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

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

Current impact factor: 3.06

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.056

Additional details

5-year impact 3.77
Cited half-life >10.0
Immediacy index 0.69
Eigenfactor 0.04
Article influence 1.15
Other titles Journal of applied physiology: respiratory, environmental and exercise physiology, JAP: Respiratory, environmental and exercise physiology, Respiratory, environmental and exercise physiology
ISSN 0161-7567
OCLC 3474500
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Physiological Society

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    • Publisher last reviewed on 03/06/2015
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Publications in this journal

  • Journal of applied physiology: respiratory, environmental and exercise physiology 01/1993; 74(2):888-896.

  • Journal of applied physiology: respiratory, environmental and exercise physiology 01/1986; 60(1):209-215.

  • Journal of applied physiology: respiratory, environmental and exercise physiology 01/1986; 60:901-907.
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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: 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: 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: 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: To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1688-95.
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    ABSTRACT: The total deposition of monodisperse, 0.026-0.19 micron (dry volume equivalent diameter) sodium chloride particles in the lungs of five healthy subjects, who breathed orally, was measured. For a tidal volume of 1,000 ml and flow rate of 500 ml/s, the percentages deposited were: 37.2 +/- 8.4% (mean +/- SD) for 0.026 micron, 23.8 +/- 3.3% for 0.051 micron, 22.8 +/- 3.1% for 0.096 micron, and 31.8 +/- 6.2% for 0.19 micron particles. The deposition minimum corresponded to a particle size of approximately 0.08 micron. Deposition did not correlate with measures of lung volume or body size but did correlate with forced expired flow rate after 75% of forced vital capacity (FVC) exhaled (FEF 75%/FVC) and with percent-predicted values for FEF 25-75% and FEF 75%. Lengthening the breathing period from 4 to 8 s/breath while maintaining flow rate at 500 ml/s caused an additional 11.3 +/- 3.1% of the inhaled particles to deposit. Sedimentation and diffusion were found to be the principal deposition mechanisms. These hygroscopic particles deposited according to sizes they would attain in air with a relative humidity between 96 and 100%.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1850-6.
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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: Eight well-trained male rowers exercised as hard as possible on a bicycle ergometer for 60 min at an ambient temperature of 18 degrees C. On 1 day (precooling test, PRET) exercise was preceded by a double cold exposure that caused starting body temperatures to be approximately 4.5, 1.0, 0.8, and 0.4 degrees C (mean skin, mean body, tympanic, and esophageal temperatures, respectively) lower than in the control test (CONT). In PRET the mean 1-h work rate (172 W) was 6.8% larger than in CONT (161 W), O2 uptake (Vo2) was 9.6% higher (2.86 vs. 2.61 1 X min-1), and O2 pulse was increased by 5.6% (18.8 vs. 17.8 ml), whereas the sweat rate was 20.3% lower in PRET (1.06 vs. 1.33 mg X cm-2.min-1). No differences in heart rate, efficiency, postexercise blood values of lactate, or acid-base status were demonstrated. It appears that the improved performance in PRET was related to an increased O2 supply to the working muscles. Although plasma levels of total beta H-endorphin immunoreactivity were in the same range under both test conditions, different components of beta H-endorphin immunoreactivity were indicated to exist in PRET and CONT.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1731-7.
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    ABSTRACT: To determine whether a portable sodium iodide (NaI) probe could provide a valid measure of the pulmonary half-life (T1/2) of aerosolized technetium-99m-diethylenetriaminepentaacetate (99mTc-DTPA, mol wt = 492) in small chests, we measured pulmonary clearance in rabbits using a gamma-scintillation camera and the portable probe. In 10 experiments the lungs of New Zealand White rabbits were insufflated with aerosolized 99mTc-DTPA (0.6 mum aerodynamic mass median diameter) and then simultaneously imaged with the gamma-camera and the probe positioned over the upper right lung. In an additional 12 experiments, alveolar-capillary membrane permeability was increased by either intratracheal instillation of 0.1 N hydrochloric acid (HCl) or intravenous injection of 100 mg/kg of oleic acid. All animals tolerated the procedure. There was a significant decrease in pulmonary T1/2 in both the HCl group (53.4 +/- 10.4 min, mean +/- SE) and the oleic acid group (14.7 +/- 2.3 min) when compared with control (127.5 +/- 18.1 min). When we compared the T 1/2 of the right lung determined by the gamma-camera with that measured by the probe, the correlation coefficient was 0.95. Potential nonpulmonary contributions to thoracic radioactivity were not significant. We conclude that a portable NaI probe is a valid means of determining T 1/2 of 99mTc-DTPA in small chests when compared with a gamma-camera and can detect increases in the permeability of the alveolar-capillary membrane to small solutes.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1908-12.
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    ABSTRACT: An apparatus and method for rearing neonatal rabbits in hypoxia is described. This technique relies on the use of hypoxia chambers that need to be serviced once a day for approximately 1 h. By use of the apparatus and procedures outlined, rabbits that exhibit standard clinical signs of hypoxemia (cyanosis and elevated hematocrit) can be reliably reared and maintained for long periods of time.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1913-6.
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    ABSTRACT: We looked for evidence of changes in lung elastic recoil and of inspiratory muscle fatigue at maximal exercise in seven normal subjects. Esophageal pressure, flow, and volume were measured during spontaneous breathing at increasing levels of cycle exercise to maximum. Total lung capacity (TLC) was determined at rest and immediately before exercise termination using a N2-washout technique. Maximal inspiratory pressure and inspiratory capacity were measured at 1-min intervals. The time course of instantaneous dynamic pressure of respiratory muscles (Pmus) was calculated for the spontaneous breaths immediately preceding exercise termination. TLC volume and lung elastic recoil at TLC were the same at the end of exercise as at rest. Maximum static inspiratory pressures at exercise termination were not reduced. However, mean Pmus of spontaneous breaths at end exercise exceeded 15% of maximum inspiratory pressure in five of the subjects. We conclude that lung elastic recoil is unchanged even at maximal exercise and that, while inspiratory muscles operate within a potentially fatiguing range, the high levels of ventilation observed during maximal exercise are not maintained for a sufficient time to result in mechanical fatigue.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1773-82.
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    ABSTRACT: The objective of this study was to determine whether changes in limb motion per se influence arterial CO2 partial pressure (PaCO2) during muscular exercise in ponies. Fifteen ponies were studied at rest and during 8 min of treadmill exercise when the work load was constant or when the work load was increased after the 4th min. Five different treadmill settings were selected to provide for a range of metabolic rate achieved with primary changes in either speed or grade (1.8 mph at 3, 8, and 15% grade; or 3 and 6 mph at 3% grade). The ponies exercised either on all four legs or on only the hindlegs. Step frequencies were 49, 66, and 99 at 1.8, 3, and 6 mph, respectively. During all work tasks PaCO2 decreased maximally 30-60 s after the work task was initiated from rest or from a less intense level of exercise. This nadir in PaCO2 was followed by some recovery with a stable level of mild hypocapnia (delta PaCO2) maintained after 3-4 min. The delta PaCO2 was directly related to O2 consumption (VO2) (P less than 0.01). The delta PaCO2-VO2 regression slopes did not differ between speed and grade VO2 changes nor between four- and two-legged exercise (P greater than 0.10). These data suggest that neither frequency of limb movement nor the number of limbs moving are major factors in the PaCO2 (and alveolar ventilation) response to exercise in ponies. We conclude that the apparent difference in PaCO2 regulation during exercise between ponies (hypocapnia) and humans (isocapnia during walking and bicycling) is not related to a species difference in the number of limbs employed in the exercise task.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1885-93.
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    ABSTRACT: Pulmonary surfactant research is considered from the perspective of interdisciplinary correlations based on information acquired from biophysics and physical chemistry, biochemistry, cell biology, physiology, and medicine. Current views of the important molecular constituents of the pulmonary surfactant system are described and related to the biophysical surface properties necessary to generate appropriate effects on respiratory physiology. The fundamental importance of multidisciplinary characterizations of lung surfactant, together with correlations between these descriptions, is stressed throughout. The primary advantage of such an approach is that it provides broad but coordinated principles and data with which to test hypotheses of lung surfactant function and roles in respiratory physiology and pathophysiology. This perspective is used to examine available information about the functional composition of lung surfactant, its surface tension-lowering properties at physiological temperature and humidity, and considerations relevant to the formulation of effective exogenous surface-active mixtures in the treatment of surfactant-deficient states. Also discussed is the biophysical state in vivo of pulmonary surfactant at the alveolar level, including current knowledge of the alveolar hypophase as well as the concept of functional surfactant acting in predominantly dry alveoli in the normal lung.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1613-24.
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    ABSTRACT: Because of its potential relevance to heavy exercise we studied the ventilatory muscle function of five normal subjects before, during, and after shortterm near-maximal voluntary normocapnic hyperpnea. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made at four levels of ventilation: 76, 79, and 86% maximal voluntary ventilation (MVV) and at MVV. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made. The pressure-stimulation frequency relationship of the diaphragm obtained by unilateral transcutaneous phrenic nerve stimulation was studied in two subjects before and after hyperpnea. Decreases in maximal inspiratory (PImax) and transdiaphragmatic (Pdimax) strength were recorded posthyperpnea at 76 and 79% MVV. Decreases in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm EMG occurred in association with decreases in Pdimax. Analysis of the pressure-time product (P X dt) for the inspiratory and expiratory muscles individually indicated the increasing contribution of expiratory muscle force to the attainment of higher levels of ventilation. Demonstrable ventilatory muscle fatigue may limit endurance at high levels of ventilation.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1742-8.
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    ABSTRACT: During dynamic exercise cardiac output (Q) normally increases approximately 5 liters per liter of increase in O2 uptake (Vo2) (i.e., delta Q/delta Vo2 approximately equal to 5), indicative of a tight coupling between systemic O2 transport and utilization. We studied four patients with muscle phosphorylase deficiency (McArdle's disease) in whom Q was normal at rest, but delta Q/delta Vo2 was 14.1 +/- 1.3 during bicycle exercise. Procedures designed to alter the availability of substrates were employed to test the hypothesis that the increased delta Q/delta Vo2 is linked to the abnormal metabolic state of skeletal muscle. Fasting plus prolonged moderate exercise was used to increase the availability of plasma free fatty acid (FFA) and resulted in a normalization of delta Q/delta Vo2 (5.3 +/- 0.4). Hyperglycemia (70% above control levels) partially normalized delta Q/delta Vo2. Nicotinic acid lowered plasma FFA concentration and dramatically increased delta Q/delta Vo2 (4.6 to 13.7) when administered after fasting plus prolonged exercise in one patient. Glucose infusion after nicotinic acid administration markedly lowered delta Q/delta Vo2. The results support the hypothesis and suggest that the metabolic state of skeletal muscle, possibly via activation of muscle afferents, participates in the regulation of systemic O2 transport.
    Journal of applied physiology: respiratory, environmental and exercise physiology 01/1985; 57(6):1749-53.