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

Atrophy and growth failure of muscle in a tail-cast suspension model were evaluated in hindlimbs of female Sprague-Dawley rats. Based on measurements of food consumption, animal growth rate, urinary excretion of urea and ammonia, and muscle size, 6 days seemed to be the optimum duration of suspension for studying muscle unloading. After 6 days, the soleus, plantaris, and gastrocnemius muscles from suspended animals were 27, 10, and 11% smaller (P less than 0.05), respectively, than those from tail-casted weight-bearing animals. The extensor digitorum longus and tibialis anterior muscles were unaffected by suspension (less than or equal to 6 days) while the triceps brachii hypertrophied (8%, P less than 0.05). Wet weight-to-dry weight ratios were smaller in the plantaris (-0.19, P less than 0.05) and gastrocnemius (-0.19, P less than 0.05) muscles from suspended rats. In the plantaris, this difference coincided with a higher protein concentration (+12 mg/g, P less than 0.001). In vitro measurements of protein metabolism in the soleus muscles of suspended rats showed both slower protein synthesis (P less than 0.05) and faster protein degradation (P less than 0.05), whereas these processes were unaltered in the extensor digitorum longus muscles.

We have produced interstitial fluid exchange in six isolated plasma-perfused canine lobes by introducing small increases in microvascular hydrostatic pressure. We measured early fast fluid exchange with a colorimetric technique and used weight changes to follow slow exchange. The observed biphasic time course suggested fluid flux across the microvascular membrane into two interstitial compartments in series (perimicrovascular and central). We related the initial rate of fluid flux into each compartment to the applied hydrostatic pressure change to obtain membrane (Kf1) and tissue conductances (Kf2) and to the exchanged volume to determine perimicrovascular (C1) and central (C2) interstitial compliances. C2 (0.25 +/- 0.193) was twice C1 (0.10 +/- 0.031 ml X cmH2O-1 X g DW-1, where DW represents dry weight. C2 increased significantly with hydration (C2 = 0.06 X WW/DW - 0.15) ml X cmH2O-1 X g DW-1 (WW/DW, wet-to-dry weight ratio), whereas C1 did not. Kf1 (0.26 +/- 0.17) was one order of magnitude larger than Kf2 (0.027 +/- 0.014 ml X min-1 X cmH2O-1 X g DW-1). Kf2 increased with hydration (Kf2 = 0.005 X WW/DW - 0.007) ml X min-1 X cmH2O-1 X g DW-1, whereas Kf1 did not. Our data point to the tissues and not the microvascular membranes as the major rate-limiting structure. Our data suggest an interstitium composed of a smaller rigid perimicrovascular space which communicates to a larger looser downstream space by a high-resistance pathway. As hydration increases, fluid accumulation becomes easier because tissue resistance to fluid flux drops and the compliance of the downstream compartment doubles.

The purpose of this work is to show mathematically the relationship between the classical maximum velocity of reaction, Vmax, for enzyme kinetics and an analogous parameter, Vmax, derived by Linehan and Dawson (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47:404-411, 1979) for the analysis of tracers which disappear by saturation kinetics from the lung circulation during the passage of indicators after bolus injection. Rederivation of the original equation for the combination of flow and reaction in a capillary showed that Vmax is equal to the product of enzyme Vmax and the volume of endothelium, Ve, in which the enzyme resides. This implies that Vmax interpreted from multiple-indicator curves in the lung by the Linehan-Dawson method is a combination of an enzyme characteristic Vmax and a measure of functioning capillary surface during passage, Ve. Lung injury could change Vmax, functioning surface (Ve), or both.

The effects of brief maximal exertion on platelet activation and reactivity have been studied in normal subjects. Although initial studies in seven subjects showed apparent exercise-induced platelet activation and enhanced platelet reactivity, these findings could not be confirmed in 13 subjects studied subsequently. There was no change in the platelet aggregate ratio, platelet fluorescent granule number or the plasma platelet factor 4 (PF4) or beta-thromboglobulin, although transient and significant increases in the platelet count and plasma heparin neutralizing activity (HNA) occurred. These results were reproducible in subjects studied more than once. It is postulated that in vitro platelet activation, most likely associated with blood collection, explained the initial results. It is concluded from the subsequent studies that in normal subjects brief maximal exercise causes neither platelet activation nor altered platelet reactivity but does cause a transient increase in the platelet count. The increase in HNA with exertion, without any accompanying increase in the PF4, demonstrates that these assays measure different substances and that the increase in HNA following exertion is most unlikely to be derived from platelets.

To reinvestigate the blood-gas CO2 equilibrium in lungs, rebreathing experiments were performed in five unanesthetized dogs prepared with a chronic tracheostomy and an exteriorized carotid loop. The rebreathing bag was initially filled with a gas mixture containing 6-8% CO2, 12, 21, or 39% O2, and 1% He in N2. During 4-6 min of rebreathing PO2 in the bag was kept constant by a controlled supply of O2 while PCO2 rose steadily from approximately 40 to 75 Torr. Spot samples of arterial blood were taken from the carotid loop; their PCO2 and PO2 were measured by electrodes and compared with the simultaneous values of end-tidal gas read from a mass spectrometer record. The mean end-tidal-to-arterial PO2 differences averaging 16, 4, and 0 Torr with bag PO2 about 260, 130, and 75 Torr, respectively, were in accordance with a venous admixture of about 1%. No substantial PCO2 differences between arterial blood and end-tidal gas (PaCO2 - PE'CO2) were found. The mean PaCO2 - PE'CO2 of 266 measurements in 70 rebreathing periods was -0.4 +/- 1.4 (SD) Torr. There was no correlation between PaCO2 - PE'CO2 and the level of arterial PCO2 or PO2. The mean PaCO2 - PE'CO2 became +0.1 Torr when the blood transit time from lungs to carotid artery (estimated at 6 s) and the rate of rise of bag PCO2 (4.5 Torr/min) were taken into account. These experimental results do not confirm the presence of significant PCO2 differences between arterial blood and alveolar gas in rebreathing equilibrium.

Postnodal lymph from the sheep caudal mediastinal node (CMN) is used by many investigators to assess lung vascular protein permeability. We explored the possibility that damage to the CMN blood-lymph barrier could produce increases in postnodal lymph flow and lymph-to-plasma protein concentration ratio (L/P) characteristic of lung vascular damage. Escherichia coli endotoxin (0.049 micrograms/min) was infused into a prenodal lymph vessel to the CMN in the conscious sheep, and postnodal lymph was collected for the next 7 h. Intranodal endotoxin caused an 80% increase in postnodal lymph flow and a 30% increase in postnodal L/P. Because there was no indication that the endotoxin had exerted a systemic effect, the lymph response to endotoxin was attributed to a direct effect of endotoxin on the blood-lymph barrier of the CMN. We conclude that significant increases in postnodal lymph flow and L/P characteristic of lung vascular damage can occur when the blood-lymph barrier of the CMN becomes damaged.

We performed morphometric studies of carotid body in acutely and chronically hypoxic rats (inspired PO2 = 70 Torr, at sea level). Acute exposure was for the duration of about 10 min, and chronic exposure lasted for 28 days. We confirmed that the total volume of the organ increased by severalfold. At the light-microscopy level we found an enlargement of the volume density of the blood sinuses from 14 to 31% due to chronic hypoxia. The morphometric hematocrit increased from 39 to 70% paralleling changes in the conventionally measured venous hematocrit. These data do not show any specific plasma skimming in the carotid body blood vessels. With the electron microscope we found that the mean average volume of type I cells increased from 320 micron3 in controls to 1,120 micron3 in the chronically hypoxic rats without hyperplasia, whereas type II cells had increased in number without alteration in size. Qualitative observations revealed that the normal appearance of clusters of ovoid type I cells interspersed by capillaries had been transformed into a pattern of individual cells forming plates between expanded blood vessels with a large increase of contact area between the cells and vessels. Type II cells appeared to have proliferated without changes in individual size to cover the enlarged periphery of type I cells. The observed structural changes in the carotid body parenchyma and vasculature appear to be physiologically adaptive and provide further support for the idea that various elements in the organ are particularly sensitive to hypoxia.

The authors investigated why intrapulmonary shunt (QS/QT) increases with sodium nitroprusside (SNP) in canine oleic acid pulmonary edema. To determine the effects of flow alone on QS/QT, a peripheral arteriovenous fistula with a variable resistor was employed to increase cardiac output (Q) 26 and 52% above base line in a stepwise fashion (P less than 0.01). To examine the direct effects of SNP, distinct from changes in flow, the drug was given to produce matched increments in Q in each dog (P less than 0.01). To control for time, base-line measurements were obtained before and after each intervention, the sequence of which was alternated. At each increment in Q, SNP and the arteriovenous fistula increased QS/QT a similar amount. The mixed venous O2 tension (P-vO2) followed Q similarly in each group. Pulmonary vascular resistance (PVR) fell more (P less than 0.01) with SNP than with the arteriovenous fistula at identical Q and P-vO2. The authors conclude that, in this model, a direct pharmacological effect of SNP does not contribute to the deterioration in QS/QT. In fact, SNP exerts a pulmonary vasoactive effect that does not adversely affect gas exchange.

To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.

Muscle fiber numbers were estimated in vivo in biceps brachii in 5 elite male bodybuilders, 7 intermediate caliber bodybuilders, and 13 age-matched controls. Mean fiber area and collagen volume density were calculated from needle biopsies and muscle cross-sectional area by computerized tomographic scanning. Contralateral measurements in a subsample of seven subjects indicated the method for estimation of fiber numbers to have adequate reliability. There was a wide interindividual range for fiber numbers in biceps (172,085-418,884), but despite large differences in muscle size both bodybuilder groups possessed the same number of muscle fibers as the group of untrained controls. Although there was a high correlation between average cross-sectional fiber area and total muscle cross-sectional area within each group, many of the subjects with the largest muscles also tended to have a large number of fibers. Since there were equally well-trained subjects with fewer than normal fiber numbers, we interpret this finding to be due to genetic endowment rather than to training-induced hyperplasia. The proportion of muscle comprised of connective and other noncontractile tissue was the same for all subjects (approximately 13%), thus indicating greater absolute amounts of connective tissue in the trained subjects. We conclude that in humans, heavy resistance training directed toward achieving maximum size in skeletal muscle does not result in an increase in fiber numbers.