bluuebunny/crossref_metadata_2025 huggingface dataset:
Altered fractal dynamics of gait: reduced stride-interval correlations with aging and Huntington’s disease
Authors: Hausdorff Jeffrey M. , Mitchell Susan L. , Firtion Renée , Peng C. K. , Cudkowicz Merit E. , Wei Jeanne Y. , Goldberger Ary L.
Published: December 2017

Hausdorff, Jeffrey M., Susan L. Mitchell, Renée Firtion, C. K. Peng, Merit E. Cudkowicz, Jeanne Y. Wei, and Ary L. Goldberger. Altered fractal dynamics of gait: reduced stride-interval correlations with aging and Huntington’s disease. J. Appl. Physiol. 82(1): 262–269, 1997.—Fluctuations in the duration of the gait cycle (the stride interval) display fractal dynamics and long-range correlations in healthy young adults. We hypothesized that these stride-interval correlations would be altered by changes in neurological function associated with aging and certain disease states. To test this hypothesis, we compared the stride-interval time series of 1) healthy elderly subjects and young controls and of 2) subjects with Huntington’s disease and healthy controls. Using detrended fluctuation analysis, we computed α, a measure of the degree to which one stride interval is correlated with previous and subsequent intervals over different time scales. The scaling exponent α was significantly lower in elderly subjects compared with young subjects (elderly: 0.68 ± 0.14; young: 0.87 ± 0.15; P < 0.003). The scaling exponent α was also smaller in the subjects with Huntington’s disease compared with disease-free controls (Huntington’s disease: 0.60 ± 0.24; controls: 0.88 ± 0.17; P < 0.005). Moreover, α was linearly related to degree of functional impairment in subjects with Huntington’s disease ( r = 0.78, P < 0.0005). These findings demonstrate that stride-interval fluctuations are more random (i.e., less correlated) in elderly subjects and in subjects with Huntington’s disease. Abnormal alterations in the fractal properties of gait dynamics are apparently associated with changes in central nervous system control.
Training intensity, blood lipids, and apolipoproteins in men with high cholesterol
Authors: Crouse Stephen F. , O’Brien Barbara C. , Grandjean Peter W. , Lowe Robert C. , Rohack J. James , Green John S. , Tolson Homer
Published: December 2017

Crouse, Stephen F., Barbara C. O’Brien, Peter W. Grandjean, Robert C. Lowe, J. James Rohack, John S. Green, and Homer Tolson.Training intensity, blood lipids, and apolipoproteins in men with high cholesterol. J. Appl. Physiol.82(1): 270–277, 1997.—Twenty-six hypercholesterolemic men (mean cholesterol, 258 mg/dl; age, 47 yr; weight, 81.9 kg) completed 24 wk of cycle ergometer training (3 days/wk, 350 kcal/session) at either high ( n = 12) or moderate ( n = 14) intensity (80 and 50% maximal O2uptake, respectively, randomly assigned) to test the influence of training intensity on blood lipid and apolipoprotein (apo) concentrations. All physiological, lipid, and apo measurements were completed at 0, 8, 16, and 24 wk. Lipid data were analyzed via two × four repeated-measures analysis of variance (∝ = 0.0031). Training produced a significant decrease in body weight and increase in maximal O2uptake. No interactions between intensity and weeks of training were noted for any lipid or apo variable, and no between-group differences were significant before or throughout training. Therefore, intensity did not affect the training response. Regardless of intensity, apo AI and apo B fell 9 and 13%, respectively, by week 16 and remained lower through week 24( P < 0.0003). Total cholesterol fell transiently (−5.5%) by week 16( P < 0.0021) but returned to initial levels by week 24. Triglyceride, low-density-lipoprotein cholesterol, and high-density-lipoprotein (HDL) cholesterol did not change with training. In contrast, HDL2cholesterol rose 79% above initial levels by week 8 and 82% above initial levels by week 24( P < 0.0018); HDL3cholesterol fell 8 and 13% over the same training intervals ( P< 0.0026). These data show that changes in blood lipid and apo concentrations that accompany training in hypercholesterolemic men are not influenced by exercise intensity when caloric expenditure is held constant.
Exhalation of gaseous nitric oxide by rats in response to endotoxin and its absorption by the lungs
Authors: Stitt John T. , Dubois Arthur B. , Douglas James S. , Shimada Steven G.
Published: December 2017

Stitt, John T., Arthur B. DuBois, James S. Douglas, and Steven G. Shimada. Exhalation of gaseous nitric oxide by rats in response to endotoxin and its absorption by the lungs. J. Appl. Physiol. 82(1): 305–316, 1997.—Rats injected with a lipopolysaccharide endotoxin produce detectable concentrations of nitric oxide gas (NO) in the expired air within 60 min. The concentration of NO reaches a plateau at 3 h. Production of the NO is dose dependent on lipopolysaccharide, and at a dose of 1 mg/kg iv, lipopolysaccharide alveolar concentrations of >260 parts per billion are observed. NO synthase inhibitors suppress this NO production in response to endotoxin. Experiments were conducted to ascertain the site of origin of this NO and to measure the capacity of the lungs to absorb NO from alveolar air. Results indicate that the endotoxin-induced NO originates from within the lungs themselves and that the lungs have the capacity to absorb >60% of NO that is presented to them. Lung tissues absorb ∼44–47% of the NO load, blood carries away between 15 and 19%, while the remainder is exhaled in the expired air. It is proposed that the exhalation of NO might prove useful as an early biomarker for acute lung injury.
Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects
Authors: Van Der Touw T. , Crawford A. B. H. , Wheatley J. R.
Published: December 2017

Van der Touw, T., A. B. H. Crawford, and J. R. Wheatley.Effects of a synthetic lung surfactant on pharyngeal patency in awake human subjects. J. Appl. Physiol. 82(1): 78–85, 1997.—We examined the effects of separate applications of saline and a synthetic lung surfactant preparation (Surf; Exosurf Neonatal) into the supraglottic airway (SA) on the anteroposterior pharyngeal diameter ( Dap) and the airway pressures required to close (Pcl) and reopen (Pop) the SA in five awake normal supine subjects. Dap, Pcl, and Pop were determined during lateral X-ray fluoroscopy and voluntary glottic closure when pressure applied to the SA lumen was decreased from 0 to −20 cmH2O and then increased to +20 cmH2O. After Surf application and relative to control, Dapwas larger for most of the applied pressures, Pcl decreased (−12.3 ± 1.9 to −18.7 ± 0.9 cmH2O; P < 0.01), Pop decreased (13.4 ± 1.9 to −6.0 ± 3.4 cmH2O; P < 0.01), and genioglossus electromyographic activity did not change ( P > 0.05). Saline had no effect. These observations suggest that pharyngeal intraluminal surface properties are important in maintaining pharyngeal patency. We propose that surfactants enhance pharyngeal patency by reducing surface tension and adhesive forces acting on intraluminal SA surfaces.
Nevill's explanation of Kleiber's 0.75 mass exponent: an artifact of collinearity problems in least squares models?
Authors: Batterham Alan M. , Tolfrey Keith , George Keith P.
Published: December 2017

Batterham, Alan M., Keith Tolfrey, and Keith P. George.Nevill’s explanation of Kleiber’s 0.75 mass exponent: an artifact of collinearity problems in least squares models? J. Appl. Physiol. 82(2): 693–697, 1997.—Intraspecific allometric modeling ( Y = a ⋅ massb, where Y is the physiological dependent variable and a is the proportionality coefficient) of peak oxygen uptake (V˙o2 peak) has frequently revealed a mass exponent ( b) greater than that predicted from dimensionality theory, approximating Kleiber’s 3/4 exponent for basal metabolic rate. Nevill ( J. Appl. Physiol. 77: 2870–2873, 1994) proposed an explanation and a method that restores the inflated exponent to the anticipated 2/3. In human subjects, the method involves the addition of “stature” as a continuous predictor variable in a multiple log-linear regression model: ln Y = ln a + c ⋅ ln stature + b ⋅ ln mass + ln ε, where c is the general body size exponent and ε is the error term. It is likely that serious collinearity confounds may adversely affect the reliability and validity of the model. The aim of this study was to critically examine Nevill’s method in modelingV˙o2 peakin prepubertal, teenage, and adult men. A mean exponent of 0.81 (95% confidence interval, 0.65–0.97) was found when scaling by mass alone. Nevill’s method reduced the mean mass exponent to 0.67 (95% confidence interval, 0.44–0.9). However, variance inflation factors and tolerance for the log-transformed stature and mass variables exceeded published criteria for severe collinearity. Principal components analysis also diagnosed severe collinearity in two principal components, with condition indexes >30 and variance decomposition proportions exceeding 50% for two regression coefficients. The derived exponents may thus be numerically inaccurate and unstable. In conclusion, the restoration of the mean mass exponent to the anticipated 2/3 may be a fortuitous statistical artifact.
Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans
Authors: Jungersten Lennart , Ambring Anneli , Wall Björn , Wennmalm Åke
Published: December 2017

Jungersten, Lennart, Anneli Ambring, Björn Wall, andÅke Wennmalm. Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans. J. Appl. Physiol. 82(3): 760–764, 1997.—We analyzed nitrate, a major stable end product of nitric oxide (NO) metabolism in vivo in plasma and urine from groups of healthy subjects with different working capacities. Resting plasma nitrate was higher in athletic subjects than in nonathletic controls [45 ± 2 vs. 34 ± 2 (SE) μM; P < 0.01]. In other subjects, both the resting plasma nitrate level ( r = 0.53; P < 0.01) and the urinary excretion of nitrate at rest ( r = 0.46; P < 0.01) correlated to the subjects’ peak work rates, as determined by bicycle ergometry. Two hours of physical exercise elevated plasma nitrate by 18 ± 4 ( P < 0.01) and 16 ± 6% ( P < 0.01), respectively, in athletes and nonathletes, compared with resting nitrate before exercise. We conclude that physical fitness and formation of NO at rest are positively linked to each other. Furthermore, a single session of exercise elicits an acute elevation of NO formation. The observed positive relation between physical exercise and NO formation may help to explain the beneficial effects of physical exercise on cardiovascular health.
Respiratory system mechanics in sedated, paralyzed, morbidly obese patients
Authors: Pelosi P. , Croci M. , Ravagnan I. , Cerisara M. , Vicardi P. , Lissoni A. , Gattinoni L.
Published: December 2017

Pelosi, P., M. Croci, I. Ravagnan, M. Cerisara, P. Vicardi, A. Lissoni, and L. Gattinoni. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients J. Appl. Physiol. 82(3): 811–818, 1997.—The effects of inspiratory flow and inflation volume on the mechanical properties of the respiratory system in eight sedated and paralyzed postoperative morbidly obese patients (aged 37.6 ± 11.8 yr who had never smoked and had normal preoperative seated spirometry) were investigated by using the technique of rapid airway occlusion during constant-flow inflation. With the patients in the supine position, we measured the interrupter resistance (Rint,rs), which in humans probably reflects airway resistance, the “additional” resistance (ΔRrs) due to viscoelastic pressure dissipation and time-constant inequalities, and static respiratory elastance (Est,rs). Intra-abdominal pressure (IAP) was measured by using a bladder catheter, and functional residual capacity was measured by the helium-dilution technique. The results were compared with a previous study on 16 normal anesthetized paralyzed humans. Compared with normal persons, we found that in obese subjects: 1) functional residual capacity was markedly lower (0.645 ± 0.208 liter) and IAP was higher (24 ± 2.2 cmH2O); 2) alveolar-arterial oxygenation gradient was increased (178 ± 59 mmHg); 3) the volume-pressure curve of the respiratory system was curvilinear with an “inflection” point; 4) Est,rs, Rint,rs, and ΔRrs were higher than normal (29.3 ± 5.04 cmH2O/l, 5.9 ± 2.4 cmH2O ⋅ l−1 ⋅ s, and 6.4 ± 1.6 cmH2O ⋅ l−1 ⋅ s, respectively); 5) Rint,rs increased with increasing inspiratory flow, Est,rs did not change, and ΔRrs decreased progressively; and 6) with increasing inflation volume, Rint,rs and Est,rs decreased, whereas ΔRrs rose progressively. Overall, our data suggest that obese subjects during sedation and paralysis are characterized by hypoxemia and marked alterations of the mechanical properties of the respiratory system, largely explained by a reduction in lung volume due to the excessive unopposed IAP.
Age and gender interactions in physiological functional capacity: insight from swimming performance
Authors: Tanaka Hirofumi , Seals Douglas R.
Published: December 2017

Tanaka, Hirofumi, and Douglas R. Seals. Age and gender interactions in physiological functional capacity: insight from swimming performance. J. Appl. Physiol. 82(3): 846–851, 1997.—One experimental approach to studying the effects of aging on physiological functional capacity in humans is to analyze the peak exercise performance of highly trained athletes with increasing age. To gain insight into the relationships among age, gender, and exercise task duration with use of this model, we performed a 5-yr (1991–1995) retrospective analysis of top freestyle performance times from the US Masters Swimming Championships. Regression analysis showed that in both men and women endurance swimming performance (i.e., 1,500 m) declined linearly from peak levels at age 35–40 yr until ∼70 yr of age, whereupon performance declined exponentially thereafter. In both genders, the variability among the top 10 winning times in each 5-yr age interval increased markedly with advancing age. Compared with the 1,500-m freestyle, performance in the 50-m freestyle (short-duration task) showed only a modest decline until ages 75 and 80 yr in women and men, respectively. The rate and magnitude of the declines in both short- and long-duration swimming performance with age were significantly ( P < 0.05) greater in women than in men. In the women, the percent decline in swimming performance over a 50-yr age period from the 19- to 24-yr to the 69- to 74-yr age groups became progressively greater from the shortest distance (50 m) to the two longest distances (800 and 1,500 m), whereas in men, no differences were observed in the magnitude of performance decline with age among the five longest distance events (i.e., 100–1,500 m). The percent gender difference in performance throughout the age range studied became progressively smaller ( P < 0.05) with increasing distance from 50 m (19 ± 1%) to 1,500 m (11 ± 1%). The findings in this cross-sectional study indicate that from peak levels at age 35–40 yr, physiological functional capacity, as assessed by swimming performance, decreases linearly until ∼70–80 yr of age, whereupon the decline becomes exponential. Moreover, the rate of decline with advancing age appears to be associated with event duration and gender.
Genetic control of differential baseline breathing pattern
Authors: Tankersley Clarke G. , Fitzgerald Robert S. , Levitt Roy C. , Mitzner Wayne A. , Ewart Susan L. , Kleeberger Steven R.
Published: December 2017

Tankersley, Clarke G., Robert S. Fitzgerald, Roy C. Levitt, Wayne A. Mitzner, Susan L. Ewart, and Steven R. Kleeberger.Genetic control of differential baseline breathing pattern. J. Appl. Physiol. 82(3): 874–881, 1997.—The purpose of the present study was to determine the genetic control of baseline breathing pattern by examining the mode of inheritance between two inbred murine strains with differential breathing characteristics. Specifically, the rapid, shallow phenotype of the C57BL/6J (B6) strain is consistently distinct from the slow, deep phenotype of the C3H/HeJ (C3) strain. The response distributions of segregant and nonsegregant progeny were compared with the two progenitor strains to determine the mode of inheritance for each ventilatory characteristic. The BXH recombinant inbred (RI) strains derived from the B6 and C3 progenitors were examined to establish strain distribution patterns for each ventilatory trait. To establish the mode of inheritance, baseline breathing frequency (f), tidal volume, and inspiratory time (Ti) were measured five times in each of 178 mature male animals from the two progenitor strains and their progeny by using whole body plethysmography. With respect to f and Ti, the two progenitor strains were consistently distinct, and segregation analyses of the inheritance pattern suggest that the most parsimonious genetic model for response distributions of f and Ti is a two-loci model. In similar experiments conducted on 82 mature male animals from 12 BXH RI strains, each parental phenotype was represented by one or more of the RI strains. Intermediate phenotypes emerged to confirm the likelihood that parental strain differences in f and Ti were determined by more than one locus. Taken together, these studies suggest that the phenotypic difference in baseline respiratory timing between male B6 and C3 mice is best explained by a genetic model that considers at least two loci as major determinants.
Cardiac output estimated noninvasively from oxygen uptake during exercise
Authors: Stringer William W. , Hansen James E. , Wasserman K.
Published: December 2017

Stringer, William W., James E. Hansen, and K. Wasserman.Cardiac output estimated noninvasively from oxygen uptake during exercise. J. Appl. Physiol. 82(3): 908–912, 1997.—Because gas-exchange measurements during cardiopulmonary exercise testing allow noninvasive measurement of oxygen uptake (V˙o 2), which is equal to cardiac output (CO) × arteriovenous oxygen content difference [C(a-[Formula: see text])], CO and stroke volume could theoretically be estimated if the C(a-[Formula: see text]) increased in a predictable fashion as a function of %maximumV˙o 2(V˙o 2 max) during exercise. To investigate the behavior of C(a-[Formula: see text]) during progressively increasing ramp pattern cycle ergometry exercise, 5 healthy subjects performed 10 studies to exhaustion while arterial and mixed venous blood were sampled. Samples were analyzed for blood gases (pH, [Formula: see text],[Formula: see text]) and oxyhemoglobin and hemoglobin concentration with a CO-oximeter. The C(a-[Formula: see text]) (ml/100 ml) could be estimated with a linear regression [C(a-[Formula: see text]) = 5.72 + 0.105 × %V˙o 2 max; r = 0.94]. The CO estimated from the C(a-[Formula: see text]) by using the above linear regression was well correlated with the CO determined by the direct Fick method ( r = 0.96). The coefficient of variation of the estimated CO was small (7–9%) between the lactic acidosis threshold and peakV˙o 2. The behavior of C(a-[Formula: see text]), as related to peakV˙o 2, was similar regardless of cardiac function compared with similar measurements from studies in the literature performed in normal and congestive heart failure patients. In summary, CO and stroke volume can be estimated during progressive work rate exercise testing from measuredV˙o 2 (in normal subjects and patients with congestive heart failure), and the resultant linear regression equation provides a good estimate of C(a-[Formula: see text]).
Effects of inhaled CO2and added dead space on idiopathic central sleep apnea
Authors: Xie Ailiang , Rankin Fiona , Rutherford Ruth , Bradley T. Douglas
Published: December 2017

Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. Effects of inhaled CO2and added dead space on idiopathic central sleep apnea. J. Appl. Physiol. 82(3): 918–926, 1997.—We hypothesized that reductions in arterial [Formula: see text]([Formula: see text]) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising[Formula: see text] would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2and transcutaneous[Formula: see text] were measured: during room air breathing ( N1), alternating room air and CO2breathing ( N2), CO2breathing all night ( N3), and addition of dead space via a face mask all night ( N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous [Formula: see text], which virtually eliminated apneas and hypopneas; they decreased from 43.7 ± 7.3 apneas and hypopneas/h on N1 to 5.8 ± 0.9 apneas and hypopneas/h during N3( P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during CO2inhalation during N2 ( P< 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 ( P< 0.005). Because raising[Formula: see text] through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in[Formula: see text] below the apnea threshold.
Lung liquid production rates and volumes do not decrease before labor in healthy fetal sheep
Authors: Lines A. , Hooper S. B. , Harding R.
Published: December 2017

Lines, A., S. B. Hooper, and R. Harding. Lung liquid production rates and volumes do not decrease before labor in healthy fetal sheep. J. Appl. Physiol. 82(3): 927–932, 1997.—Previous studies have suggested that the volume and production rate of fetal lung liquid decrease late in gestation, before the onset of labor, in preparation for the clearance of lung liquid at birth. In contrast, our earlier studies have not shown a decrease in lung liquid volume near term, although these studies were not continued to the onset of labor. Our aim was to determine the changes in lung liquid volume and production rate in fetal sheep during the last 2 wk of gestation up to the onset of labor at term (∼147 days). In eight chronically catheterized fetal sheep, the volume and production rate of fetal lung liquid were measured at 130, 135, and 140 days of gestation and then on every 2nd day until the onset of labor. Labor was detected by monitoring uterine muscle activity and intrauterine pressure changes. On the day of labor onset, which occurred at 147 ± 1 days of gestation, fetuses weighed 5.0 ± 0.2 kg. The volume of fetal lung liquid was 40.4 ± 2.7 ml/kg at 19 ± 1 days before labor onset and had not significantly changed by 0.7 ± 0.2 days (44.8 ± 5.1 ml/kg) before labor. Similarly, lung liquid production rates at 19 ± 1 days before labor (5.1 ± 1.8 ml ⋅ h−1 ⋅ kg−1) were not significantly different from those at 0.7 ± 0.2 days before labor (3.4 ± 0.7 ml ⋅ h−1 ⋅ kg−1). We conclude that, in healthy ovine fetuses, lung liquid volumes and production rates do not decrease before the onset of labor. Our results indicate that the entire volume of fetal lung liquid (∼222.5 ± 36.6 ml) must be cleared after the onset of labor.
Shunt and ventilation-perfusion distribution during partial liquid ventilation in healthy piglets
Authors: Mates Elisabeth A. , Hildebrandt Jacob , Jackson J. Craig , Tarczy-Hornoch Peter , Hlastala Michael P.
Published: December 2017

Mates, Elisabeth A., Jacob Hildebrandt, J. Craig Jackson, Peter Tarczy-Hornoch, and Michael P. Hlastala. Shunt and ventilation-perfusion distribution during partial liquid ventilation in healthy piglets. J. Appl. Physiol.82(3): 933–942, 1997.—Replacing gas in the lung with perfluorocarbon fluids (PFC) and periodically ventilating with a gas [partial liquid ventilation (PLV)] has been shown to improve oxygenation in models of respiratory distress syndrome. We hypothesized that the addition of PFC to healthy lungs would result in shunt, diffusion impairment, and increased ventilation-perfusion (V˙a/Q˙) heterogeneity. Previously, Mates et al. showed that O2 shunt and arterial-alveolar CO2 difference increased linearly with dose in piglets given graded intratracheal doses of PFC (10, 20, and 30 ml/kg followed by mechanical ventilation with 100% O2) (E. A. Mates, J. C. Jackson, J. Hildebrandt, W. E. Truog, T. A. Standaert, and M. P. Hlastala. In: Oxygen Transport to Tissue XVI, 1994, p. 427–435). Here we reportV˙a/Q˙ distribution in the same animals, showing a 50% increase inV˙a/Q˙ heterogeneity during PLV independent of PFC dose. Ventilation heterogeneity was the major factor in this increase, and there was no significant change in dead space ventilation. We also report on five animals given a single 20 ml/kg dose of PFC and followed for 3 h. They showed an increase in shunt during PLV but no change in arterial-alveolar CO2 difference.
Branching design of the bronchial tree based on a diameter-flow relationship
Authors: Kitaoka Hiroko , Suki Béla
Published: December 2017

Kitaoka, Hiroko, and Béla Suki. Branching design of the bronchial tree based on a diameter-flow relationship. J. Appl. Physiol. 82(3): 968–976, 1997.—We propose a method for designing the bronchial tree where the branching process is stochastic and the diameter ( d) of a branch is determined by its flow rate (Q). We use two principles: the continuum equation for flow division and a power-law relationship between d and Q, given by Q ∼ d n, where n is the diameter exponent. The value of n has been suggested to be ∼3. We assume that flow is divided iteratively with a random variable for the flow-division ratio, defined as the ratio of flow in the branch to that in its parent branch. We show that the cumulative probability distribution function of Q, P(>Q) is proportional to Q−1. We analyzed prior morphometric airway data (O. G. Raabe, H. C. Yeh, H. M. Schum, and R. F. Phalen, Report No. LF-53, 1976) and found that the cumulative probability distribution function of diameters, P(> d), is proportional to d −n, which supports the validity of Q ∼ d n since P(>Q) ∼ Q−1. This allowed us to assign diameters to the segments of the flow-branching pattern. We modeled the bronchial trees of four mammals and found that their statistical features were in good accordance with the morphometric data. We conclude that our design method is appropriate for robust generation of bronchial tree models.
Three-dimensional reconstruction of human diaphragm with the use of spiral computed tomography
Authors: Pettiaux Nicolas , Cassart Marie , Paiva Manuel , Estenne Marc
Published: December 2017

Pettiaux, Nicolas, Marie Cassart, Manuel Paiva, and Marc Estenne. Three-dimensional reconstruction of human diaphragm with the use of spiral computed tomography. J. Appl. Physiol. 82(3): 998–1002, 1997.—We developed a technique of diaphragm imaging by using spiral computed tomography, and we studied four normal subjects who had been previously investigated with magnetic resonance imaging (A. P. Gauthier, S. Verbanck, M. Estenne, C. Segebarth, P. T. Macklem, and M. Paiva. J. Appl. Physiol. 76: 495–506, 1994). One acquisition of 15- to 25-s duration was performed at residual volume, functional residual capacity, functional residual capacity plus one-half inspiratory capacity, and total lung capacity with the subject holding his breath and relaxing. From these acquisitions, 20 coronal and 30 sagittal images were reconstructed at each lung volume; on each image, diaphragm contour in the zone of apposition and in the dome was digitized with the software Osiris, and the digitized silhouettes were used for three-dimensional reconstruction with Matlab. Values of length and surface area for the diaphragm, the dome, and the zone of apposition were very similar to those obtained with magnetic resonance imaging. We conclude that satisfactory three-dimensional reconstruction of the in vivo diaphragm may be obtained with spiral computed tomography, allowing accurate measurements of muscle length, surface area, and shape.
Nitric oxide and thermoregulation during exercise in the horse
Authors: Mills Paul C. , Marlin David J. , Scott Caroline M. , Smith Nicola C.
Published: December 2017

Mills, Paul C., David J. Marlin, Caroline M. Scott, and Nicola C. Smith. Nitric oxide and thermoregulation during exercise in the horse. J. Appl. Physiol. 82(4): 1035–1039, 1997.—The effect of inhibition of nitric oxide production on sweating rate (SR) and on core, rectal, and tail skin temperatures was measured in five Thoroughbred horses during exercise of variable intensity on a high-speed treadmill. A standard exercise test consisting of three canters [∼55% maximum O2uptake (V˙o2 max)], with walking (∼9%V˙o2 max) and trotting (∼22% V˙o2 max) between each canter, was performed twice (control or test), in random order, by each horse. NG-nitro-l-arginine methyl ester (l-NAME; 20 mg/kg), a competitive inhibitor of nitric oxide synthase, was infused into the central circulation and induced a significant reduction in the SR measured on the neck (31.6 ± 6.4 vs. 9.7 ± 4.2 g ⋅ min−1⋅ m−2; 69%) and rump (14.7 ± 5.2 vs. 4.8 ± 1.6 g ⋅ min−1⋅ m−2; 67%) of the horses during canter ( P< 0.05). Significant increases in core, rectal, and tail skin temperatures were also measured ( P < 0.05).l-Arginine (200 mg/kg iv) partially reversed the inhibitory effects ofl-NAME on SR, but core, rectal, and tail skin temperatures continued to increase ( P < 0.05), suggesting a cumulation of body heat. The results support the contention that nitric oxide synthase inhibition diminishes SR, resulting in elevated core and peripheral temperatures leading to deranged thermoregulation during exercise. The inhibition of sweating byl-NAME may be related to peripheral vasoconstriction but may also involve the neurogenic control of sweating.
Spirometry with a Fleisch pneumotachograph: upstream heat exchanger replaces heating requirement
Authors: Miller Martin R. , Pedersen Ole F. , Sigsgaard Torben
Published: December 2017

Miller, Martin R., Ole F. Pedersen, and Torben Sigsgaard.Spirometry with a Fleisch pneumotachograph: upstream heat exchanger replaces heating requirement. J. Appl. Physiol. 82(4): 1053–1057, 1997.—The exact temperature of the head of an unheated Fleisch pneumotachograph (PT) during recording is not known, and variation in its temperature may lead to errors in measuring spirometric indexes. We measured PT head temperature during blows from five normal subjects, recorded by using a PT with and without an upstream heat exchanger to condition the air to the ambient temperature that was set in a climate chamber. Group mean (±SD) temperature of a thermocouple (TC) placed inside the PT head was 11.8 ± 1.9°C with 7°C ambient, 25.4 ± 1.3°C at 23°C, and was 37.2 ± 0.3°C at 37°C. The between-subject range of temperature for this TC was 7.5° at 7°C, 5.5° at 23°C, and 1.1° at 37°C. The mean within-subject within-blow variation of temperature for this TC was 10.0° and 3.3°C for ambient of 7° and 23°C, respectively. At the usual ambient temperature in a laboratory, these differences in temperature lead to a 3.6% between-subject bias in recording, and the within-subject differences lead to 2.6% underreading of peak expiratory flow and a 0.5% overreading later in the blow, which makesatps-to-btpscorrection erroneous or difficult to perform. With the use of an upstream heat exchanger, the group mean temperature was 8.7 ± 0.4°, 23.2 ± 0.2°, and 37.1 ± 0.2°C at the three ambient temperatures, respectively, and the within-subject within-blow variation was reduced to <1°C. A heat exchanger placed upstream of the PT satisfactorily conditioned expired air to the ambient temperature and removed the error.
Hypoxic vasoconstriction in pulmonary arterioles and venules
Authors: Hillier Simon C. , Graham Jacquelyn A. , Hanger Christopher C. , Godbey Patricia S. , Glenny Robb W. , Wagner Wiltz W.
Published: December 2017

Hillier, Simon C., Jacquelyn A. Graham, Christopher C. Hanger, Patricia S. Godbey, Robb W. Glenny, and Wiltz W. Wagner, Jr.Hypoxic vasoconstriction in pulmonary arterioles and venules. J. Appl. Physiol. 82(4): 1084–1090, 1997.—Pulmonary microvessels (<70 μm) lack a complete muscular media. We tested the hypothesis that these thin-walled vessels do not participate in the hypoxic pressor response. Isolated canine lobes were pump perfused at precisely known microvascular pressures. A videomicroscope, coupled to a computerized image-enhancement system, permitted accurate diameter measurements of subpleural arterioles and venules, with each vessel serving as its own control. While vascular pressure was maintained constant throughout the protocol, hypoxia caused an average reduction of 25% of microvessel diameters. The constriction was reversed when nitric oxide was added to the hypoxic gas mixture. The nitric oxide reversal, combined with a lack of lobar blood flow redistribution as measured by fluorescent microspheres, shows that the constriction was active. This response suggests the unexpected potential for active intra-acinar ventilation-perfusion matching.
Age, fitness, and regional blood flow during exercise in the heat
Authors: Ho C. W. , Beard J. L. , Farrell P. A. , Minson C. T. , Kenney W. L.
Published: December 2017

Ho, C. W., J. L. Beard, P. A. Farrell, C. T. Minson, and W. L. Kenney. Age, fitness, and regional blood flow during exercise in the heat. J. Appl. Physiol. 82(4): 1126–1135, 1997.—During dynamic exercise in warm environments, the requisite increase in skin blood flow (SkBF) is supported by an increase in cardiac output (Q˙c) and decreases in splanchnic (SBF) and renal blood flows (RBF). To examine interactions between age and fitness in determining this integrated response, 24 men, i.e., 6 younger fit (YF), 6 younger sedentary (YS), 6 older fit (OF), and 6 older sedentary (OS) rested for 50 min, then exercised at 35 and 60% maximal O2 consumption (V˙o 2 max) at 36°C ambient temperature. YF had a significantly higherQ˙c and SkBF than any other group during exercise, but fitness level had no significant effect on any measured variable in the older men. At 60%V˙o 2 max, younger subjects had significantly greater decreases in SBF and RBF than the older men, regardless of fitness level. Total flow redirected from these two vascular beds (ΔSBF + ΔRBF) followed YF >> YS > OF > OS. A rigorous 4-wk endurance training program increased exercise SkBF in OS, but ΔSBF and ΔRBF were unchanged. Under these conditions, older men distribute Q˙c differently to regional circulations, i.e., smaller increases in SkBF and smaller decreases in SBF and RBF. In younger subjects, the higher SkBF associated with a higher fitness level is a function of both a higher Q˙c and a greater redistribution of flow from splanchnic and renal circulations, but the attenuated splanchnic and renal vasoconstriction in older men does not appear to change with enhanced aerobic fitness.
Na+channel and acetylcholine receptor changes in muscle at sites distant from burns do not simulate denervation
Authors: Nosek M. T. , Martyn J. A. J.
Published: December 2017

Nosek, M. T., and J. A. J. Martyn.Na+channel and acetylcholine receptor changes in muscle at sites distant from burns do not simulate denervation. J. Appl. Physiol. 82(4): 1333–1339, 1997.—Muscle weakness and aberrant responses to neuromuscular relaxants after burn injury are associated with upregulation of acetylcholine receptors (AChRs). Typically, these functional, pharmacological, and biochemical changes occur after denervation, in which transcriptionally mediated qualitative changes in AChRs and Na+channels and of myogenic regulatory proteins MyoD and myogenin also occur. This study in rats, by an examination of changes in the above-enumerated proteins or their transcripts in the gastrocnemius muscle distant from the burn, verifies whether a denervation-like state exists after burns. Scatchard analysis of [3H]saxitoxin binding revealed no changes in the affinity ( Kd) and total number (Bmax) of Na+channels between control and burn-injured animals at both 7 and 14 days after injury. The mRNA levels of the immature proteins, SkM2 of the Na+channels and the γ-subunits of AChRs, the increase of which is pathognomic of denervation, were assessed by Northern analysis and were unchanged. The transcripts of mature Na+channels, SkM1, were significantly increased at day 14after the burn (1.24 ± 0.10 in burn-injured vs. 1.06 ± 0.12 in sham animals, arbitrary units, P= 0.006). Although MyoD levels were increased in burn-injured animals at 14 days (0.21 ± 0.02 vs. 0.15 ± 0.07 arbitrary units, P = 0.05), myogenin levels were unaltered. The absence of changes in AChR transcripts, including α-, δ-, and γ-subunits, indicates that the upregulation of AChR in burns is not transcriptionally mediated. The unaltered levels of transcripts of myogenin, SkM2 of Na+channels and γ-subunit of AChR, confirm that there is no denervation-like prejunctional (nerve-related) component to explain the muscle weakness or the upregulation of AChRs at sites distant from burns.
Retention of soluble99mTc-DTPA in the human lung: 24-h postdeposition
Authors: Foster W. Michael , Stetkiewicz Pamela T. , Freed Arthur N.
Published: December 2017

Foster, W. Michael, Pamela T. Stetkiewicz, and Arthur N. Freed. Retention of soluble99mTc-DTPA in the human lung: 24-h postdeposition. J. Appl. Physiol.82(4): 1378–1382, 1997.—Clearance of low-molecular-weight solutes, e.g., radiolabeled chelate diethylenetriaminepentaacetate (DTPA), across epithelial surfaces of distal airways and the lung parenchyma is a broadly used technique to assess epithelial integrity. It has been generally assumed that clearance of solute follows a simple first-order process and that DTPA clearance through the respiratory epithelium and into blood and lymphatic channels is complete within a few hours. Using γ-camera imaging and a radiolabeled aerosol of99mTc-labeled DTPA, we observed in eight healthy subjects lung retention of radioisotope ∼24 h postdeposition of the 99mTc-DTPA. Residual lung retention at the 24-h end point averaged 6.0 ± 1.8 (SD)% of the amount of radioisotope initially deposited in the lung. This suggests that for normal healthy subjects a small amount of the99mTc radioisotope, either in a dissociated or chelated form, is nonpermeable or slowly cleared from respiratory tisssues.
Short-term exercise training alters responses of porcine femoral and brachial arteries
Authors: McAllister Richard M. , Laughlin M. Harold
Published: December 2017

McAllister, Richard M., and M. Harold Laughlin.Short-term exercise training alters responses of porcine femoral and brachial arteries. J. Appl. Physiol. 82(5): 1438–1444, 1997.—The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity ( P < 0.05). Vascular rings ∼3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 ± 0.09 (−log M); Trn, 9.07 ± 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 ± 0.17 (−log M); Trn, 8.97 ± 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.
Dobutamine as a countermeasure for reduced exercise performance of rats exposed to simulated microgravity
Authors: Tipton Charles M. , Sebastian Lisa A.
Published: December 2017

Tipton, Charles M., and Lisa A. Sebastian. Dobutamine as a countermeasure for reduced exercise performance of rats exposed to simulated microgravity. J. Appl. Physiol. 82(5): 1607–1615, 1997.—Post-spaceflight results and findings from humans and rodents after conditions of bed rest or simulated microgravity indicate maximum exercise performance is significantly compromised. However, the chronic administration of dobutamine (a synthetic adrenomimetic) to humans in relevant experiments improves exercise performance by mechanisms that prevent the decline in peak O2 consumption (V˙o 2 peak) and reduce the concentration of lactic acid measured in the blood. Although dobutamine restores maximumV˙o 2values in animals participating in simulated microgravity studies, it is unknown whether injections of this α1-, β1-, and β2-adrenoceptor agonist in rats will enhance exercise performance. To investigate this, adult male rats were assigned to three experimental groups: caged control receiving saline; head-down, tail-suspended (HDS) receiving saline (HDS-S); and an HDS group receiving dobutamine hydrochloride injections (1.8 mg/kg twice daily per rat). Treadmill tests were performed before suspension, at 14 days, and after 21 days.V˙o 2 peak, run time, and the rate of rise in colonic temperature (heating index) were evaluated after 14 days, whereas at 21 days, hemodynamic responses (heart rate, systolic blood pressure, and double product) were determined during submaximal exercise with blood pH, blood gases, and lactic acid concentration values obtained during maximal exercise. In contrast to the results for the HDS-S rats, dobutamine administration did restore V˙o 2 peakand “normalized” lactic acid concentrations during maximal exercise. However, daily injections were unable to enhance exercise performance aspects associated with treadmill run time, the mechanical efficiency of running, the heating index, or the retention of muscle and body mass. These simulated microgravity findings suggest that dobutamine’s potential value as a countermeasure for postflight maximal performance or for egress emergencies is limited and that other countermeasures must be considered.
Effects of transverse fiber stiffness and central tendon on displacement and shape of a simple diaphragm model
Authors: Boriek Aladin M. , Rodarte Joseph R.
Published: December 2017

Boriek, Aladin M., and Joseph R. Rodarte. Effects of transverse fiber stiffness and central tendon on displacement and shape of a simple diaphragm model. J. Appl. Physiol. 82(5): 1626–1636, 1997.—Our previous experimental results (A. M. Boriek, S. Lui, and J. R. Rodarte. J. Appl. Physiol. 75: 527–533, 1993 and A. M. Boriek, T. A. Wilson, and J. R. Rodarte. J. Appl. Physiol. 76: 223–229, 1994) showed that 1) costal diaphragm shape is similar at functional residual capacity and end inspiration regardless of whether the diaphragm muscle shortens actively (increased tension) or passively (decreased tension); 2) diaphragmatic muscle length changes minimally in the direction transverse to the muscle fibers, suggesting the diaphragm may be inextensible in that direction; and 3) the central tendon is not stretched by physiological stresses. A two-dimensional orthotropic material has two different stiffnesses in orthogonal directions. In the plane tangent to the muscle surface, these directions are along the fibers and transverse to the fibers. We wondered whether orthotropic material properties in the muscular region of the diaphragm and inextensibility of the central tendon might contribute to the constancy of diaphragm shape. Therefore, in the present study, we examined the effects of stiffness transverse to muscle fibers and inextensibility of the central tendon on diaphragmatic displacement and shape. Finite element hemispherical models of the diaphragm were developed by using pressurized isotropic and orthotropic membranes with a wide range of stiffness ratios. We also tested heterogeneous models, in which the muscle sheet was an orthotropic material, having transverse fiber stiffness greater than that along the fibers, with the central tendon being an inextensible isotropic cap. These models revealed that increased transverse stiffness limits the shape change of the diaphragm. Furthermore, an inextensible cap simulating the central tendon dramatically limits the change in shape as well as the membrane displacement in response to pressure. These findings provide a plausible mechanism by which the diaphragm maintains similar shapes despite different physiological loads. This study suggests that changes of diaphragm shape are restricted because the central tendon is essentially inextensible and stiffness in the direction transverse to the muscle fibers is greater than stiffness along the fibers.
Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction
Authors: Yamato H. , Sun J. P. , Churg A. , Wright J. L.
Published: December 2017

Yamato, H., J. P. Sun, A. Churg, and J. L. Wright.Guinea pig pulmonary hypertension caused by cigarette smoke cannot be explained by capillary bed destruction. J. Appl. Physiol. 82(5): 1644–1653, 1997.—Chronic exposure to cigarette smoke is known to produce pulmonary hypertension in humans and in animal models, but the etiology of this process is controversial. To evaluate whether alterations in the structure of the pulmonary capillary bed or the peribronchiolar arterioles could be correlated with the pulmonary arterial pressure (Ppa), we examined the pulmonary vasculature in guinea pigs that had developed pulmonary hypertension after being exposed to cigarette smoke for 6 mo. The smoke-exposed animals had a significant increased Ppa compared with the control (air-exposed) animals (14.4 ± 2.4 vs. 9.9 ± 0.9 cmH2O). In the smoke-exposed animals, there was an increased percentage of muscularized peribronchiolar arterioles (33.5 ± 5.8% smoke exposed vs. 56.1 ± 5.8% control), and the capillary diameter and density were significantly decreased in both the center and periphery of the lobule (center diameter 8.8 ± 1.9, periphery diameter 10.0 ± 2.0 μm, center density 79 ± 5, and periphery density 84 ± 4 in smoked exposed vs. center diameter 7.7 ± 1.9, periphery diameter 8.6 ± 2.0 μm, center density 73 ± 6, and periphery density 77 ± 6 in controls). Neither group showed any correlation between these values and the Ppa. We conclude that although chronic exposure to cigarette smoke produces alteration of the capillary bed and pulmonary arterioles secondary to emphysematous air-space enlargement, these structural findings cannot explain the increase in Ppa. It appears that pulmonary hypertension due to chronic cigarette smoke exposure is a result of a primary alteration of capillary or muscular arteriolar vascular structure but instead may be secondary to alterations of the dynamic properties of the vascular bed with subsequent increase in vascular resistance.