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Biomedical subjects

P B Rock

Publications and source records attributed to P B Rock.

At least 19 recordsLinked to original sources
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↗
PubMed1991

Cardiocirculatory responses to upright tilt at sea level and high altitude.

A collaborative study was conducted to measure the cardiocirculatory responses to upright tilt in eight young men at sea level (SL); after 1h at 4300m simulated altitude (SA) and at 18h, 66h and 114h during residence at 4300m (HA). Heart rate (HR), stroke volume (SV), cardiac output (CO), calf blood flow (CBF), blood pressure (BP) and total peripheral resistance (TPR) were obtained during supine rest and after 13 min of 60 degrees head-up tilt using an impedance monitor and an electrosphygmomanometer. SL to HA changes in blood volume (BV) were calculated from hematocrit and hemoglobin values. Supine HR, TPR and BP were increased while SV, CO and CBP were reduced SL to HA (P less than .05). HR and BP in the upright position were increased SL to HA (P less than .05). The responses to tilt (delta supine to upright) were unaltered SL vs SA. With prolonged exposure, SV, CO, TPR and CBP responses to tilt were reduced (P less than .05). The reduced responses to tilt at HA were associated with a 10% decline in BV (P less than .01). It was concluded that the reduction in SV during tilt at SL and SA was compensated for by increases in HR and TPR in order to maintain BP. After 18h HA, BP in the upright position was maintained only by an increase in HR.

Adult↗
PubMed1991

Effects of dexamethasone and high terrestrial altitude on cognitive performance and affect.

This study examined the effects of dexamethasone and exposure to high terrestrial altitude on cognitive performance, affect, and personality. Cognitive performance was evaluated by five cognitive tasks, affect was evaluated by the Clyde Mood Scale and the Multiple Affect Adjective Check List, and personality was examined using the Minnesota Multiphasic Personality Inventory. Sixteen healthy young men received either dexamethasone (4 mg every 6 h) (n = 7) or placebo (n = 9) for 34 h prior to and 52 h after ascent to 4,300 m. Subjects treated with dexamethasone correctly performed more computer interaction and addition problems than did placebo-treated subjects. They also were less sleepy, dizzy, depressed, and anxious than placebo-treated subjects at altitude. No adverse effects on cognitive performance, affect, or personality were noted after dexamethasone was discontinued on the third day at altitude. Results indicate that dexamethasone at the present dose positively influences cognitive performance and mood states at altitude, but has no residual effect on personality.

Adult↗
PubMed1990

Symptomatology during hypoxic exposure to flame-retardant chamber atmospheres.

Hypoxia was studied in 12 men during 63-h exposures to 17 and 13% O2, with the subjects serving as their own controls by repeating the measurements in 21% O2. All test atmospheres were contaminated with 0.9% CO2 to simulate the condition of living aboard submarines. The mean SaO2's were 97-98% in all conditions of 21% O2, 96% in 17% O2 (n.s.), and 92% in 13% O2 (P less than 0.05). The blood concentrations of 2,3-diphosphoglycerate were elevated in 13 and 17% O2 (P less than 0.05). Seventeen percent O2 did not cause significant symptoms of environmental stress; however, 13% O2 caused symptoms of acute mountain sickness in 5 of 12 men. In the last 7 h of exposure to 17% O2, reduction of the barometric pressure to 576 Torr reduced the ambient PO2 to 98 Torr (similar to the PO2 of 13% O2 at normobaric pressure). This induced symptoms of acute mountain sickness in 3 of 11 men. All symptomatology and physiologic changes were reversed during recovery in 21% O2. Monitoring devices indicated the presence of volatile organic contaminants at a mean concentration of 6.1 ppm in the chamber atmosphere. Combustion tests in the occupied chamber showed that flame propagation was retarded by lowering the O2 concentration from 21 to 13-17%. We conclude that men can live comfortably in a normobaric, flame-retardant atmosphere consisting of 17% O2-0.9% CO2-6.1 ppm volatile organic compounds-balance N2.

2,3-Diphosphoglycerate↗
PubMed1990

The use of tympanometry to detect aerotitis media in hypobaric chamber operations.

Diagnosis and quantification of aerotitis media were performed using a modified commercially-available tympanometer under hypobaric conditions. Subjects were 22 males and 9 females, 22-43 years of age, who were tested in each ear with the tympanometer prior to and after exposure, sequentially at the barometric pressure plateaus of 706, 656, 609, 586, 564, and 522 mm Hg, and following an induced ear block during a 1-min descent from 522 to 586 mm Hg. Each subject was examined once either alone or in pairs during a 90-min exposure. Aerotitis media was detected using tympanometry at simulated altitude as evidenced by the difference between measurements made during induced ear blocks and those made prior to inducement, as well as following relief of the pressure differential with the Valsalva maneuver. There were no significant differences between pre- and post-induced aerotitis media values at 586 mm Hg, or between pre- and post-hypobaria. Our study suggests that tympanometry can be a valuable tool in managing aerotitis media in the aeromedical environment.

Acoustic Impedance Tests↗
PubMed1989

Atropine-induced cutaneous vasodilation decreases esophageal temperature during exercise.

Four healthy adult males volunteered for this study, which followed informed-consent procedures administered by our local Human Use Committee. Esophageal (Tes) and mean skin (Tsk, eight site) temperatures, forearm sweating rate (ms), metabolism (M), heart rate (HR), and forearm blood flow (FBF) were measured at rest and during forearm blood flow (FBF) were measured at rest and during exercise [55% oxygen consumption (Vo2) peak] during control experiments and after 2 mg im atropine (ATR). Experiments were randomized and separated by at least 72 h. ATR increased heart rate at rest by 15 beats/min and during exercise by 24 beats/min. ATR decreased whole body sweating by 57%. All eight local skin temperatures were higher in ATR than in control. Tsk was 32.6 degrees C in ATR and 31.0 degrees C in control (P less than 0.01). During exercise, ATR increased vasodilation of the forearm compared with control. The slope of FBF to Tes increased over 300% in ATR experiments compared with control (P less than 0.05). The higher sensible heat flux from this vasodilation decreased Tes during exercise, which further decreased sweating. Skin blood flow remained elevated as Tes decreased, suggesting that local vasodilatory factors promoted atropine-induced cutaneous vasodilation.

Adult↗
PubMed1989

Operation Everest II: maximal oxygen uptake at extreme altitude.

Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188-1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1-15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.

Adult↗
PubMed1989

Operation Everest II: comparison of four instruments for measuring blood O2 saturation.

The bias and precision of four different methods for determining O2 saturation (SO2) were evaluated during a study of hypobaric hypoxia conducted with seven male subjects exposed progressively over a 40-day period to simulated altitudes from sea level (760 Torr) to 8,840 m (240 Torr). SO2 of arterial and mixed venous blood samples were measured with the Instrumentation Laboratory 282 CO-oximeter (CO-OX), the Radiometer ABL-300 (ABL), and the Lex-O2-Con-K (LEX). Noninvasive measurements of arterial SO2 were made with a Hewlett-Packard 47201A ear oximeter (EAR-OX). The CO-OX method was used as a secondary standard for comparison with the other methods because it has been validated against the classical Van Slyke method over a wide physiological range (Maas et al., Clin. Chim. Acta 29: 303-309, 1970). The LEX results most closely approximated but consistently underestimated those of the CO-OX: LEX = 0.93 CO-OX -0.86, standard error of the estimate (SEE) = 5.17, r = 0.98, n = 670. The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486. The EAR-OX results were found to approximate those of the CO-OX at SO2 values only greater than 65%: EAR-OX = 1.07 CO-OX -6.12, SEE = 7.71, r = 0.98, n = 326.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Dexamethasone as prophylaxis for acute mountain sickness. Effect of dose level.

Rapid exposure of unacclimatized persons to high altitude causes the syndrome acute mountain sickness (AMS). Prophylactic treatment with frequent high doses of dexamethasone has been shown to prevent AMS. To determine whether lower, less frequent doses were effective in preventing AMS, 28 men between the ages of 18 and 32 were exposed to a simulated altitude of 4,570 m for 45 h in a hypobaric chamber on two occasions while taking one of three doses of dexamethasone (4 mg, 1 mg, or .25 mg every 12 h) or a placebo in a double-blind, crossover design. The 4-mg dose of dexamethasone reduced the incidence of AMS symptoms compared with placebo and the other dose levels. Dexamethasone did not alter fluid balance or plasma volume changes, but treatment with 1 mg and 4 mg suppressed cortisol secretion. There was no evidence of adrenal cortical suppression after treatment with dexamethasone or placebo 48 h after discontinuing altitude exposure and drug treatment. The results indicate that 4 mg of dexamethasone twice daily is an effective prophylactic treatment for AMS, while lower doses are relatively ineffective.

Adolescent↗
PubMed1989

Effects of propranolol on acute mountain sickness (AMS) and well-being at 4,300 meters of altitude.

A number of physiological responses and adjustments occur at high altitude to compensate for hypoxia. We hypothesized that interference with one component of the normal compensatory process, the sympathetic nervous system, would hinder altitude acclimatization and thereby exacerbate acute mountain sickness (AMS) and compromise well-being. Twelve young males (21.2 +/- 0.4 years) received either 80 mg propranolol (PRO; n = 6) or placebo (PLA; n = 6), t.i.d. at sea level (SL) and during the first 15 d of a 19-d residence at 4,300 m (HA). Individuals were randomly assigned to each group. The Environmental Symptoms Questionnaire (ESQ) was administered at SL and twice daily (AM and PM) during the entire altitude exposure in order to assess AMS symptoms and subjective feelings of well-being. Supine heart rate (HR) was determined at rest twice at SL and four times at HA. HR in the PLA group increased 40% over SL values (57 +/- 3 to 80 +/- 4 beats/min) by day 7 at HA (p less than 0.01). HR in the PRO group did not increase above SL values during medication at HA. By 4 d after the medication administration was terminated, HR in the PRO group had increased and did not differ from the PLA group. Throughout the entire altitude exposure, ESQ scores for the PRO group were lower than or similar to the PLA group. Furthermore, cessation of PRO treatment did not result in a change in well-being. These findings suggested that interference with the normal acclimatization process by beta-adrenergic blockade did not exacerbate AMS or reduce feelings of well-being.

Acute Disease↗
PubMed1989

Propranolol and the compensatory circulatory responses to orthostasis at high altitude.

Tachycardia has been shown to be an important response involved in the maintenance of cardiac output during orthostasis at high altitude. This study was undertaken to determine if tachycardia, mediated by beta-adrenergic sympathetic stimulation, actually represents an essential response. Twelve young, healthy male subjects were administered either 80 mg propranolol (n = 6) or placebo (n = 6), t.i.d. at sea level and for 3 days (d) prior to and during the first 15 d of a 19-d altitude sojourn (On Treatment). Individuals were randomly assigned to each group. Upright tilt tests were performed at sea level and at high altitude during days 2, 7, and 15 On Treatment. Subjects were also tilt-tested at sea level and on day 19 of the altitude exposure without placebo or propranolol administration (Off Treatment). Heart rate, stroke volume, calf blood flow, and blood pressure were obtained during supine rest and after 12 min of 60 degrees tilt. We found no differences between groups in any of the circulatory measurements at sea level and altitude while Off Treatment. During the On Treatment phases at sea level and altitude, propranolol caused reductions in heart rate and blood pressure values in each position (p less than 0.05). Supine and upright cardiac output, however, were found not altered due to compensatory increases in stroke volume (p less than 0.05). We concluded that tachycardia, both at rest and during upright tilt at high altitude is important, but not essential to maintain cardiac output.

Adult↗
PubMed1988

Responses of plasma human atrial natriuretic factor to high intensity submaximal exercise in the heat.

No data exists regarding responses of human atrial natriuretic factor (ANF) to exercise in the heat. The purpose of this study was to examine the responses of plasma ANF to high intensity submaximal (71% +/- 0.9 VO2max) exercise in the heat over an eight day acclimation period. Fourteen healthy males volunteered to participate in the study. Subjects performed intermittent exercises on a treadmill (0% grade) during 50 min of each 100 min trial in an environmental chamber maintained at 41.2 +/- 0.5 degrees C, 39.0 +/- 1.7% relative humidity. Blood was obtained from an antecubital vein after standing 20 min in the heat prior to exercise, and immediately after exercise. Measures were compared on days 1, 4 and 8. ANF did not change pre- to post-exercise nor did it change over the eight day heat acclimation period despite other heat acclimation adaptations. Conversely, plasma aldosterone (ALDO), renin activity (PRA) and cortisol (COR) all increased (p less than 0.05) pre- to post-exercise on each day but again no changes were observed over the eight day period. These data support that ANF may not increase when ALDO and PRA increases are observed.

Acclimatization↗
PubMed1988

Maximal cardiorespiratory responses to one- and two-legged cycling during acute and long-term exposure to 4300 meters altitude.

During exposure to altitudes greater than about 2200 m, maximal oxygen uptake (VO2max) is immediately diminished in proportion to the reduction in the partial pressure of oxygen in the inspired air. If the exposure lasts longer than a couple of days, an increase in arterial oxygen content (CaO2), due to a hemoconcentration and an increase in arterial oxygen saturation, occurs. However, there is also a reduction in maximal cardiac output (Qmax) at altitude which offsets the increase in CaO2 and, therefore, VO2max does not improve. The purpose of this investigation was to study the contribution of the increase in CaO2 to the working muscles without the potentially confounding problem of a reduced Qmax. The approach used was to have seven male subjects (aged 17 to 24 years) perform one- and two-legged VO2max tests on a cycle ergometer at sea level (SL, PIO2 = 159 Torr), after 1 h at 4300 m simulated altitude (SA, PIO2 = 94 Torr) and during two weeks of residence on the summit of Pikes Peak, CO. (PP, 4300 m, PIO2 = 94 Torr). Cardiac output limits maximal performance during two-legged cycling but does not limit performance during one-legged cycling. During the study, CaO2 changed from 189 +/- 3 (mean +/- SE) at SL to 161 +/- 4 ml.L-1 during SA (SL vs. SA, p less than 0.01) and to 200 +/- 6 ml.L-1 at PP (SL vs. PP, p less than 0.05; SA vs. PP, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Operation Everest II: oxygen transport during exercise at extreme simulated altitude.

A decrease in maximal O2 uptake has been demonstrated with increasing altitude. However, direct measurements of individual links in the O2 transport chain at extreme altitude have not been obtained previously. In this study we examined eight healthy males, aged 21-31 yr, at rest and during steady-state exercise at sea level and the following inspired O2 pressures (PIO2): 80, 63, 49, and 43 Torr, during a 40-day simulated ascent of Mt. Everest. The subjects exercised on a cycle ergometer, and heart rate was recorded by an electrocardiograph; ventilation, O2 uptake, and CO2 output were measured by open circuit. Arterial and mixed venous blood samples were collected from indwelling radial or brachial and pulmonary arterial catheters for analysis of blood gases, O2 saturation and content, and lactate. As PIO2 decreased, maximal O2 uptake decreased from 3.98 +/- 0.20 l/min at sea level to 1.17 +/- 0.08 l/min at PIO2 43 Torr. This was associated with profound hypoxemia and hypocapnia; at 60 W of exercise at PIO2 43 Torr, arterial PO2 = 28 +/- 1 Torr and PCO2 = 11 +/- 1 Torr, with a marked reduction in mixed venous PO2 [14.8 +/- 1 (SE) Torr]. Considering the major factors responsible for transfer of O2 from the atmosphere to the tissues, the most important adaptations occurred in ventilation where a fourfold increase in alveolar ventilation was observed. Diffusion from alveolus to end-capillary blood was unchanged with altitude. The mass circulatory transport of O2 to the tissue capillaries was also unaffected by altitude except at PIO2 43 Torr where cardiac output was increased for a given O2 uptake. Diffusion from the capillary to the tissue mitochondria, reflected by mixed venous PO2, was also increased with altitude. With increasing altitude, blood lactate was progressively reduced at maximal exercise, whereas at any absolute and relative submaximal work load, blood lactate was higher. These findings suggest that although glycogenolysis may be accentuated at low work loads, it may not be maximally activated at exhaustion.

2,3-Diphosphoglycerate↗
PubMed1988

Hemodynamic and sympathoadrenal responses to altitude in humans: effect of dexamethasone.

Altitude exposure alters hemodynamics and sympathoadrenal function and elicits acute mountain sickness (AMS). Since dexamethasone prevents AMS and influences responsiveness to catecholamines, we studied hemodynamic and sympathoadrenal responses to 4,570 m simulated altitude in 8 subjects treated with dexamethasone or placebo. Mean pulse rates were less at altitude with dexamethasone (96.1 for placebo and 84.1 for dexamethasone; treatment-altitude interaction, p = 0.0045). Altitude led to a postural decline in mean arterial pressure (posture-altitude interaction, p = 0.0026), but this was not affected by dexamethasone. Dexamethasone reduced urinary epinephrine to a greater extent during altitude exposure (from 9.41 ng.mg-1 creatinine with placebo to 4.16 with dexamethasone) when compared with sea level (from 3.24 to 3.08). Urinary excretion of norepinephrine was unchanged at altitude. We conclude that acute altitude exposure is associated with stimulation of the adrenal medulla and not the sympathetic nervous system. Dexamethasone blocks the adrenal medullary response and blunts the pulse rate increase at altitude.

Adrenal Medulla↗
PubMed1987

Propranolol blocks metabolic rate increase but not ventilatory acclimatization to 4300 m.

Previously, we found resting metabolic rate increased at high altitude but the mechanism and consequences of this increase were unclear. We sought to test the role of beta-sympathetic activation for increasing metabolic rate and the contribution of an increase in metabolic rate to raising total ventilation at altitude. Following baseline studies at sea level, two groups of six healthy male subjects received either placebo or propranolol (80 mg/8 h) for 3 days prior to ascent to Pikes Peak (4300 m) where treatment was continued for 15 days. O2 consumption increased in placebo-treated subjects with a rise of 20 +/- 5% (X +/- SEM) on day 1 and no change 0 +/- 7% in propranolol-treated subjects (difference between groups, P less than 0.05). The increase in total ventilation upon ascent was 28 +/- 2% in the placebo group vs 9 +/- 7% in the propranolol group (P less than 0.05) and was correlated with metabolic rate in individual subjects. Decreasing end-tidal PCO2, taken as an index of ventilatory acclimatization, was similar in both groups. Thus, beta-sympathetic activation appears to increase metabolic rate upon ascent to high altitude and lead to a proportionate elevation in total ventilation but does not alter ventilatory acclimatization.

Acclimatization↗
PubMed1987

Oxygen transport during exercise at extreme altitude: Operation Everest II.

Eight male volunteers had rest and exercise measurement to determine the mechanisms of oxygen transport during a 40-day chamber decompression simulating high-altitude exposure equivalent to the summit of Mt Everest. Five subjects completing the study decreased their maximum oxygen uptake by 72%. During maximal or near-maximal exercise, arterial PCO2 fell as low as 8 mm Hg, defending the alveolar PO2 and confirming marked hyperventilation. Alveolar-arterial diffusion did not improve and V/Q worsened. Cardiac function was unimpaired. Circulatory oxygen transport resembled that at sea level. The decrease in mixed venous PO2 was not enough to preserve fractional oxygen utilization "on the summit." The PO2 gradients from atmosphere to alveolus, alveolus to arterial blood, arterial to venous blood, and from venous (capillary) blood to mitochondria all decreased. However, hyperventilation appeared to be the primary adaptation that defended the maximum oxygen uptake.

Adult↗