Journal of applied physiology: respiratory, environmental and exercise physiology (J Appl Physiol Respir Environ Exerc Physiol )

Publisher: American Physiological Society (1887- ), American Physical Society


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    Journal of applied physiology: respiratory, environmental and exercise physiology, JAP: Respiratory, environmental and exercise physiology, Respiratory, environmental and exercise physiology
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Publications in this journal

  • Journal of applied physiology: respiratory, environmental and exercise physiology 01/1986; 60:901-907.
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    ABSTRACT: We produced pulmonary fibrin microembolism using an infusion of a prothrombin activator (Echis carinatus venom, 30 min, 0.5 NIH thrombin equivalent units/kg) in open-chest mongrel dogs. To determine the nonclotting effects of this venom on edemagenesis we infused an irreversible thrombin inhibitor, D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone (PPACK, 57 nmol X kg-1 X min-1 for 120 min), alone (n = 5) or with venom (Echis + PPACK, n = 5). The control group (n = 5) was given 1 ml of 0.9% NaCl. A decline in left atrial pressure (means +/- SE, 5.3 +/- 0.4 to 4.0 +/- 0.5 mmHg, P less than 0.05) and cardiac index (149 +/- 10 to 82 +/- 13 ml X min-1 X kg-1, P less than 0.01) in association with a marked increase in pulmonary arterial pressure (14.5 +/- 0.6 to 26.6 +/- 2.5 mmHg, P less than 0.001) and pulmonary vascular resistance (64 +/- 5 to 304 +/- 42 mmHg X ml-1 X min-1 X kg-1, P less than 0.001) was observed after 20 min of venom infusion. During this interval, pulmonary artery wedge pressure increased (4 +/- 1 to 12 +/- 4 mmHg, P less than 0.01) in four of eight animals. Fibrinogen declined below measurable levels and fibrin microemboli were seen in many pulmonary arterioles. These changes were not observed in the Echis + PPACK, PPACK, or control groups. Leukopenia and thrombocytopenia were observed in the Echis and Echis + PPACK groups.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1824-8.
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    ABSTRACT: Female rats were exercised by swimming up to 4 h/day either 2, 4, or 6 days/wk. After 7 wk they continued to train at these frequencies or had their training reduced from 6 to 4, 2, or 0 days/wk for an additional 9 wk. Ventricular weights and maximum O2 uptake (VO2max) were increased by 5-10% after training 2 days/wk, 15-17% after 4 days/wk, and 25-30% after 6 days/wk. Following reduced training, VO2max was similar when the 4- or 2-day/wk reduced training groups are compared with their 4- or 2-day/wk continued training counterparts. In contrast, VO2max was greater in the 0-day reduced than in the sedentary control group. No differences in mitochondrial markers or myoglobin content in red or mixed skeletal muscles were found between training 2 or 4 days/wk vs. reduced training at comparable frequencies. O2 uptake capacity of plantaris muscles and myoglobin concentration in fast-twitch red vastus lateralis muscles were greater in the 0-day reduced group than in the sedentary controls. These data show that VO2max and certain markers of aerobic metabolism in skeletal muscles of rats are lost at a slower rate than their rate of increase from the untrained state. However, a reduction of swimming frequency from 6 to 4 or 2 days/wk is not a sufficient stimulus to maintain VO2max, cardiac enlargement, or the increased aerobic potential of skeletal muscle at the 6-day/wk levels.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1834-41.
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    ABSTRACT: To investigate the effect of different levels of central blood volume on cardiac performance during exercise, M-mode echocardiography was utilized to determine left ventricular size and performance during cycling exercise in the upright posture (UP), supine posture (SP), and head-out water immersion (WI). At submaximal work loads requiring a mean O2 consumption (Vo2) of 1.2 1/min and 1.5 1/min, mean left ventricular end-diastolic and end-systolic dimensions were significantly greater (P less than 0.05) with WI than UP. In the SP during exercise, left ventricular dimensions were intermediate between UP and WI. Heart rate did not differ significantly among the three conditions at rest and at submaximal exercise up to a mean Vo2 of 1.8 1/min. However, at a mean Vo2 of 2.4 1/min, heart rate in the UP was significantly greater than WI (P less than 0.01) and the SP (P less than 0.05). Maximal Vo2 did not differ statistically in the three conditions. These data indicate that a change in central blood volume results in alterations in left ventricular end-diastolic and end-systolic dimensions during moderate levels of exercise and a change in heart rate at heavy levels of exercise.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1662-7.
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    ABSTRACT: Changes in expired alveolar O2 and CO2 were measured breath-by-breath in six healthy male subjects (mean age 30 yr, mean weight 80 kg) at rest, 600 kpm/min, and 1,200 kpm/min. Changes were expressed in relation to expired volume (liters) and time (s) and separated into an initial dead-space component using the Fowler method applied to expired CO2 and O2, and alveolar slope. The alveolar slopes with respect to time (dPACO2, dPAO2, Torr/s) increased in relation to CO2 output (VCO2, 1/min, STPD) and O2 intake (VO2, 1/min, STPD) but were reduced by increasing tidal volume (VT, liters, BTPS): dPACO2 = 2.7 + 4.6(VCO2) - 1.9(VT) (r = 0.97); and dPAO2 = 2.3 + 5.5(VO2) - 1.9(VT) (r = 0.96). From the alveolar slopes, tidal volume, and airway dead-space volume, mean expired alveolar PO2 and PCO2 (PAO2, PACO2) were calculated. There was no change in arterialized capillary PCO2 (PaCO2) between rest (38.9 +/- 0.66 Torr) and heavy exercise (38.2 +/- 2.18 Torr), but mean PACO2 rose from 36.7 +/- 0.55 to 40.8 +/- 1.67 Torr during heavy exercise. There was no change in arterialized capillary (mean = 84.3 +/- 0.7 Torr) or alveolar (mean = 107.2 +/- 1.03 Torr) PO2. Exercise increases the fluctuations in alveolar gas composition leading to discrepancies between the PCO2 in mean alveolar gas and arterial blood to an extent that is dependent on VCO2 and VT.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1704-9.
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    ABSTRACT: Recording from pulmonary stretch receptors in the intact cervical vagus nerve revealed a novel interaction between stretch receptors and smooth muscle in the lungs of anesthetized paralyzed cats. Firing rates of pulmonary stretch receptors were modulated in step with the inflation-deflation cycle of the mechanical respirator, as expected. Firing rates of most slowly adapting receptors, but not rapidly adapting receptors, were also strongly modulated in step with the phrenic nerve activity even when the respirator was turned off and the cat motionless. The modulation of some receptors' firing rates by the inspiratory motor output was as great as the change in firing-rate in response to a lung inflation of 20 ml of air (one tidal volume). Atropine blocked the inspiratory-related modulation of slowly adapting/receptor firing rates; it did not block the inflation-related modulation. Pulmonary resistance was modulated in step with the inspiratory activity on the phrenic nerve. Hyperventilation to neural apnea (no phrenic nerve activity) reduced pulmonary resistance to its lowest level, a level equal to that produced by an injection of isoproterenol or atropine. Hypoxia during hypocapnic apnea caused bursts of inspiratory activity on the phrenic nerve accompanied by one-to-one increases in airway resistance. We conclude that the intrathoracic airway smooth muscle contracts with each neural inspiration, that the modulation of the pulmonary stretch receptors is due to a mechanical interaction with the intrathoracic airway smooth muscle, and that through the mechanical link with airway smooth muscle, stretch receptor sensitivity depends on inspiratory output, a closed loop.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1842-9.
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    ABSTRACT: Hypoxia causes severe disruption of both rapid-eye-movement (REM) and non-REM (NREM) sleep. Experiments were performed on rats to determine if hypoxic insomnia is mediated by peripheral chemoreceptors and if normal sleep is restored during acclimatization to low O2. Novel methods were devised to measure distribution of amplitudes of cortical slow waves during NREM sleep and to detect REM sleep from the ratio of amplitudes of theta-to delta-frequency bands in the hippocampal electroencephalogram (EEG). Acute exposure of rats to 10.5% O2 (5,030 m altitude equivalent) during daylight hours virtually abolished REM sleep and shifted the distribution of amplitudes of slow-wave sleep EEG toward awake values. Similar disruption of sleep occurred during inhalation of 0.05% CO with steady-state carboxyhemoglobin of approximately 35%. Respiratory rate and alveolar ventilation were greatly increased by 10.5% O2 but were unaffected by CO. Therefore, hypoxic disruption of sleep was not mediated by peripheral chemoreceptors regulating breathing. Partial recovery of sleep occurred after 1-2 wk of hypoxia, but both REM and NREM were still subnormal after 1 mo. Decreased intensity of NREM sleep during hypoxia, measured by amplitude of cortical slow waves, may explain the disparity between subjective complaints of insomnia at altitude and evaluations of sleep by direct observation or by conventional EEG. Loss of appetite, loss of weight, irritability, and other symptoms of altitude sickness may be related to hypoxic insomnia.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1696-703.
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    ABSTRACT: The response of colonic and tail-skin temperatures to treadmill exercise was assessed in female Sprague-Dawley rats using incremental and single-stage exercise protocols to investigate the relationship between deep body temperature and work rate. O2 uptake (VO2) was measured by flow-through technique to evaluate the exercise intensity. Experiments were performed in ambient temperatures below (22-25 degrees C) and above (33-35 degrees C) the thermoneutral zone of the rat. During graded incremental exercise there was a linear relationship between colonic temperature (Tco) and VO2 in both the cooler and warmer ambient temperatures. However, Tco and tail-skin temperature (Tsk) at comparable work rates in the cooler and warmer environments were 40.22 +/- 0.59, 34.84 +/- 1.10 degrees C and 42.04 +/- 0.57, 38.39 +/- 1.54 degrees C, indicating that the rise in Tco was unrelated to the severity of exercise. During single-stage exercise the rats were able to achieve thermal equilibrium but only at low work rates and in the cool environment (22-25 degrees C). There were no significant differences in Tco at the first three levels of single-stage exercise (stage 1, 39.63 +/- 0.34 degrees C; stage 2, 39.67 +/- 0.49 degrees C; stage 3, 39.75 +/- 0.50 degrees C) despite significant differences in VO2 (stage 1, 4.3 +/- 0.7 ml X min-1 X 100 g-1; stage 2, 5.3 +/- 0.6 ml X min X 100 g-1; stage 3, 7.6 +/- 1.2 ml X min-1 X 100 g-1). This demonstrates that there was no relationship between the level of Tco maintained during exercise and the work intensity.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1872-7.
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    ABSTRACT: Dogs with indwelling catheters in the jugular vein and in the carotid artery ran on the treadmill (slope: 15%, speed: 133 m/min). Lactate turnover and glucose turnover were measured using [U-14C]lactate and [3-3H]glucose as tracers, according to the primed constant-rate infusion method. In addition, the participation of plasma glucose in lactate production (Ra-L) was measured with [U-14C]glucose. Propranolol was given either (A) before exercise (250 micrograms/kg, iv) or (B) in form of a primed infusion administered to the dog running at a steady rate. Measurements of plasma propranolol concentration showed that in type A experiments plasma propranolol fell in 45 min below the lower limit of the complete beta-blockade. In the first 15 min of work Ra-L rose rapidly; then it fell below that of the control (exercise) values. During steady exercise, the elevated Ra-L was decreased by propranolol infusion close to resting values. beta-Blockade doubled the response of glucose production, utilization, and metabolic clearance rate to exercise. In exercising dogs approximately 40-50% of Ra-L arises from plasma glucose. This value was increased by the blockade to 85-90%. It is concluded that glycogenolysis in the working muscle has a dual control: 1) an intracellular control operating at the beginning of exercise, and 2) a hormonal control involving epinephrine and the beta-adrenergic receptors.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1754-9.
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    ABSTRACT: Previously we observed what appeared to be augmented D-glucose transport across the pulmonary epithelium. To investigate this phenomenon we placed fluid containing L-[3H]glucose and D-[U-14C]glucose in the alveoli of isolated Ringer-perfused lungs from 4-wk-old rabbits. The appearance of radioactivity in recirculating glucose-free perfusate was measured. 3H appearing in the perfusate was associated with L-glucose. 14C, however, was associated with three compounds, with approximate molecular weights of 180 (glucose), 300, and 560. The nonglucose species were not identified. This 14C movement was inhibited by phlorizin, but not phloretin, in the alveolar fluid. A similar pattern of 14C movement occurred when D-[U-14C]glucose was replaced with 2-deoxy-D-[U14C]-glucose, but not with methyl-alpha-D-[U-14C]glucopyranoside. The activation energy of the 14C metabolism-transport process was found to be 34 kcal/mol, and L-glucose transport showed an unusual temperature dependence, with maximum conductance at 15 degrees C. It appears that some D-glucose crosses the pulmonary epithelium as does L-glucose. However, most enters epithelial cells and is incorporated into larger molecules which enter the vascular but not the alveolar space.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1722-30.
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    ABSTRACT: The suitability of an isolated lung, perfused under carefully monitored conditions, for the study of the biosynthesis of glycosaminoglycans was examined for the rat lung using either [35S]-sulfate or [6-3H]glucosamine. Metabolic and electron-microscopic studies after 3 h of perfusion showed that under the conditions of this study the isolated lung showed no anatomical or metabolic derangements. All glycosaminoglycans normally synthesized in the intact lung were identified. The predominant glycosaminoglycan was heparan sulfate (40% of total). Approximately 14% of the glucosamine incorporated into the glycosaminoglycans was found in hyaluronic acid. Less than 5% of either label was in heparin. The remainder of the synthesized glycosaminoglycans, with the exception of 10% which could not be identified, consisted of the chondroitin sulfates and dermatan sulfate. The relative proportions of the newly synthesized glycosaminoglycans, including the low amounts of heparin, are similar to those found in isolation of endogenous lung glycosaminoglycans. The isolated perfused rat lung appears to be a useful model for the study of glycosaminoglycan biosynthesis by the intact lung.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1648-54.
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    ABSTRACT: In seven unanesthetized cats, radiolabeled microspheres were used to determine regional brain blood flow (rBBF) to the medulla-pons (M-P), midbrain-thalamus (M-T), cerebellum (Cb), and cortex (Cx) during three conditions: 1) control [arterial O2 tension (PaO2) = 81 Torr, arterial CO2 tension (PaCO2) = 26 Torr]; 2) hypocapnic hypoxia (PaO2 = 39 Torr, PaCO2 = 22 Torr); and 3) isocapnic hypoxia (PaO2 = 47 Torr, PaCO2 = 26 Torr). Hypoxia increased blood flow significantly more in the caudal brain stem (M-P) than in the Cx (P less than 0.05) during both hypocapnic hypoxia (M-P/Cx: +33/ +17 ml X min-1 X 100 g-1) and isocapnic hypoxia (M-P/Cx: +13/ -2 ml X min-1 X 100 g-1). Since sympathetic innervation is greater anatomically to rostral than to caudal vessels, we examined the rBBF response to hypocapnic hypoxia in seven additional cats after unilateral superior cervical gangliectomy. All seven cats had a reduction in the cortical-to-caudal brain stem trend on the denervated side of the brain (M-P/Cx: +27/+28 ml X min-1 X 100 g-1) compared with the intact side of the brain (M-P/Cx: +34/+24 ml X min-1 X 100 g-1) owing to both increases in Cx and decreases in M-P flows. We conclude that in unanesthetized cats hypoxia causes a greater increase in the caudal brain stem compared with cortical blood flow, and this differential response is related to modulation by the sympathetic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1803-8.
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    ABSTRACT: In rabbits exposed to 100% O2 at 1 ATA from 48 to 72 h, we measured the accumulation of intravenously injected 125I-bovine albumin, [57Co]cyanocobalamin, and 51Cr-erythrocytes in the intestine, skeletal muscle, heart, and lungs. From these data, we calculated the extravascular albumin and cyanocobalamin spaces (EVAS, EVECS) and the partition of water among vascular, interstitial, and cellular compartments in these organs. All variables remained at their base-line levels at 48 h in O2. At 64-66 h, the lung EVECS remained unchanged, but its EVAS increased by 210%. This change occurred after the previously documented increase of the alveolar epithelial permeability to solute and of the pulmonary conductance to water but before the appearance of pulmonary edema and arterial hypoxemia. The only change in the systemic circulation was a 17% increase of the heart EVAS. The increased heart and lung EVAS values, in the absence of any fluid volume shifts, are consistent with damage to the tissue polysaccharides of these organs by the toxic O2 species.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1767-72.
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    ABSTRACT: The hemodynamic and metabolic effects of exercise were measured in Crotalaria-induced pulmonary hypertension in rats. The Crotalaria group had increased preexercise heart rate, mean pulmonary arterial pressure (PAP), arteriovenous O2 content difference, right ventricular work index (RVWI), and total pulmonary vascular resistance index (TPVRI) and decreased mean systemic blood pressure (BP), arterial O2 content (CaO2), venous O2 content (CvO2), cardiac index (CI), stroke volume index (SVI), and left ventricular work index (LVWI). The Crotalaria group during exercise had increased PAP, RVWI, TPVRI, and total systemic vascular resistance index and decreased BP, O2 consumption, CaO2, CvO2, CI, SVI, LVWI, O2 pulse index, and exercise duration. It is hypothesized that abnormal right ventricular function was a primary factor in the reduced exercise tolerance of the Crotalaria group.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1829-33.
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    ABSTRACT: Thirty experiments were performed in two goats at an air temperature of +35 degrees C and a relative humidity of 33%. By means of heat exchangers, body core temperature (Tpaor) was adjusted to 39, 40.5, or 42 degrees C and maintained at these levels for 120 min. During the last 60 min the animals worked at a rate of 1.2 W/kg (treadmill, 3 km/h, 15%). Blood gases (arteriovenous O2 difference, Po2, Pco2), hemoglobin (Hb), blood lactate (LA), cardiac output (CO), blood pressure (MAP), heart rate (HR), metabolic rate (M), and respiratory evaporative heat loss (REHL) were determined. M, CO, HR, and Hb increased with exercise and were independent of Tpaor. At rest and exercise, REHL increased and Pco2 decreased at higher levels of Tpaor resulting in a respiratory alkalosis. During exercise this was accompanied by an increase in LA. At all instants, the concentrations of LA were higher at higher Tpaor. It is concluded that in a virtually nonsweating species like the goat the overall stress on the circulatory system caused by hyperthermia during exercise is relatively small while the behavior of blood LA is indicative of a temperature-dependent accumulation of LA also in the exercising muscle.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1655-61.
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    ABSTRACT: The position of small metallic markers embedded within the lung parenchyma and glued to the pleural surface of four excised right caudal dog lobes were determined during stepwise deflation from an airway opening pressure of 25 cmH2O in air-filled suspended lobes and 8 cmH2O in saline-filled lobes submerged in saline. Changes in the volumes of tetrahedrons formed by four noncoplanar markers were taken as regional lung volume changes at the centroids of the tetrahedron. In both air- and saline-filled lobes at all volumes below total lobe capacity (TLC) there was considerable variability in regional volume. The variability occurred at the first step below TLC and increased with deflation. Regions behaved consistently; regions that were proportionally larger or smaller than the overall lobe at any step tended to be larger or smaller, respectively, at all steps. There was a significant correlation between the regional behavior of the air- and saline-filled lobes. The variability of regional volume did not follow any clear topographical orientation. These results indicate there is considerable variability of lung compliance within small regions. This heterogeneity of regional parenchymal properties may be the anatomical basis of the nonuniformity of regional ventilation known to occur in intact animals and excised lobes within small regions at the same vertical height.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1710-4.
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    ABSTRACT: Specific airway conductance (sGaw) was measured during quiet breathing and during panting in 21 normal subjects and 10 patients with obstructive lung disease. The direct method used does not require measuring thoracic gas volume (TGV). Coefficients of variation were 5.5% for panting and 5.1% for quiet breathing. Interobserver variability was 4.7% in the quiet-breathing method and 6.3% in the panting method. The two methods gave equivalent results for sGaw. A slightly greater sGaw was found by the panting method in normal subjects with the highest sGaw values, probably due to widening of the oropharynx-glottis during panting. In six normal subjects studied for intrasubject variability over time, no significant diurnal or day-to-day variability was seen by either method. We conclude that the quiet-breathing method is a simple valid means of determining sGaw and utilizes a physiological respiratory maneuver. Obviation of the need to measure TGV is advantageous. Results are equivalent to those of the panting method and variability is similar.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1917-22.
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    ABSTRACT: Studies using tissue homogenates have demonstrated an increase in pulmonary beta-receptors during development. However, techniques using disrupted tissue have not permitted the precise anatomic localization of pulmonary beta-receptors or identification of structures where increases occur. Using L-[3H]dihydroalprenolol, beta-receptors were radioautographically localized and quantitated in sections of newborn (NB) and adult (A) guinea pig lung. Scatchard analysis showed a single class of binding sites with a maximum binding capacity of 189 +/- 3 (NB) and 305 +/- 37 (A) fmol X mg-1 protein (P less than 0.02). Binding was of high affinity with the dissociation constant (Kd) = 1.46 +/- 0.2 (NB) and 1.26 +/- 0.3 (A) nM (NS). The majority of beta-receptors were localized in alveolar wall and airway epithelia (alveolar much greater than bronchiolar greater than bronchial) (P less than 0.0001). Airway and vascular smooth muscle had significantly fewer demonstrable beta-receptors. The increased number of beta-receptors in the adult appeared to be due primarily to a 2.0 +/- 0.12-fold increase in alveolar wall and airway epithelia as opposed to only a 1.3 +/- 0.18-fold increase in the already low number in airway and vascular smooth muscle (P less than 0.05). While apparent receptor density may not necessarily correlate with physiological response or importance, radioautographic localization of pulmonary beta-receptors may significantly enhance our understanding of their role in normal and pathologic states.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1901-7.
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    ABSTRACT: This study 1) quantitates the effect of a 42.2-km footrace (marathon) on leg extensor strength (maximal peak torque, MPT) and work capacity (WC, measured during a leg extensor fatigue test), and 2) describes the effect of either a rest or exercise regimen for 1 wk after the marathon on the recovery of MPT and WC. Ten trained male runners performed personal records in a marathon and were then randomly assigned to either a rest or exercise-recovery group. The rest group did not train, whereas the exercise group ran 20-45 min/day at their selected intensity of exercise [50-60% maximal O2 consumption (Vo2max)] during the recovery week. MPT was measured at 1.1, 3.2, and 5.3 rad X s-1. The total work generated during a 50-contraction active extension-passive flexion fatigue test conducted at 3.2 rad X s-1 was defined as WC. Reports of perceived soreness of the quadriceps were obtained before each strength-testing session. These measurements were obtained before the marathon and 15-20 min and 1, 3, 5, and 7 days postmarathon. A significant reduction in MPT and WC resulted and continued 1 day postmarathon. MPT of both groups improved through day 5 postmarathon at 1.1 and 3.2 rad X s-1. MPT of the rest group improved through day 7 postmarathon but remained less than premarathon MPT. Recovery of MPT was impaired in the exercise group through days 5-7 postmarathon after 40-45 min exercise at 60% Vo2max. WC was recovered 3 days postmarathon in the rest group but was still impaired 7 days postmarathon in the exercise group.(ABSTRACT TRUNCATED AT 250 WORDS)
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1668-73.
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    ABSTRACT: With airways obstruction, panting frequency affects plethysmographically determined thoracic gas volume (Vtg) because the extrathoracic airway acts as a shunt capacitor. Stanescu et al. (19) suggested that in the calculation of Vtg, use of esophageal (delta Pes) rather than mouth pressure (delta Pm) swings might eliminate the problem. We measured total lung capacity (TLC) plethysmographically in 10 subjects with chronic airways obstruction (CAO) and in four normal subjects. TLC (using delta Pm) was derived from Vtg obtained from slow-(approximately 1 Hz) and fast- (approximately 4 Hz) panting frequencies. In the normal subjects and four subjects with CAO, TLC was also obtained using delta Pes. In these subjects abdominal gas compression and decompression did not contribute significantly to the frequency dependence of TLC. In CAO, TLC was frequency dependent in direct proportion to the severity of obstruction. Although the frequency dependence was greater using delta Pm to calculate Vtg, it also occurred using delta Pes. Thus it could not be explained entirely by the shunt capacitor effect of the extrathoracic airways. The residual and significant overestimations of TLC (reflected by frequency dependency of TLC derived from Vtg calculated from delta Pes) may be explained by interregional nonhomogeneities during the panting maneuver.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1865-71.

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