Journal of applied physiology: respiratory, environmental and exercise physiology最新文献

To examine the role of cardiopulmonary receptors in arterial blood pressure regulation during and after exercise, conscious dogs with chronic sinoaortic denervation were subjected to 12 min of light exercise and 12 min of exercise that increased in severity every 3 min. Hemodynamic measurements were made before and after interruption of cardiopulmonary afferents by bilateral cervical vagotomy. During both exercise protocols, after an initial transient decrease, the arterial blood pressure remained close to resting values before and after vagotomy. On cessation of the graded exercise, the arterial blood pressure did not change before, but a rapid and sustained increase in pressure occurred after vagotomy. At the time of this increase the cardiac output and heart rate were returning rapidly to the resting level. The study demonstrates that in the chronic absence of arterial baroreflexes, vagal afferents prevent a rise in arterial blood pressure after vigorous exercise presumably by the action of cardiopulmonary receptors causing a rapid dilatation of systemic resistance vessels.

The frequency dependence of pulmonary compliance and resistance was investigated in 27 patients with obstructive lung disease. Compliance and resistance were determined either by the conventional zero crossing (Cdyn) and isovolume (RL) technique or by a modified Fourier analysis following a smoothing procedure (auto- and cross-correlation function) yielding an effective compliance and resistance, CL and RL. The latter technique was used to calculate CL and RL from the fundamental and third and fourth harmonics present in the flow and transpulmonary pressure signals. Three breathing frequencies were investigated: 0.5, 1, and 2 Hz. Both Cdyn and CL, calculated from the fundamental component, decreased progressively with frequency. However, Cdyn showed less frequency dependence than CL. CL calculated from the harmonics was significantly smaller than CL from the fundamental at the same breathing frequency. RL, as well as RL calculated from the fundamental, tended to increase with frequency. A decline of resistance with frequency became apparent, however, when RL from the fundamental was compared with RL obtained from the corresponding higher order harmonics. These results suggest that the frequency dependence of resistance can be masked by the usual procedure of breathing at several frequencies. Instead the measurements should be performed at a single frequency, for instance spontaneous breathing, by computing resistance from the higher order harmonics present in the breathing signals.

To determine whether plasma catecholamine concentrations (a measure of sympathetic nervous activity [SNA]) rise above normoxic levels during exercise with hypoxemia, we exercised seven men for 15 min at three loads that required from 40 to 88% of maximal O2 uptake (VO2max). Subjects breathed room air on one day and 11-12% O2 on another with relative work loads corrected for the 24% fall in VO2max during hypoxemia. Hypoxemia caused large increments in norepinephrine (NE) concentration (radioenzyme technique) to 1.21 +/- 0.20 ng/ml (mean +/- SE), 2.79 +/- 0.38, and up to 5.90 +/- 0.75 (hypoxemia) compared with 0.89 +/- 0.06, 1.66 +/- 0.16, and 3.95 +/- 0.39 in normoxia at the three loads, respectively (P less than 0.001). Epinephrine (E) concentration approximately doubled (P less than 0.001) in hypoxemia at each load when compared with normoxic levels (i.e., 0.10 +/- 0.01 ng/ml, 0.23 +/- 0.03, and 0.46 +/- 0.06 in normoxia). However, hypoxemia did not significantly alter linear relationships between log plasma NE concentration and either heart rate (HR) or percent VO2max utilized, or between HR and percent VO2max. Thus NE concentration, like HR, appeared to reflect relative severity of exercise and overall SNA in both hypoxemia and normoxia. Above 40% VO2max during hypoxemia, circulating NE and E far exceeded levels known to have direct vasoconstrictor and metabolic effects in normoxic humans, but hypoxemia may blunt vasoconstriction in some regions.

The purpose of this investigation was to determine the age-related metabolic responses to chronic exercise. Female Fischer 344 rats 3, 12, and 24 mo of age were trained for 8 wks by treadmill running at 75% of their maximal oxygen uptake (VO2max). Values of VO2max were 74.5 +/- 3.1, 63.3 +/- 3.9, and 54.6 +/- 2.3 ml X kg-1 X min-1 in the untrained 3-, 12-, and 24-mo groups, respectively. In response to training, VO2max increased significantly (P less than 0.05) by 11.9, 18.6, and 20.4% in the three groups. The 24-mo animals also demonstrated the greatest improvement in the treadmill speed eliciting VO2max (71%) when compared with the 12-mo (64%) and 3-mo (57%) age groups. While large increases in endurance times were recorded for all trained groups (456, 806, and 324% in 3, 12, and 24 mo, respectively) relative to the controls, the older animals exhibited a diminished response, comparatively. Body weights did not differ between the trained (Tr) and sedentary controls for 3- and 12-mo animals, but the 24-mo Tr rats demonstrated a more rapid decline in body weight with age than did the age-matched controls. While no differences in absolute or relative heart weights existed for the 3- and 12-mo groups with training, both of these parameters in the 24-mo Tr animals were significantly greater than sedentary controls. It was concluded that compared with younger animals the 24-mo group demonstrated a similar relative adaptation to training in terms of aerobic power but a diminished response comparatively in endurance capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied the effect of mild hypoxia (15% O2) and low ambient temperature (Ta = 15 degrees C) on the rat's sleep-waking pattern (SWP) and maximum-minimum core temperature (max-min Tb). Mild hypoxia at neutral Ta (29 degrees C) disrupted the SWP in the same way as low Ta during normoxia: both affected the pattern of frequency of state changes (P less than 0.01), not the pattern of epoch durations. Mild hypoxia and low Ta together caused a degree of disruption of the SWP which was the sum of each alone, i.e., additive. Although both mild hypoxia and low Ta significantly depressed max-min Tb, low Ta exerted a greater effect than mild hypoxia. Together they further depressed max-min Tb in an additive way. We conclude that mild hypoxia disrupts the rat's SWP independent of central thermoregulatory mechanisms at neutral Ta, that the effects of mild hypoxia and low Ta on the SWP are additive at the stimulus levels used, and that Ta, not inspired O2, determines Tb.

Functional innervation of cat airways smooth muscle was examined in isolated segments of trachea and bronchi using electrical field stimulation (EFS) techniques. Field stimulation caused contraction in tissues at resting tone and biphasic responses (contraction followed by relaxation) in tissues precontracted with 5-hydroxytryptamine (5-HT). Contractions were abolished by 10(-6) M atropine. Inhibitory responses were dependent on impulse voltage, duration, and frequency. At low voltages (less than or equal to 10 V) and pulse durations (less than or equal to 0.3 ms), EFS induced relaxations were abolished by 3 X 10(-6) M tetrodotoxin (TTX). Greater stimulus parameters elicited TTX-resistant relaxations. Pretreatment of the tissues with 10(-6) M propranolol and 10(-5) M guanethidine caused rightward shifts in relaxation frequency-response curves. These findings indicate that cat airways are innervated by excitatory cholinergic, inhibitory adrenergic, and inhibitory nonadrenergic noncholinergic (NANC) nerves. Pretreatment of the tissues with hexamethonium, cimetidine, indomethacin, or nordihydroguaiaretic acid did not affect NANC relaxation responses. It is concluded that NANC inhibitory responses in cat airway smooth muscle are mediated through intrinsic postganglionic nerve fibers and occur independently of histamine H2-receptor activation and without involvement of cyclooxygenase or lipoxygenase products of arachidonic acid metabolism.

This paper describes a simple apparatus enabling the O2 consumption of small animals to be monitored. The system consists of a sensitive solid-state pressure transducer linked via a relay to a small peristaltic pump. While the animal breathes air in its closed chamber the CO2 expired is removed by an absorber; hence the pressure falls. The signal is sensed by the transducer triggering the pump to deliver a set volume of O2 to the chamber. The number of pump operations per unit time necessary to keep the system equilibrated is a measure of the O2 consumption rate. Each device is built as a module, up to four being mounted in one assembly controlled by a microcomputer. A balance control, priming switch, pump-volume setting, and electromagnetic counter are built into each front panel. Calibration is achieved be removing a known volume of air from the system with no animal present and counting the number of operations to return the chamber to equilibrium.

We studied the ultrastructural damage caused by venous air embolization in anesthetized sheep by morphological techniques after monitoring hemodynamics and lymph dynamics. Lung lymph flow and protein flux increased during 1 and 4 h of venous air embolization, results consistent with increased microvascular permeability. Histologically, the air emboli were restricted to the small pulmonary arterial vessels (1,000 to 100 micron in diam). Neutrophils accumulated around the air bubbles and formed intravascular clumps. Ultrastructurally, at the air embolus-blood interface, neutrophils appeared attached to a layer a proteinaceous material. Many neutrophils were in close contact with the pulmonary arterial endothelial cells. We found gaps (0.1-3 micron in width) between the endothelial cells of the pulmonary arterial microvessels. Beneath these gaps the basal lamina was disrupted. Other vessel types were unaffected. Some lymphocytes were seen near the air bubbles and the endothelial cell gaps. Platelets remained discoid, and fibrin clots were not observed. These results indicate that venous air embolization in sheep damages the pulmonary arterial microvessels. Neutrophils are closely associated to both the air emboli and the endothelial cell gaps.

The direct contribution of forces in tree structures in the lung to lung recoil pressure and changes in recoil pressure induced by alterations of the forces are analyzed. The analysis distinguishes the contributions of axial and circumferential tensions in the trees and indicates that only axial tensions directly contribute to static recoil. This contribution is derived from analysis of the axial forces transmitted across a random plane transecting the lung. The change in recoil pressure induced by changes in axial tension is similarly derived. Alterations of circumferential tensions in the trees indirectly change recoil by causing nonuniform deformations of the surrounding lung parenchyma, and a continuum elasticity solution for the stress induced by the deformations is derived. Sample calculations are presented for the airway tree based on available data on airway morphometric and mechanical properties. The increase in recoil pressure accompanying increases in axial and circumferential tensions with contraction of airway smooth muscle is also analyzed. The calculations indicate that axial stresses in the airway tree out to bronchioles directly contribute only a small fraction of the static recoil pressure. However, it is found that contraction of smooth muscle in these airways can increase recoil pressure appreciably (10-20%), mainly by the deformation of the parenchyma with increases in circumferential tension in smaller airways. The results indicate that the geometric and mechanical properties of the airway tree are such that only peripheral elements of the tree can substantially affect the elastic properties of the lung. The possible contributions of vascular trees for which data on mechanical and morphometric properties are more limited are also discussed.

Numerous studies have reported that following intense exercise the rate of blood lactate (La) disappearance is greater during continuous aerobic work than during passive recovery. Recent work indicates that a combination of high- and low-intensity work may be optimal in reducing blood La. We tested this hypothesis by measuring the changes in blood La levels following maximal exercise during four different recovery patterns. Immediately following 50 S of maximal work, subjects (n = 7) performed one of the following recovery treatments for 40 min: 1) passive recovery (PR); 2) cycling at 35% maximal O2 uptake (VO2 max) (35% R); 3) cycling at 65% VO2 max (65% R); 4) cycling at 65% for 7 min followed by cycling at 35% for 33 min (CR). The treatment order was counterbalanced with each subject performing all treatments. Serial blood samples were obtained throughout recovery treatments and analyzed for La. The rate of blood La disappearance was significantly greater (P less than 0.05) in both the 35% R and CR when compared with either the 65% R or PR. No significant difference (P greater than 0.05) existed in the rate of blood La disappearance between the 35% R and CR. These data do not support the hypothesis that exercise recovery at a combination of intensities is superior to a recovery involving continuous submaximal exercise in lowering blood La following maximal work.