectively. Arterial saturations after exhaustive exercise were decreased to 63% at 380 Torr and 39% at 282 Torr. At 380 and 282 Torr, postexercise plasma concentrations of glucose and free fatty acids were not increased, whereas plasma glycerol concentrations were decreased relative to SL (145 +/- 24 microM at 380 Torr and 77 +/- 10 microM at 282 Torr vs. 213 +/- 24 microM at SL). Preexercise plasma insulin concentrations were elevated at both 380 and 282 Torr (87 +/- 16 pM at 380 Torr and 85 +/- 18 pM at 282 Torr vs. 41 +/- 30 pM at SL). In general, postexercise concentrations of plasma catecholamines were decreased at altitude compared with SL. Preexercise lactate and ammonium concentrations were not different at any simulated altitude. From these data neither substrate availability nor metabolic product accumulation limited exercise capacity at extreme simulated altitude.

Adult↗

PubMed1992

Operation Everest II: arterial oxygen saturation and sleep at extreme simulated altitude.

Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

Adult↗

PubMed1992

Effects of high altitude and exercise on marksmanship.

The effects of exercise and high altitude (3,700 m to 4,300 m) on marksmanship accuracy and sighting time were quantified in 16 experienced marksmen. Subjects dry-fired a disabled rifle equipped with a laser-based system from a free-standing position. The 2.3-cm circular target was at a distance of 5 m. Marksmanship was assessed under the following conditions: 1) at rest at sea level; 2) immediately after a 21-km run/walk ascent from 1,800 m to 4,300 m elevation; 3) at rest during days 1 to 3 at altitude; 4) at rest during days 14 to 16 at altitude; and 5) immediately after a second ascent after 17 d at altitude. Exercise reduced marksmanship accuracy (p less than 0.05) but did not affect sighting time. Acute altitude exposure reduced marksmanship accuracy, and decreased sighting time (p less than 0.05). However, after residence at altitude, accuracy and sighting time at rest returned to sea level values. Exercise and acute altitude exposure had similar but independent detrimental effects on marksmanship.

Adolescent↗

PubMed1991

Increased vital and total lung capacities in Tibetan compared to Han residents of Lhasa (3,658 m).

Larger chest dimensions and lung volumes have been reported for Andean high-altitude natives compared with sea-level residents and implicated in raising lung diffusing capacity. Studies conducted in Nepal suggested that lifelong Himalayan residents did not have enlarged chest dimensions. To determine if high-altitude Himalayans (Tibetans) had larger lung volumes than acclimatized newcomers (Han "Chinese"), we studied 38 Tibetan and 43 Han residents of Lhasa, Tibet Autonomous Region, China (elevation 3,658 m) matched for age, height, weight, and smoking history. The Tibetan compared with the Han subjects had a larger total lung capacity [6.80 +/- 0.19 (mean +/- SEM) vs 6.24 +/- 0.18 l BTPS, P less than 0.05], vital capacity (5.00 +/- 0.08 vs 4.51 +/- 0.10 1 BTPS, P less than 0.05), and tended to have a greater residual volume (1.86 +/- 0.12 vs 1.56 +/- 0.09 1 BTPS, P less than 0.06). Chest circumference was greater in the Tibetan than the Han subjects (85 +/- 1 vs 82 +/- 1 cm, P less than 0.05) and correlated with vital capacity in each group as well as in the two groups combined (r = 0.69, P less than 0.05). Han who had migrated to high altitude as children (less than or equal to 5 years old, n = 6) compared to Han adult migrants (greater than or equal to 18 years old, n = 26) were shorter but had similar lung volumes and capacities when normalized for body size. The Tibetans' vital capacity and total lung capacity in relation to body size were similar to values reported previously for lifelong residents of high altitude in South and North America. Thus, Tibetans, like North and South American high-altitude residents, have larger lung volumes. This may be important for raising lung diffusing capacity and preserving arterial oxygen saturation during exercise.

Adult↗

PubMed1991

Effect of beta-adrenergic blockade on plasma lactate concentration during exercise at high altitude.

When unacclimatized lowlanders exercise at high altitude, blood lactate concentration rises higher than at sea level, but lactate accumulation is attenuated after acclimatization. These responses could result from the effects of acute and chronic hypoxia on beta-adrenergic stimulation. In this investigation, the effects of beta-adrenergic blockade on blood lactate and other metabolites were studied in lowland residents during 30 min of steady-state exercise at sea level and on days 3, 8, and 20 of residence at 4300 m. Starting 3 days before ascent and through day 15 at high altitude, six men received propranolol (80 mg three times daily) and six received placebo. Plasma lactate accumulation was reduced in propranolol- but not placebo-treated subjects during exercise on day 3 at high altitude compared to sea-level exercise of the same percentage maximal oxygen uptake (VO2max). Plasma lactate accumulation exercise on day 20 at high altitude was reduced in both placebo- and propranolol-treated subjects compared to exercise of the same percentage VO2max performed at sea level. The blunted lactate accumulation during exercise on day 20 at high altitude was associated with reduced muscle glycogen utilization. Thus, increased plasma lactate accumulation in unacclimatized lowlanders exercising at high altitude appears to be due to increased beta-adrenergic stimulation. However, acclimatization-induced changes in muscle glycogen utilization and plasma lactate accumulation are not adaptations to chronically increased beta-adrenergic activity.

Adrenergic beta-Antagonists↗

PubMed1991

Operation Everest II: structural adaptations in skeletal muscle in response to extreme simulated altitude.

Alterations in skeletal muscle structure were investigated in 6 male subjects who underwent 40 days of progressive decompression in a hypobaric chamber simulating an ascent to the summit of Mount Everest. Needle biopsies were obtained from vastus lateralis of 5 subjects before and immediately after confinement in the chamber, and were examined for various structural and ultrastructural parameters. In addition, total muscle area was calculated in 6 subjects from CT scans of the thighs and upper arms. Muscle area at these sites was found to decrease significantly (by 13 and 15%) as a result of the hypobaric confinement. This was substantiated by significant (25%) decreases in cross sectional fibre areas of the Type I fibres and 26% decreases (non significant) in Type II fibre area. Capillary to fibre ratios remained unchanged following hypoxia as did capillary density although there was a trend (non significant) towards an increase in capillary density. There were no significant increases in mitochondrial volume density or other morphometric parameters. These data indicate that chronic, severe hypoxia on its own does not result in an increase in absolute muscle capillary number or a de novo synthesis of mitochondria. The trends toward an increase in capillary density and mitochondrial volume density were interpreted as being secondary occurrences in response to the pronounced muscle atrophy which occurred.

Acclimatization↗

PubMed1991

Doubly labeled water measurement of human energy expenditure during strenuous exercise.

The energy expenditures (EE) of 23 adult male Marines were measured during a strenuous 11-day cold-weather field exercise at 2,200- to 2,550-m elevation by both doubly labeled water (2H2 18O, DLW) and intake balance methods. The DLW EE calculations were corrected for changes in baseline isotopic abundances in a control group that did not receive 2H2 18O. Intake balance EE was estimated from the change in body energy stores and food intake. Body energy-store changes were calculated from anthropometric [-1,574 +/- 144 (SE) kcal/day] and isotope dilution (-1,872 +/- 293 kcal/day) measurements made before and after the field exercise. The subjects kept daily logbook records of ration consumption (3,132 +/- 165 kcal/day). Mean DLW EE (4,919 +/- 190 kcal/day) did not differ significantly from intake balance EE estimated from food intake and either anthropometric (4,705 +/- 181 kcal/day) or isotope dilution (5,004 +/- 240 kcal/day) estimates of the change in body energy stores. The DLW method can be used with at least the same degree of confidence as the intake balance method to measure the EE of active free-living humans.

Adult↗

PubMed1991

Hypobaric hypoxia (380 Torr) decreases intracellular and total body water in goats.

The effects of prolonged hypoxia on body water distribution was studied in four unanesthetized adult goats (Capra lircus) at sea level and after 16 days in a hypobaric chamber [(380 Torr, 5,500 m, 24 +/- 1 degrees C); arterial PO2 = 27 +/- 2 (SE) Torr]. Total body water (TBW), extracellular fluid volume (ECF), and plasma volume (PV) were determined with 3H2O, [14C]inulin, and indocyanine green dye, respectively. Blood volume (BV) [BV = 100PV/(100 - hematocrit)], erythrocyte volume (RCV) (RCV = BV - PV), and intracellular fluid (ICF) (ICF = TBW - ECF) and interstitial fluid (ISF) (ISF = ECF - PV) volumes were calculated. Hypoxia resulted in increased pulmonary ventilation and arterial pH and decreased arterial PCO2 and PO2 (P less than 0.05). In addition, body mass (-7.1%), TBW (-9.1%), and ICF volume (-14.4%) all decreased, whereas ECF (+11.7%) and ISF (+27.7%) volumes increased (P less than 0.05). The decrease in TBW accounted for 89% of the loss of body mass. Although PV decreased significantly (-15.3%), BV was unchanged because of an offsetting increase in RCV (+39.5%; P less than 0.05). We conclude that, in adult goats, prolonged hypobaric hypoxia results in decreases in TBW volume, ICF volume, and PV, with concomitant increases in ECF and ISF volumes.

Animals↗

PubMed1991

Internal carotid flow velocity with exercise before and after acclimatization to 4,300 m.

Cerebral blood flow and O2 delivery during exercise are important for well-being at altitude but have not been studied. We expected flow to increase on arrival at altitude and then to fall as O2 saturation and hemoglobin increased, thereby maintaining cerebral O2 delivery. We used Doppler ultrasound to measure internal carotid artery flow velocity at sea level and on Pikes Peak, CO (4,300 m). In an initial study (1987, n = 7 men) done to determine the effect of brief (5-min) exercises of increasing intensity, we found at sea level that velocity [24.8 +/- 1.4 (SE) cm/s rest] increased by 15 +/- 7, 30 +/- 6, and 22 +/- 8% for cycle exercises at 33, 71, and 96% of maximal O2 uptake, respectively. During acute hypobaric hypoxia in a decompression chamber (inspired PO2 = 83 Torr), velocity (23.2 +/- 1.4 cm/s rest) increased by 33 +/- 6, 20 +/- 5, and 17 +/- 9% for exercises at 45, 72, and 98% of maximal O2 uptake, respectively. After 18 days on Pikes Peak (inspired PO2 = 87 Torr), velocity (26.6 +/- 1.5 cm/s rest) did not increase with exercise. A subsequent study (1988, n = 7 men) of the effect of prolonged exercise (45 min at approximately 100 W) found at sea level that velocity (24.8 +/- 1.7 cm/s rest) increased by 22 +/- 6, 13 +/- 5, 17 +/- 4, and 12 +/- 3% at 5, 15, 30, and 45 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1991

Plasma changes in beta-endorphin to acute hypobaric hypoxia and high intensity exercise.

The purpose of this study was to examine the immediate post-exercise effects of acute exposure to a simulated altitude of 4,300 m on plasma concentrations of beta-endorphin (beta-EP) and associated changes of adrenocorticotropin (ACTH), and cortisol to high intensity cycle exercise (i.e., stages of 90 and 100% peak Vo2). Exercise intensities were assigned relative to peak O2 uptake both under sea level conditions and under acute hypobaric hypoxic conditions. Plasma beta-EP concentrations significantly increased from pre- to immediately post-exercise at both 90 and 100% peak Vo2 in both the sea level and acute hypobaric hypoxic trials. No associated exercise-induced changes were observed for ACTH or cortisol pre- to immediately post-exercise at either sea level or during hypoxic conditions. Exercise at acute hypobaric hypoxia elicited no significantly different responses in plasma beta-EP, ACTH, or cortisol than those elicited by the same relative exercise intensities under normobaric normoxic conditions. Additionally, no changes in the beta-EP/ACTH molar ratio for exercise or between conditions were observed. These data indicate that acute simulated high altitude exposure neither diminishes nor augments the physiological stimuli involved with high relative exercise intensity activation mechanisms of these hormones.

Adaptation, Physiological↗