bluuebunny/crossref_metadata_2025 huggingface dataset:
Prolongation in expiration evoked from ventrolateral pons of adult rats
Authors: Jodkowski Józef S. , Coles Sharon K. , Dick Thomas E.
Published: December 2017

Jodkowski, Józef S., Sharon K. Coles, and Thomas E. Dick. Prolongation in expiration evoked from ventrolateral pons of adult rats. J. Appl. Physiol. 82(2): 377–381, 1997.—Activation of neurons in the ventrolateral (vl) pons was hypothesized to alter the breathing pattern because previous studies demonstrated apneusis after inhibiting neuronal activity with bilateral muscimol (10 mM) microinjections into the vl pons (17). The excitatory amino acid l-glutamate (10 mM) was microinjected (10–100 nl) into the vl pons in anesthetized, vagotomized, paralyzed, and ventilated adult rats ( n = 8). In four of these animals, the target site was approached from the ventral surface of the pons to avoid penetrating the dorsolateral (dl) pons. The expiratory phase was prolonged transiently and concurrently with the microinjection. The location of the injection sites included the A5 area, was independent of the approach, and was distinct from the dl pons. These results complement our previous data and indicate that neurons located in the vl pons influence respiration specifically by prolonging expiration when activated and by delaying the inspiratory-to-expiratory phase transition when inhibited.
Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin
Authors: Ermert L. , Duncker H.-R. , Brückner H. , Grimminger F. , Hansen T. , Rössig R. , Aktories K. , Seeger W.
Published: December 2017

Ermert, L., H.-R. Duncker, H. Brückner, F. Grimminger, T. Hansen, R. Rössig, K. Aktories, and W. Seeger.Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin. J. Appl. Physiol. 82(2): 382–388, 1997.—The role of the endothelial cytoskeleton for the structural integrity of the pulmonary gas exchange area was probed with the use of Clostridium botulinumC2toxin. This agent causes selective loss of nonmuscle F-actin. In buffer-perfused rabbit lungs, vascular pressures were kept within physiological ranges. In different groups, low-dose [0.3 (C2,I)/0.6 (C2,II) ng/ml] and high-dose [10 (C2,I)/20 (C2,II) ng/ml] toxin were applicated into the buffer fluid; experiments were terminated after a total weight gain of either 1 or 7.5 g. Electron microscopy revealed extensive attenuations, undulations, and protrusions of the endothelial layer, suggestive of “remodeling” and “flowing” of the cell membrane in low C2toxin-treated lungs accompanied by few disruptions of the endothelial layer and edema formation. In addition, endothelial cells displayed vesiculation and bleb formation. Lungs that were exposed to high-toxin doses displayed marked attenuations of the endothelial layer in addition to large endothelial cell disruptions, which did not include interendothelial junctions. Interestingly, type II epithelial cells displayed fusion of lamellar bodies. Collectively, these data suggest that the actin microfilament system is instrumental in supporting endothelial cell membrane configuration and integrity and maintains the intimal barrier function of the lung microvasculature.
Lactate inhibits Ca2+-activated Ca2+-channel activity from skeletal muscle sarcoplasmic reticulum
Authors: Favero Terence G. , Zable , Anthony C. , Colter , David , Abramson Jonathan J.
Published: December 2017

Favero, Terence G., Anthony C. Zable, David Colter, and Jonathan J. Abramson. Lactate inhibits Ca2+-activated Ca2+-channel activity from skeletal muscle sarcoplasmic reticulum. J. Appl. Physiol. 82(2): 447–452, 1997.—Sarcoplasmic reticulum (SR) Ca2+-release channel function is modified by ligands that are generated during about of exercise. We have examined the effects of lactate on Ca2+- and caffeine-stimulated Ca2+release, [3H]ryanodine binding, and single Ca2+-release channel activity of SR isolated from rabbit white skeletal muscle. Lactate, at concentrations from 10 to 30 mM, inhibited Ca2+- and caffeine-stimulated [3H]ryanodine binding to and inhibited Ca2+- and caffeine-stimulated Ca2+release from SR vesicles. Lactate also inhibited caffeine activation of single-channel activity in bilayer reconstitution experiments. These findings suggest that intense muscle activity, which generates high concentrations of lactate, will disrupt excitation-contraction coupling. This may lead to decreases in Ca2+transients promoting a decline in tension development and contribute to muscle fatigue.
Voluntary exercise training enhances glucose transport in muscle stimulated by insulin-like growth factor I
Authors: Hokama Jason Y. , Streeper Ryan S. , Henriksen Erik J.
Published: December 2017

Hokama, Jason Y., Ryan S. Streeper, and Erik J. Henriksen.Voluntary exercise training enhances glucose transport in muscle stimulated by insulin-like growth factor I. J. Appl. Physiol. 82(2): 508–512, 1997.—Skeletal muscle glucose transport can be regulated by hormonal factors such as insulin and insulin-like growth factor I (IGF-I). Although it is well established that exercise training increases insulin action on muscle glucose transport, it is currently unknown whether exercise training leads to an enhancement of IGF-I-stimulated glucose transport in skeletal muscle. Therefore, we measured glucose transport activity [by using 2-deoxy-d-glucose (2-DG) uptake] in the isolated rat epitrochlearis muscle stimulated by submaximally and maximally effective concentrations of insulin (0.2 and 13.3 nM) or IGF-I (5 and 50 nM) after 1, 2, and 3 wk of voluntary wheel running (WR). After 1 wk of WR, both submaximal and maximal insulin-stimulated 2-DG uptake rates were significantly ( P < 0.05) enhanced (43 and 31%) compared with those of sedentary controls, and these variables were further increased after 2 (86 and 57%) and 3 wk (71 and 70%) of WR. Submaximal and maximal IGF-I-stimulated 2-DG uptake rates were significantly enhanced after 1 wk of WR (82 and 61%), and these increases did not expand substantially after 2 (71 and 58%) and 3 wk (96 and 70%) of WR. This enhancement of hormone-stimulated 2-DG uptake in WR muscles preceded any alteration in glucose transporter (GLUT-4) protein level, which increased only after 2 (24%) and 3 wk (54%) of WR. Increases in GLUT-4 protein were significantly correlated ( r = 0.844) with increases in citrate synthase. These results indicate that exercise training can enhance both insulin-stimulated and IGF-I-stimulated muscle glucose transport activity and that these improvements can develop without an increase in GLUT-4 protein.
Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis in young sedentary men
Authors: Burg P. J. M. Van Den , Hospers J. E. H. , Van Vliet M. , Mosterd W. L. , Bouma B. N. , Huisveld I. A.
Published: December 2017

Van den Burg, P. J. M., J. E. H. Hospers, M. Van Vliet, W. L. Mosterd, B. N. Bouma, and I. A. Huisveld. Effect of endurance training and seasonal fluctuation on coagulation and fibrinolysis in young sedentary men. J. Appl. Physiol.82(2): 613–620, 1997.—The effect of 12 wk of submaximal training on hemostatic variables was studied in 20 young sedentary men (Tr) and 19 nontraining matched controls (Con). After training, a more pronounced increase in factor VIII coagulant activity ( P < 0.01), reflected in a decrease in activated partial thromboplastin time ( P < 0.01) during maximal exercise, was seen. Both basal plasminogen activator inhibitor 1 antigen (PAI-1 Ag) and activity (PAI-1 Act; P < 0.05), as well as basal and exercise-induced tissue-type plasminogen activator antigen (t-PA Ag; P < 0.05), were decreased after training. The overall effect on fibrinolysis was reflected in an increase in the t-PA Act/t-PA Ag ratio in the Tr group. In contrast, during the same period (February-June), the Con group demonstrated an increase in basal PAI-1 Ag and PAI-1 Act ( P < 0.05), together with an increase in basal and exercise-induced t-PA Ag ( P < 0.05). Both basal and exercise-induced t-PA Act were unchanged, but t-PA Act/t-PA Ag was decreased ( P < 0.05) in the Con group. We conclude that physical training promotes both coagulation and fibrinolytic potential during exercise and may reverse unfavorable seasonal effects on fibrinolysis.
Effect of endurance exercise training on muscle glycogen supercompensation in rats
Authors: Nakatani Akira , Han Dong-Ho , Hansen Polly A. , Nolte Lorraine A. , Host Helen H. , Hickner Robert C. , Holloszy John O.
Published: December 2017

Nakatani, Akira, Dong-Ho Han, Polly A. Hansen, Lorraine A. Nolte, Helen H. Host, Robert C. Hickner, and John O. Holloszy.Effect of endurance exercise training on muscle glycogen supercompensation in rats. J. Appl. Physiol. 82(2): 711–715, 1997.—The purpose of this study was to test the hypothesis that the rate and extent of glycogen supercompensation in skeletal muscle are increased by endurance exercise training. Rats were trained by using a 5-wk-long swimming program in which the duration of swimming was gradually increased to 6 h/day over 3 wk and then maintained at 6 h/day for an additional 2 wk. Glycogen repletion was measured in trained and untrained rats after a glycogen-depleting bout of exercise. The rats were given a rodent chow diet plus 5% sucrose in their drinking water ad libitum during the recovery period. There were remarkable differences in both the rates of glycogen accumulation and the glycogen concentrations attained in the two groups. The concentration of glycogen in epitrochlearis muscle averaged 13.1 ± 0.9 mg/g wet wt in the untrained group and 31.7 ± 2.7 mg/g in the trained group ( P < 0.001) 24 h after the exercise. This difference could not be explained by a training effect on glycogen synthase. The training induced ∼50% increases in muscle GLUT-4 glucose transporter protein and in hexokinase activity in epitrochlearis muscles. We conclude that endurance exercise training results in increases in both the rate and magnitude of muscle glycogen supercompensation in rats.
High-energy phosphates and tension production in rabbit tibialis anterior/extensor digitorum longus muscles
Authors: Ryschon T. W. , Jarvis J. C. , Salmons S. , Balaban R. S.
Published: December 2017

Ryschon, T. W., J. C. Jarvis, S. Salmons, and R. S. Balaban.High-energy phosphates and tension production in rabbit tibialis anterior/extensor digitorum longus muscles. J. Appl. Physiol. 82(3): 1024–1029, 1997.—The effects of repetitive muscle contraction on energy state and tension production were studied in rabbit tibialis anterior/extensor digitorum longus muscles that had been subjected to 90 days of continuous indirect electrical stimulation at 10 Hz. Anesthetized chronically stimulated and control rabbits were challenged with 15 min of stimulation at 4 and 15 tetani/min. Pi-to-phosphocreatine (PCr) ratio (Pi/PCr) was measured in vivo before, during, and after acute stimulation by31P-magnetic resonance spectroscopy, and tension was recorded at the same time. Although Pi/PCr was low at rest, it was significantly higher in chronically stimulated muscle than in control muscle (0.20 ± 0.02 vs. 0.05 ± 0.01, P < 0.05). Stimulation of control muscle for 15 min at both 4 and 15 tetani/min induced a significant rise in Pi/PCr, whereas the same conditions in chronically stimulated muscle did not produce any significant departure from initial levels. The tension produced by control muscle fell to 93 ± 3% of its initial value during stimulation at 4 tetani/min and to 61 ± 7% at 15 tetani/min, respectively. In chronically stimulated muscle, on the other hand, tension was potentiated above its initial level at both stimulation rates (135 ± 15 and 138 ± 11%, respectively) and remained significantly elevated throughout each trial. The ability of chronically stimulated muscle to sustain high levels of activity with minimal perturbations in Pi/PCr or decrement in tension is attributable to cellular adaptations that include a well-documented increase in oxidative capacity.
Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs
Authors: Chen H. F. , Lee B. P. , Kou Y. R.
Published: December 2017

Chen, H. F., B. P. Lee, and Y. R. Kou. Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs. J. Appl. Physiol. 82(3): 765–771, 1997.—We investigated the involvement of the cyclooxygenase metabolites and hydroxyl radical (⋅ OH) in the stimulation of vagal pulmonary C fibers (PCs) by pulmonary air embolism (PAE). Impulses were recorded from PCs in 51 anesthetized, open-chest, and artificially ventilated dogs. Fifty of 59 PCs were stimulated by infusion of air into the right atrium (0.2 ml ⋅ kg−1⋅ min−1for 10 min). As a group ( n = 59), PC activity increased from a baseline of 0.4 ± 0.1 to a peak of 1.7 ± 0.2 impulses/s during the period from 1 min before to 2 min after the termination of PAE induction. In PCs initially stimulated by PAE induction, PAE was repeated after the intervening treatment (iv) with saline ( n = 9), ibuprofen (a cyclooxygenase inhibitor; n = 11), or dimethylthiourea (a ⋅ OH scavenger; n = 12). The responses of PCs to PAE were not altered by saline vehicle but were abolished by ibuprofen and significantly attenuated by dimethylthiourea. Although hyperinflation of the lungs reversed the PAE-induced bronchomotor responses, it did not reverse the stimulation of PCs ( n= 8). These results suggest that 1) cyclooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional importance of cyclooxygenase products may be mediated in part through the formation of ⋅ OH.
Changes in regional lung mechanics and ventilation distribution after unilateral pulmonary artery occlusion
Authors: Simon Brett A. , Tsuzaki Koichi , Venegas Jose G.
Published: December 2017

Simon, Brett A., Koichi Tsuzaki, and Jose G. Venegas.Changes in regional lung mechanics and ventilation distribution after unilateral pulmonary artery occlusion. J. Appl. Physiol. 82(3): 882–891, 1997.—Regional pneumoconstriction induced by alveolar hypocapnia is an important homeostatic mechanism for optimization of ventilation-perfusion matching. We used positron imaging of13NN-equilibrated lungs to measure the distribution of regional tidal volume (Vt), lung volume (Vl), and lung impedance ( Z) before and after left (L) pulmonary artery occlusion (PAO) in eight anesthetized, open-chest dogs. Measurements were made during eucapnic sinusoidal ventilation at 0.2 Hz with 4-cmH2O positive end expiratory pressure. Right (R) and L lung impedances ( Z rand Z l) were determined from carinal pressure and positron imaging of dynamic regional Vl. LPAO caused an increase in ‖ Z l‖ relative to ‖ Z r‖, resulting in a shift in Vt away from the PAO side, with a L/R ‖ Z‖ ratio changing from 1.20 ± 0.07 (mean ± SE) to 2.79 ± 0.85 after LPAO ( P < 0.05). Although mean L lung Vl decreased slightly, theVl normalized parameters specific admittance and specific compliance both significantly decreased with PAO. Lung recoil pressure at 50% total lung capacity also increased after PAO. We conclude that PAO results in an increase in regional lung Z that shifts ventilation away from the affected area at normal breathing frequencies and that this effect is not due to a change in Vl but reflects mechanical constriction at the tissue level.
Oxygen pulse in guinea pigs in hyperbaric helium and hydrogen
Authors: Kayar Susan R. , Parker Erich C.
Published: December 2017

Kayar, Susan R., and Erich C. Parker. Oxygen pulse in guinea pigs in hyperbaric helium and hydrogen. J. Appl. Physiol. 82(3): 988–997, 1997.—We analyzed O2 pulse, the total volume of O2 consumed per heart beat, in guinea pigs at pressures from 10 to 60 atmospheres. Animals were placed in a hyperbaric chamber and breathed 2% O2 in either helium (heliox) or hydrogen (hydrox). Oxygen consumption rate (V˙o 2) was measured by gas chromatographic analysis. Core temperature and heart rate were measured by using surgically implanted radiotelemeters. TheV˙o 2 was modulated over a fourfold range by varying chamber temperature from 25 to 36°C. There was a direct correlation betweenV˙o 2 and heart rate, which was significantly different for animals in heliox vs. hydrox ( P = 0.003). By using multivariate regression analysis, we identified variables that were significant to O2 pulse: body surface area, chamber temperature, core temperature, and pressure. After normalizing for all nonpressure variables, the residual O2 pulse was found to decrease significantly ( P = 0.02) with pressure for animals in heliox but did not decrease significantly ( P = 0.38) with pressure for animals in hydrox over the range of pressures studied. This amounted to a roughly 25% lower O2 pulse for normothermic animals in 60 atmospheres heliox vs. hydrox. These results suggest that reduction of cardiovascular efficiency in a hyperbaric environment can be mitigated by the choice of breathing gas.
Prevention of ischemia-reperfusion lung injury by sulfated Lewisapentasaccharide
Authors: Reignier Jean , Sellak Hassan , Lemoine Rémy , Lubineau André , Mazmanian Guy Michel , Detruit Hélène , Chapelier Alain , Hervé Philippe , Group The Paris-Sud University Lung Trans
Published: December 2017

Reignier, Jean, Hassan Sellak, Rémy Lemoine, André Lubineau, Guy Michel Mazmanian, Hélène Detruit, Alain Chapelier, Philippe Hervé, and The Paris-Sud University Lung Transplantation Group. Prevention of ischemia-reperfusion lung injury by sulfated Lewisapentasaccharide. J. Appl. Physiol.82(4): 1058–1063, 1997.—Inhibition of polymorphonuclear neutrophil (PMN) adhesion to the pulmonary endothelium attenuates ischemia-reperfusion (I/R) lung injury. We hypothesized that 3′-sulfated Lewisa(SuLa), a potent ligand for the selectin adhesion molecules, may have a beneficial effect on I/R lung injury, as measured by the filtration coefficient ( Kfc), and reduce pulmonary sequestration of PMN as assessed by the lung myeloperoxidase (MPO) activity. Blood-perfused rat lungs were subjected to 30 min of perfusion, 60 min of warm ischemia, and 90 min of reperfusion after treatment with either SuLa (200 μg) or saline. Effects of SuLa on PMN adhesion to cultured human umbilical vein endothelial cells (HUVEC) stimulated with tumor necrosis factor-α and calcium ionophore were also investigated. Compared with preischemia conditions, I/R induced a significant increase in Kfc, which was attenuated with SuLa (80 ± 8 vs. 30 ± 5%; P < 0.001). SuLa reduced lung MPO and PMN adhesion to stimulated HUVEC. These results indicate that SuLa reduces I/R-induced lung injury and PMN accumulation in lung. This protective effect might be related to inhibition of PMN adhesion to endothelial cells.
Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans?
Authors: Maeda Seiji , Miyauchi Takashi , Sakane Michiko , Saito Makoto , Maki Shinichi , Goto Katsutoshi , Matsuda Mitsuo
Published: December 2017

Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto Saito, Shinichi Maki, Katsutoshi Goto, and Mitsuo Matsuda. Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans? J. Appl. Physiol. 82(4): 1107–1111, 1997.—Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide that potentiates contractions to norepinephrine in human vessels. We previously reported that the circulating plasma concentration of ET-1 is significantly increased after exercise (S. Maeda, T. Miyauchi, K. Goto, and M. Matsuda. J. Appl. Physiol. 77: 1399–1402, 1994). To study the roles of ET-1 during and after exercise, we investigated whether endurance exercise affects the production of ET-1 in the circulation of working muscles and nonworking muscles. Male athletes performed one-leg cycle ergometer exercise of 30-min duration at intensity of 110% of their individual ventilatory threshold. Plasma concentrations of ET-1 in both sides of femoral veins (veins in the working leg and nonworking leg) and in the femoral artery (artery in the nonworking leg) were measured before and after exercise. The plasma ET-1 concentration in the femoral vein in the nonworking leg was significantly increased after exercise, whereas that in femoral vein in the working leg was not changed. The arteriovenous difference in ET-1 concentration was significantly increased after exercise in the circulation of the nonworking leg but not of the working leg, which suggests that the production of ET-1 was increased in the circulation of the nonworking leg by exercise. The present study also demonstrated that the plasma norepinephrine concentrations were elevated by exercise in the femoral veins of both the working and nonworking legs, suggesting that the sympathetic nerve activity was augmented in both legs during exercise. Therefore, the present study demonstrates the possibility that the increase in production of ET-1 in nonworking muscles may cause vasoconstriction and hence decrease blood flow in nonworking muscles through its direct vasoconstrictive action or through an indirect effect of ET-1 to enhance vasoconstrictions to norepinephrine and that these responses may be helpful in increasing blood flow in working muscles. We propose that endogenous ET-1 contributes to the exercise-induced redistribution of blood flow in muscles.
Respiratory-related neurons of the fastigial nucleus in response to chemical and mechanical challenges
Authors: Xu Fadi , Frazier Donald T.
Published: December 2017

Xu, Fadi, and Donald T. Frazier. Respiratory-related neurons of the fastigial nucleus in response to chemical and mechanical challenges. J. Appl. Physiol. 82(4): 1177–1184, 1997.—Responses of cerebellar respiratory-related neurons (CRRNs) within the rostral fastigial nucleus and the phrenic neurogram to activation of respiratory mechano- and chemoreceptors were recorded in anesthetized, paralyzed, and ventilated cats. Respiratory challenges included the following: 1) cessation of the ventilator for a single breath at the end of inspiration (lung inflation) or at functional residual capacity, 2) cessation of the ventilator for multiple breaths, and 3) exposure to hypercapnia. Nineteen CRRNs having spontaneous activity during control conditions were characterized as either independent (basic, n = 14) or dependent (pump, n = 5) on the ventilator movement. Thirteen recruited CRRNs showed no respiratory-related activity until breathing was stressed. Burst durations of expiratory CRRNs were prolonged by sustained lung inflation but were inhibited when the volume was sustained at functional residual capacity; it was vice versa for inspiratory CRRNs. Multiple-breath cessation of the ventilator and hypercapnia significantly increased the firing rate and/or burst duration concomitant with changes noted in the phrenic neurogram. We conclude that CRRNs respond to respiratory inputs from CO2 chemo- and pulmonary mechanoreceptors in the absence of skeletal muscle contraction.
Effects of hypothermia on energy metabolism in rat and Richardson’s ground squirrel hearts
Authors: Belke Darrell D. , Wang Lawrence C. H. , Lopaschuk Gary D.
Published: December 2017

Belke, Darrell D., Lawrence C. H. Wang, and Gary D. Lopaschuk. Effects of hypothermia on energy metabolism in rat and Richardson’s ground squirrel hearts. J. Appl. Physiol. 82(4): 1210–1218, 1997.—Glycolysis, glucose oxidation, palmitate oxidation, and cardiac function were measured in isolated working hearts from ground squirrels and rats subjected to a hypothermia-rewarming protocol. Hearts were perfused initially for 30 min at 37°C, followed by 2 h of hypothermic perfusion at 15°C, after which hearts were rewarmed to 37°C and further perfused for 30 min. Functional recovery in ground squirrel hearts was greater than in rat hearts after rewarming. Hypothermia-rewarming had a similar general effect on the various metabolic pathways in both species. Despite these similarities, total energy substrate metabolic rates were greater in rat than ground squirrel hearts during hypothermia despite a lower level of work being performed by the rat hearts, indicating that rat hearts are less efficient than ground squirrel hearts during hypothermia. After rewarming, energy substrate metabolism recovered completely in both species, although cardiac work remained depressed in rat hearts. The difference in functional recovery between rat and ground squirrel hearts after rewarming cannot be explained by general differences in energy substrate metabolism during hypothermia or after rewarming.
In vivo assessment of changes in air and tissue volumes after pneumonectomy
Authors: Takeda S. , Wu E. Y. , Epstein R. H. , Estrera A. S. , Hsia C. C. W.
Published: December 2017

Takeda, S., E. Y. Wu, R. H. Epstein, A. S. Estrera, and C. C. W. Hsia. In vivo assessment of changes in air and tissue volumes after pneumonectomy. J. Appl. Physiol. 82(4): 1340–1348, 1997.—We examined the progression and topographical distribution of postpneumonectomy volume changes in immature foxhounds undergoing right pneumonectomy (R-Pnx, n = 5) or sham pneumonectomy (Sham, n = 6) at 2 mo of age and subsequently raised to maturity. Volumes of lung air (Vair) and tissue (Vti) were estimated by computerized tomography (CT) scan at 7, 22, and 52 wk after surgery at a transpulmonary pressure of 20 cmH2O. Estimates of Vti by CT scan included both septal tissue as well as nonseptal tissue (small- and medium-sized airways and blood vessels); these were compared with estimates of septal Vti by an acetylene rebreathing (Rb) method. We found significant correlations between these techniques (VairCT = 0.83 VairRb + 275, R = 0.97; VtiCT = 1.62 VtiRb − 30, R = 0.81). Extravascular septal Vti returned to normal 7 wk after R-Pnx and remained normal up to maturity. Nonseptal Vti remained significantly below normal. The greatest increase in Vti occurred in the midlung region just cephalad and caudal to the heart. After an early period of accelerated tissue growth after R-Pnx, the rate of septal tissue growth matched that of somatic growth, whereas nonseptal tissue growth lagged behind. Compensatory growth of the remaining left lung was not associated with selective alterations in thoracic development.
Training-induced alterations of glucose flux in men
Authors: Friedlander Anne L. , Casazza Gretchen A. , Horning Michael A. , Huie Melvin J. , Brooks George A.
Published: December 2017

Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (V˙o 2 peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra (4.63 ± 0.25), Rd (4.65 ± 0.24), Rox (3.77 ± 0.43), and Rd E (15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Rox was lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.
Nitric oxide–endothelin-1 interaction in humans
Authors: Ahlborg Gunvor , Lundberg Jan M.
Published: December 2017

Ahlborg, Gunvor, and Jan M. Lundberg. Nitric oxide–endothelin-1 interaction in humans. J. Appl. Physiol. 82(5): 1593–1600, 1997.—Healthy men received NG-monomethyl-l-arginine (l-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1.l-NMMA effects were that heart rate (17%), cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean arterial blood pressure (6%), and systemic (28%) and pulmonary (40%) vascular resistances increased ( P < 0.05 to 0.001). Arterial ET-1 levels (21%) increased due to a pulmonary net ET-1 release ( P < 0.05 to 0.01). Splanchnic glucose output (SGO) fell (26%, P < 0.01). Arterial insulin and glucagon were unchanged. Subsequent ET-1 infusion caused no change in mean arterial pressure, heart rate, or cardiac output, as found in the present controls, or in splanchnic and renal blood flow or splanchnic glucose output as previously found with ET-1 infusion (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 79: 141–145, 1995). In conclusion, l-NMMA like ET-1, induces prolonged cardiovascular effects and suppresses SGO.l-NMMA causes pulmonary ET-1 release and blocks responses to ET-1 infusion. The results indicate that nitric oxide inhibits ET-1 production and thereby interacts with ET-1 regarding increase in vascular tone and reduction of SGO in humans.
Otolithic and tonic neck receptors control of limb blood flow in humans
Authors: Normand Hervé , Etard Olivier , Denise Pierre
Published: December 2017

Normand, Hervé, Olivier Etard, and Pierre Denise.Otolithic and tonic neck receptors control of limb blood flow in humans. J. Appl. Physiol. 82(6): 1734–1738, 1997.—The aim of this study was to evaluate the role of otolithic receptors and neck mechanoreceptors on the control of the cardiovascular system. We measured calf (CBF) and forearm blood flow (FBF) by strain-gauge plethysmography, mean arterial pressure (MAP), and heart rate (HR) in 12 healthy subjects in two body positions (lying prone and on the left side) and three head positions (reference, flexion, and extension). When the subjects were lying prone, CBF and FBF were lower in head flexion (5.2 ± 0.6 and 3.2 ± 0.4 ml ⋅ min−1 ⋅ 100 ml−1, respectively) than in reference position (5.8 ± 0.4 and 3.8 ± 0.3 ml ⋅ min−1 ⋅ 100 ml−1; P < 0.05), with no significant difference in MAP and HR. When the subjects were lying on the side, changing the head position from reference to flexion significantly increased FBF (from 3.7 ± 0.2 to. 4.2 ± 0.4 ml ⋅ min−1 ⋅ 100 ml−1), MAP (from 97.2 ± 3.3 to 102.4 ± 5.8 mmHg), and HR (from 63.7 ± 1.4 to 65.9 ± 2.5 beats/min; P < 0.05). Because otolithic receptors and neck mechanoreceptors are involved when the subjects are lying prone, and otolithic receptors are not involved when the subjects are lying on the side, the results suggest that otolithic and neck mechanoreceptors exert significant influences over the cardiovascular system.
Fibrinolytic responses to acute physical activity in older hypertensive men
Authors: Desouza Christopher A. , Dengel Donald R. , Rogers Marc A. , Cox Kim , Macko Richard F.
Published: December 2017

DeSouza, Christopher A., Donald R. Dengel, Marc A. Rogers, Kim Cox, and Richard F. Macko. Fibrinolytic responses to acute physical activity in older hypertensive men. J. Appl. Physiol. 82(6): 1765–1770, 1997.—We tested the hypothesis that the fibrinolytic response to acute physical activity is impaired in sedentary older hypertensive men, which may contribute to the risk of exertion-triggered acute myocardial infarction in this population. Tissue-type plasminogen activator (t-PA) antigen and activity and plasminogen activator inhibitor-1 (PAI-1) antigen and activity were measured in 12 hypertensive (69 ± 1 yr) and 11 normotensive (64 ± 1 yr) men before and after an acute bout of submaximal exercise. Contrary to our hypothesis, there were no differences between the two groups in the fibrinolytic response to exercise. t-PA antigen and activity were significantly elevated in both the hypertensive (38 and 172%, respectively) and normotensive (45 and 130%, respectively) groups immediately after exercise but they returned to resting levels within 30 min. There was no change in PAI-1 antigen levels immediately after exercise in either group; however, PAI-1 antigen was significantly lower at 30 and 60 min postexercise in both the hypertensive (31 and 16%, respectively) and normotensive (35 and 20%, respectively) groups. PAI-1 activity was significantly lower immediately after exercise in both the hypertensive (25%) and normotensive (22%) groups and remained lower than preexercise levels at 30 min (23 and 26%, respectively) and 60 min (16 and 12%, respectively) postexercise in both groups. The results of this study demonstrate that the fibrinolytic response to an acute bout of moderate physical activity is not impaired in sedentary older hypertensive men.
A 33-yr follow-up of peak oxygen uptake and related variables of former physical education students
Authors: Åstrand Per-Olof , Bergh Ulf , Kilbom Åsa
Published: December 2017

Åstrand, Per-Olof, Ulf Bergh, and Åsa Kilbom. A 33-yr follow-up of peak oxygen uptake and related variables of former physical education students. J. Appl. Physiol. 82(6): 1844–1852, 1997.—In 1949, 27 female and 26 male physical education students were studied at a mean age of 22 and 25 yr, respectively. They were restudied in 1970 and 1982. Measurements included oxygen uptake, heart rate, and pulmonary ventilation during submaximal and maximal exercise on a cycle ergometer and treadmill. After 21 yr, peak aerobic power was significantly reduced, from 2.90 to 2.18 l/min and from 4.09 to 3.28 l/min for women and men, respectively. After another 12 yr, the 1970 maxima were not reduced further. From 1949 to 1982 there was a decrease in peak heart rate from 196 to 177 beats/min in women and from 190 to 175 beats/min in men ( P < 0.05). Highest pulmonary ventilation did not change significantly. At an oxygen uptake of 1.5 l/min, the heart rate was the same in 1949 as in 1982. In conclusion, the physical fitness level of the subjects was well above average for these ages. From 1970 to 1982 there was no decline in the average peak aerobic power, a finding possibly related to increased habitual physical activity.
Norepinephrine spillover at rest and during submaximal exercise in young and old subjects
Authors: Mazzeo Robert S. , Rajkumar Chakravarthi , Jennings Garry , Esler Murray
Published: December 2017

Mazzeo, Robert S., Chakravarthi Rajkumar, Garry Jennings, and Murray Esler. Norepinephrine spillover at rest and during submaximal exercise in young and old subjects. J. Appl. Physiol. 82(6): 1869–1874, 1997.—Aging is associated with elevations in plasma norepinephrine concentrations. The purpose of this investigation was to examine total body and regional norepinephrine spillover as an indicator of sympathetic nerve activity. Eight young (26 ± 3 yr) and seven old (69 ± 5 yr) male subjects were studied at rest and during 20 min of submaximal cycling exercise at 50% of peak work capacity. Norepinephrine spillover was determined by continuous intravenous infusion of [3H]norepinephrine. Arterial norepinephrine concentrations were significantly greater at rest for old vs. young subjects (280 ± 36 vs. 196 ± 27 ng/ml, respectively). Whereas total norepinephrine spillover did not differ between groups at rest, hepatomesenteric norepinephrine spillover was 50% greater in old subjects compared with their young counterparts (51 ± 7 vs. 34 ± 5 ng/min, respectively). Additionally, norepinephrine clearance rates at rest were significantly lower for the old subjects (−23%). During exercise, plasma norepinephrine concentrations increased compared with rest, with old subjects again demonstrating greater values than the young group. Hepatomesenteric norepinephrine spillover was significantly greater (+36%) during exercise for old subjects compared with young; however, no difference was found for whole body spillover rates between age groups. Norepinephrine clearance rates remained depressed (−30%) in the old subjects during exercise. Clearance of epinephrine mirrored that for norepinephrine both at rest and during exercise across age groups. It was concluded that in old subjects, a reduction in norepinephrine clearance and an increase in regional norepinephrine spillover can account for the higher plasma norepinephrine concentrations observed at rest. This relationship is not exacerbated by the stress imposed during an acute bout of exercise.
Norepinephrine-induced contraction of isolated rabbit bronchial artery: role of α1- and α2-adrenoceptor activation
Authors: Zschauer A. O. A. , Sielczak M. W. , Smith D. A. S. , Wanner A.
Published: December 2017

Zschauer, A. O. A., M. W. Sielczak, D. A. S. Smith, and A. Wanner. Norepinephrine-induced contraction of isolated rabbit bronchial artery: role of α1- and α2-adrenoceptor activation. J. Appl. Physiol. 82(6): 1918–1925, 1997.—The contractile effect of norepinephrine (NE) on isolated rabbit bronchial artery rings (150–300 μm in diameter) and the role of α1- and α2-adrenoceptors (AR) on smooth muscle and endothelium were studied. In intact arteries, NE increased tension in a dose-dependent manner, and the sensitivity for NE was further increased in the absence of endothelium. In intact but not in endothelium-denuded arteries, the response to NE was increased in the presence of both indomethacin (Indo; cyclooxygenase inhibitor) and N G-nitro-l-arginine methyl ester [l-NAME; nitric oxide (NO) synthase inhibitor], indicating that two endothelium-derived factors, NO and a prostanoid, modulate the NE-induced contraction. The α1-AR antagonist prazosin shifted the NE dose-response curve to the right, and phenylephrine (α1-AR agonist) induced a dose-dependent contraction that was potentiated byl-NAME or removal of the endothelium. The sensitivity to NE was increased slightly by the α2-AR antagonists yohimbine and idazoxan, and this effect was abolished by Indo or removal of the endothelium. Similarly, contractions induced by UK-14304 (α2-AR agonist) were potentiated by Indo or removal of the endothelium. These results suggest that NE-induced contraction is mediated through activation of α1- and α2-ARs on both smooth muscle and endothelium. Activation of the α1- and α2-ARs on the smooth muscle causes contraction, whereas activation of the endothelial α1- and α2-ARs induces relaxation through release of NO (α1-ARs) and a prostanoid (α2-ARs).
Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects
Authors: McKenzie D. K. , Allen G. M. , Butler J. E. , Gandevia S. C.
Published: December 2017

McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects. J. Appl. Physiol. 82(6): 2011–2019, 1997.—Task failure during inspiratory resistive loading is thought to be accompanied by substantial peripheral fatigue of the inspiratory muscles. Six healthy subjects performed eight resistive breathing trials with loads of 35, 50, 75 and 90% of maximal inspiratory pressure (MIP) with and without supplemental oxygen. MIP measured before, after, and at every minute during the trial increased slightly during the trials, even when corrected for lung volume (e.g., for 24 trials breathing air, 12.5% increase, P < 0.05). In some trials, task failure occurred before 20 min (end point of trial), and in these trials there was an increase in end-tidal[Formula: see text]( P < 0.01), despite the absence of peripheral muscle fatigue. In four subjects (6 trials with task failure), there was no decline in twitch amplitude with bilateral phrenic stimulation or in voluntary activation of the diaphragm, even though end-tidal [Formula: see text] rose by 1.6 ± 0.9%. These results suggest that hypoventilation, CO2 retention, and ultimate task failure during resistive breathing are not simply dependent on impaired force-generating capacity of the diaphragm or impaired voluntary activation of the diaphragm.
Anaerobic capacity and muscle activation during horizontal and uphill running
Authors: Sloniger Mark A. , Cureton Kirk J. , Prior Barry M. , Evans Ellen M.
Published: December 2017

Sloniger, Mark A., Kirk J. Cureton, Barry M. Prior, and Ellen M. Evans. Anaerobic capacity and muscle activation during horizontal and uphill running. J. Appl. Physiol. 83(1): 262–269, 1997.—Anaerobic capacity as measured by the maximal or peak oxygen deficit is greater during uphill than during horizontal running. The objective of this study was to determine whether the greater peak oxygen deficit determined during uphill compared with horizontal running is related to greater muscle volume or mass activated in the lower extremity. The peak oxygen deficit in 12 subjects was determined during supramaximal treadmill running at 0 and 10% grade. Exercise-induced contrast shifts in magnetic resonance images were obtained before and after exercise and used to determine the percentage of muscle volume activated. The mean peak oxygen deficit determined for uphill running [2.96 ± 0.63 (SD) liters or 49 ± 6 ml/kg] was significantly greater ( P < 0.05) than for horizontal running (2.45 ± 0.51 liters or 41 ± 7 ml/kg) by 21%. The mean percentage of muscle volume activated for uphill running [73.1 ± 7.4% (SD)] was significantly greater ( P < 0.05) than for horizontal running (67.0 ± 8.3%) by 9%. The differences in peak oxygen deficit (liters) between uphill and horizontal running were significantly related ( y = 8.05 × 10−4x + 0.35; r = 0.63, SE of estimate = 0.29 liter, P < 0.05) to the differences in the active muscle volume (cm3) in the lower extremity. We conclude that the higher peak oxygen deficit during uphill compared with horizontal running is due in part to increased mass of skeletal muscle activated in the lower extremity.
Oxidation of lactate and acetate in rat skeletal muscle: analysis by13C-nuclear magnetic resonance spectroscopy
Authors: Bertocci Loren A. , Jones John G. , Malloy Craig R. , Victor Ronald G. , Thomas Gail D.
Published: December 2017

Bertocci, Loren A., John G. Jones, Craig R. Malloy, Ronald G. Victor, and Gail D. Thomas. Oxidation of lactate and acetate in rat skeletal muscle: analysis by13C-nuclear magnetic resonance spectroscopy. J. Appl. Physiol. 83(1): 32–39, 1997.—The balance between carbohydrate and fatty acid utilization in skeletal muscle previously has been studied in vivo by using a variety of methods such as arteriovenous concentration differences and radioactive isotope tracer techniques. However, these methodologies provide only indirect estimates of substrate oxidation. We used13C-nuclear magnetic resonance (NMR) spectroscopy and non-steady-state isotopomer analysis to directly quantify the relative oxidation of two competing exogenous substrates in rat skeletal muscles. We infused [1,2-13C]acetate and [3-13C]lactate intravenously in anesthetized rats during the final 30 min of 35 ( n = 10) or 95 ( n = 10) min of intense, unilateral, rhythmic hindlimb contractions.13C-NMR spectroscopy and isotopomer analysis were performed on extracts of gastrocnemius and soleus muscles from both the contracting and contralateral resting hindlimbs. We found that 1) [13C]lactate and [13C]acetate were taken up and oxidized by both resting and contracting skeletal muscles; and 2) high-intensity muscle contractions altered the pattern of substrate utilization such that the relative oxidation of acetate decreased while that of lactate remained unchanged or increased. Based on these findings, we propose that13C-NMR spectroscopy in combination with isotopomer analysis can be used to study the general dynamics of substrate competition between carbohydrates and fats in rat skeletal muscle.
Motor innervation of the cricopharyngeus muscle by the recurrent laryngeal nerve
Authors: Hammond Carol Smith , Davenport Paul W. , Hutchison Alastair , Otto Randall A.
Published: December 2017

Hammond, Carol Smith, Paul W. Davenport, Alastair Hutchison, and Randall A. Otto. Motor innervation of the cricopharyngeus muscle by the recurrent laryngeal nerve. J. Appl. Physiol. 83(1): 89–94, 1997.—Patients with recurrent laryngeal nerve (RLN) paresis demonstrate impaired function of laryngeal muscles and swallowing. The cricopharyngeus muscle (CPM) is a major component of the upper esophageal sphincter. It was hypothesized that the RLN innervates this muscle. A nerve branch leading from the RLN to the CPM was found in adult sheep by anatomic dissection. Electrical stimulation of the RLN elicited a muscle action potential recorded by electrodes placed in the ipsilateral CPM. Swallowing was investigated by mechanical stimulation of oropharynx pre- and postsectioning of the RLN. Severing of the RLN resulted in a loss of the early phases of swallow-related CPM electromyographic activity; however, late-phase CPM electromyographic activity persisted. The RLN provides motor innervation of the CPM, which also has innervation from the pharyngeal plexus.
Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure
Authors: Mathew Oommen P.
Published: December 2017

Mathew, Oommen P. Effects of transient intrathoracic pressure changes (hiccups) on systemic arterial pressure. J. Appl. Physiol. 83(2): 371–375, 1997.—The purpose of the study was to determine the effect of transient changes in intrathoracic pressure on systemic arterial pressure by utilizing hiccups as a tool. Values of systolic and diastolic pressures before, during, and after hiccups were determined in 10 intubated preterm infants. Early-systolic hiccups decreased systolic blood pressure significantly ( P < 0.05) compared with control (39.38 ± 2.72 vs. 46.46 ± 3.41 mmHg) and posthiccups values, whereas no significant change in systolic blood pressure occurred during late-systolic hiccups. Diastolic pressure immediately after the hiccups remained unchanged during both early- and late-systolic hiccups. In contrast, diastolic pressure decreased significantly ( P < 0.05) when hiccups occurred during diastole (both early and late). Systolic pressures of the succeeding cardiac cycle remained unchanged after early-diastolic hiccups, whereas they decreased after late-diastolic hiccups. These results indicate that transient decreases in intrathoracic pressure reduce systemic arterial pressure primarily through an increase in the volume of the thoracic aorta. A reduction in stroke volume appears to contribute to the reduction in systolic pressure.