bluuebunny/crossref_metadata_2025 huggingface dataset:
Effects of muscle kinematics on surface EMG amplitude and frequency during fatiguing dynamic contractions
Authors: Potvin J. R.
Published: December 2017

Potvin, J. R. Effects of muscle kinematics on surface EMG amplitude and frequency during fatiguing dynamic contractions. J. Appl. Physiol. 82(1): 144–151, 1997.—Fifteen male subjects performed a repetitive elbow flexion/extension task with a 7-kg mass until exhaustion. Average joint angle, angular velocity, and biceps brachii surface electromyographic (EMG) amplitude (aEMG) and mean power frequency (MPF) were calculated with each consecutive 250-ms segment of data during the entire trial. Data were separated into concentric or eccentric phases and into seven 20°-ranges from 0 to 140° of elbow flexion. A regression analysis was used to estimate the rested and fatigued aEMG and MPF values. aEMG values were expressed as a percentage of amplitudes from maximum voluntary contractions (MVC). Under rested dynamic conditions, the average concentric aEMG amplitude was 10% MVC higher than average eccentric values. Rested MPF values were similar for concentric and eccentric phases, although values increased ∼20 Hz from the most extended to flexed joint angles. Fatigue resulted in an average increase in concentric and eccentric aEMG of 35 and 10% MVC, respectively. The largest concentric aEMG increases (up to 58% MVC) were observed at higher joint velocities, whereas eccentric increases appeared to be related to decreases in velocity. Fatigue had a similar effect on MPF during both concentric and eccentric phases. Larger MPF decreases were observed at shorter muscle lengths such that values within each angle range were very similar by the end of the trial. It was hypothesized that this finding may reflect a biological minimum in conduction velocity before propagation failure occurs.
Lisofylline prevents leak, but not neutrophil accumulation, in lungs of rats given IL-1 intratracheally
Authors: Hybertson Brooks M. , Bursten Stuart L. , Leff Jonathan A. , Lee Young M. , Jepson Eric K. , Dewitt Chris R. , Zagorski John , Cho Hyun G. , Repine John E.
Published: December 2017

Hybertson, Brooks M., Stuart L. Bursten, Jonathan A. Leff, Young M. Lee, Eric K. Jepson, Chris R. Dewitt, John Zagorski, Hyun G. Cho, and John E. Repine. Lisofylline prevents leak, but not neutrophil accumulation, in lungs of rats given IL-1 intratracheally. J. Appl. Physiol.82(1): 226–232, 1997.—Interleukin-1 (IL-1) is increased in lung lavages from patients with the acute respiratory distress syndrome, and administering IL-1 intratracheally causes neutrophil accumulation and a neutrophil-dependent oxidative leak in lungs of rats. In the present study, we found that rats pretreated intraperitoneally with lisofylline [( R)-1-(5-hydroxyhexyl)-3,7-dimethylxanthine (LSF)], an inhibitor of lysophosphatidic acid acyl transferase, which reduces the production of unsaturated phosphatidic acid species, did not develop the lung leak or the related ultrastructural abnormalities that occur after intratracheal administration of IL-1. However, rats pretreated with LSF and then given IL-1 intratracheally did develop the same elevations of lung lavage cytokine-induced neutrophil chemoattractant (CINC) levels and the same increased numbers of lung lavage neutrophils as rats given IL-1 intratracheally. Lungs of rats given IL-1 intratracheally also had increased unsaturated phosphatidic acid and free acyl (linoleate, linolenate) concentrations compared with untreated rats, and these lipid responses were prevented by pretreatment with LSF. Our results reveal that LSF decreases lung leak and lung lipid alterations without decreasing neutrophil accumulation or lung lavage CINC increases in rats given IL-1 intratracheally.
A distributed nonlinear model of lung tissue elasticity
Authors: Maksym Geoffrey N. , Bates Jason H. T.
Published: December 2017

Maksym, Geoffrey N., and Jason H. T. Bates. A distributed nonlinear model of lung tissue elasticity. J. Appl. Physiol. 82(1): 32–41, 1997.—- We present a theory relating the static stress-strain properties of lung tissue strips to the stress-bearing constituents, collagen and elastin. The fiber pair is modeled as a Hookean spring (elastin) in parallel with a nonlinear string element (collagen), which extends to a maximum stop length. Based on a series of fiber pairs, we develop both analytical and numerical models with distributed constituent properties that account for nonlinear tissue elasticity. The models were fit to measured stretched stress-strain curves of five uniaxially stretched tissue strips, each from a different dog lung. We found that the distributions of stop length and spring stiffness follow inverse power laws, and we hypothesize that this results from the complex fractal-like structure of the constituent fiber matrices in lung tissue. We applied the models to representative pressure-volume (PV) curves from patients with normal, emphysematous, and fibrotic lungs. The PV curves were fit to the equation V = A − Bexp(− KP), where V is volume, P is transpulmonary pressure, and A, B, and K are constants. Our models lead to a possible mechanistic explanation of the shape factor K in terms of the structural organization of collagen and elastin fibers.
Eglin-c prevents monocrotaline-induced ventilatory dysfunction
Authors: Lai Y. L. , Zhou K.-R.
Published: December 2017

Lai, Y. L., and K.-R. Zhou. Eglin-c prevents monocrotaline-induced ventilatory dysfunction. J. Appl. Physiol. 82(1): 324–328, 1997.—The present study was carried out to investigate the relationship between elastase and monocrotaline (MCT)-induced ventilatory dysfunction in rats. To accomplish this, we used an elastase inhibitor eglin-c to suppress the activity of endogenous elastase. Thirty-five young Sprague-Dawley rats were randomly divided into six groups: control, MCT, eglin-c (1), eglin-c (2), eglin-c (1)+MCT, and eglin-c (2)+MCT. Rats in the control group received no treatment. Each MCT rat received a single subcutaneous injection of MCT (60 mg/kg) 1 wk before the functional test. Each eglin-c (1) rat was intratracheally instilled with eglin-c (9 mg/rat) twice in 1 wk. Each eglin-c (2) rat was intratracheally instilled with eglin-c (9 mg/rat) five times in 1 wk. Both eglin-c+MCT groups were treated with the combination of eglin-c (1) or eglin-c (2) and MCT. In the MCT group, there were significant decreases in dynamic respiratory compliance, maximal expiratory flow rate at 50% total lung capacity, and the slopes of the maximal expiratory flow-%total lung capacity curve and the maximal expiratory flow-static recoil pressure curve. However, in the eglin-c (1)+MCT and eglin-c (2)+MCT groups, all of the above-mentioned MCT-induced changes were prevented. All ventilatory values of the eglin-c (1) and eglin-c (2) groups were not significantly different from those of the control group. These results demonstrate that eglin-c treatment prevents MCT-induced ventilatory dysfunction and suggest that endogenous elastase may play an important role in MCT-induced inflammation-mediated ventilatory abnormality.
A model for phosphocreatine resynthesis
Authors: Nevill Alan M. , Jones David A. , McIntyre David , Bogdanis Gregory C. , Nevill Mary E.
Published: December 2017

Nevill, Alan M., David A. Jones, David McIntyre, Gregory C. Bogdanis, and Mary E. Nevill. A model for phosphocreatine resynthesis. J. Appl. Physiol. 82(1): 329–335, 1997.—A model for phosphocreatine (PCr) resynthesis is proposed based on a simple electric circuit, where the PCr store in muscle is likened to the stored charge on the capacitor. The solution to the second-order differential equation that describes the potential around the circuit suggests the model for PCr resynthesis is given by PCr( t) = R − [ d 1 ⋅ exp(− k 1 ⋅ t) ± d 2 ⋅ exp(− k 2 ⋅ t)], where R is PCr concentration at rest, d 1, d 2, k 1, and k 2 are constants, and t is time. By using nonlinear least squares regression, this double-exponential model was shown to fit the PCr recovery data taken from two studies involving maximal exercise accurately. In study 1, when the muscle was electrically stimulated while occluded, PCr concentrations rose during the recovery phase to a level above that observed at rest. In study 2, after intensive dynamic exercise, PCr recovered monotonically to resting concentrations. The second exponential term in the double-exponential model was found to make a significant additional contribution to the quality of fit in both study 1( P < 0.05) and study 2( P < 0.01).
Evidence that nitric oxide increases glucose transport in skeletal muscle
Authors: Balon Thomas W. , Nadler Jerry L. ,   (With the Technical Assistance of Arnie Jasman)
Published: December 2017

Balon, Thomas W., and Jerry L. Nadler. Evidence that nitric oxide increases glucose transport in skeletal muscle. J. Appl. Physiol. 82(1): 359–363, 1997.—Nitric oxide synthase (NOS) is expressed in skeletal muscle. However, the role of nitric oxide (NO) in glucose transport in this tissue remains unclear. To determine the role of NO in modulating glucose transport, 2-deoxyglucose (2-DG) transport was measured in rat extensor digitorum longus (EDL) muscles that were exposed to either a maximally stimulating concentration of insulin or to an electrical stimulation protocol, in the presence of NG-monomethyl-l-arginine, a NOS inhibitor. In addition, EDL preparations were exposed to sodium nitroprusside (SNP), an NO donor, in the presence of submaximal and maximally stimulating concentrations of insulin. NOS inhibition reduced both basal and exercise-enhanced 2-DG transport but had no effect on insulin-stimulated 2-DG transport. Furthermore, SNP increased 2-DG transport in a dose-responsive manner. The effects of SNP and insulin on 2-DG transport were additive when insulin was present in physiological but not in pharmacological concentrations. Chronic treadmill training increased protein expression of both type I and type III NOS in soleus muscle homogenates. Our results suggest that NO may be a potential mediator of exercise-induced glucose transport.
Testosterone and cortisol in relationship to dietary nutrients and resistance exercise
Authors: Volek Jeff S. , Kraemer William J. , Bush Jill A. , Incledon Thomas , Boetes Mark
Published: December 2017

Volek, Jeff S., William J. Kraemer, Jill A. Bush, Thomas Incledon, and Mark Boetes. Testosterone and cortisol in relationship to dietary nutrients and resistance exercise. J. Appl. Physiol. 82(1): 49–54, 1997.—Manipulation of resistance exercise variables (i.e., intensity, volume, and rest periods) affects the endocrine response to exercise; however, the influence of dietary nutrients on basal and exercise-induced concentrations of hormones is less understood. The present study examined the relationship between dietary nutrients and resting and exercise-induced blood concentrations of testosterone (T) and cortisol (C). Twelve men performed a bench press exercise protocol (5 sets to failure using a 10-repetitions maximum load) and a jump squat protocol (5 sets of 10 repetitions using 30% of each subject’s 1-repetition maximum squat) with 2 min of rest between all sets. A blood sample was obtained at preexercise and 5 min postexercise for determination of serum T and C. Subjects also completed detailed dietary food records for a total of 17 days. There was a significant ( P ≤ 0.05) increase in postexercise T compared with preexercise values for both the bench press (7.4%) and jump squat (15.1%) protocols; however, C was not significantly different from preexercise concentrations. Significant correlations were observed between preexercise T and percent energy protein ( r = −0.71), percent energy fat ( r = 0.72), saturated fatty acids (g ⋅ 1,000 kcal−1⋅ day−1; r = 0.77), monounsaturated fatty acids (g ⋅ 1,000 kcal−1⋅ day−1; r = 0.79), the polyunsaturated fat-to-saturated fat ratio ( r = −0.63), and the protein-to-carbohydrate ratio ( r = −0.59). There were no significant correlations observed between any nutritional variables and preexercise C or the absolute increase in T and C after exercise. These data confirm that high-intensity resistance exercise results in elevated postexercise T concentrations. A more impressive finding was that dietary nutrients may be capable of modulating resting concentrations of T.
Long-term facilitation of upper airway muscle activities in vagotomized and vagally intact cats
Authors: Mateika J. H. , Fregosi R. F. ,   (With the Technical Assistance of E. G. Essif )
Published: December 2017

Mateika, J. H., and R. F. Fregosi. Long-term facilitation of upper airway muscle activities in vagotomized and vagally intact cats. J. Appl. Physiol.82(2): 419–425, 1997.—The primary purpose of the present investigation was to determine whether long-term facilitation (LTF) of upper airway muscle activities occurs in vagotomized and vagally intact cats. Tidal volume and diaphragm, genioglossus, and nasal dilator muscle activities were recorded before, during, and after one carotid sinus nerve was stimulated five times with 2-min trains of constant current. Sixty minutes after stimulation, nasal dilator and genioglossus muscle activities were significantly greater than control in the vagotomized cats but not in the vagally intact cats. Tidal volume recorded from the vagotomized and vagally intact cats was significantly greater than control during the poststimulation period. In contrast, diaphragm activities were not significantly elevated in the poststimulation period in either group of animals. We conclude that 1) LTF of genioglossus and nasal dilator muscle activities can be evoked in vagotomized cats; 2) vagal mechanisms inhibit LTF in upper airway muscles; and 3) LTF can be evoked in accessory inspiratory muscles because LTF of inspired tidal volume was greater than LTF of diaphragm activity.
Effect of lung inflation in vivo on airways with smooth muscle tone or edema
Authors: Brown Robert H. , Mitzner Wayne , Bulut Yonca , Wagner Elizabeth M.
Published: December 2017

Brown, Robert H., Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner. Effect of lung inflation in vivo on airways with smooth muscle tone or edema. J. Appl. Physiol. 82(2): 491–499, 1997.—Fibrous attachments to the airway wall and a subpleural surrounding pressure can create an external load against which airway smooth muscle must contract. A decrease in this load has been proposed as a possible cause of increased airway narrowing in asthmatic individuals. To study the interaction between the airways and the surrounding lung parenchyma, we investigated the effect of lung inflation on relaxed airways, airways contracted with methacholine, and airways made edematous by infusion of bradykinin into the bronchial artery. Measurements were made in anesthetized sheep by using high-resolution computed tomography to visualize changes in individual airways. During methacholine infusion, airway area was decreased but increased minimally with increases in transpulmonary pressure. Bradykinin infusion caused a 50% increase in airway wall area and a small decrease in airway luminal area. In contrast to airways contracted with methacholine, the luminal area after bradykinin increased substantially with increases in transpulmonary pressure, reaching 99% of the relaxed area at total lung capacity. Thus airway edema by itself did not prevent full distension of the airway at lung volumes approaching total lung capacity. Therefore, we speculate that if a deep inspiration fails to relieve airway narrowing in vivo, this must be a manifestation of airway smooth muscle contraction and not airway wall edema.
Comparison of energy expenditure elevations after submaximal and supramaximal running
Authors: Laforgia J. , Withers R. T. , Shipp N. J. , Gore C. J.
Published: December 2017

Laforgia, J., R. T. Withers, N. J. Shipp, and C. J. Gore.Comparison of energy expenditure elevations after submaximal and supramaximal running. J. Appl. Physiol. 82(2): 661–666, 1997.—Although exercise intensity has been identified as a major determinant of the excess postexercise oxygen consumption (EPOC), no studies have compared the EPOC after submaximal continuous running and supramaximal interval running. Eight male middle-distance runners [age = 21.1 ± 3.1 (SD) yr; mass = 67.8 ± 5.1 kg; maximal oxygen consumption (V˙o 2 max) = 69.2 ± 4.0 ml ⋅ kg−1 ⋅ min−1] therefore completed two equated treatments of treadmill running (continuous running: 30 min at 70%V˙o 2 max; interval running: 20 × 1-min intervals at 105%V˙o 2 max with intervening 2-min rest periods) and a control session (no exercise) in a counterbalanced research design. The 9-h EPOC values were 6.9 ± 3.8 and 15.0 ± 3.3 liters ( t-test: P = 0.001) for the submaximal and supramaximal treatments, respectively. These values represent 7.1 and 13.8% of the net total oxygen cost of both treatments. Notwithstanding the higher EPOC for supramaximal interval running compared with submaximal continuous running, the major contribution of both to weight loss is therefore via the energy expended during the actual exercise.
Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation
Authors: Charan Nirmal B. , Johnson Shane R. , Lakshminarayan S. , Thompson William H. , Carvalho Paula
Published: December 2017

Charan, Nirmal B., Shane R. Johnson, S. Lakshminarayan, William H. Thompson, and Paula Carvalho. Nitric oxide and β-adrenergic agonist-induced bronchial arterial vasodilation. J. Appl. Physiol. 82(2): 686–692, 1997.—In anesthetized sheep, we measured bronchial blood flow (Q˙br) by an ultrasonic flow probe to investigate the interaction between inhaled nitric oxide (NO; 100 parts/million) given for 5 min and 5 ml of aerosolized isoetharine (1.49 × 10−2 M concentration). NO and isoetharine increased Q˙br from 26.5 ± 6.5 to 39.1 (SE) ± 10.6 and 39.7 ± 10.7 ml/min, respectively ( n = 5). Administration of NO immediately after isoetharine further increasedQ˙br to 57.3 ± 15.1 ml/min. NO synthase inhibitor N ω-nitro-l-arginine methyl ester hydrochloride (l-NAME; 30 mg/kg, in 20 ml saline given iv) decreased Q˙br to 14.6 ± 2.6 ml/min. NO given three times alternately with isoetharine progressively increased Q˙br from 14.6 ± 2.6 to 74.3 ± 17.0 ml/min, suggesting that NO and isoetharine potentiate vasodilator effects of each other. In three other sheep, afterl-NAME, three sequential doses of isoetharine increased Q˙br from 10.2 ± 3.4 to 11.5 ± 5.7, 11.7 ± 4.7, and 13.3 ± 5.7 ml/min, respectively, indicating that effects of isoetharine are predominantly mediated through synthesis of NO. When this was followed by three sequential administrations of NO, Q˙br increased by 146, 172, and 185%, respectively. Thus in the bronchial circulation there seems to be a close interaction between adenosine 3′,5′-cyclic monophosphate- and guanosine 3′,5′-cyclic monophosphate-mediated vasodilatation.
Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation
Authors: Hayashi Yoshihiro , Ikata Takaaki , Takai Hiroaki , Takata Shinjiro , Sogabe Takayuki , Koga Keiko
Published: December 2017

Hayashi, Yoshihiro, Takaaki Ikata, Hiroaki Takai, Shinjiro Takata, Takayuki Sogabe, and Keiko Koga. Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation. J. Appl. Physiol. 82(3): 732–737, 1997.—This study examined the time course of recovery from nerve injury on energy state assessed by phosphorus-31 magnetic resonance spectroscopy and local circulation dynamics by fluorine-19 magnetic resonance spectroscopy in skeletal muscles of rats. The hindlimb muscles that had undergone unilateral sciatic nerve compression for 2 wk (CN) were compared with sham-operated (SO) muscles and with muscles that had the compression removed after 2 wk and were allowed to recover for 4 wk (R4) or for 6 wk (R6). The energy state and local circulation dynamics of CN muscles were less than those of SO muscles ( P< 0.01). The energy state of R4 muscles remained at levels similar to CN muscles, whereas the local circulation dynamics improved but not back to SO values. In R6 muscles, both parameters returned to SO values. These results showed that the recovery processes of circulation precede those of energy state in skeletal muscles.
Resistance exercise maintains skeletal muscle protein synthesis during bed rest
Authors: Ferrando Arny A. , Tipton Kevin D. , Bamman Marcas M. , Wolfe Robert R.
Published: December 2017

Ferrando, Arny A., Kevin D. Tipton, Marcas M. Bamman, and Robert R. Wolfe. Resistance exercise maintains skeletal muscle protein synthesis during bed rest. J. Appl. Physiol. 82(3): 807–810, 1997.—Spaceflight results in a loss of lean body mass and muscular strength. A ground-based model for microgravity, bed rest, results in a loss of lean body mass due to a decrease in muscle protein synthesis (MPS). Resistance training is suggested as a proposed countermeasure for spaceflight-induced atrophy because it is known to increase both MPS and skeletal muscle strength. We therefore hypothesized that scheduled resistance training throughout bed rest would ameliorate the decrease in MPS. Two groups of healthy volunteers were studied during 14 days of simulated microgravity. One group adhered to strict bed rest (BR; n = 5), whereas a second group engaged in leg resistance exercise every other day throughout bed rest (BREx; n = 6). MPS was determined directly by the incorporation of infusedl-[ ring-13C6]phenylalanine into vastus lateralis protein. After 14 days of bed rest, MPS in the BREx group did not change and was significantly greater than in the BR group. Thus moderate-resistance exercise can counteract the decrease in MPS during bed rest.
Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats
Authors: Fitzgerald Robert S. , Shirahata Machiko , Ide Tohru
Published: December 2017

Fitzgerald, Robert S., Machiko Shirahata, and Tohru Ide.Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats. J. Appl. Physiol.82(3): 819–827, 1997.—From the 1930s into the 1970s, the role of acetylcholine (ACh) in the carotid body’s chemotransduction of hypoxia was debated. Since the late 1970s, the issue has been pursued only intermittently or not at all. The purpose of this study was to test again with a new preparation the hypothesis that ACh is an excitatory neurotransmitter in the cat carotid body’s chemotransduction of hypoxia. We tested the effect of the specific nicotinic blocker mecamylamine and the muscarinic blocker of all five muscarinic receptors, atropine. We further tested the effects of M1 and M2 muscarinic-receptor blockers. The carotid body region was selectively perfused with hypoxic Krebs-Ringer bicarbonate (KRB) solutions that were blocker free or contained varying doses of the blockers. Both mecamylamine and atropine reduced the response to hypoxic KRB in a dose-related manner. The M2 muscarinic-receptor blockers gallamine and AFDX 116 increased the response to hypoxic KRB, whereas the M1 muscarinic-receptor blocker pirenzepine reduced the response to hypoxic KRB. These data are consistent with an excitatory role for ACh in the carotid body chemotransduction of hypoxia in the cat.
Bronchial vasodilatory response to ionic and nonionic contrast media
Authors: Baile Elisabeth M. , Wang Lu , Verburgt Lorraine , Paré Peter D.
Published: December 2017

Baile, Elisabeth M., Lu Wang, Lorraine Verburgt, and Peter D. Paré. Bronchial vasodilatory response to ionic and nonionic contrast media. J. Appl. Physiol. 82(3): 841–845, 1997.—It has recently been shown that bronchial arterial injection of conventional contrast medium causes a significant increase in bronchial blood flow (Q˙br) and that this response is partially attenuated after infusion of N ω-nitro-l-arginine (l-NNA). However, the precise mechanism for this increase in Q˙br is unknown. In this study we examined the effect of bronchial arterial injection of conventional ionic as well as nonionic contrast media. We measuredQ˙br in nine anesthetized, ventilated, open-chest sheep. Q˙br was recorded before (baseline) and at the peak response to injection of 0.5 ml of either 0.9% saline (control; isosmolar with plasma), Omnipaque 300 (iohexol; nonionic), Conray 66 (sodium iothalamate; ionic), or 50% dextrose (viscous control).
Segmental pulmonary vascular responses to ATP in rat lungs: role of nitric oxide
Authors: Hakim Tawfic S. , Ferrario Lara , Freedman Jeffrey C. , Carlin Robert E. , Camporesi Enrico M.
Published: December 2017

Hakim, Tawfic S., Lara Ferrario, Jeffrey C. Freedman, Robert E. Carlin, and Enrico M. Camporesi. Segmental pulmonary vascular responses to ATP in rat lungs: role of nitric oxide. J. Appl. Physiol. 82(3): 852–858, 1997.—ATP exhibits vascular pressor and depressor responses in a dose- and tone-dependent manner. The vascular site of ATP-induced contraction or dilation has not previously been characterized. Using the vascular occlusion technique, we investigated the effects of ATP in isolated rat lungs perfused with autologous blood (hematocrit = 20%) and described its action during resting and elevated tone in terms of changes in resistances of the small and large arteries and veins. During resting tone, ATP (10−5M)
Frequency dependence of forced oscillatory respiratory mechanics in horses with heaves
Authors: Young S. S. , Tesarowski D. , Viel L.
Published: December 2017

Young, S. S., D. Tesarowski, and L. Viel. Frequency dependence of forced oscillatory respiratory mechanics in horses with heaves. J. Appl. Physiol. 82(3): 983–987, 1997.—The effect of measurement frequency on respiratory mechanics was investigated in six horses with reversible allergic airway disease. Total respiratory impedance was measured at 1.5, 2.0, 3.0, and 5.0 Hz by using the forced oscillation technique with the horses in remission, after acute antigenic challenge producing clinical heaves, and with heaves but after the administration of 2 mg fenoterol by inhalation. The slopes of the magnitude (‖Zrs‖) and real part (R) of total respiratory impedance over the frequency range 1.5–3 Hz changed significantly after antigenic challenge and fenoterol. The ratio of R at 2 Hz to R at 3 Hz, however, discriminated better among the three conditions. Compliance and resonant frequency (calculated by using a three-element model) changed significantly after antigenic challenge and fenoterol, but inertance did not. We concluded that horses with heaves showed frequency dependence of R and ‖Zrs‖ at frequencies up to 3 Hz and that parameters derived from a three-element model were useful indicators of small airway obstruction in the horse.
Interactive effects of K+, acid, norepinephrine, and ischemia on the heart: implications for exercise
Authors: O’Neill Mark , Sears Claire E. , Paterson David J.
Published: December 2017

O’Neill, Mark, Claire E. Sears, and David J. Paterson.Interactive effects of K+, acid, norepinephrine, and ischemia on the heart: implications for exercise. J. Appl. Physiol. 82(4): 1046–1052, 1997.—We tested the hypothesis that cardiac ischemia uncouples the beneficial interaction among hyperkalemia, acidosis, and raised plasma catecholamines when these chemicals are changed to mimic their exercise levels. Potassium chloride, lactic acid, and norepinephrine (NE) were infused intravenously for 2 min into anesthetized, artificially ventilated, thoracotomized rabbits during either occlusion of the left circumflex artery (3 min; n = 10) or after a period of prolonged ischemia (20 min; n = 7) that led to a small infarction. NE (1 μg ⋅ kg−1 ⋅ min−1iv) offset the negative cardiac effects of hyperkalemia (up to 8.7 ± 0.7 mM) and acidosis (arterial pH 7.09 ± 0.03) in normal hearts. Cardiac performance was not significantly depressed by either acute or chronic ischemia before any infusions. However, the protective effect of NE during acute ischemia or after prolonged ischemia with hyperkalemia and acidosis was substantially reduced. These results show that cardiac ischemia attenuates the protective action of NE and increases the depressive effects of hyperkalemia and acidosis. Whether myocardial ischemia amplifies the cardiotoxic effects of hyperkalemia and acidosis during vigorous exercise by attenuating the beneficial effect of catecholamines remains to be determined.
Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo
Authors: Reiser Peter J. , Kline William O. , Vaghy Pal L.
Published: December 2017

Reiser, Peter J., William O. Kline, and Pal L. Vaghy.Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo. J. Appl. Physiol. 82(4): 1250–1255, 1997.—Fast-twitch skeletal muscles contain more neuronal-type nitric oxide synthase (nNOS) than slow-twitch muscles because nNOS is present only in fast (type II) muscle fibers. Chronic in vivo electrical stimulation of tibialis anterior and extensor digitorum longus muscles of rabbits was used as a method of inducing fast-to-slow fiber type transformation. We have studied whether an increase in muscle contractile activity induced by electrical stimulation alters nNOS expression, and if so, whether the nNOS expression decreases to the levels present in slow muscles. Changes in the expression of myosin heavy chain isoforms and maximum velocity of shortening of skinned fibers indicated characteristic fast-to-slow fiber type transformation after 3 wk of stimulation. At the same time, activity of NOS doubled in the stimulated muscles, and this correlated with an increase in the expression of nNOS shown by immunoblot analysis. These data suggest that nNOS expression in skeletal muscle is regulated by muscle activity and that this regulation does not necessarily follow the fast-twitch and slow-twitch pattern during the dynamic phase of phenotype transformation.
A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics
Authors: Ursino Mauro , Lodi Carlo Alberto
Published: December 2017

Ursino, Mauro, and Carlo Alberto Lodi. A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics. J. Appl. Physiol. 82(4): 1256–1269, 1997.—A simple mathematical model of intracranial pressure (ICP) dynamics oriented to clinical practice is presented. It includes the hemodynamics of the arterial-arteriolar cerebrovascular bed, cerebrospinal fluid (CSF) production and reabsorption processes, the nonlinear pressure-volume relationship of the craniospinal compartment, and a Starling resistor mechanism for the cerebral veins. Moreover, arterioles are controlled by cerebral autoregulation mechanisms, which are simulated by means of a time constant and a sigmoidal static characteristic. The model is used to simulate interactions between ICP, cerebral blood volume, and autoregulation. Three different related phenomena are analyzed: the generation of plateau waves, the effect of acute arterial hypotension on ICP, and the role of cerebral hemodynamics during pressure-volume index (PVI) tests. Simulation results suggest the following: 1) ICP dynamics may become unstable in patients with elevated CSF outflow resistance and decreased intracranial compliance, provided cerebral autoregulation is efficient. Instability manifests itself with the occurrence of self-sustained plateau waves. 2) Moderate acute arterial hypotension may have completely different effects on ICP, depending on the value of model parameters. If physiological compensatory mechanisms (CSF circulation and intracranial storage capacity) are efficient, acute hypotension has only negligible effects on ICP and cerebral blood flow (CBF). If these compensatory mechanisms are poor, even modest hypotension may induce a large transient increase in ICP and a significant transient reduction in CBF, with risks of secondary brain damage. 3) The ICP response to a bolus injection (PVI test) is sharply affected, via cerebral blood volume changes, by cerebral hemodynamics and autoregulation. We suggest that PVI tests may be used to extract information not only on intracranial compliance and CSF circulation, but also on the status of mechanisms controlling CBF.
Immune response to heavy exertion
Authors: Nieman David C.
Published: December 2017

Nieman, David C. Immune response to heavy exertion. J. Appl. Physiol. 82(5): 1385–1394, 1997.—Epidemiological data suggest that endurance athletes are at increased risk for upper respiratory tract infection during periods of heavy training and the 1- to 2-wk period following race events. There is growing evidence that, for several hours subsequent to heavy exertion, several components of both the innate (e.g., natural killer cell activity and neutrophil oxidative burst activity) and adaptive (e.g., T and B cell function) immune system exhibit suppressed function. At the same time, plasma pro- and anti-inflammatory cytokines are elevated, in particular interleukin-6- and interleukin-1-receptor antagonist. Various mechanisms explaining the altered immunity have been explored, including hormone-induced trafficking of immune cells and the direct influence of stress hormones, prostaglandin-E2, cytokines, and other factors. The immune response to heavy exertion is transient, and further research on the mechanisms underlying the immune response to prolonged and intensive endurance exercise is necessary before meaningful clinical applications can be drawn. Some attempts have been made through chemical or nutritional means (e.g., indomethacin, glutamine, vitamin C, and carbohydrate supplementation) to attenuate immune changes following intensive exercise.
Pregnancy alters body-core temperature response to a simulated open field in rats
Authors: Fewell James E. , Tang Patricia A.
Published: December 2017

Fewell, James E., and Patricia A. Tang. Pregnancy alters body-core temperature response to a simulated open field in rats. J. Appl. Physiol. 82(4): 1406–1410, 1997.—Exposure of a rat to a novel environment (e.g., a simulated open field) induces a transient increase in body-core temperature, which is often called stress-induced hyperthermia. Although pregnancy is known to influence thermoregulatory control, its effect on stress-induced hyperthermia is unknown. Therefore, 24 Sprague-Dawley rats (8 nonpregnant and 16 pregnant) were studied to test the hypothesis that pregnancy would alter the development of stress-induced hyperthermia after exposure to a simulated open field. Body-core temperature index increased significantly after exposure to a simulated open field in nonpregnant and gestation day-10 rats but not in gestation day-15 and day-20 rats. Thus our data provide evidence that pregnancy influences the body-core temperature response of rats exposed to a simulated open field in a gestation-dependent fashion. The functional consequences as well as the mechanisms involved remain to be determined.
TNF-α in smoke inhalation lung injury
Authors: Hales Charles A. , Elsasser T. H. , Ocampo Peter , Efimova Olga
Published: December 2017

Hales, Charles A., T. H. Elsasser, Peter Ocampo, and Olga Efimova. TNF-α in smoke inhalation lung injury. J. Appl. Physiol. 82(5): 1433–1437, 1997.—Adult respiratory distress syndrome is a major cause of morbidity in fire victims. Tumor necrosis factor-α (TNF-α) is edematogenic and has been associated with the etiology of other forms of adult respiratory distress syndrome. In the sheep lymph fistula model, we measured TNF-α after 48 ( n = 7) or 128 ( n = 3) breaths of cotton smoke and compared this with sham controls ( n = 5) or controls in which left atrial pressure was elevated to 20 mmHg ( n = 5) to increase lymph flow in the absence of inflammation. Smoke induced a rise in lymph flow and pulmonary arterial pressure with either no fall in lymph-to-plasma protein ratio (128 breaths) or a modest fall in lymph-to-plasma protein ratio (48 breaths), consistent with a change in microvascular permeability as well as a rise in microvascular pressure. Lymph concentration of TNF-α fell in both groups, although lymph flux (concentration × flow) transiently rose in both. In neither case did TNF-α flux exceed that induced by left atrial pressure elevation. TNF-α was detectable in only one out of five sheep in alveolar lavage. Thus, by utilizing a sensitive and specific radioimmunoassay, we were unable to demonstrate a role for TNF-α in smoke-induced microvascular lung injury in sheep.
Complement-mediated lung injury and neutrophil retention after intestinal ischemia-reperfusion
Authors: Xiao Feng , Eppihimer Michael J. , Willis Bradley H. , Carden Donna L.
Published: December 2017

Xiao, Feng, Michael J. Eppihimer, Bradley H. Willis, and Donna L. Carden. Complement-mediated lung injury and neutrophil retention after intestinal ischemia-reperfusion. J. Appl. Physiol. 82(5): 1459–1465, 1997.—Complement-mediated neutrophil activation appears to play an important role in ischemia-reperfusion (I/R) injury in a variety of tissues, including the heart, lung, and small bowel. The objective of this study was to determine whether inhibition of the alternative and classic complement cascades by administration of soluble complement receptor 1 (sCR1) prevents the increased neutrophil stiffness, lung neutrophil retention, and pulmonary microvascular injury elicited by a systemic inflammatory insult. Isolated lungs were perfused with blood obtained from animals subjected to 2 h of intestinal ischemia and 20 min of reperfusion (I/R) or control (nonischemic) surgery. Intestinal I/R resulted in a significant increase in neutrophil stiffness, lung neutrophil retention, and increased pulmonary microvascular permeability, effects that were prevented by administration of sCR1 before intestinal reperfusion. The results of this study suggest that I/R injury in the gut is a potent systemic inflammatory stimulus that induces complement-mediated neutrophil stiffness, lung neutrophil entrapment, and pulmonary microvascular dysfunction.
Distribution of blood flow and neutrophil kinetics in bronchial vasculature of sheep
Authors: Baile Elisabeth M. , Paré Peter D. , Ernest David , Dodek Peter M.
Published: December 2017

Baile, Elisabeth M., Peter D. Paré, David Ernest, and Peter M. Dodek. Distribution of blood flow and neutrophil kinetics in bronchial vasculature of sheep. J. Appl. Physiol. 82(5): 1466–1471, 1997.—The bronchial circulation, as opposed to the pulmonary circulation, is the likely source of the edema and inflammatory cells that contribute to airflow obstruction and airway narrowing associated with asthma and pulmonary edema. The purpose of this study was to understand the mechanism of edema formation and inflammation in airway walls. Therefore, we sought first to determine the normal bronchial venous drainage pathways. In anesthetized, ventilated, open-chest sheep we measured the relative distribution of 51Cr-labeled red blood cells to the right and left ventricles after injection into the bronchial artery ( n = 7). Using this information, we then studied the kinetics of leukocytes in the bronchial vascular bed. We measured the extraction of111In-labeled neutrophils during their first pass through the microvasculature after injection into the bronchial artery or right ventricle ( n= 6). In the first set of experiments, we found >85% of the systemic blood flow to the lung returns to the left ventricle. In the second set of experiments, we found that extraction of neutrophils in the bronchial vasculature (50–60%) was less ( P < 0.05) than that in the pulmonary vasculature (80%). This finding may be explained by differences in the anatomy and/or hydrodynamic dispersal forces between the pulmonary and bronchial vascular beds or may reflect sequestration of neutrophils within the pulmonary microvasculature while traversing bronchial-to-pulmonary anastomotic pathways.
Effect of stochastic heterogeneity on lung impedance during acute bronchoconstriction: a model analysis
Authors: Thorpe C. William , Bates Jason H. T.
Published: December 2017

Thorpe, C. William, and Jason H. T. Bates. Effect of stochastic heterogeneity on lung impedance during acute bronchoconstriction: a model analysis. J. Appl. Physiol. 82(5): 1616–1625, 1997.—In a previous study (J. H. T. Bates, A. M. Lauzon, G. S. Dechman, G. N. Maksym, and T. F. Schuessler. J. Appl. Physiol. 76: 616–626, 1994), we investigated the acute changes in isovolume lung mechanics immediately after a bolus injection of histamine. We found that dynamic resistance and elastance increased progressively in the 80-s period after injection, whereas the estimated tissue hysteresivity reached a stable plateau after ∼25 s. In the present study, we developed a computer model of the lung to investigate the mechanisms responsible for these observations. The model conforms to Horsfield’s morphometry, with the addition of compliant airways and structural damping tissue units. Using this model, we simulated the time course of acute bronchoconstriction after intravenous administration of a bolus of bronchial agonist. Heterogeneity was induced by randomly varying the values of the maximal airway smooth muscle contraction and the tissue response to the agonist. Our results demonstrate that much of the increase in lung impedance observed in our previous study can be produced purely by the effects of airway heterogeneity. However, we were only able to reproduce the plateauing of hysteresivity by assigning a minimum radius to each airway, beyond which it would immediately snap completely shut. We propose that airway closure played an important role in our experimental observations.
Effects of fatigue duration and muscle type on voluntary and evoked contractile properties
Authors: Behm D. G. , St-Pierre D. M. M.
Published: December 2017

Behm, D. G., and D. M. M. St-Pierre. Effects of fatigue duration and muscle type on voluntary and evoked contractile properties. J. Appl. Physiol. 82(5): 1654–1661, 1997.—The effects of fatigue duration and muscle type on voluntary and evoked contractile properties were investigated with an isometric, intermittent, submaximal fatigue protocol. Four groups performed contractions of the plantar flexors and quadriceps at various intensities to produce long (LDF; 19 min 30 s)- and short-duration fatigue (SDF; 4 min 17 s). The LDF group had a significantly greater decrease in muscle activation than did the SDF group (12 vs. 5.8%) during recovery, although there was no difference in the impairment of maximum voluntary contraction force beyond 30 s of recovery. The significant decrease in the compound muscle action potential of the LDF group (M-wave amplitude; 14.7%) contrasted with the M-wave potentiation of the SDF group (15.7%), suggesting changes in membrane excitation may affect LDF. The quadriceps group performing contractions at 50% MVC experienced a smaller decrease in agonist electromyograph activity than did other groups, indicating both muscle and fatigue duration specificity. Impairments in excitation-contraction coupling were indicated by changes in quadriceps peak twitch and time to peak twitch while decreases in PF M-wave amplitudes suggested a disruption of membrane potentials. Results suggest that fatigue mechanisms may be duration (activation, half relaxation time) or muscle specific (electromyograph, twitch torque) or a combination of both (M wave, time to peak twitch torque).
A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing
Authors: Schuessler Thomas F. , Gottfried Stewart B. , Bates Jason H. T.
Published: December 2017

Schuessler, Thomas F., Stewart B. Gottfried, and Jason H. T. Bates. A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing. J. Appl. Physiol. 82(5): 1694–1703, 1997.—Intrinsic positive end-expiratory pressure (PEEPi) and inspiratory work of breathing (Wi) are important factors in the management of severe obstructive respiratory disease. We used a computer model of spontaneously breathing patients with chronic obstructive pulmonary disease to assess the sensitivity of measurement techniques for dynamic PEEPi(PEEPi dyn) and Wi to expiratory muscle activity (EMA) and cardiogenic oscillations (CGO) on esophageal pressure. Without EMA and CGO, both PEEPi dynand Wi were accurately estimated ( r = 0.999 and 0.95, respectively). Addition of moderate EMA caused PEEPi dynand Wi to be systematically overestimated by 141 and 52%, respectively. Furthermore, CGO introduced large random errors, obliterating the correlation between the true and estimated values for both PEEPi dyn( r = 0.29) and Wi( r = 0.38). Thus the accurate estimation of PEEPi dynand Wi requires steps to be taken to ameliorate the adverse effects of both EMA and CGO. Taking advantage of our simulations, we also investigated the relationship between PEEPi dynand static PEEPi(PEEPi stat). The PEEPi dyn/PEEPi statratio decreased as stress adaptation in the lung was increased, suggesting that heterogeneity of expiratory flow limitation is responsible for the discrepancies between PEEPi dynand PEEPi statthat have been reported in patients with severe airway obstruction.
cAMP production in rabbit carotid body: role of adenosine
Authors: Chen J. , Dinger B. , Fidone S. J.
Published: December 2017

Chen, J., B. Dinger, and S. J. Fidone. cAMP production in rabbit carotid body: role of adenosine. J. Appl. Physiol. 82(6): 1771–1775, 1997.—In the present study, we have investigated the possible role of adenosine in the hypoxia-mediated increase in adenosine 3′,5′-cyclic monophosphate (cAMP) in the carotid body. cAMP levels in rabbit carotid bodies superfused in vitro for 10 min were increased in the presence of adenosine (100 μM and 1.0 mM; maximum increase = 127%, P < 0.01). These effects were reduced by the nonspecific adenosine-receptor antagonist 1,3-dipropyl-8[ p-sulfophenyl]xanthine (DPSPX; 10 μM). The specific A2-receptor agonist 2-[4′(2-carboxymethyl)phenylethylamino]-5′- N-ethylcarboxamido adenosine (CGS-21680; 100 nM) also elevated carotid body cAMP levels, an effect that was blocked by the specific A2-antagonist 3,7-dimethyl-l-propargyl-xanthine (DMPX; 50 μM). Hypoxia-evoked elevations in cAMP were potentiated in the presence of the adenosine-uptake inhibitor dipyridamole (100 nM) and blocked by exposure to adenosine-receptor antagonists. Our data suggest that the rabbit carotid body contains specific adenosine receptors (A2 subtype) that are positively coupled to adenylate cyclase and that increases in cAMP associated with hypoxia are mediated by the release of endogenous adenosine.