bluuebunny/crossref_metadata_2025 huggingface dataset:
Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy
Authors: Colin Patrice , Slama Michel , Vahanian Alec , Lecarpentier Yves , Motté Gilbert , Chemla Denis
Published: December 2017

Colin, Patrice, Michel Slama, Alec Vahanian, Yves Lecarpentier, Gilbert Motté, and Denis Chemla. Hemodynamic correlates of effective arterial elastance in mitral stenosis before and after balloon valvotomy. J. Appl. Physiol. 83(4): 1083–1089, 1997.—This study had the purpose of documenting the hemodynamic correlates of effective arterial elastance (Ea; i.e., an accurate estimate of hydraulic load) in mitral stenosis (MS) patients. The main hypothesis tested was that Ea relates to the total vascular resistance (R)-to-pulse interval duration ( T) ratio (R/ T) in MS patients both before and after successful balloon mitral valvotomy (BMV). High-fidelity aortic pressure recordings were obtained in 10 patients (40 ± 12 yr) before and 15 min after BMV. Ea value was calculated as the ratio of the steady-state end-systolic aortic pressure (ESAP) to stroke volume (thermodilution). Ea increased after BMV (from 1.55 ± 0.63 to 1.83 ± 0.71 mmHg/ml; P < 0.05). Throughout the procedure, there was a strong linear relationship between Ea and R/ T: Ea = 1.09R/ T − 0.01 mmHg/ml, r = 0.99, P = 0.0001. This ultimately depended on the powerful link between ESAP and mean aortic pressure [MAP; r = 0.99, 95% confidence interval for the difference (MAP − ESAP) from −18.5 to +4.5 mmHg]. Ea was also related to total arterial compliance (area method) and to wave reflections (augmentation index), although to a lesser extent. After BMV, enhanced and anticipated wave reflections were observed, and this was likely to be explained by decreased arterial compliance. The present study indicated that Ea depended mainly on the steady component of hydraulic load (i.e., R) and on heart period (i.e., T) in MS patients.
Experimental murine acid aspiration injury is mediated by neutrophils and the alternative complement pathway
Authors: Weiser Martin R. , Pechet Taine T. V. , Williams Julian P. , Ma Minghe , Frenette Paul S. , Moore Francis D. , Kobzik Lester , Hines Richard O. , Wagner Denisa D. , Carroll Michael C. , Hechtman Herbert B.
Published: December 2017

Weiser, Martin R., Taine T. V. Pechet, Julian P. Williams, Minghe Ma, Paul S. Frenette, Francis D. Moore, Lester Kobzik, Richard O. Hines, Denisa D. Wagner, Michael C. Carroll, and Herbert B. Hechtman. Experimental murine acid aspiration injury is mediated by neutrophils and the alternative complement pathway. J. Appl. Physiol. 83(4): 1090–1095, 1997.—Acid aspiration may result in the development of the acute respiratory distress syndrome, an event associated with significant morbidity and mortality. Although once attributed to direct distal airway injury, the pulmonary failure after acid aspiration is more complex and involves an inflammatory injury mediated by complement (C) and polymorphonuclear leukocytes. This study examines the injurious inflammatory cascades that are activated after acid aspiration. The role of neutrophils was defined by immunodepletion before aspiration, which reduced injury by 59%. The injury was not modified in either P- or E-selectin-knockout mice, indicating that these adhesion molecules were not operative. C activation after aspiration was documented with immunochemistry by C3 deposition on injured alveolar pneumocytes. Animals in which C activation was inhibited with soluble C receptor type 1 (sCR1) had a 54% reduction in injury, similar to the level of protection seen in C3-knockout mice (58%). However C4-knockout mice were not protected from injury, indicating that C activation is mediated by the alternative pathway. Finally, an additive effect of neutrophils and C was demonstrated whereby neutropenic animals that were treated with sCR1 showed an 85% reduction in injury. Thus acid aspiration injury is mediated by neutrophils and the alternative C pathway.
Restoration of fluid balance after exercise-induced dehydration: effects of alcohol consumption
Authors: Shirreffs Susan M. , Maughan Ronald J.
Published: December 2017

Shirreffs, Susan M., and Ronald J Maughan. Restoration of fluid balance after exercise-induced dehydration: effects of alcohol consumption. J. Appl. Physiol. 83(4): 1152–1158, 1997.—The effect of alcohol consumption on the restoration of fluid and electrolyte balance after exercise-induced dehydration [2.01 ± 0.10% (SD) of body mass] was investigated. Drinks containing 0, 1, 2, and 4% alcohol were consumed over 60 min beginning 30 min after the end of exercise; a different beverage was consumed in each of four trials. The volume consumed (2,212 ± 153 ml) was equivalent to 150% of body mass loss. Peak urine flow rate occurred later ( P = 0.024) with the 4% beverage. The total volume of urine produced over the 6 h after rehydration, although not different between trials ( P = 0.307), tended to increase as the quantity of alcohol ingested increased. The increase in blood ( P = 0.013) and plasma ( P = 0.050) volume with rehydration was slower when the 4% beverage was consumed and did not increase to values significantly greater than the dehydrated level ( P = 0.013 and P = 0.050 for blood volume and plasma volume, respectively); generally, the increase was an inverse function of the quantity of alcohol consumed. These results suggest that alcohol has a negligible diuretic effect when consumed in dilute solution after a moderate level of hypohydration induced by exercise in the heat. There appears to be no difference in recovery from dehydration whether the rehydration beverage is alcohol free or contains up to 2% alcohol, but drinks containing 4% alcohol tend to delay the recovery process.
Simulation of motor unit recruitment and microvascular unit perfusion: spatial considerations
Authors: Fuglevand Andrew J. , Segal Steven S.
Published: December 2017

Fuglevand, Andrew J., and Steven S. Segal. Simulation of motor unit recruitment and microvascular unit perfusion: spatial considerations. J. Appl. Physiol.83(4): 1223–1234, 1997.—Muscle fiber activity is the principal stimulus for increasing capillary perfusion during exercise. The control elements of perfusion, i.e., microvascular units (MVUs), supply clusters of muscle fibers, whereas the control elements of contraction, i.e., motor units, are composed of fibers widely scattered throughout muscle. The purpose of this study was to examine how the discordant spatial domains of MVUs and motor units could influence the proportion of open capillaries (designated as perfusion) throughout a muscle cross section. A computer model simulated the locations of perfused MVUs in response to the activation of up to 100 motor units in a muscle with 40,000 fibers and a cross-sectional area of 100 mm2. The simulation increased contraction intensity by progressive recruitment of motor units. For each step of motor unit recruitment, the percentage of active fibers and the number of perfused MVUs were determined for several conditions: 1) motor unit fibers widely dispersed and motor unit territories randomly located (which approximates healthy human muscle), 2) regionalized motor unit territories, 3) reversed recruitment order of motor units, 4) densely clustered motor unit fibers, and 5) increased size but decreased number of motor units. The simulations indicated that the widespread dispersion of motor unit fibers facilitates complete capillary (MVU) perfusion of muscle at low levels of activity. The efficacy by which muscle fiber activity induced perfusion was reduced 7- to 14-fold under conditions that decreased the dispersion of active fibers, increased the size of motor units, or reversed the sequence of motor unit recruitment. Such conditions are similar to those that arise in neuromuscular disorders, with aging, or during electrical stimulation of muscle, respectively.
Respiratory muscle reserve in rats during heavy exercise
Authors: Gosselin Luc E. , Megirian David , Rodman Joshua , Mueller Donna , Farkas Gaspar A.
Published: December 2017

Gosselin, Luc E., David Megirian, Joshua Rodman, Donna Mueller, and Gaspar A. Farkas. Respiratory muscle reserve in rats during heavy exercise. J. Appl. Physiol. 83(4): 1405–1409, 1997.—The extent to which the respiratory pump muscles limit maximal aerobic capacity in quadrupeds is not entirely clear. To examine the effect of reduced respiratory muscle reserve on aerobic capacity, whole body peak oxygen consumption (V˙o 2 peak) was measured in healthy Sprague-Dawley rats before and after Sham, unilateral, or bilateral hemidiaphragm denervation (Dnv) surgery.V˙o 2 peak was determined by using a graded treadmill running test. Hemidiaphragm paralysis was verified after testing by recording the absence of electromyographic activity during inspiration. Before surgery,V˙o 2 peak averaged 86, 87, and 92 ml ⋅ kg−1 ⋅ min−1for the Sham, unilateral, and bilateral Dnv groups, respectively. Two weeks after surgery, there was no significant change inV˙o 2 peak for either the Sham or unilateral Dnv group. However,V˙o 2 peak decreased ∼19% in the bilateral Dnv group 2 wk after surgery. These findings strongly suggest that the pulmonary system in rats is designed such that during heavy exercise, the remaining respiratory pump muscles are able to compensate for the loss of one hemidiaphragm, but not of both.
Central neural correlates of learned heart rate control during exercise: central command demystified
Authors: Chefer Svetlana I. , Talan Mark I. , Engel Bernard T.
Published: December 2017

Chefer, Svetlana I., Mark I. Talan, and Bernard T. Engel.Central neural correlates of learned heart rate control during exercise: central command demystified. J. Appl. Physiol. 83(5): 1448–1453, 1997.—To identify the brain areas involved in central command, four monkeys were trained to attenuate the tachycardia of exercise while different brain sites affecting heart rate (HR) were simultaneously stimulated electrically. Among 24 brain sites located mostly in the limbic structures, we have identified four types of control systems that mediate cardiovascular and motor behavior during exercise. One system increases HR equivalently during both exercise and operantly controlled HR, whereas another increases HR during both tasks and abolishes operant HR control. In the third system, the effect of brain stimulation on HR is attenuated during exercise and during exercise with operantly controlled HR. The fourth system increases HR in both tasks, but its effect is significantly attenuated during operant HR control. We believe that this last system, which includes the mediodorsal nucleus, nucleus ventralis anterior, and cingulate cortex, plays a significant role in central command.
Impaired muscle glycogen resynthesis after a marathon is not caused by decreased muscle GLUT-4 content
Authors: Asp Sven , Rohde Thomas , Richter Erik A.
Published: December 2017

Asp, Sven, Thomas Rohde, and Erik A. Richter. Impaired muscle glycogen resynthesis after a marathon is not caused by decreased muscle GLUT-4 content. J. Appl. Physiol. 83(5): 1482–1485, 1997.—Our purpose was to investigate whether the slow rate of muscle glycogen resynthesis after a competitive marathon is associated with a decrease in the total muscle content of the muscle glucose transporter (GLUT-4). Seven well-trained marathon runners participated in the study, and muscle biopsies were obtained from the lateral head of the gastrocnemius muscle before, immediately after, and 1, 2, and 7 days after the marathon, as were venous blood samples. Muscle GLUT-4 content was unaltered over the experimental period. Muscle glycogen concentration was 758 ± 53 mmol/kg dry weight before the marathon and decreased to 148 ± 39 mmol/kg dry weight immediately afterward. Despite a carbohydrate-rich diet (containing at least 7 g carbohydrate ⋅ kg body mass−1 ⋅ day−1), the muscle glycogen concentration remained 30% lower than before-race values 2 days after the race, whereas it had returned to before-race levels 7 days after the race. We conclude that the total GLUT-4 protein content is unaltered in the lateral gastrocnemius after a competitive marathon and that the slow recovery of muscle glycogen after the race apparently involves factors other than changes in the total content of this protein.
Gas compression in lungs decreases peak expiratory flow depending on resistance of peak flowmeter
Authors: Pedersen O. F. , Pedersen T. F. , Miller M. R.
Published: December 2017

Pedersen, O. F., T. F. Pedersen, and M. R. Miller. Gas compression in lungs decreases peak expiratory flow depending on resistance of peak flowmeter. J. Appl. Physiol. 83(5): 1517–1521, 1997.—It has recently been shown (O. F. Pedersen T. R. Rasmussen, Ø. Omland, T. Sigsgaard, P. H. Quanjer, and M. R. Miller. Eur. Respir. J. 9: 828–833, 1996) that the added resistance of a mini-Wright peak flowmeter decreases peak expiratory flow (PEF) by ∼8% compared with PEF measured by a pneumotachograph. To explore the reason for this, 10 healthy men (mean age 43 yr, range 33–58 yr) were examined in a body plethysmograph with facilities to measure mouth flow vs. expired volume as well as the change in thoracic gas volume (Vb) and alveolar pressure (Pa). The subjects performed forced vital capacity maneuvers through orifices of different sizes and also a mini-Wright peak flowmeter. PEF with the meter and other added resistances were achieved when flow reached the perimeter of the flow-Vb curves. The mini-Wright PEF meter decreased PEF from 11.4 ± 1.5 to 10.3 ± 1.4 (SD) l/s ( P < 0.001), Pa increased from 6.7 ± 1.9 to 9.3 ± 2.7 kPa ( P < 0.001), an increase equal to the pressure drop across the meter, and caused Vb at PEF to decrease by 0.24 ± 0.09 liter ( P < 0.001). We conclude that PEF obtained with an added resistance like a mini-Wright PEF meter is a wave-speed-determined maximal flow, but the added resistance causes gas compression because of increased Pa at PEF. Therefore, Vb at PEF and, accordingly, PEF decrease.
Mechanical impedance of the lung periphery
Authors: Hantos Z. , Peták F. , Adamicza Á. , Asztalos T. , Tolnai J. , Fredberg J. J.
Published: December 2017

Hantos, Z., F. Peták, Á. Adamicza, T. Asztalos, J. Tolnai, and J. J. Fredberg. Mechanical impedance of the lung periphery. J. Appl. Physiol.83(5): 1595–1601, 1997.—The mechanics of the regional airways and tissues was studied in isolated dog lobes by means of a modified wave-tube technique. Small-amplitude pseudorandom forced oscillations between 0.1 and 48 Hz were applied through catheters wedged in 2-mm-diameter bronchi in three regions of each lobe at translobar pressures (Pl) of 10, 7, 5, 3, 2, and 1 cmH2O. The measured regional input impedances were fitted by a model containing the resistance (R1) and inertance (I) of the regular (segmental) airways, the resistance of the collateral channels (R2), and the damping (G) and elastance (H) of the local tissues. This model gave far better fits to the data on impedance of the lung periphery than when G and H were replaced by a single tissue compliance, which explains why interruption of segmental flow did not lead to monoexponential pressure decay in previous studies. The interlobar and intralobar variances of the parameters were equally significant, and poor correlations were found between the airway parameters R1 and R2 and between any airway and tissue parameter (e.g., R1 and H). R2 was on average ∼10 times higher than R1, although the R2-to-R1ratios and their dependencies on Pl were regionally highly variable. However, for the total of 33 regions studied, the Pl dependence was the same for R1 and R2, which may reflect similar morphological structures for the regular and collateral airways. The dependencies of G and H on Plshowed high interregional variations; generally, however, they assumed their minima at medium Pl values (∼5 cmH2O).
Flow-induced responses in cat isolated pulmonary arteries
Authors: Shimoda Larissa A. , Norins Nan A. , Madden Jane A.
Published: December 2017

Shimoda, Larissa A., Nan A. Norins, and Jane A. Madden. Flow-induced responses in cat isolated pulmonary arteries. J. Appl. Physiol.83(5): 1617–1622, 1997.—Isolated, cannulated, endothelium-intact cat pulmonary arteries, averaging 692 ± 104 μm in diameter, were set at a transmural pressure of 10 mmHg and monitored with a video system. Intraluminal flow was increased in steps from 0 to 1.6 ml/min by using a syringe pump. An electronic system held pressure constant by changing outflow resistance. Flow-diameter curves were generated in physiological saline solution. At constant transmural pressure, the arteries constricted in response to increased intraluminal flow. Constriction was not affected by removing extracellular Ca2+ but was abolished after treatment with ryanodine to deplete intracellular Ca2+ stores, with the endothelin-1 synthesis inhibitor phosphoramidon, with the endothelin A-receptor antagonist BQ-123, with the protein kinase C inhibitor staurosporine, or with glutaraldehyde to reduce endothelial cell deformability. The results indicate that isolated pulmonary arteries can constrict in response to intraluminal flow and suggest that constriction is mediated by endothelin-1 and depends on intracellular Ca2+ release and protein kinase C activation.
Raising P50 increases tissue P O 2 in canine skeletal muscle but does not affect critical O2extraction ratio
Authors: Curtis Scott E. , Walker Thomas A. , Bradley W. E. , Cain Stephen M.
Published: December 2017

Curtis, Scott E., Thomas A. Walker, W. E. Bradley, and Stephen M. Cain. Raising P50increases tissue [Formula: see text] in canine skeletal muscle but does not affect critical O2 extraction ratio. J. Appl. Physiol. 83(5): 1681–1689, 1997.—Affinity of hemoglobin (Hb) for O2 determines in part the rate of O2 diffusion from capillaries to myocytes by altering capillary [Formula: see text]. We hypothesized that a decrease in Hb O2 affinity (increased P50) would increase capillary and tissue [Formula: see text](P[Formula: see text]) and improve O2 consumption during ischemia. To test this hypothesis, blood flow to the pump-perfused left hindlimb of 18 anesthetized and paralyzed dogs was progressively decreased over 90 min while hindlimb O2 consumption and O2 delivery (Q˙o 2) and P[Formula: see text] were measured at the muscle surface. Arterial[Formula: see text] was maintained at 150 ± 10 Torr in all dogs. We increased P50by 12.3 ± 0.9 (SE) Torr in nine dogs with RSR-13, an allosteric modifier of Hb. This decreased arterial O2 saturation to 90–92% but increased mean P[Formula: see text] from 35.5 ± 11.6 to 44.1 ± 15.2 (SD) Torr ( P < 0.05) with no change in controls ( n = 9). O2 extraction ratio at criticalQ˙o 2was 74 ± 2% in controls and 79 ± 1% in RSR-13-treated dogs ( P = not significant). P[Formula: see text] was 30–40% higher in the RSR-13-treated group at anyQ˙o 2above critical but did not differ between groups below criticalQ˙o 2. Perfusion heterogeneity and convergence of the dissociation curves near criticalQ˙o 2may have mitigated any effect of increased P50 on O2 diffusion. Still, increasing P50 by 12 Torr with RSR-13 significantly increased P[Formula: see text] atQ˙o 2values above critical.
Wave-speed-determined flow limitation at peak flow in normal and asthmatic subjects
Authors: Pedersen O. F. , Brackel H. J. L. , Bogaard J. M. , Kerrebijn K. F.
Published: December 2017

Pedersen, O. F., H. J. L. Brackel, J. M. Bogaard, and K. F. Kerrebijn. Wave-speed-determined flow limitation at peak flow in normal and asthmatic subjects. J. Appl. Physiol. 83(5): 1721–1732, 1997.—The purpose of this study was to examine whether peak expiratory flow is determined by the wave-speed flow-limiting mechanism. We examined 17 healthy subjects and 11 subjects with stable asthma, the latter treated with inhaled bronchodilators and corticosteroids. We used an esophageal balloon and a Pitot-static probe positioned at five locations between the right lower lobe and midtrachea to obtain dynamic area-transmural pressure ( A-Ptm) curves as described (O. F. Pedersen, B. Thiessen, and S. Lyager. J. Appl. Physiol. 52: 357–369, 1982). From these curves we obtained cross-sectional area ( A) and airway compliance (Caw = d A/dPtm) at PEF, calculated flow at wave speed {V˙ws = A[ A/(Caw∗ρ)0.5], where ρ is density} and speed index is (SI =V˙/V˙ws). In 13 of 15 healthy and in 4 of 10 asthmatic subjects, who could produce satisfactory curves, SI at PEF was >0.9 at one or more measured positions. Alveolar pressure continued to increase after PEF was achieved, suggesting flow limitation somewhere in the airway in all of these subjects. We conclude that wave speed is reached in central airways at PEF in most subjects, but it cannot be excluded that wave speed is also reached in more peripheral airways.
Postexercise protein-carbohydrate and carbohydrate supplements increase muscle glycogen in men and women
Authors: Tarnopolsky M. A. , Bosman M. , Macdonald J. R. , Vandeputte D. , Martin J. , Roy B. D.
Published: December 2017

Tarnopolsky, M. A., M. Bosman, J. R. MacDonald, D. Vandeputte, J. Martin, and B. D. Roy. Postexercise protein-carbohydrate and carbohydrate supplements increase muscle glycogen in men and women. J. Appl. Physiol. 83(6): 1877–1883, 1997.—We have previously demonstrated that women did not increase intramuscular glycogen in response to an increased percent of dietary carbohydrate (CHO) (from 60 to 75% of energy intake) (M. A. Tarnopolsky, S. A. Atkinson, S. M. Phillips, and J. D. MacDougall. J. Appl. Physiol. 78: 1360–1368, 1995). CHO and CHO-protein (Pro) supplementation postexercise can potentiate glycogen resynthesis compared with placebo (K. M. Zawadzki, B. B. Yaspelkis, and J. L. Ivy. J. Appl. Physiol. 72: 1854–1859, 1992). We studied the effect of isoenergetic CHO and CHO-Pro-Fat supplements on muscle glycogen resynthesis in the first 4 h after endurance exercise (90 min at 65% peak O2 consumption) in trained endurance athletes (men, n= 8; women, tested in midfollicular phase, n = 8). Each subject completed three sequential trials separated by 3 wk; a supplement was provided immediately and 1-h postexercise: 1) CHO (0.75 g/kg) + Pro (0.1 g/kg) + Fat (0.02 g/kg), 2) CHO (1 g/kg), and 3) placebo (Pl; artificial sweetener). Subjects were given prepackaged, isoenergetic, isonitrogenous diets, individualized to their habitual diet, for the day before and during the exercise trial. During exercise, women oxidized more lipid than did men ( P< 0.05). Both of the supplement trials resulted in greater postexercise glucose and insulin compared with Pl ( P < 0.01), with no gender differences. Similarly, both of these trials resulted in increased glycogen resynthesis (37.2 vs. 24.6 mmol ⋅ kg dry muscle−1 ⋅ h−1, CHO vs. CHO-Pro-Fat, respectively) compared with Pl (7.5 mmol ⋅ kg dry muscle−1 ⋅ h−1; P < 0.001) with no gender differences. We conclude that postexercise CHO and CHO-Pro-Fat nutritional supplements can increase glycogen resynthesis to a greater extent than Pl for both men and women.
Hyperventilation-induced airway injury and vascular leakage in dogs: effects of α1-adrenergic agonists
Authors: Freed Arthur N. , Taskar Varsha , Schofield Brian , Omori Chiharu
Published: December 2017

Freed, Arthur N., Varsha Taskar, Brian Schofield, and Chiharu Omori. Hyperventilation-induced airway injury and vascular leakage in dogs: effects of α1-adrenergic agonists. J. Appl. Physiol. 83(6): 1884–1889, 1997.—α1-Adrenergic agonists inhibit hyperventilation-induced bronchoconstriction (HIB) in dogs. We tested the hypothesis that α-agonists inhibit HIB by reducing bronchovascular leakage and edema that theoretically could cause airway obstruction. Peripheral airways were isolated by using a bronchoscope; pretreated with either methoxamine (Mx), norepinephrine (NE), or saline aerosol; and then exposed to a 2,000 ml/min dry-air challenge (DAC) for 2 min. Colloidal carbon was injected before DAC and used to quantify bronchovascular permeability. Mx-, NE-, and vehicle-treated airways were prepared for morphometric analysis within 1 h after DAC. Light microscopy revealed that the 2-min DAC produced minimal bronchovascular leakage and little epithelial damage. However, pretreatment with either Mx or NE significantly enhanced dry air-induced bronchovascular hyperpermeability and mucosal injury. The increased damage associated with these α1-agonists implicates a protective role for the bronchial circulation. The fact that α1-agonists inhibit HIB suggests that neither dry air-induced leakage nor injury directly contributes to the development of airway obstruction. In addition, our data suggest that α-agonists attenuate HIB in part by augmenting hyperventilation-induced bronchovascular leakage and by replacing airway water lost during a DAC.
Cardiovascular adaptations to 10 days of cycle exercise
Authors: Mier Constance M. , Turner Michael J. , Ehsani Ali A. , Spina Robert J.
Published: December 2017

Mier, Constance M., Michael J. Turner, Ali A. Ehsani, and Robert J. Spina. Cardiovascular adaptations to 10 days of cycle exercise. J. Appl. Physiol. 83(6): 1900–1906, 1997.—We hypothesized that 10 days of training would enhance cardiac output (CO) and stroke volume (SV) during peak exercise and increase the inotropic response to β-adrenergic stimulation. Ten subjects [age 26 ± 2 (SE) yr] trained on a cycle ergometer for 10 days. At peak exercise, training increased O2 uptake, CO, and SV ( P < 0.001). Left ventricular (LV) size and function at rest were assessed with two-dimensional echocardiography before (baseline) and after atropine injection (1.0 mg) and during four graded doses of dobutamine. LV end-diastolic diameter increased with training ( P< 0.02), whereas LV wall thickness was unchanged. LV contractile performance was assessed by relating fractional shortening (FS) to the estimated end-systolic wall stress (ςES). Training increased the slope of the FS-ςES relationship ( P < 0.05), indicating enhanced systolic function. The increase in slope correlated with increases in CO ( r = −0.71, P < 0.05) and SV ( r = −0.70, P < 0.05). The increase in blood volume also correlated with increases in CO ( r = 0.80, P < 0.01) and SV ( r= 0.85, P < 0.004). These data show that 10 days of training enhance the inotropic response to β-adrenergic stimulation, associated with increases in CO and SV during peak exercise.
Gender differences in airway resistance during sleep
Authors: Trinder John , Kay Amanda , Kleiman Jan , Dunai Judith
Published: December 2017

Trinder, John, Amanda Kay, Jan Kleiman, and Judith Dunai.Gender differences in airway resistance during sleep. J. Appl. Physiol. 83(6): 1986–1997, 1997.—At the onset of non-rapid-eye-movement (NREM) sleep there is a fall in ventilation and an increase in upper airway resistance (UAR). In healthy men there is a progressive increase in UAR as NREM sleep deepens. This study compared the pattern of change in UAR and ventilation in 14 men and 14 women (aged 18–25 yr) both during sleep onset and over the NREM phase of a sleep cycle (from wakefulness to slow-wave sleep). During sleep onset, fluctuations between electroencephalographic alpha and theta activity were associated with mean alterations in inspiratory minute ventilation and UAR of between 1 and 4.5 l/min and between 0.70 and 5.0 cmH2O ⋅ l−1 ⋅ s, respectively, with no significant effect of gender on either change ( P > 0.05). During NREM sleep, however, the increment in UAR was larger in men than in women ( P < 0.01), such that the mean levels of UAR at peak flow reached during slow-wave sleep were ∼25 and 10 cmH2O ⋅ l−1 ⋅ s in men and women, respectively. We speculate that the greater increase in UAR in healthy young men may represent a gender-related susceptibility to sleep-disordered breathing that, in conjunction with other predisposing factors, may contribute to the development of obstructive sleep apnea.
Strength, skeletal muscle composition, and enzyme activity in multiple sclerosis
Authors: Kent-Braun J. A. , Ng A. V. , Castro M. , Weiner M. W. , Gelinas D. , Dudley G. A. , Miller R. G.
Published: December 2017

Kent-Braun, J. A., A. V. Ng, M. Castro, M. W. Weiner, D. Gelinas, G. A. Dudley, and R. G. Miller. Strength, skeletal muscle composition and enzyme activity in multiple sclerosis. J. Appl. Physiol. 83(6): 1998–2004, 1997.—This study examined functional, biochemical, and morphological characteristics of skeletal muscle in nine multiple sclerosis (MS) patients and eight healthy controls in an effort to ascertain whether intramuscular adaptations could account for excessive fatigue in this disease. Analyses of biopsies of the tibialis anterior muscle showed that there were fewer type I fibers (66 ± 6 vs. 76 ± 6%), and that fibers of all types were smaller (average ↓26%) and had lower succinic dehydrogenase (SDH; average ↓40%) and SDH/α-glycerol-phosphate dehydrogenase (GPDH) but not GPDH activities in MS vs. control subjects, suggesting that muscle in this disease is smaller and relies more on anaerobic than aerobic-oxidative energy supply than does muscle of healthy individuals. Maximal voluntary isometric force for dorsiflexion was associated with both average fiber cross-sectional area ( r = 0.71, P = 0.005) and muscle fat-free cross-sectional area by magnetic resonance imaging ( r = 0.80, P < 0.001). Physical activity, assessed by accelerometer, was associated with average fiber SDH/GPDH ( r = 0.78, P = 0.008). There was a tendency for symptomatic fatigue to be inversely associated with average fiber SDH activity ( r = −0.57, P = 0.068). The results of this study suggest that the inherent characteristics of skeletal muscle fibers per se and of skeletal muscle as a whole are altered in the direction of disuse in MS. They also suggest that changes in skeletal muscle in MS may significantly affect function.
Correlation between ventilation and EEG-defined arousal during sleep onset in young subjects
Authors: Trinder John , Van Beveren John A. , Smith Philip , Kleiman Jan , Kay Amanda
Published: December 2017

Trinder, John, John A. Van Beveren, Philip Smith, Jan Kleiman, and Amanda Kay. Correlation between ventilation and EEG-defined arousal during sleep onset in young subjects. J. Appl. Physiol. 83(6): 2005–2011, 1997.—In studies of elderly individuals, ventilation and EEG-defined arousal have been shown to vary periodically and synchronously. Such results have been interpreted as indicating the primacy of sleep/wake state in causing ventilatory instability during sleep onset. However, because the elderly individuals studied were periodic breathers, the results do not unequivocally support this conclusion. In this study the relationship between ventilation and EEG-defined arousal was assessed in a group of 21 young, healthy men in whom ventilatory instability during sleep onset was not periodic. Ventilation and EEG (O1-A2) recordings were collected, and the longest uncontaminated periods from early and late in sleep onset were selected for subsequent analysis. The 84 time series (21 subjects, 2 variables, and 2 occasions in sleep onset) were subjected to spectral analysis to identify periodicity, and the relationship between the two variables was determined by cross-correlational methods. The results indicated that the time series were nonperiodic, yet significant correlations were observed between the two variables. The data support the view that during sleep onset ventilatory instability is driven primarily by variations in sleep/wake arousal level.
Improving energy expenditure estimation by using a triaxial accelerometer
Authors: Chen Kong Y. , Sun Ming
Published: December 2017

Chen, Kong Y., and Ming Sun. Improving energy expenditure estimation by using a triaxial accelerometer. J. Appl. Physiol. 83(6): 2112–2122, 1997.—In our study of 125 subjects (53 men and 72 women) for two 24-h periods, we validated energy expenditure (EE), estimated by a triaxial accelerometer (Tritrac-R3D), by using a whole-room indirect calorimeter under close-to-normal living conditions. The estimated EE was correlated with the measured total EE for the 2 days ( r = 0.925 and r = 0.855; P < 0.001) and in minute-by-minute EE ( P < 0.01). Resting EE formulated by the Tritrac was found to be similar to the measured values [standard errors of estimation (SEE) = 0.112 W/kg; P = 0.822]. The Tritrac significantly underestimated total EE, EE for physical activities, EE of sedentary and light-intensity activities, and EE for exercise such as stepping (all P < 0.001). We developed a linear and a nonlinear model to predict EE by using the acceleration components from the Tritrac. Predicted EE was significantly improved with both models in estimating total EE, total EE for physical activities, EE in low-intensity activities, minute-by-minute averaged relative difference, and minute-by-minute SEE (all P < 0.05). Furthermore, with our generalized models and by using subjects’ physical characteristics and body acceleration, EE can be estimated with higher accuracy (averaged SEE = 0.418 W/kg) than with the Tritrac model.
Effect of selective phosphodiesterase inhibitors on response of ovine pulmonary arteries to prostaglandin E2
Authors: Gao Yuansheng , Tolsa Jean-François , Shen Hai , Raj J. Usha
Published: December 2017

Gao, Yuansheng, Jean-François Tolsa, Hai Shen, and J. Usha Raj. Effect of selective phosphodiesterase inhibitors on response of ovine pulmonary arteries to prostaglandin E2. J. Appl. Physiol. 84(1): 13–18, 1998.—Several adenosine 3′,5′-cyclic monophosphate (cAMP)-hydrolyzing phosphodiesterase isozymes are present in the pulmonary vasculature. The present study was designed to determine the effect of selective inhibitors of phosphodiesterase subtypes on prostaglandin E2(PGE2)-induced relaxation of isolated fourth- generation pulmonary arteries of newborn lambs. PGE2 and forskolin caused pulmonary arteries to relax and induced an increase in the intracellular cAMP content in the vessels. The relaxation and change in cAMP content were augmented by milrinone and rolipram, inhibitors of phosphodiesterase type 3 (PDE3) and type 4 (PDE4), respectively. The augmentation in relaxation and the increase in cAMP content caused by milrinone plus rolipram was greater than the sum of the responses caused by either of the inhibitors alone. 8-Methoxymethyl-1-methyl-3-(2-methylpropyl)xanthine, an inhibitor of phosphodiesterase type 1, had no effect on relaxation and change in cAMP induced by PGE2 and forskolin. Acetylcholine alone had no effect on cAMP content in the vessels but augmented the relaxation and the increase in cAMP induced by PGE2 and forskolin in arteries with endothelium. This effect was not observed in arteries without endothelium or in arteries with endothelium treated with N G-nitro-l-arginine. These results suggest that PDE3 and PDE4 are the primary enzymes hydrolyzing cAMP of pulmonary arteries of newborn lambs and that an inhibition of both PDE3 and PDE4 would result in a greater effect than that caused by inhibition of either one of the subtype isozymes alone. Furthermore, endothelium-derived nitric oxide may enhance cAMP-mediated relaxation by inhibition of PDE3.
Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude
Authors: Gonzalez Norberto C. , Clancy Richard L. , Moue Yoshihiro , Richalet Jean-Paul
Published: December 2017

Gonzalez, Norberto C., Richard L. Clancy, Yoshihiro Moue, and Jean-Paul Richalet. Increasing maximal heart rate increases maximal O2 uptake in rats acclimatized to simulated altitude. J. Appl. Physiol. 84(1): 164–168, 1998.—Maximal exercise heart rate (HRmax) is reduced after acclimatization to hypobaric hypoxia. The low HRmax contributes to reduce maximal cardiac output (Q˙max) and may limit maximal O2 uptake (V˙o 2 max). The objective of these experiments was to test the hypothesis that the reduction inQ˙max after acclimatization to hypoxia, due, in part, to the low HRmax, limitsV˙o 2 max. If this hypothesis is correct, an increase inQ˙max would result in a proportionate increase inV˙o 2 max. Rats acclimatized to hypobaric hypoxia [inspired[Formula: see text]([Formula: see text]) = 69.8 ± 3 Torr for 3 wk] exercised on a treadmill in hypoxic ([Formula: see text] = 71.7 ± 1.1 Torr) or normoxic conditions ([Formula: see text] = 142.1 ± 1.1 Torr). Each rat ran twice: in one bout the rat was allowed to reach its spontaneous HRmax, which was 505 ± 7 and 501 ± 5 beats/min in hypoxic and normoxic exercise, respectively; in the other exercise bout, HRmax was increased by 20% to the preacclimatization value of 600 beats/min by atrial pacing. This resulted in an ∼10% increase inQ˙max, since the increase in HRmax was offset by a 10% decrease in stroke volume, probably due to shortening of diastolic filling time. The increase inQ˙max was accompanied by a proportionate increase in maximal rate of convective O2 delivery (Q˙max × arterial O2 content), maximal work rate, and V˙o 2 max in hypoxic and normoxic exercise. The data show that increasing HRmax to preacclimatization levels increasesV˙o 2 max, supporting the hypothesis that the low HRmax tends to limitV˙o 2 maxafter acclimatization to hypoxia.
Choroidal readaptation to gravity in rats after spaceflight and head-down tilt
Authors: Davet Julien , Clavel Benoit , Datas Lucien , Mani-Ponset Laurence , Maurel Daniel , Herbuté Serge , Viso Michel , Hinds William , Jarvi Joellen , Gabrion Jacqueline
Published: December 2017

Davet, Julien, Benoit Clavel, Lucien Datas, Laurence Mani-Ponset, Daniel Maurel, Serge Herbuté, Michel Viso, William Hinds, Joellen Jarvi, and Jacqueline Gabrion.Choroidal readaptation to gravity in rats after spaceflight and head-down tilt. J. Appl. Physiol.84(1): 19–29, 1998.—To determine when choroidal structures were restored after readaptation to Earth gravity or orthostatic position, fine structure and protein distribution were studied in rat choroid plexus dissected either 6 h [Space Life Sciences-2 (SLS-2) experiments] or 2 days [National Institutes of Health-Rodent 1 (NIH-R1) experiments] after a spaceflight, or 6 h after head-down tilt (HDT) experiments. Apical alterations were noted in choroidal cells from SLS-2 and HDT animals, confirming that weightlessness impaired choroidal structures and functions. However, the presence of small apical microvilli and kinocilia and the absence of vesicle accumulations showed that the apical organization began to be restored rapidly after landing. Very enlarged apical microvilli appeared after 2 days on Earth, suggesting increased choroidal activity. However, as distributions of ezrin and carbonic anhydrase II remained altered in both flight and suspended animals after readaptation to Earth gravity, it was concluded that choroidal structures and functions were not completely restored, even after 2 days in Earth’s gravity.
Effects of NREM sleep on dynamic within-breath changes in upper airway patency in humans
Authors: Morrell M. J. , Badr M. S.
Published: December 2017

Morrell, M. J., and M. S. Badr. Effects of NREM sleep on dynamic within-breath changes in upper airway patency in humans. J. Appl. Physiol. 84(1): 190–199, 1998.—The purpose of our study was to compare inspiratory- and expiratory-related changes in retropalatal cross-sectional area (CSA) during wakefulness to those during non-rapid-eye-movement (NREM) sleep. We studied 18 subjects in whom the severity of sleep-disordered breathing varied. Relative changes in CSA were visualized by using fiber-optic endoscopy. For each breath analyzed (wakefulness n = 4–13; sleep n = 7–16), the CSA was measured at fixed points within inspiration and expiration (0, 25, 50, and 100% of the inspiratory and expiratory duration); these measurements were expressed as a percentage of the CSA that occurred at the start of inspiration. During wakefulness, there was a statistically significant increase in the retropalatal CSA (compared with the start of inspiration) only during early expiration (group mean: expiration, 0% = 112.6 ± 3.2 (SE) %; 25% = 122.8 ± 6.2%; 50% = 110.6 ± 3.8%). In contrast, during sleep, significant changes in CSA occurred during both inspiration and expiration (group mean: inspiration, 25% = 75.3 ± 6.0%; 50% = 66.7 ± 7.7%; 75% = 64.6 ± 8.1%; expiration, 0% = 126.8 ± 11.8%; 25% = 125.3 ± 6.9%). The expiratory-related increase in CSA was followed by narrowing such that at end expiration the caliber of the airway was returned to that occurring at the beginning of inspiration (group mean at end expiration = 98.6 ± 3.1%). The largest changes in CSA occurred in the subjects with an increased body mass index (BMI). We conclude that, during NREM sleep, significant changes in CSA occur during both inspiration and expiration and that the magnitude of these changes is significantly influenced by BMI.
Contractile function of single muscle fibers after hindlimb unweighting in aged rats
Authors: Thompson L. V. , Shoeman J. A.
Published: December 2017

Thompson, L. V., and J. A. Shoeman. Contractile function of single muscle fibers after hindlimb unweighting in aged rats. J. Appl. Physiol. 84(1): 229–235, 1998.—This investigation determined how muscle atrophy produced by hindlimb unweighting (HU) alters the contractile function of single muscle fibers from older animals (30 mo). After 1 wk of HU, small bundles of fibers were isolated from the soleus muscles and the deep region of the lateral head of the gastrocnemius muscles. Single glycerinated fibers were suspended between a motor lever and force transducer, functional properties were studied, and the myosin heavy chain (MHC) composition was determined electrophoretically. After HU, the diameter of type I MHC fibers of the soleus declined (88 ± 2 vs. 80 ± 4 μm) and reductions were observed in peak active force (47 ± 3 vs. 28 ± 3 mg) and peak specific tension (Po; 80 ± 5 vs. 56 ± 5 kN/m2). The maximal unloaded shortening velocity increased. The type I MHC fibers from the gastrocnemius showed reductions in diameter (14%), peak active force (41%), and Po(24%), whereas the type IIa MHC fibers showed reductions in peak active force and Po. Thus 1 wk of inactivity has a significant effect on the force-generating capacity of single skeletal muscle fibers from older animals in a fiber type-specific manner (type I MHC > type IIa MHC > type I-IIa MHC). The decline in the functional properties of single skeletal muscle fibers in the older animals appears to be more pronounced than what has been reported in younger animal populations.
Multiple-breath washin of helium and sulfur hexafluoride in sustained microgravity
Authors: Prisk G. Kim , Elliott Ann R. , Guy Harold J. B. , Verbanck Sylvia , Paiva Manuel , West John B.
Published: December 2017

Prisk, G. Kim, Ann R. Elliott, Harold J. B. Guy, Sylvia Verbanck, Manuel Paiva, and John B. West. Multiple-breath washin of helium and sulfur hexafluoride in sustained microgravity. J. Appl. Physiol. 84(1): 244–252, 1998.—We performed multiple-breath washouts of N2 and simultaneous washins of He and SF6 with fixed tidal volume (∼1,250 ml) and preinspiratory lung volume (approximately the subject’s functional residual capacity in the standing position) in four normal subjects (mean age 40 yr) standing and supine in normal gravity (1 G) and during exposure to sustained microgravity (μG). The primary objective was to examine the influence of diffusive processes on the residual, nongravitational ventilatory inhomogeneity in the lung in μG. We calculated several indexes of convective ventilatory inhomogeneity from each gas species. A normal degree of ventilatory inhomogeneity was seen in the standing position at 1 G that was largely unaltered in the supine position. When we compared the standing position in 1 G with μG, there were reductions in phase III slope in all gases, consistent with a reduction in convection-dependent inhomogeneity in the lung in μG, although considerable convective inhomogeneity persisted in μG. The reductions in the indexes of convection-dependent inhomogeneity were greater for He than for SF6, suggesting that the distances between remaining nonuniformly ventilated compartments in μG were short enough for diffusion of He to be an effective mechanism to reduce gas concentration differences between them.
Mechanism controlling sleep organization of the obese Zucker rats
Authors: Megirian David , Dmochowski Jacek , Farkas Gaspar A.
Published: December 2017

Megirian, David, Jacek Dmochowski, and Gaspar A. Farkas. Mechanism controlling sleep organization of the obese Zucker rat. J. Appl. Physiol. 84(1): 253–256, 1998.—We tested the hypothesis that the obese ( fa/fa) Zucker rat has a sleep organization that differs from that of lean Zucker rats. We used the polygraphic technique to identify and to quantify the distribution of the three main states of the rat: wakefulness (W), non-rapid-eye-movement (NREM), and rapid-eye-movement (REM) sleep states. Assessment of states was made with light present (1000–1600), at the rats thermoneutral temperature of 29°C. Obese rats, compared with lean ones, did not show significant differences in the total time spent in the three main states. Whereas the mean durations of W and REM states did not differ statistically, that of NREM did ( P = 0.046). However, in the obese rats, the frequencies of switching from NREM sleep to W, which increased, and from NREM to REM sleep, which decreased, were statistically significantly different ( P = 0.019). Frequency of switching from either REM or W state was not significantly different. We conclude that sleep organization differs between lean and obese Zucker rats and that it is due to a disparity in switching from NREM sleep to either W or REM sleep and the mean duration of NREM sleep.
Control of breathing during sleep assessed by proportional assist ventilation
Authors: Meza S. , Giannouli E. , Younes M.
Published: December 2017

Meza, S., E. Giannouli, and M. Younes. Control of breathing during sleep assessed by proportional assist ventilation. J. Appl. Physiol. 84(1): 3–12, 1998.—We used proportional assist ventilation (PAV) to evaluate the sources of respiratory drive during sleep. PAV increases the slope of the relation between tidal volume (Vt) and respiratory muscle pressure output (Pmus). We reasoned that if respiratory drive is dominated by chemical factors, progressive increase of PAV gain should result in only a small increase in Vt because Pmus would be downregulated substantially as a result of small decreases in[Formula: see text]. In the presence of substantial nonchemical sources of drive [believed to be the case in rapid-eye-movement (REM) sleep] PAV should result in a substantial increase in minute ventilation and reduction in [Formula: see text] as the output related to the chemically insensitive drive source is amplified severalfold. Twelve normal subjects underwent polysomnography while connected to a PAV ventilator. Continuous positive air pressure (5.2 ± 2.0 cmH2O) was administered to stabilize the upper airway. PAV was increased in 2-min steps from 0 to 20, 40, 60, 80, and 90% of the subject’s elastance and resistance. Vt, respiratory rate, minute ventilation, and end-tidal CO2pressure were measured at the different levels, and Pmus was calculated. Observations were obtained in stage 2 sleep ( n = 12), slow-wave sleep ( n = 11), and REM sleep ( n = 7). In all cases, Pmus was substantially downregulated with increase in assist so that the increase in Vt, although significant ( P < 0.05), was small (0.08 liter at the highest assist). There was no difference in response between REM and non-REM sleep. We conclude that respiratory drive during sleep is dominated by chemical control and that there is no fundamental difference between REM and non-REM sleep in this regard. REM sleep appears to simply add bidirectional noise to what is basically a chemically controlled respiratory output.