bluuebunny/crossref_metadata_2025 huggingface dataset:
“Living high-training low”: effect of moderate-altitude acclimatization with low-altitude training on performance
Authors: Levine Benjamin D. , Stray-Gundersen James
Published: December 2017

Levine, Benjamin D., and James Stray-Gundersen.“Living high-training low”: effect of moderate-altitude acclimatization with low-altitude training on performance. J. Appl. Physiol. 83(1): 102–112, 1997.—The principal objective of this study was to test the hypothesis that acclimatization to moderate altitude (2,500 m) plus training at low altitude (1,250 m), “living high-training low,” improves sea-level performance in well-trained runners more than an equivalent sea-level or altitude control. Thirty-nine competitive runners (27 men, 12 women) completed 1) a 2-wk lead-in phase, followed by 2) 4 wk of supervised training at sea level; and 3) 4 wk of field training camp randomized to three groups: “high-low” ( n = 13), living at moderate altitude (2,500 m) and training at low altitude (1,250 m); “high-high” ( n = 13), living and training at moderate altitude (2,500 m); or “low-low” ( n = 13), living and training in a mountain environment at sea level (150 m). A 5,000-m time trial was the primary measure of performance; laboratory outcomes included maximal O2 uptake (V˙o 2 max), anaerobic capacity (accumulated O2 deficit), maximal steady state (MSS; ventilatory threshold), running economy, velocity at V˙o 2 max, and blood compartment volumes. Both altitude groups significantly increased V˙o 2 max(5%) in direct proportion to an increase in red cell mass volume (9%; r = 0.37, P < 0.05), neither of which changed in the control. Five-kilometer time was improved by the field training camp only in the high-low group (13.4 ± 10 s), in direct proportion to the increase inV˙o 2 max( r = 0.65, P < 0.01). Velocity atV˙o 2 max and MSS also improved only in the high-low group. Four weeks of living high-training low improves sea-level running performance in trained runners due to altitude acclimatization (increase in red cell mass volume and V˙o 2 max) and maintenance of sea-level training velocities, most likely accounting for the increase in velocity atV˙o 2 max and MSS.
Influence of treadmill running on femoral bone in young orchidectomized rats
Authors: Horcajada M.-N. , Coxam V. , Davicco M.-J. , Gaumet N. , Pastoureau P. , Leterrier C. , Culioli J. , Barlet J.-P.
Published: December 2017

Horcajada, M.-N., V. Coxam, M.-J. Davicco, N. Gaumet, P. Pastoureau, C. Leterrier, J. Culioli, and J.-P. Barlet. Influence of treadmill running on femoral bone in young orchidectomized rats. J. Appl. Physiol. 83(1): 129–133, 1997.—Forty 6-wk-old male Wistar rats weighing 308 ± 24 g were divided into two groups. On day 0, the 20 animals in one group were surgically castrated and the other group was sham operated. Within each group, 10 rats were selected for treadmill running (60% maximal O2consumption, 1 h/day, 6 days/wk for 15 wk). The 20 sedentary rats were used as controls. At the time the rats were killed ( day 105), running had no significant effect on femoral mechanical properties either in castrated or in sham-operated rats. Femoral bone density was lower in orchidectomized than in sham-operated rats. Nevertheless, it was higher in exercised than in sedentary rats. Femoral Ca content paralleled changes in bone density. Treadmill running had no significant effect on plasma osteocalcin concentration but inhibited the increase in urinary deoxypyridinoline excretion observed in castrated rats. Image analysis (measured at the distal femoral diaphysis) revealed that these effects mainly resulted from decreased trabecular bone resorption in castrated exercised rats.
Physiological adaptations to a weight-loss dietary regimen and exercise programs in women
Authors: Kraemer William J. , Volek Jeff S. , Clark Kristine L. , Gordon Scott E. , Incledon Thomas , Puhl Susan M. , Triplett-McBride N. Travis , McBride Jeffrey M. , Putukian Margot , Sebastianelli Wayne J.
Published: December 2017

Kraemer, William J., Jeff S. Volek, Kristine L. Clark, Scott E. Gordon, Thomas Incledon, Susan M. Puhl, N. Travis Triplett-McBride, Jeffrey M. McBride, Margot Putukian, and Wayne J. Sebastianelli.Physiological adaptations to a weight-loss dietary regimen and exercise programs in women. J. Appl. Physiol. 83(1): 270–279, 1997.—Thirty-one women (mean age 35.4 ± 8.5 yr) who were overweight were matched and randomly placed into either a control group (Con; n = 6), a diet-only group (D; n = 8), a diet+aerobic endurance exercise training group (DE; n = 9), or a diet+aerobic endurance exercise training+strength training group (DES; n = 8). After 12 wk, the three dietary groups demonstrated a significant ( P ≤ 0.05) reduction in body mass, %body fat, and fat mass. No differences were observed in the magnitude of loss among groups, in fat-free mass, or in resting metabolic rate. The DE and DES groups increased maximal oxygen consumption, and the DES group demonstrated increases in maximal strength. Weight loss resulted in a similar reduction in total serum cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol among dietary groups. These data indicate that weight loss during moderate caloric restriction is not altered by inclusion of aerobic or aerobic+resistance exercise, but diet in conjunction with training can induce remarkable adaptations in aerobic capacity and muscular strength despite significant reductions in body mass.
Differences between estimates and measured Pa CO 2 during rest and exercise in older subjects
Authors: Williams J. S. , Babb T. G.
Published: December 2017

Williams, J. S., and T. G. Babb. Differences between estimates and measured [Formula: see text] during rest and exercise in older subjects. J. Appl. Physiol. 83(1): 312–316, 1997.—Arterial[Formula: see text]([Formula: see text]) has been estimated during exercise with good accuracy in younger individuals by using the Jones equation (PJ co 2) ( J. Appl. Physiol. 47: 954–960, 1979). The purpose of this project was to determine the utility of estimating [Formula: see text] from end-tidal[Formula: see text]([Formula: see text]) or PJ co 2at rest, ventilatory threshold (V˙Th), and maximal exercise (Max) in older subjects.[Formula: see text] was determined from respired gases simultaneously (MGA 1100) with arterial blood gases (radial arterial catheter) in 12 older and 11 younger subjects at rest and during exercise. Mean differences were analyzed with paired t-tests, and relationships between the estimated [Formula: see text] values and the actual values of [Formula: see text] were determined with correlation coefficients. In the older subjects,[Formula: see text] was not significantly different from [Formula: see text] at rest (−1.2 ± 4.3 Torr), V˙Th (0.4 ± 2.5), or Max (−0.8 ± 2.7), and the two were significantly ( P < 0.05) correlated atV˙th ( r = 0.84) and Max ( r = 0.87) but not at rest ( r = 0.47). PJ co 2was similar to [Formula: see text] at rest (−1.0 ± 3.9) and V˙th (−1.3 ± 2.3) but significantly lower at Max (−3.0 ± 2.6), and the two were significantly correlated at V˙th ( r = 0.86) and Max ( r = 0.80) but not at rest ( r = 0.54).[Formula: see text] was significantly higher than [Formula: see text] during exercise in the younger subjects but similar to [Formula: see text] at rest. PJ co 2was similar to [Formula: see text] at rest andV˙th but significantly lower at Max in younger subjects. In conclusion, our data demonstrate that[Formula: see text] during exercise is better estimated by [Formula: see text] than by PJ co 2in older subjects, contrary to what is observed in younger subjects. This appears to be related to the finding that[Formula: see text] does not exceed[Formula: see text] during exercise in older subjects, as occurs in the younger subjects. However,[Formula: see text] at rest is best estimated by PJ co 2in both younger and older subjects.
Decreased [3H]ouabain binding sites in skeletal muscle of rats with chronic heart failure
Authors: Pickar Joel G. , Mattson John P. , Lloyd Steve , Musch Timothy I.
Published: December 2017

Pickar, Joel G., John P. Mattson, Steve Lloyd, and Timothy I. Musch. Decreased [3H]ouabain binding sites in skeletal muscle of rats with chronic heart failure. J. Appl. Physiol. 83(1): 323–329, 1997.—Abnormalities intrinsic to skeletal muscle are thought to contribute to decrements in exercise capacity found in individuals with chronic heart failure (CHF). Na+-K+-adenosinetriphosphatase (the Na+ pump) is essential for maintaining muscle excitability and contractility. Therefore, we investigated the possibility that the number and affinity of Na+ pumps in locomotor muscles of rats with CHF are decreased. Myocardial infarction (MI) was induced in 8 rats, and a sham operation was performed in 12 rats. The degree of CHF was assessed ∼180 days after surgery. Soleus and plantaris muscles were harvested, and Na+pumps were quantified by using a [3H]ouabain binding assay. At the time of muscle harvest, MI and sham-operated rats were similar in age (458 ± 54 vs. 447 ± 34 days old, respectively). Compared with their sham-operated counterparts, MI rats had a significant amount of heart failure, right ventricular-to-body weight ratio was greater (48%), and the presence of pulmonary congestion was suggested by an elevated lung-to-body weight ratio (29%). Left ventricular end-diastolic pressure was significantly increased in the MI rats (11 ± 1 mmHg) compared with the sham-operated controls (1 ± 1 mmHg). In addition, mean arterial blood pressure was lower in the MI rats compared with their control counterparts. [3H]ouabain binding sites were reduced 18% in soleus muscle (136 ± 12 vs. 175 ± 13 pmol/g wet wt, MI vs. sham, respectively) and 22% in plantaris muscle (119 ± 12 vs. 147 ± 8 pmol/g wet wt, MI vs. sham, respectively). The affinity of these [3H]ouabain binding sites was similar for the two groups. The relationship between the reduction in Na+ pump number and the reduced exercise capacity in individuals with CHF remains to be determined.
Neuromuscular factors contributing to in vivo eccentric moment generation
Authors: Webber Sandra , Kriellaars Dean
Published: December 2017

Webber, Sandra, and Dean Kriellaars. Neuromuscular factors contributing to in vivo eccentric moment generation. J. Appl. Physiol. 83(1): 40–45, 1997.—Muscle series elasticity and its contribution to eccentric moment generation was examined in humans. While subjects [male, n = 30; age 26.3 ± 4.8 (SD) yr; body mass 78.8 ± 13.1 kg] performed an isometric contraction of the knee extensors at 60° of knee flexion, a quick stretch was imposed with a 12°-step displacement at 100°/s. The test was performed at 10 isometric activation levels ranging from 1.7 to 95.2% of maximal voluntary contraction (MVC). A strong linear relationship was observed between the peak imposed eccentric moment derived from quick stretch and the isometric activation level ( y = 1.44 x + 7.08; r = 0.99). This increase in the eccentric moment is consistent with an actomyosin-dependent elasticity located in series with the contractile element of muscle. By extrapolating the linear relationship to 100% MVC, the predicted maximum eccentric moment was found to be 151% MVC, consistent with in vitro data. A maximal voluntary, knee extensor strength test was also performed (5–95°, 3 repetitions, ±50, 100, 150, 200, and 250°/s). The predicted maximum eccentric moment was 206% of the angle- and velocity-matched, maximal voluntary eccentric moments. This was attributed to a potent neural regulatory mechanism that limits the recruitment and/or discharge of motor units during maximal voluntary eccentric contractions.
Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm
Authors: McGuire Michelle , Carey Michael F. , O’Connor John J.
Published: December 2017

McGuire, Michelle, Michael F. Carey, and John J. O’Connor.Almitrine and doxapram decrease fatigue and increase subsequent recovery in isolated rat diaphragm. J. Appl. Physiol. 83(1): 52–58, 1997.—The effects of almitrine bimesylate and doxapram HCl on isometric force produced by in vitro rat diaphragm were studied during direct muscle activation at 37°C. Doxapram and almitrine ameliorate respiratory failure clinically by indirectly increasing phrenic nerve activity. This study was carried out to investigate possible direct actions of these agents on the diaphragm before and after fatigue of the fibers. Two age groups of animals were chosen [6–14 wk ( group 1) and 50–55 wk ( group 2)] because it is known that increasing age decreases a muscle fiber’s resistance to fatigue. Muscle strips were isolated from both group 1 and group 2 and directly stimulated (2-ms pulse duration, 5–15 V) to produce twitch tensions of 1.3 and 2.1 N/cm2, respectively. At low concentrations, doxapram (≤20 μg/ml) and almitrine (≤12 μg/ml) had no effect on twitch contraction or 100-Hz tetanic tension. However, 40 μg/ml doxapram and 30 μg/ml almitrine increased twitch tension by 9.0 ± 1.4 and 11.6 ± 1.9%, respectively, in animals of group 2( n = 5). A fatigue protocol consisting of low-frequency stimulation (30-Hz trains, 250-ms duration every 2 s for 5 min) caused a reduction of twitch tension in animals of group 1 (48 ± 4% of control) and group 2 (28 ± 4% of control). At 90 min postfatigue, the twitch tension recovered to 72 ± 3 and 42 ± 2% of control values in group 1 and group 2, respectively. In the presence of doxapram (20 μg/ml), there was a significant increase in the recovery of twitch tension at 90 min in group 1 and group 2 (84.5 ± 3.2 and 80.1 ± 2.8%, respectively) compared with controls at 90 min postfatigue. In the presence of almitrine (12 μg/ml), there was a full recovery from fatigue in group 1 animals (100% of control) and a recovery to 95.6 ± 2.1% of control in group 2 animals at 90 min. These results demonstrate a significant improvement in the rapidity and magnitude of recovery from fatigue in the rat diaphragm muscle in the presence of both doxapram and, especially, almitrine. These effects may be due to changes in intracellular calcium, ADP/ATP ratios, or oxygen free radical scavenging.
Expression of nitric oxide synthase isoforms in normal ventilatory and limb muscles
Authors: Hussain Sabah N. A. , El-Dwairi Qasim , Abdul-Hussain Mohammed N. , Sakkal Dalia
Published: December 2017

Hussain, Sabah N. A., Qasim El-Dwairi, Mohammed N. Abdul-Hussain, and Dalia Sakkal. Expression of nitric oxide synthase isoforms in normal ventilatory and limb muscles. J. Appl. Physiol. 83(2): 348–353, 1997.—Nitric oxide (NO), an important messenger molecule with widespread actions, is synthesized by NO synthases (NOS). In this study, we investigated the correlation between fiber type and NOS activity among ventilatory and limb muscles of various species. We also assessed the presence of the three NOS isoforms in normal skeletal muscles and how various NOS inhibitors influence muscle NOS activity. NOS activity was detected in various muscles; however, NOS activity in rabbits and rats varied significantly among different muscles. Immunoblotting of muscle samples indicated the presence of both the neuronal NOS and the endothelial NOS isoforms but not the cytokine-inducible NOS isoform. However, these isoforms were expressed to different degrees in various muscles. Although the neuronal NOS isoform was detectable in the canine diaphragm, very weak expression was detected in rabbit, rat, and mouse diaphragms. The endothelial NOS isoform was detected in the rat and mouse diaphragms but not in the canine and rabbit diaphragms. We also found that NG-nitro-l-arginine methyl ester, 7-nitroindazole, and S-methylisothiourea were stronger inhibitors of muscle NOS activity than was aminoguanidine. These results indicate the presence of different degrees of constitutive NOS expression in normal ventilatory and limb muscles of various species. Our data also indicate that muscle NOS activity is not determined by fiber type distribution but by other not yet identified factors. The functional significance of this expression remains to be assessed.
Effects of renal denervation on cardiovascular and renal responses to ACE inhibition in conscious lambs
Authors: Smith Francine G. , Chan Suzanne , De Wildt Saskia N.
Published: December 2017

Smith, Francine G., Suzanne Chan, and Saskia N. De Wildt.Effects of renal denervation on cardiovascular and renal responses to ACE inhibition in conscious lambs. J. Appl. Physiol. 83(2): 414–419, 1997.—Cardiovascular and renal effects of either the angiotensin-converting enzyme inhibitor captopril or vehicle were measured in chronically instrumented lambs in the presence (intact; n = 6) and absence of renal sympathetic nerves (denervated; n = 5) to determine whether there was an interaction between the renin-angiotensin system and renal sympathetic nerves early in life. Captopril caused a similar decrease in mean arterial pressure ( P < 0.001) in intact and denervated lambs, predominantly through a decrease in diastolic pressure. Heart rate was increased from 177 ± 34 to 213 ± 22 (SD) beats/min during captopril compared with vehicle infusion in intact lambs. In denervated lambs, basal heart rates were elevated to 218 ± 33 beats/min; there was no further increase in heart rate during captopril compared with vehicle infusion. Captopril infusion caused a decrease in renal vascular resistance but only in the absence of renal nerves. These findings provide evidence to suggest that early in life there is an interaction between renal sympathetic nerves and the renin-angiotensin system in regulating renal hemodynamics and the baroreflex control of the heart.
Effect of hypoxia on respiratory system impedance in dogs
Authors: Simon B. A. , Zanaboni P. B. , Nyhan D. P.
Published: December 2017

Simon, B. A., P. B. Zanaboni, and D. P. Nyhan. Effect of hypoxia on respiratory system impedance in dogs. J. Appl. Physiol. 83(2): 451–458, 1997.—The effects of hypoxia on lung and airway mechanics remain controversial, possibly because of the confounding effects of competing reflexes caused by systemic hypoxemia. We compared the effects of systemic hypoxemia with those of unilateral alveolar hypoxia (with systemic normoxemia) on unilateral respiratory system impedance (Z) in intact, anesthetized dogs. Independent lung ventilation was obtained with a Kottmeier endobronchial tube. Individual left and right respiratory system Z was measured during sinusoidal forcing with 45 ml of volume at frequencies of 0.2–2.1 Hz during control [100% inspired O2 fraction ([Formula: see text])], systemic hypoxemia (10% [Formula: see text]), and unilateral alveolar hypoxia (0%[Formula: see text] to left lung, 100%[Formula: see text] to right lung). During systemic hypoxemia, there was a mean Z magnitude increase of 18%. This change was entirely attributable to a decrease in the imaginary component of Z; there was no change in the real component of Z. Administration of atropine (0.2 mg/kg) did not block the increase in Z with systemic hypoxemia. In contrast, there was no change in Z in the lung subjected to unilateral alveolar hypoxia. We conclude that alveolar hypoxia has no direct effect on lung mechanical properties in intact dogs. In contrast, systemic hypoxemia does increase lung impedance, apparently through a noncholinergic mechanism.
Reflex apneic response evoked by laryngeal exposure to wood smoke in rats: neural and chemical mechanisms
Authors: Lin Y. S. , Kou Y. R.
Published: December 2017

Lin, Y. S., and Y. R. Kou. Reflex apneic response evoked by laryngeal exposure to wood smoke in rats: neural and chemical mechanisms. J. Appl. Physiol. 83(3): 723–730, 1997.—We investigated the neural and chemical mechanisms contributing to the immediate ventilatory responses to laryngeal exposure to wood smoke in anesthetized Sprague-Dawley rats. Five milliliters of wood smoke were delivered into a functionally isolated larynx at a constant flow rate of 1.4 ml/s while the animals breathed spontaneously. Within 1 s after exposure, laryngeal wood smoke consistently triggered an apnea in each of the 42 rats tested. The apneic duration reached 1,636.4 ± 105.4 (SE) % ( n = 42) of the baseline expiratory duration. This apneic response was not affected by denervation of recurrent laryngeal nerves ( n = 6) or by removal of smoke particulates ( n = 14), but it was totally eliminated by topical application of an anesthetic ( n = 8; lidocaine hydrochloride, 8%) to the laryngeal mucosa or by sectioning of the superior laryngeal nerves ( n = 42). Furthermore, laryngeal application of a hydroxyl radical scavenger (dimethylthiourea; 500 mg/ml; n = 8) greatly diminished or abolished the smoke-induced apneic response, but it did not affect the apneic response evoked by laryngeal exposure to air saturated with 6% ammonia. These results suggest that the immediate apneic response to laryngeal wood smoke is a reflex resulting from the stimulation of the superior laryngeal afferents by the gas phase of wood smoke and that the stimulation is mediated through a hydroxyl radical mechanism.
Relationship between resistive loads and P1 peak of respiratory-related evoked potential
Authors: Knafelc Marie , Davenport Paul W.
Published: December 2017

Knafelc, Marie, and Paul W. Davenport. Relationship between resistive loads and P1peak of respiratory-related evoked potential. J. Appl. Physiol. 83(3): 918–926, 1997.—This study investigated the relationship between resistive-load (ΔR) magnitude, the first positive peak (P1) amplitude of the respiratory-related evoked potential (RREP), and load-magnitude estimation (ME). The first experiments determined the subject’s ( n = 9) ME of five ΔR magnitudes randomly presented at the onset of an inspiration or by interrupting an inspiration. No significant differences were found in the slopes of the two different presentations, but the subjects estimated the interrupted inspiratory loads to be of lesser magnitude than loads presented at the onset of the breath. In the second series of experiments, the subject’s ( n = 6) RREPs were recorded in response to three ΔR magnitudes. The amplitude of the short-latency P1 peak of the RREP significantly increased with increases in the ΔR magnitude. A log-log plot of the group-averaged P1 amplitudes showed a linear relationship with ΔR. These results were consistent with the hypothesis that the perceptual magnitude of the respiratory load was related to the P1 amplitude of the RREP, suggesting the physical magnitude of the load-related stimulus was correlated with the amplitude of the cortical neural activation.
Kinematics and mechanics of midcostal diaphragm of dog
Authors: Boriek Aladin M. , Rodarte Joseph R. , Wilson Theodore A.
Published: December 2017

Boriek, Aladin M., Joseph R. Rodarte, and Theodore A. Wilson. Kinematics and mechanics of midcostal diaphragm of dog. J. Appl. Physiol. 83(4): 1068–1075, 1997.—Radiopaque markers were attached to the peritoneal surface of three neighboring muscle bundles in the midcostal diaphragm of four dogs, and the locations of the markers were tracked by biplanar video fluoroscopy during quiet spontaneous breathing and during inspiratory efforts against an occluded airway at three lung volumes from functional residual capacity to total lung capacity in both the prone and supine postures. Length and curvature of the muscle bundles were determined from the data on marker location. Muscle lengths for the inspiratory states, as a fraction of length at functional residual capacity, ranged from 0.89 ± 0.04 at end inspiration during spontaneous breathing down to 0.68 ± 0.07 during inspiratory efforts at total lung capacity. The muscle bundles were found to have the shape of circular arcs, with the three bundles forming a section of a right circular cylinder. With increasing lung volume and diaphragm displacement, the circular arcs rotate around the line of insertion on the chest wall, the arcs shorten, but the radius of curvature remains nearly constant. Maximal transdiaphragmatic pressure was calculated from muscle curvature and maximal tension-length data from the literature. The calculated maximal transdiaphragmatic pressure-length curve agrees well with the data of Road et al. ( J. Appl. Physiol. 60: 63–67, 1986).
Nonspecific endothelin-receptor antagonist blunts monocrotaline-induced pulmonary hypertension in rats
Authors: Hill Nicholas S. , Warburton Rod R. , Pietras Linda , Klinger James R.
Published: December 2017

Hill, Nicholas S., Rod R. Warburton, Linda Pietras, and James R. Klinger. Nonspecific endothelin-receptor antagonist blunts monocrotaline-induced pulmonary hypertension in rats. J. Appl. Physiol. 83(4): 1209–1215, 1997.—Endothelin-1 (ET-1), a potent vasoactive and mitogenic peptide, has been implicated in the pathogenesis of several forms of pulmonary hypertension. We hypothesized that nonspecific blockade of ET receptors would blunt the development of monocrotaline (MCT)-induced pulmonary hypertension in rats. A single dose of the nonspecific ET blocker bosentan (100 mg/kg) given to intact rats by gavage completely blocked the pulmonary vasoconstrictor actions of Big ET-1 and partially blunted hypoxic pulmonary vasoconstriction. After 3 wk, MCT-injected (105 mg/kg sc) rats gavaged once daily with bosentan (200 mg/kg) had lower right ventricular (RV) systolic pressure (RVSP), RV-to-body weight (RV/BW) and RV-to-left ventricular (LV) plus septal (S) weight [RV/(LV+S)] ratios and less percent medial thickness of small pulmonary arteries than control MCT-injected rats. Lower dose bosentan (100 mg/kg) had no effect on these parameters after MCT or saline injection. Bosentan raised plasma ET-1 levels but had no effect on lung ET-1 levels. Bosentan (200 mg/kg) also had no effect on wet-to-dry lung weight ratios 6 days after MCT injection. When given during the last 10 days, but not the first 11 days of a 3-wk period after MCT injection, bosentan reduced RV/(LV+S) compared with MCT-injected controls. We conclude that ET-1 contributes to the pathogenesis of MCT-induced pulmonary hypertension and acts mainly during the later inflammatory rather than the acute injury phase after injection.
Theory of diaphragm structure and shape
Authors: Angelillo Maurizio , Boriek Aladin M. , Rodarte Joe R. , Wilson Theodore A.
Published: December 2017

Angelillo, Maurizio, Aladin M. Boriek, Joe R. Rodarte, and Theodore A. Wilson. Theory of diaphragm structure and shape. J. Appl. Physiol. 83(5): 1486–1491, 1997.—The muscle bundles of the diaphragm form a curved sheet that extends from the chest wall to the central tendon. Each muscle bundle exerts a force in the direction of its curvature; the magnitude of this force is proportional to the curvature of the bundle. The contribution of this force to transdiaphragmatic pressure is maximal if the direction of bundle curvature is orthogonal to the surface and the curvature is maximal. That is, the contribution of muscle tension to transdiaphragmatic pressure is maximal if the muscle bundles lie along lines that are both geodesics and lines of maximal principal curvature of the surface. A theory of diaphragm shape is developed from the assumption that all muscle bundles have these optimal properties. The class of surfaces that are formed of line elements that are both geodesics and lines of principal curvature is described. This class is restricted. The lines that form the surface must lie in planes, and all lines must have the same shape. In addition, the orientation of the lines is restricted. An example of this class that is similar to the shape of the canine diaphragm is described, and the stress distribution in this example is analyzed.
Respiratory-related pharyngeal constrictor muscle activity in decerebrate cats
Authors: Kuna Samuel T. , Vanoye Christi R.
Published: December 2017

Kuna, Samuel T., and Christi R. Vanoye.Respiratory-related pharyngeal constrictor muscle activity in decerebrate cats. J. Appl. Physiol.83(5): 1588–1594, 1997.—Respiratory-related activity of the hyopharyngeus (middle pharyngeal constrictor) and thyropharyngeus (inferior pharyngeal constrictor) muscles was determined in decerebrate, tracheotomized adult cats and compared with the electromyographic activity of the thyroarytenoid, a vocal cord adductor. During quiet breathing, the hyopharyngeus and usually the thyroarytenoid exhibited phasic activity during expiration and tonic activity throughout the respiratory cycle. Respiratory-related thyropharyngeus activity was absent under these conditions. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia increased phasic expiratory activity in both pharyngeal constrictor (PC) muscles but tended to suppress thyroarytenoid activity. Passively induced hypocapnia and the central apnea that followed the cessation of the mechanical hyperventilation were associated with tonic activation of the hyopharyngeus and thyroarytenoid but no recruitment in thyropharyngeus activity. The expiratory phase of a sigh and progressive pneumothorax were associated with an increase in phasic thyroarytenoid activity but no change in phasic PC activity. The results indicate that a variety of stimuli modulate respiratory-related PC activity, suggesting that the PC muscles may have a role in the regulation of upper airway patency during respiration.
Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis
Authors: Shah Ashish R. , Keens Thomas G. , Gozal David
Published: December 2017

Shah, Ashish R., Thomas G. Keens, and David Gozal.Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis. J. Appl. Physiol. 83(5): 1641–1647, 1997.—The effects of supplemental O2on recovery from supramaximal exercise and subsequent performance remain unknown. If recovery from exercise could be enhanced in individuals with chronic lung disease, subsequent supramaximal exercise performance could also be improved. Recovery from supramaximal exercise and subsequent supramaximal exercise performance were assessed after 10 min of breathing 100% O2or room air (RA) in 17 cystic fibrosis (CF) patients [25 ± 10 (SD) yr old, 53% men, forced expired volume in 1 s = 62 ± 21% predicted] and 17 normal subjects (25 ± 8 yr old, 59% men, forced expired volume in 1 s = 112 ± 15% predicted). Supramaximal performance was assessed as the work of sustained bicycling at a load of 130% of the maximum load achieved during a graded maximal exercise. Peak minute ventilation (V˙e) and heart rate (HR) were lower in CF patients at the end of each supramaximal bout than in controls. In CF patients, single-exponential time decay constants indicated faster recovery of HR (τHR= 86 ± 8 and 73 ± 6 s in RA and O2, respectively, P < 0.01). Similarly, fast and slow time constants of two-exponential equations providing the best fit for ventilatory recovery were improved in CF patients during O2breathing ([Formula: see text]= 132.1 ± 10.5 vs. 82.5 ± 10.4 s;[Formula: see text]= 880.3 ± 300.1 vs. 368.6 ± 107.1 s, P < 0.01). However, no such improvements occurred in controls. Supramaximal performance after O2improved in CF patients (109 ± 6% of the 1st bout after O2vs. 94 ± 6% in RA, P < 0.01). O2supplementation had no effect on subsequent performance in controls (97 ± 3% in O2vs. 93 ± 3% in RA). We conclude that supplemental O2after a short bout of supramaximal exercise accelerates recovery and preserves subsequent supramaximal performance in patients with CF.
Blood flow, vascular resistance, and blood volume after hemorrhage in conscious adrenalectomized rat
Authors: Darlington Daniel N. , Tehrani Majid J.
Published: December 2017

Darlington, Daniel N., and Majid J. Tehrani. Blood flow, vascular resistance, and blood volume after hemorrhage in conscious adrenalectomized rat. J. Appl. Physiol. 83(5): 1648–1653, 1997.—Hemorrhage leads to cardiovascular collapse and death in adrenal-insufficient animals. To determine whether the cardiovascular collapse is due to vasodilation and/or failure to restore blood volume, we used radiolabeled microspheres and 125I-labeled albumin to measure blood flow and blood volume in conscious adrenalectomized (ADX) rats after 15 ml ⋅ kg−1 ⋅ 3 min−1 hemorrhage. In ADX rats, hemorrhage led to a greater fall than in sham rats in blood flow in the stomach, small intestines, cecum, colon, spleen, hepatic portal vein, kidney, testis, lung, thymus, bone, fat, forebrain, cerebellum, and brainstem. The greater fall in blood flow was caused by an increase in vascular resistance in these organs except brain and hepatic artery. Sham rats maintained or increased brain and hepatic artery blood flow after hemorrhage whereas flow decreased and remained depressed in ADX rats. ADX rats failed to restore blood volume, whereas sham rats completely restored blood flow by 2 h. We conclude that cardiovascular collapse in ADX rats does not result from vasodilatation but may result from a failure to restore blood volume. The failure to restore blood volume and the low blood flow to organs, especially brain and liver, may contribute to mortality in ADX rats after hemorrhage.
Ventilation distribution during histamine provocation
Authors: Verbanck S. , Schuermans D. , Van Muylem A. , Paiva M. , Noppen M. , Vincken W.
Published: December 2017

Verbanck, S., D. Schuermans, A. Van Muylem, M. Paiva, M. Noppen, and W. Vincken. Ventilation distribution during histamine provocation. J. Appl. Physiol. 83(6): 1907–1916, 1997.—We investigated ventilation inhomogeneity during provocation with inhaled histamine in 20 asymptomatic nonsmoking subjects. We used N2multiple-breath washout (MBW) to derive parameters S condand S acin as a measurement of ventilation inhomogeneity in conductive and acinar zones of the lungs, respectively. A 20% decrease of forced expiratory volume in 1 s (FEV1) was used to distinguish responders from nonresponders. In the responder group, average FEV1 decreased by 26%, whereas S condincreased by 390% with no significant change in S acin. In the nonresponder group, FEV1 decreased by 11%, whereas S cond increased by 198% with no significant S acin change. Despite the absence of change in S acin during provocation, baseline S acin was significantly larger in the responder vs. the nonresponder group. The main findings of our study are that during provocation large ventilation inhomogeneities occur, that the small airways affected by the provocation process are situated proximal to the acinar zone where the diffusion front stands, and that, in addition to overall decrease in airway caliber, there is inhomogeneous narrowing of parallel airways.
Nitric oxide and endothelial permeability
Authors: Hinder Frank , Booke Michael , Traber Lillian D. , Traber Daniel L.
Published: December 2017

Hinder, Frank, Michael Booke, Lillian D. Traber, and Daniel L. Traber. Nitric oxide and endothelial permeability. J. Appl. Physiol. 83(6): 1941–1946, 1997.—Nitric oxide synthase inhibition reverses systemic vasodilation during sepsis but may increase endothelial permeability. To assess adverse effects on the pulmonary vasculature, 12 sheep were chronically instrumented with lung lymph fistulas and hydraulic pulmonary venous occluders. Escherichia coli endotoxin (lipopolysaccharide; 10 ng ⋅ kg−1⋅ min−1) was continuously infused for 32 h. After 24 h, six animals received 25 mg/kg of Nω-nitro-l-arginine methyl ester (l-NAME), and six received saline. All sheep developed a hyperdynamic circulatory response and elevated lymph flows by 24 h of lipopolysaccharide infusion. l-NAME reversed systemic vasodilation, increased pre- and postcapillary pulmonary vascular resistance index, pulmonary arterial pressure, and, transiently, effective pulmonary capillary pressure. Lung lymph flows were not different between groups at 24 h or thereafter. Calculated as changes from baseline, however, lung lymph flow was higher in thel-NAME group than in the control animals, with a trend toward lower lymph-to-plasma protein concentration ratio at 25 h. Permeability analysis at 32 h by the venous occlusion technique showed normal reflection coefficients and elevated filtration coefficients without differences between groups. Reversal by l-NAME of the systemic vasodilation during endotoxemia was associated with high pulmonary vascular resistance without evidence of impaired pulmonary endothelial barrier function.
Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women
Authors: Tanaka Hirofumi , Desouza Christopher A. , Jones Pamela P. , Stevenson Edith T. , Davy Kevin P. , Seals Douglas R.
Published: December 2017

Tanaka, Hirofumi, Christopher A. DeSouza, Pamela P. Jones, Edith T. Stevenson, Kevin P. Davy, and Douglas R. Seals. Greater rate of decline in maximal aerobic capacity with age in physically active vs. sedentary healthy women. J. Appl. Physiol. 83(6): 1947–1953, 1997.—Using a meta-analytic approach, we recently reported that the rate of decline in maximal oxygen uptake (V˙o 2 max) with age in healthy women is greatest in the most physically active and smallest in the least active when expressed in milliliters per kilogram per minute per decade. We tested this hypothesis prospectively under well-controlled laboratory conditions by studying 156 healthy, nonobese women (age 20–75 yr): 84 endurance-trained runners (ET) and 72 sedentary subjects (S). ET were matched across the age range for age-adjusted 10-km running performance. Body mass was positively related with age in S but not in ET. Fat-free mass was not different with age in ET or S. Maximal respiratory exchange ratio and rating of perceived exertion were similar across age in ET and S, suggesting equivalent voluntary maximal efforts. There was a significant but modest decline in running mileage, frequency, and speed with advancing age in ET.V˙o 2 max(ml ⋅ kg−1 ⋅ min−1) was inversely related to age ( P < 0.001) in ET ( r = −0.82) and S ( r = −0.71) and was higher at any age in ET. Consistent with our meta-analysic findings, the absolute rate of decline inV˙o 2 max was greater in ET (−5.7 ml ⋅ kg−1 ⋅ min−1 ⋅ decade−1) compared with S (−3.2 ml ⋅ kg−1 ⋅ min−1 ⋅ decade−1; P < 0.01), but the relative (%) rate of decline was similar (−9.7 vs −9.1%/decade; not significant). The greater absolute rate of decline inV˙o 2 max in ET compared with S was not associated with a greater rate of decline in maximal heart rate (−5.6 vs. −6.2 beats ⋅ min−1 ⋅ decade−1), nor was it related to training factors. The present cross-sectional findings provide additional evidence that the absolute, but not the relative, rate of decline in maximal aerobic capacity with age may be greater in highly physically active women compared with their sedentary healthy peers. This difference does not appear to be related to age-associated changes in maximal heart rate, body composition, or training factors.
Changes in insulin-stimulated glucose transport and GLUT-4 protein in rat skeletal muscle after training
Authors: Kawanaka Kentaro , Tabata Izumi , Katsuta Shigeru , Higuchi Mitsuru
Published: December 2017

Kawanaka, Kentaro, Izumi Tabata, Shigeru Katsuta, and Mitsuru Higuchi. Changes in insulin-stimulated glucose transport and GLUT-4 protein in rat skeletal muscle after training. J. Appl. Physiol. 83(6): 2043–2047, 1997.—After running training, which increased GLUT-4 protein content in rat skeletal muscle by <40% compared with control rats, the training effect on insulin-stimulated maximal glucose transport (insulin responsiveness) in skeletal muscle was short lived (24 h). A recent study reported that GLUT-4 protein content in rat epitrochlearis muscle increased dramatically (∼2-fold) after swimming training (J.-M. Ren, C. F. Semenkovich, E. A. Gulve, J. Gao, and J. O. Holloszy. J. Biol. Chem. 269, 14396–14401, 1994). Because GLUT-4 protein content is known to be closely related to skeletal muscle insulin responsiveness, we thought it possible that the training effect on insulin responsiveness may remain for >24 h after swimming training if GLUT-4 protein content decreases gradually from the relatively high level and still remains higher than control level for >24 h after swimming training. Therefore, we examined this possibility. Male Sprague-Dawley rats swam 2 h a day for 5 days with a weight equal to 2% of body mass. Approximately 18, 42, and 90 h after cessation of training, GLUT-4 protein concentration and 2-[1,2-3H]deoxy-d-glucose transport in the presence of a maximally stimulating concentration of insulin (2 mU/ml) were examined by using incubated epitrochlearis muscle preparation. Swimming training increased GLUT-4 protein concentration and insulin responsiveness by 87 and 85%, respectively, relative to age-matched controls when examined 18 h after training. Forty-two hours after training, GLUT-4 protein concentration and insulin responsiveness were still higher by 52 and 51%, respectively, in muscle from trained rats compared with control. GLUT-4 protein concentration and insulin responsiveness in trained muscle returned to sedentary control level within 90 h after training. We conclude that 1) the change in insulin responsiveness during detraining is directly related to muscle GLUT-4 protein content, and 2) consequently, the greater the increase in GLUT-4 protein content that is induced by training, the longer an effect on insulin responsiveness persists after the training.
Ventilation and hypoxic ventilatory responsiveness in Chinese-Tibetan residents at 3,658 m
Authors: Curran Linda S. , Zhuang Jianguo , Sun Shin Fu , Moore Lorna G.
Published: December 2017

Curran, Linda S., Jianguo Zhuang, Shin Fu Sun, and Lorna G. Moore. Ventilation and hypoxic ventilatory responsiveness in Chinese-Tibetan residents at 3,658 m. J. Appl. Physiol. 83(6): 2098–2104, 1997.—When breathing ambient air at rest at 3,658 m altitude, Tibetan lifelong residents of 3,658 m ventilate as much as newcomers acclimatized to high altitude; they also ventilate more and have greater hypoxic ventilatory responses (HVRs) than do Han (“Chinese”) long-term residents at 3,658 m. This suggests that Tibetan ancestry is advantageous in protecting resting ventilation levels during years of hypoxic exposure and is of interest in light of the permissive role of hypoventilation in the development of chronic mountain sickness, which is nearly absent among Tibetans. The existence of individuals with mixed Tibetan-Chinese ancestry (Han-Tibetans) residing at 3,658 m affords an opportunity to test this hypothesis. Eighteen men born in Lhasa, Tibet, China (3,658 m) to Tibetan mothers and Han fathers were compared with 27 Tibetan men and 30 Han men residing at 3,658 m who were previously studied. We used the same study procedures (minute ventilation was measured with a dry-gas flowmeter during room air breathing and hyperoxia and with a 13-liter spirometer-rebreathing system during the hypoxic and hypercapnic tests). During room air breathing at 3,658 m (inspired O2 pressure = 93 Torr), Han-Tibetans resembled Tibetans in ventilation (12.1 ± 0.6 vs. 11.5± 0.5 l/min btps, respectively) but had HVR that were blunted (63 ± 16 vs. 121 ± 13, respectively, for HVR shape parameter A) and declined with increasing duration of high-altitude residence. During administered hyperoxia (inspired O2 pressure = 310 Torr) at 3,658 m, the paradoxical hyperventilation previously seen in Tibetan but not Han residents at 3,658 m (11.8 ± 0.5 vs. 10.1 ± 0.5 l/min btps) was absent in these Han-Tibetans (9.8 ± 0.6 l/minbtps). Thus, although longer duration of high-altitude residence appears to progressively blunt HVR among Han-Tibetans born and residing at 3,658 m, their Tibetan ancestry appears protective in their maintenance of high resting ventilation levels despite diminished chemosensitivity.
Does adipose tissue influence bioelectric impedance in obese men and women?
Authors: Baumgartner Richard N. , Ross Robert , Heymsfield Steven B.
Published: December 2017

Baumgartner, Richard N., Robert Ross, and Steven B. Heymsfield. Does adipose tissue influence bioelectric impedance in obese men and women? J. Appl. Physiol.84(1): 257–262, 1998.—Bioelectric-impedance analysis overestimates fat-free mass in obese people. No clear hypotheses have been presented or tested that explain this effect. This study tested the hypothesis that adipose tissue affects measurements of resistance by using data for whole body and body segment resistance and by using muscle, adipose tissue, and bone volumes from magnetic resonance imaging for 86 overweight and obese men and women (body mass index >27 kg/m2; age 38.5 ± 10.2 yr). In multiple-regression analysis, muscle volumes had strong associations with resistance, confirming that the electric currents are conducted primarily in the lean soft tissues. Subcutaneous adipose tissue had a slight but statistically significant effect in women, primarily for the leg, suggesting that adipose tissue can affect measured resistance when the volume of adipose tissue is greater than muscle volume, as may occur in obese women in particular. This resulted in a slight overestimation of fat-free mass (e.g., +3 kg) when a bioelectric- impedance-analysis equation calibrated for nonobese female subjects was applied.
Neuromuscular fatigue after maximal stretch-shortening cycle exercise
Authors: Strojnik V. , Komi P. V.
Published: December 2017

Strojnik, V., and P. V. Komi. Neuromuscular fatigue after maximal stretch-shortening cycle exercise. J. Appl. Physiol. 84(1): 344–350, 1998.—To examine some possible sites of fatigue during short-lasting maximally intensive stretch-shortening cycle exercise, drop jumps on an inclined sledge apparatus were analyzed. Twelve healthy volunteers performed jumps until they were unable to maintain jumping height >90% of their maximum. After the workout, the increases in the blood lactate concentration and serum creatine kinase activation were statistically significant ( P < 0.001 and P < 0.05, respectively) but rather small in physiological terms. The major changes after the workout were as follows: the single twitch was characterized by smaller peak torque ( P < 0.05) and shorter time to peak ( P < 0.05) and half-relaxation time ( P < 0.01). The double-twitch torque remained at the same level ( P > 0.05), but with a steeper maximal slope of torque rise ( P < 0.05); during 20- and 100-Hz stimulation the torque declined (both P < 0.01) and the maximal voluntary torque changed nonsignificantly but with a smaller maximal slope of torque rise ( P < 0.01) and a higher activation level ( P < 0.05), accompanied by an increased electromyogram amplitude. These findings indicate that the muscle response after the short-lasting consecutive maximum jumps on the sledge apparatus may involve two distinct mechanisms acting in opposite directions: 1) The contractile mechanism seems to be potentiated through a shorter Ca2+transient and faster cross-bridge cycling, as implied by twitch changes. 2) High-frequency action potential propagation shows an impairment, which is suggested as the possible dominant reason for fatigue in exercise of this type.
The alcohol breath test—a review
Authors: Hlastala Michael P.
Published: December 2017

Hlastala, Michael P. The alcohol breath test—a review. J. Appl. Physiol.84(2): 401–408, 1998.—The alcohol breath test (ABT) is evaluated for variability in response to changes in physiological parameters. The ABT was originally developed in the 1950s, at a time when understanding of pulmonary physiology was quite limited. Over the past decade, physiological studies have shown that alcohol is exchanged entirely within the conducting airways via diffusion from the bronchial circulation. This is in sharp contrast to the old idea that alcohol exchanges in the alveoli in a manner similar to the lower solubility respiratory gases (O2and CO2). The airway alcohol exchange process is diffusion (airway tissue) and perfusion (bronchial circulation) limited. The dynamics of airway alcohol exchange results in a positively sloped exhaled alveolar plateau that contributes to considerable breathing pattern-dependent variation in measured breath alcohol concentration measurements.