bluuebunny/crossref_metadata_2025 huggingface dataset:
Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise
Authors: Coker Robert H. , Krishna Mahesh G. , Lacy D. Brooks , Allen Eric J. , Wasserman David H.
Published: December 2017

Coker, Robert H., Mahesh G. Krishna, D. Brooks Lacy, Eric J. Allen, and David H. Wasserman. Sympathetic drive to liver and nonhepatic splanchnic tissue during heavy exercise. J. Appl. Physiol. 82(4): 1244–1249, 1997.—The contribution of sympathetic drive and vascular catecholamine delivery to the splanchnic bed during heavy exercise was studied in dogs that underwent a laparotomy during which flow probes were implanted onto the portal vein and hepatic artery and catheters were inserted into the carotid artery, portal vein, and hepatic vein. At least 16 days after surgery, dogs completed a 20-min heavy exercise protocol (mean work rate of 5.7 ± 1 miles/h, 20 ± 2% grade). Arterial epinephrine (Epi) and norepinephrine (NE) increased by ∼500 and ∼900 pg/ml, respectively, after 20 min of heavy exercise. Because Epi is not released from the splanchnic bed and because Epi fractional extraction (FX) = NE FX, NE uptake by splanchnic tissue can be calculated despite simultaneous release of NE. Basal nonhepatic splanchnic (NHS) FX increased from a basal rate of 0.52 ± 0.09 to a peak of 0.64 ± 0.05 at 10 min of exercise. Hepatic Epi FX increased from a basal rate of 0.68 ± 0.10 to 0.81 ± 0.09 at 20 min of exercise. Even though NHS extraction of Epi reduced portal vein Epi levels by ∼60%, the release of NE from NHS tissue maintained portal vein NE at levels similar to those in arterial blood. NHS NE spillover increased from a basal rate of 5.7 ± 1.4 to 11.7 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 20 min of exercise. Hepatic NE spillover increased from a basal rate of 5.0 ± 1.2 ng ⋅ kg−1 ⋅ min−1to a peak of 14.2 ± 2.8 ng ⋅ kg−1 ⋅ min−1at 15 min of exercise. These results show that 1) approximately two- and threefold increases in NHS and hepatic NE spillover occur during heavy exercise, demonstrating that sympathetic drive to these tissues contributes to the increase in circulating NE; 2) the high catecholamine FX by the NHS tissues results in an Epi level at the liver that is considerably lower than that in the arterial blood; and 3) circulating NE delivery to the liver is sustained despite high catecholamine FX due to simultaneous NHS NE release.
Resistance and aerobic training in older men: effects onV˙o 2 peak and the capillary supply to skeletal muscle
Authors: Hepple R. T. , Mackinnon S. L. M. , Goodman J. M. , Thomas S. G. , Plyley M. J.
Published: December 2017

Hepple, R. T., S. L. M. Mackinnon, J. M. Goodman, S. G. Thomas, and M. J. Plyley. Resistance and aerobic training in older men: effects onV˙o 2 peak and the capillary supply to skeletal muscle. J. Appl. Physiol. 82(4): 1305–1310, 1997.—Both aerobic training (AT) and resistance training (RT) may increase aerobic power (V˙o 2 peak) in the older population; however, the role of changes in the capillary supply in this response has not been evaluated. Twenty healthy men (age 65–74 yr) engaged in either 9 wk of lower body RT followed by 9 wk of AT on a cycle ergometer (RT→AT group) or 18 wk of AT on a cycle ergometer (AT→AT group). RT was performed three times per week and consisted of three sets of four exercises at 6–12 repetitions maximum. AT was performed three times per week for 30 min at 60–70% heart rate reserve.V˙o 2 peak was increased after both RT and AT ( P < 0.05). Biopsies (vastus lateralis) revealed that the number of capillaries per fiber perimeter length was increased after both AT and RT ( P < 0.05), paralleling the changes in V˙o 2 peak, whereas capillary density was increased only after AT ( P < 0.01). These results, and the finding of a significant correlation between the change in capillary supply and V˙o 2 peak( r = 0.52), suggest the possibility that similar mechanisms may be involved in the increase ofV˙o 2 peak after high-intensity RT and AT in the older population.
Influence of pregnancy on the febrile response to ICV administration of PGE1 in rats studied in a thermocline
Authors: Eliason Heather L. , Fewell James E.
Published: December 2017

Eliason, Heather L., and James E. Fewell. Influence of pregnancy on the febrile response to ICV administration of PGE1 in rats studied in a thermocline. J. Appl. Physiol. 82(5): 1453–1458, 1997.—Rats near term of pregnancy have an attenuated febrile response to intracerebroventricular (ICV) injection of prostaglandin E1(PGE1) when they are studied at an ambient temperature below their thermoneutral zone. Given that nonshivering thermogenesis in brown adipose tissue is impaired in rodents near term of pregnancy, it is possible that the attenuated febrile response is forced by impairment of this component of the autonomic thermoregulatory response. If this were the case, then near-term pregnant rats should develop a “normal” fever after PGE1 administration if they were studied in a thermocline where they could utilize behavioral as well as autonomic thermoregulatory effectors to increase their body core temperature (Tbc). Experiments were, therefore, carried out on 13 nonpregnant and 14 pregnant chronically instrumented rats in a thermocline (temperature gradient 10–40°C) to investigate their Tbc responses to ICV injection of PGE1. ICV injection of 0.2 μg PGE1 produced significant increases in Tbc and fever index in both nonpregnant and pregnant animals ( day 19 of gestation); the increases, however, were significantly attenuated in the pregnant compared with the nonpregnant rats. Behavioral (e.g., selected ambient temperature) and autonomic (e.g., oxygen consumption) thermoregulatory effectors were activated to increase Tbc after ICV PGE1 in both groups of animals, but the duration of activation was shortened in pregnant compared with nonpregnant rats. The abbreviated thermoregulatory effector responses and the resulting attenuated febrile response to PGE1 in the pregnant rats may have resulted from a pregnancy-related activation of an endogenous antipyretic system.
Effects of hypoxia on diaphragm relaxation rate during fatigue
Authors: Van Lunteren Erik , Torres Augusto , Moyer Michelle
Published: December 2017

Van Lunteren, Erik, Augusto Torres, and Michelle Moyer.Effects of hypoxia on diaphragm relaxation rate during fatigue. J. Appl. Physiol. 82(5): 1472–1478, 1997.—Skeletal muscle fatigue is associated with a slowing of relaxation rate. Hypoxia may increase the rate at which fatigue occurs, but, surprisingly, mild to moderate hypoxia has not been found to augment the degree of slowing of relaxation during fatigue. The present study tested the hypothesis that severe hypoxia interacts with fatigue in slowing the rate of muscle relaxation and that this can be modulated by altering membranous ionic conductances. Rat diaphragm muscle strips were studied in vitro while aerated with 95% O2-5% CO2 (normoxia) or 95% N2-5% CO2 (hypoxia). During continuous 0.1-Hz stimulation, relaxation rate and force remained stable over time, and relaxation rate was not slowed by hypoxia. Hypoxia accelerated force decline during continuous 5-Hz but not intermittent 20-Hz stimulation. During both 5- and 20-Hz stimulation, relaxation rate became slower over time as force declined, the extent of which was increased significantly by hypoxia. The extent of hypoxia-augmented slowing of relaxation rate during fatigue increased over time and was greater than expected for a given degree of force loss. 4-Aminopyridine did not attenuate or partially attenuated, whereas lowering extracellular Cl−concentration fully attenuated, the hypoxia-induced prolongation of relaxation rate during repetitive stimulation. Thus hypoxia slows relaxation rate to a greater extent than expected for a given degree of force decline, an effect that increases over time, is at most partially attenuated by lowering K+ conductance, and is fully attenuated by lowering membranous Cl− conductance.
Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating
Authors: Ray Chester A. , Gracey Kathryn H.
Published: December 2017

Ray, Chester A., and Kathryn H. Gracey. Augmentation of exercise-induced muscle sympathetic nerve activity during muscle heating. J. Appl. Physiol. 82(6): 1719–1725, 1997.—The muscle metabo- and mechanoreflexes have been shown to increase muscle sympathetic nerve activity (MSNA) during exercise. Group III and IV muscle afferents, which are believed to mediate this response, have been shown to be thermosensitive in animals. The purpose of the present study was to evaluate the effect of muscle temperature on MSNA responses during exercise. Eleven subjects performed ischemic isometric handgrip at 30% of maximal voluntary contraction to fatigue, followed by 2 min of postexercise muscle ischemia (PEMI), with and without local heating of the forearm. Local heating of the forearm increased forearm muscle temperature from 34.4 ± 0.2 to 38.9 ± 0.3°C ( P = 0.001). Diastolic and mean arterial pressures were augmented during exercise in the heat. MSNA responses were greater during ischemic handgrip with local heating compared with control (no heating) after the first 30 s. MSNA responses at fatigue were greater during local heating. MSNA increased by 16 ± 2 and 20 ± 2 bursts per 30 s for control and heating, respectively ( P = 0.03). When expressed as a percent change in total activity (total burst amplitude), MSNA increased 531 ± 159 and 941 ± 237% for control and heating, respectively ( P = 0.001). However, MSNA was not different during PEMI between trials. This finding suggests that the augmentation of MSNA during exercise with heat was due to the stimulation of mechanically sensitive muscle afferents. These results suggest that heat sensitizes skeletal muscle afferents during muscle contraction in humans and may play a role in the regulation of MSNA during exercise.
Inhibition of CD18 or CD11b attenuates acute lung injury after acid instillation in rabbits
Authors: Folkesson Hans G. , Matthay Michael A.
Published: December 2017

Folkesson, Hans G., and Michael A. Matthay. Inhibition of CD18 or CD11b attenuates acute lung injury after acid instillation in rabbits. J. Appl. Physiol. 82(6): 1743–1750, 1997.—Acid-induced lung injury is mediated primarily by activated neutrophils. Although a prior study demonstrated that acid-induced neutrophil influx into the air spaces was not CD18 dependent, we hypothesized that either a neutralizing anti-CD18 monoclonal antibody (MHM23) or a neutrophil inhibitory factor (NIF), NIF (CD11b,18), might attenuate acid-induced lung injury in rabbits by interfering with neutrophil activation. This hypothesis derived from in vitro studies that reported that anti-CD18 therapy prevented tumor necrosis factor-α-induced neutrophil activation. Hydrochloric acid (pH = 1.5 in one-third normal saline) or one-third normal saline (4 ml/kg) was instilled into the lungs of ventilated, anesthetized rabbits. The rabbits were studied for 6 h. In acid-instilled rabbits without the anti-CD18 monoclonal antibody or NIF (CD11b,18), severe lung injury developed. In acid-instilled rabbits, pretreatment (5 min before acid) with the anti-CD18 monoclonal antibody (2 mg/kg iv) or pretreatment with the NIF (anti-CD11b,18, 10 mg/kg iv) prevented 50–70% of acid-induced abnormalities in oxygenation, the increase in extravascular lung water, and extravascular protein accumulation. The anti-CD18 monoclonal antibody was associated with a significant increase in air space neutrophils by bronchoalveolar lavage, suggesting that the neutrophils respond normally to chemotactic stimuli but that the neutrophils did not injure the lung even though they accumulated in the air spaces. In summary, neutralization of CD18 attenuates the acute lung injury after acid instillation without reducing the number of neutrophils in the air spaces, suggesting that anti-CD18 therapy may be beneficial because of its capacity to reduce neutrophil activation.
Weight loss and wrestling training: effects on nutrition, growth, maturation, body composition, and strength
Authors: Roemmich James N. , Sinning Wayne E.
Published: December 2017

Roemmich, James N., and Wayne E. Sinning. Weight loss and wrestling training: effects on nutrition, growth, maturation, body composition, and strength. J. Appl. Physiol. 82(6): 1751–1759, 1997.—Adolescent wrestlers ( n = 9, 15.4 yr) and recreationally active control adolescent males ( n = 7, 15.7 yr) were measured before, at the end (late season), and 3.5–4 mo after a wrestling season to assess the influence of dietary restriction on growth, maturation, body composition, protein nutrition, and muscular strength. Controls consumed adequate amounts of energy, carbohydrate (CHO), protein, and fat, and demonstrated normal gains in weight, fat mass (FM) and fat-free mass (FFM). Wrestlers consumed a high-CHO (61 ± 2% kcal), low-fat (24 ± 2% kcal) diet during the season but did not consume adequate energy (24.7 ± 3.5 kcal ⋅ kg−1⋅ day−1) or protein (0.9 g ⋅ kg−1⋅ day−1). Deficient dietary intake reduced prealbumin levels (26.0 ± 1.9 vs. 20.2 ± 0.9 mg/dl) and slowed the accrual of lean arm and thigh cross-sectional muscle areas (AXSECT, TXSECT, respectively). For wrestlers, dietary deficiency also decreased weight (60.3 ± 3.5 to 58.0 ± 3.3 kg), relative fat (9.9 ± 0.5 to 8.0 ± 0.7%), and FM (6.0 ± 0.5 to 4.7 ± 0.6 kg). Postseason, wrestlers and controls consumed similar diets, and wrestlers had significant increases in prealbumin, AXSECT, and TXSECT. Wrestlers also increased their weight (6.1 ± 0.6 kg), FFM (3.0 ± 0.6 kg), and FM (3.2 ± 0.5 kg) postseason. Rates of bone maturation and segmental growth were not different between the groups. The wrestlers had reductions in elbow and knee strength from preseason to late season but increases postseason. Lean tissue changes were associated with the changes in strength and power ( r = 0.72–0.91, P < 0.001). After covariance for FFM or limb-specific cross section, few significant changes remained. In conclusion, dietary restriction reduced protein nutrition and muscular performance but produced little effect on linear growth and maturation. Prealbumin levels and the rate of lean tissue accrual were positively related ( r = 0.43, P ≤ 0.05).
Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass
Authors: Zanaboni Paul , Murray Paul A. , Simon Brett A. , Zehr Kenton , Fleischer Kirk , Tseng Elaine , Nyhan Daniel P.
Published: December 2017

Zanaboni, Paul, Paul A. Murray, Brett A. Simon, Kenton Zehr, Kirk Fleischer, Elaine Tseng, and Daniel P. Nyhan. Selective endothelial dysfunction in conscious dogs after cardiopulmonary bypass. J. Appl. Physiol. 82(6): 1776–1784, 1997.—It has previously been demonstrated that cardiopulmonary bypass (CPB) causes prolonged pulmonary vascular hyperreactivity (D. P. Nyhan, J. M. Redmond, A. M. Gillinov, K. Nishiwaki, and P. A. Murray. J. Appl. Physiol. 77: 1584–1590, 1994). This study investigated the effects of CPB on endothelium-dependent (acetylcholine and bradykinin) and endothelium-independent (sodium nitroprusside) pulmonary vasodilation in conscious dogs. Continuous left pulmonary vascular pressure-flow (LP-Q˙) plots were generated in conscious dogs before CPB and again in the same animals 3–4 days post-CPB. The dose of U-46619 used to acutely preconstrict the pulmonary circulation to similar levels pre- and post-CPB was decreased (0.13 ± 0.01 vs. 0.10 ± 0.01 mg ⋅ kg−1 ⋅ min−1, P < 0.01) after CPB. Acetylcholine, bradykinin, and sodium nitroprusside all caused dose-dependent pulmonary vasodilation pre-CPB. The pulmonary vasodilator response to acetylcholine was completely abolished post-CPB. For example, at left pulmonary blood flow of 80 ml ⋅ kg−1 ⋅ min−1acetylcholine (10 μg ⋅ kg−1 ⋅ min−1) resulted in 72 ± 15% reversal ( P< 0.01) of U-46619 preconstriction pre-CPB but caused no change post-CPB. However, the responses to bradykinin and sodium nitroprusside were unchanged post-CPB. The impaired pulmonary vasodilator response to acetylcholine, but not to bradykinin, suggests a selective endothelial defect post-CPB. The normal response to sodium nitroprusside indicates that cGMP-mediated vasodilation is unchanged post-CPB.
Effect of glucose supplement timing on protein metabolism after resistance training
Authors: Roy B. D. , Tarnopolsky M. A. , Macdougall J. D. , Fowles J. , Yarasheski K. E.
Published: December 2017

Roy, B. D., M. A. Tarnopolsky, J. D. MacDougall, J. Fowles, and K. E. Yarasheski. Effect of glucose supplement timing on protein metabolism after resistance training. J. Appl. Physiol. 82(6): 1882–1888, 1997.—We determined the effect of the timing of glucose supplementation on fractional muscle protein synthetic rate (FSR), urinary urea excretion, and whole body and myofibrillar protein degradation after resistance exercise. Eight healthy men performed unilateral knee extensor exercise (8 sets/∼10 repetitions/∼85% of 1 single maximal repetition). They received a carbohydrate (CHO) supplement (1 g/kg) or placebo (Pl) immediately ( t = 0 h) and 1 h ( t = +1 h) postexercise. FSR was determined for exercised (Ex) and control (Con) limbs by incrementall-[1-13C]leucine enrichment into the vastus lateralis over ∼10 h postexercise. Insulin was greater ( P < 0.01) at 0.5, 0.75, 1.25, 1.5, 1.75, and 2 h, and glucose was greater ( P < 0.05) at 0.5 and 0.75 h for CHO compared with Pl condition. FSR was 36.1% greater in the CHO/Ex leg than in the CHO/Con leg ( P = not significant) and 6.3% greater in the Pl/Ex leg than in the Pl/Con leg ( P = not significant). 3-Methylhistidine excretion was lower in the CHO (110.43 ± 3.62 μmol/g creatinine) than Pl condition (120.14 ± 5.82, P < 0.05) as was urinary urea nitrogen (8.60 ± 0.66 vs. 12.28 ± 1.84 g/g creatinine, P < 0.05). This suggests that CHO supplementation (1 g/kg) immediately and 1 h after resistance exercise can decrease myofibrillar protein breakdown and urinary urea excretion, resulting in a more positive body protein balance.
Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure
Authors: Peters Jochen K. , Lister George , Nadel Ethan R. , Mack Gary W.
Published: December 2017

Peters, Jochen K., George Lister, Ethan R. Nadel, and Gary W. Mack. Venous and arterial reflex responses to positive-pressure breathing and lower body negative pressure. J. Appl. Physiol. 82(6): 1889–1896, 1997.—We examined the relative importance of arteriolar and venous reflex responses during reductions in cardiac output provoked by conditions that increase [positive end-expiratory pressure (PEEP)] or decrease [lower body negative pressure (LBNP)] peripheral venous filling. Five healthy subjects were exposed to PEEP (10, 15, 20, and 25 cmH2O) and LBNP (−10, −15, −20, and −25 mmHg) to induce progressive but comparable reductions in right atrial transmural pressure (control to minimum): from 5.9 ± 0.4 to 1.8 ± 0.7 and from 6.5 ± 0.6 to 2.0 ± 0.2 mmHg with PEEP and LBNP, respectively. Cardiac output (impedance cardiography) fell less during PEEP than during LBNP (from 3.64 ± 0.21 to 2.81 ± 0.21 and from 3.39 ± 0.21 to 2.14 ± 0.24 l ⋅ min−1 ⋅ m−2with PEEP and LBNP, respectively), and mean arterial pressure increased. We observed sustained increases in forearm vascular resistance (i.e., forearm blood flow by venous occlusion plethysmography) and systemic vascular resistance that were greater during LBNP: from 19.7 ± 2.91 to 27.97 ± 5.46 and from 20.56 ± 2.48 to 50.25 ± 5.86 mmHg ⋅ ml−1 ⋅ 100 ml tissue−1 ⋅ min ( P < 0.05) during PEEP and LBNP, respectively. Venomotor responses (venous pressure in the hemodynamically isolated limb) were always transient, significant only with the greatest reduction in right atrial transmural pressure, and were similar for LBNP and PEEP. Thus arteriolar rather than venous responses are predominant in blood volume mobilization from skin and muscle, and venoconstriction is not intensified with venous engorgement during PEEP.
Stabilized bubbles in the body: pressure-radius relationships and the limits to stabilization
Authors: Van Liew Hugh D. , Raychaudhuri Soumya
Published: December 2017

Van Liew, Hugh D., and Soumya Raychaudhuri. Stabilized bubbles in the body: pressure-radius relationships and the limits to stabilization. J. Appl. Physiol.82(6): 2045–2053, 1997.—We previously outlined the fundamental principles that govern behavior of stabilized bubbles, such as the microbubbles being put forward as ultrasound contrast agents. Our present goals are to develop the idea that there are limits to the stabilization and to provide a conceptual framework for comparison of bubbles stabilized by different mechanisms. Gases diffuse in or out of stabilized bubbles in a limited and reversible manner in response to changes in the environment, but strong growth influences will cause the bubbles to cross a threshold into uncontrolled growth. Also, bubbles stabilized by mechanical structures will be destroyed if outside influences bring them below a critical small size. The in vivo behavior of different kinds of stabilized bubbles can be compared by using plots of bubble radius as a function of forces that affect diffusion of gases in or out of the bubble. The two ends of the plot are the limits for unstabilized growth and destruction; these and the curve’s slope predict the bubble’s practical usefulness for ultrasonic imaging or O2 carriage to tissues.
Altered glycolytic and oxidative capacities of skeletal muscle contribute to insulin resistance in NIDDM
Authors: Simoneau Jean-Aimé , Kelley David E.
Published: December 2017

Simoneau, Jean-Aimé, and David E. Kelley. Altered glycolytic and oxidative capacities of skeletal muscle contribute to insulin resistance in NIDDM. J. Appl. Physiol. 83(1): 166–171, 1997.—The insulin resistance of skeletal muscle in glucose-tolerant obese individuals is associated with reduced activity of oxidative enzymes and a disproportionate increase in activity of glycolytic enzymes. Because non-insulin-dependent diabetes mellitus (NIDDM) is a disorder characterized by even more severe insulin resistance of skeletal muscle and because many individuals with NIDDM are obese, the present study was undertaken to examine whether decreased oxidative and increased glycolytic enzyme activities are also present in NIDDM. Percutaneous biopsy of vatus lateralis muscle was obtained in eight lean (L) and eight obese (O) nondiabetic subjects and in eight obese NIDDM subjects and was assayed for marker enzymes of the glycolytic [phosphofructokinase, glyceraldehyde phosphate dehydrogenase, hexokinase (HK)] and oxidative pathways [citrate synthase (CS), cytochrome- c oxidase], as well as for a glycogenolytic enzyme (glycogen phosphorylase) and a marker of anaerobic ATP resynthesis (creatine kinase). Insulin sensitivity was measured by using the euglycemic clamp technique. Activity for glycolytic enzymes (phosphofructokinase, glyceraldehye phosphate dehydrogenase, HK) was highest in subjects with subjects with NIDDM, following the order of NIDDM > O > L, whereas maximum velocity for oxidative enzymes (CS, cytochrome- c oxidase) was lowest in subjects with NIDDM. The ratio between glycolytic and oxidative enzyme activities within skeletal muscle correlated negatively with insulin sensitivity. The HK/CS ratio had the strongest correlation ( r = −0.60, P < 0.01) with insulin sensitivity. In summary, an imbalance between glycolytic and oxidative enzyme capacities is present in NIDDM subjects and is more severe than in obese or lean glucose-tolerant subjects. The altered ratio between glycolytic and oxidative enzyme activities found in skeletal muscle of individuals with NIDDM suggests that a dysregulation between mitochondrial oxidative capacity and capacity for glycolysis is an important component of the expression of insulin resistance.
Respiratory impedances and acinar gas transfer in a canine model for emphysema
Authors: Barnas George M. , Delaney Paul A. , Gheorghiu Ileana , Mandava Srinivas , Russell Robert G. , Kahn Renée , Mackenzie Colin F.
Published: December 2017

Barnas, George M., Paul A. Delaney, Ileana Gheorghiu, Srinivas Mandava, Robert G. Russell, Renée Kahn, and Colin F. Mackenzie. Respiratory impedances and acinar gas transfer in a canine model for emphysema. J. Appl. Physiol. 83(1): 179–188, 1997.—We examined how the changes in the acini caused by emphysema affected gas transfer out of the acinus (Taci) and lung and chest wall mechanical properties. Measurements were taken from five dogs before and 3 mo after induction of severe bilateral emphysema by exposure to papain aerosol (170–350 mg/dose) for 4 consecutive wk. With the dogs anesthetized, paralyzed, and mechanically ventilated at 0.2 Hz and 20 ml/kg, we measured Taciby the rate of washout of133Xe from an area of the lung with occluded blood flow. Measurements were repeated at positive end-expiratory pressures (PEEP) of 10, 5, 15, 0, and 20 cmH2O. We also measured dynamic elastances and resistances of the lungs (El and Rl, respectively) and chest wall at the different PEEP and during sinusoidal forcing in the normal range of breathing frequency and tidal volume. After final measurements, tissue sections from five randomly selected areas of the lung each showed indications of emphysema. Taciduring emphysema was similar to that in control dogs. Eldecreased by ∼50% during emphysema ( P < 0.05) but did not change its dependence on frequency or tidal volume. Rl did not change ( P > 0.05) at the lowest frequency studied (0.2 Hz), but in some dogs it increased compared with control at the higher frequencies. Chest wall properties were not changed by emphysema ( P > 0.05). We suggest that although large changes in acinar structure and El occur during uncomplicated bilateral emphysema, secondary complications must be present to cause several of the characteristic dysfunctions seen in patients with emphysema.
Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise
Authors: Sen Chandan K. , Atalay Mustafa , Ågren Jyrki , Laaksonen David E. , Roy Sashwati , Hänninen Osmo
Published: December 2017

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren, David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise. J. Appl. Physiol.83(1): 189–195, 1997.—Fish oil supplementation and physical exercise may induce oxidative stress. We tested the effects of 8 wk of α-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats ( n = 80) were divided into groups supplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO and vitamin E (SOVE), and for FOVE and SOVE they were divided into corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipid peroxidation [thiobarbituric acid-reacting substances (TBARS)] was 33% higher in FO compared with SO in the liver, but oxidative protein damage (carbonyl levels) remained similar in both liver and red gastrocnemius muscle (RG). Vitamin E supplementation, compared with FO and SO, markedly decreased liver and RG TBARS, but liver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E also markedly decreased liver and RG protein carbonyl levels, although levels in FOVE and SOVE were similar. Exercise increased liver and RG TBARS and RG protein carbonyl levels markedly, with similar levels in FOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not protein oxidation in a tissue-specific manner. Vitamin E markedly decreased lipid peroxidation and protein oxidation in both FOVE and SOVE, although liver lipid peroxidation remained higher in FOVE. Despite higher levels of hepatic lipid peroxidation at rest in FOVE compared with SOVE, liver appeared to be relatively less susceptible to exercise-induced oxidative stress in FOVE.
Endurance exercise modulates neuromuscular junction of C57BL/6NNia aging mice
Authors: Fahim Mohamed A.
Published: December 2017

Fahim, Mohamed A. Endurance exercise modulates neuromuscular junction of C57BL/6NNia aging mice. J. Appl. Physiol. 83(1): 59–66, 1997.—The effect of age and endurance exercise on the physiology and morphology of neuromuscular junctions (NMJ) of gluteus maximus muscle was studied in C57BL/6NNia mice. Mice were exercised, starting at 7 or 25 mo of age, at 28 m/min for 60 min/day, 5 days/wk for 12 wk, on a rodent treadmill. Intracellular recordings of spontaneous miniature endplate potentials (MEPP) and the quantal content of endplate potentials (EPP) were recorded from NMJ of 10- and 28-mo-old control and exercised mice. Endurance exercise resulted in significant increases in MEPP amplitudes (23%), quantal content, and safety margin, and a significant decrease in MEPP frequency of young mice, with no change in resting membrane potential or membrane capacitance. Three months of endurance exercise resulted in an increase in MEPP frequency (41%) and decreases in MEPP amplitudes (15%), quantal content, and safety margin of old mice. Endurance exercise resulted in significantly larger nerve terminals (24%) in young animals, suggesting functional adaptation. Nerve terminals in exercised 28-mo-old mice were smaller than in the corresponding control mice, an indication that exercise minimized age-related nerve terminal elaboration. It is concluded that the different physiological responses of young and old gluteus maximus muscles to endurance exercise parallel their morphological responses. This suggests that the mouse NMJ undergoes a process of physiological and morphological remodeling during aging, and such plasticity could be modulated differently by endurance exercise.
Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system
Authors: Bao Gang , Metreveli Naira , Li Rena , Taylor Addison , Fletcher Eugene C.
Published: December 2017

Bao, Gang, Naira Metreveli, Rena Li, Addison Taylor, and Eugene C. Fletcher. Blood pressure response to chronic episodic hypoxia: role of the sympathetic nervous system. J. Appl. Physiol. 83(1): 95–101, 1997.—Previous studies in several strains of rats have demonstrated that 35 consecutive days of recurrent episodic hypoxia (7 h/day) cause an 8- to 13-mmHg persistent increase in diurnal systemic blood pressure (BP). Carotid chemoreceptors and the sympathetic nervous system have been shown to be necessary for development of this BP increase. The present study was undertaken to further define the role of renal artery sympathetic nerves and the adrenal medulla in this BP increase. Male Sprague-Dawley rats had either adrenal medullectomy, bilateral renal artery denervation, or sham surgery. Rats from each of these groups were subjected to episodic hypoxia for 35 days. Control groups received either compressed air or were left unhandled. Adrenal demedullation or renal artery denervation eliminated the chronic diurnal mean BP response (measured intra-arterially) to episodic hypoxia, whereas sham-operated controls continued to showed persistent elevation of systemic BP. Plasma and renal tissue catecholamine levels at the end of the experiment confirmed successful adrenal demedullation or renal denervation in the respective animals. The chronic episodic hypoxia-mediated increase in diurnal BP requires both intact renal artery nerves as well as an intact adrenal medulla.
Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery
Authors: Verbitsky O. , Mizrahi J. , Levin M. , Isakov E.
Published: December 2017

Verbitsky, O., J. Mizrahi, M. Levin, and E. Isakov.Effect of ingested sodium bicarbonate on muscle force, fatigue, and recovery. J. Appl. Physiol. 83(2): 333–337, 1997.—The influence of acute ingestion of NaHCO3 on fatigue and recovery of the quadriceps femoris muscle after exercise was studied in six healthy male subjects. A bicycle ergometer was used for exercising under three loading conditions: test A, load corresponding to maximal oxygen consumption; test B, load in test A + 17%; test C, load in test B but performed 1 h after acute ingestion of NaHCO3. Functional electrical stimulation (FES) was applied to provoke isometric contraction of the quadriceps femoris. The resulting knee torque was monitored during fatigue (2-min chronic FES) and recovery (10-s FES every 10 min, for 40 min). Quadriceps torques were higher in the presence of NaHCO3( P < 0.05): with NaHCO3 the peak, residual, and recovery (after 40 min) normalized torques were, respectively, 0.68 ± 0.05 (SD), 0.58 ± 0.05, and 0.73 ± 0.05; without NaHCO3 the values were 0.45 ± 0.04, 0.30 ± 0.06, and 0.63 ± 0.06. The increased torques obtained after acute ingestion of NaHCO3 indicate the possible existence of improved nonoxidative glycolysis in isometric contraction, resulting in reduced fatigue and enhanced recovery.
Focal central chemoreceptor sensitivity in the RTN studied with a CO2 diffusion pipette in vivo
Authors: Li Aihua , Nattie Eugene E.
Published: December 2017

Li, Aihua, and Eugene E. Nattie. Focal central chemoreceptor sensitivity in the RTN studied with a CO2 diffusion pipette in vivo. J. Appl. Physiol. 83(2): 420–428, 1997.—We describe and use a CO2diffusion pipette to produce a quickly reversible focal acidosis in the retrotrapezoid nucleus region of the rat brain stem. No tissue injection is made. Instead, artificial cerebrospinal fluid (aCSF) equilibrated with CO2 circulates within the micropipette, providing a source for continued CO2 diffusion into the tissue from the pipette tip. Tissue pH electrodes show the acidosis is limited to 500 μm from the tip. In controls (aCSF equilibrated with air), 1-min pipette perfusions increased tissue pH slightly and decreased phrenic nerve amplitude. In moderate- and high-CO2 groups (aCSF equilibrated with 50 or 100% CO2), 1-min perfusions significantly decreased tissue pH and increased phrenic nerve amplitude in a dose-dependent manner. The responses developed and reversed within minutes. Compared with our prior use of medullary acetazolamide injections to produce a focal acidosis, in this approach the acidosis 1) arises and reverses quickly and 2) its intensity can be varied. This allows study of sensitivity and mechanism. We conclude from this initial experiment that retrotrapezoid nucleus region chemoreceptors operate within the normal physiological range of CO2-induced tissue pH changes.
PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury
Authors: Chiang Chi-Huei , Hsu Kang , Yan Horng-Chin , Harn Horng-Jyh , Chang Deh-Ming
Published: December 2017

Chiang, Chi-Huei, Kang Hsu, Horng-Chin Yan, Horng-Jyh Harn, and Deh-Ming Chang.PGE1, dexamethasone, U-74389G, or Bt2-cAMP as an additive to promote protection by UW solution in I/R injury. J. Appl. Physiol. 83(2): 583–590, 1997.—A method to reduce ischemia-reperfusion (I/R) injury can be an important criterion to improve the preservation solution. Although University of Wisconsin solution (UW) works as a lung preservation solution, its attenuation effect on I/R injury has not been investigated. We attempted to determine whether, by adding various protective agents, modified UW solutions will enhance the I/R attenuation by UW. We examined the I/R injury in an isolated rat lung model. Various solutions, e.g., physiological salt solution (PSS), UW, and modified UW solutions containing various protective agents such as prostaglandin E1, dexamethasone, U-74389G, or dibutyryl adenosine 3′,5′-cyclic monophosphate were perfused individually to evaluate the I/R injury. Isolated rat lung experiments, with ischemia for 45 min, then reperfusion for 60 min, were conducted in a closed circulating system. Hemodynamic changes, lung weight gain (LWG), capillary filtration coefficient ( Kfc), protein content of lavage fluid, concentration of cytokines, and lung histopathology were analyzed. Results showed that the acute I/R lung injury with immediate permeability pulmonary edema was associated with an increase in tumor necrosis factor-α (TNF-α) production. A significant correlation existed between TNF-α and Kfc( r = 0.8, P < 0.0001) and TNF-α and LWG ( r = 0.9, P < 0.0001), indicating that TNF-α is an important cytokine modulating early I/R injury. Significantly lower levels of Kfc, LWG, TNF-α, and protein concentration of lung lavage ( P < 0.05) were found in the UW-perfused group than in the control group perfused with PSS. Modified UW promoted the protective effect of UW to further decrease Kfc, LWG, and TNF-α ( P < 0.05). Histopathological observations also substantiated this evidence. In the UW+U-74389G group, bronchial alveolar lavage fluid contained lowest protein concentration. We conclude that the UW solution attenuates I/R injury of rat lung and that the modified UW solutions further enhance the effect of UW in reducing I/R injury. Among modified solutions, UW+U-74389G is the best. Further investigation of the improved effects of the modified UW solutions would be beneficial in lung transplantation.
Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans
Authors: Ramires P. R. , Forjaz C. L. M. , Strunz C. M. C. , Silva M. E. R. , Diament J. , Nicolau W. , Liberman B. , Negrão C. E.
Published: December 2017

Ramires, P. R., C. L. M. Forjaz, C. M. C. Strunz, M. E. R. Silva, J. Diament, W. Nicolau, B. Liberman, and C. E. Negrão.Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans. J. Appl. Physiol. 83(2): 608–614, 1997.—The effects of an oral glucose administration (1 g/kg) 30 min before exercise on endurance capacity and metabolic responses were studied in 21 type I diabetic patients [insulin-dependent diabetes mellitus (IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55–60% of maximal O2uptake) was performed until exhaustion. Glucose administration significantly increased endurance capacity in Con (112 ± 7 vs. 125 ± 6 min, P < 0.05) but only in IDDM patients whose blood glucose decreased during exercise (70.8 ± 8.2 vs. 82.8 ± 9.4 min, P < 0.05). Hyperglycemia was normalized at 15 min of exercise in Con (7.4 ± 0.2 vs. 4.8 ± 0.2 mM) but not in IDDM patients (12.4 ± 0.7 vs. 15.6 ± 0.9 mM). In Con, insulin and C-peptide levels were normalized during exercise. Glucose administration decreased growth hormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in some IDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.
In vivo validation of whole body composition estimates from dual-energy X-ray absorptiometry
Authors: Prior Barry M. , Cureton Kirk J. , Modlesky Christopher M. , Evans Ellen M. , Sloniger Mark A. , Saunders Michael , Lewis Richard D.
Published: December 2017

Prior, Barry M., Kirk J. Cureton, Christopher M. Modlesky, Ellen M. Evans, Mark A. Sloniger, Michael Saunders, and Richard D. Lewis. In vivo validation of whole body composition estimates from dual-energy X-ray absorptiometry. J. Appl. Physiol. 83(2): 623–630, 1997.—We validated whole body composition estimates from dual-energy X-ray absorptiometry (DEXA) against estimates from a four-component model to determine whether accuracy is affected by gender, race, athletic status, or musculoskeletal development in young adults. Measurements of body density by hydrostatic weighing, body water by deuterium dilution, and bone mineral by whole body DEXA were obtained in 172 young men ( n = 91) and women ( n = 81). Estimates of body fat (%Fat) from DEXA (%FatDEXA) were highly correlated with estimates of body fat from the four-component model [body density, total body water, and total body mineral (%Fatd,w,m); r = 0.94, standard error of the estimante (SEE) = 2.8% body mass (BM)] with no significant difference between methods [mean of the difference ± SD of the difference = −0.4 ± 2.9 (SD) % BM, P = 0.10] in women and men. On the basis of the comparison with %Fatd,w,m, estimates of %FatDEXA were slightly more accurate than those from body density ( r = 0.91, SEE = 3.4%; mean of the difference ± SD of the difference = −1.2 ± 3.4% BM). Differences between %FatDEXA and %Fatd,w,m were weakly related to body thickness, as reflected by BMI ( r= −0.34), and to the percentage of water in the fat-free mass ( r = −0.51), but were not affected by race, athletic status, or musculoskeletal development. We conclude that body composition estimates from DEXA are accurate compared with those from a four-component model in young adults who vary in gender, race, athletic status, body size, musculoskeletal development, and body fatness.
Water transport and the distribution of aquaporin-1 in pulmonary air spaces
Authors: Effros R. M. , Darin C. , Jacobs E. R. , Rogers R. A. , Krenz G. , Schneeberger E. E.
Published: December 2017

Effros, R. M., C. Darin, E. R. Jacobs, R. A. Rogers, G. Krenz, and E. E. Schneeberger. Water transport and the distribution of aquaporin-1 in pulmonary air spaces. J. Appl. Physiol. 83(3): 1002–1016, 1997.—Recent evidence suggests that water transport between the pulmonary vasculature and air spaces can be inhibited by HgCl2, an agent that inhibits water channels (aquaporin-1 and -5) of cell membranes. In the present study of isolated rat lungs, clearances of labeled (3HOH) and unlabeled water were compared after instillation of hypotonic or hypertonic solutions into the air spaces or injection of a hypotonic bolus into the pulmonary artery. The clearance of3HOH between the air spaces and perfusate after intratracheal instillation and from the vasculature to the tissues after pulmonary arterial injections was invariably greater than that of unlabeled water, indicating that osmotically driven transport of water is limited by permeability of the tissue barriers rather than the rate of perfusion. Exposure to 0.5 mM HgCl2in the perfusate and air-space solution reduced the product of the filtration coefficient and surface area ( PfS) of water from the air spaces to the perfusate by 28% after instillation of water into the trachea. In contrast, perfusion of 0.5 mM HgCl2in air-filled lungs reduced PfSof the endothelium by 86% after injections into the pulmonary artery, suggesting that much of the action of this inhibitor is on the endothelial surfaces. Confocal laser scanning microscopy demonstrated that aquaporin-1 is on mouse pulmonary endothelium. No aquaporin-1 was found on alveolar type I cells with immunogold transmission electron microscopy, but small amounts were present on some type II cells.
Lateral pharyngeal fat pad pressure during breathing in anesthetized pigs
Authors: Winter W. Christopher , Gampper Tom , Gay Spencer B. , Suratt Paul M.
Published: December 2017

Winter, W. Christopher, Tom Gampper, Spencer B. Gay, and Paul M. Suratt. Lateral pharyngeal fat pad pressure during breathing in anesthetized pigs. J. Appl. Physiol. 83(3): 688–694, 1997.—It has been hypothesized that the pressure in tissues surrounding the upper airway is one of the determinants of the size and shape of the upper airway. To our knowledge, this pressure has not been measured. The purpose of this study was to test whether the pressure in a tissue lateral to the upper airway, the lateral pharyngeal fat pad pressure (Pfp), differs from atmospheric and pharyngeal pressures and whether it changes with breathing. We studied six male lightly sedated pigs by inserting a transducer tipped catheter into their fat pad space by using computerized tomographic scan guidance. We measured airflow with a pneumotachograph attached to a face mask and pharyngeal pressure with a balloon catheter. Pfp differed from atmospheric pressure, generally exceeding it, and from pharyngeal pressure. Pfp correlated positively with airflow and with pharyngeal pressure, decreasing during inspiration and increasing during expiration. Changes in Pfp with ventilation were eliminated by oropharyngeal intubation. We conclude that Pfp differs from atmospheric and pharyngeal pressures and that it changes with breathing.
Muscle glycogen accumulation after endurance exercise in trained and untrained individuals
Authors: Hickner R. C. , Fisher J. S. , Hansen P. A. , Racette S. B. , Mier C. M. , Turner M. J. , Holloszy J. O.
Published: December 2017

Hickner, R. C., J. S. Fisher, P. A. Hansen, S. B. Racette, C. M. Mier, M. J. Turner, and J. O. Holloszy. Muscle glycogen accumulation after endurance exercise in trained and untrained individuals. J. Appl. Physiol. 83(3): 897–903, 1997.—Muscle glycogen accumulation was determined in six trained cyclists (Trn) and six untrained subjects (UT) at 6 and either 48 or 72 h after 2 h of cycling exercise at ∼75% peak O2uptake (V˙o2 peak), which terminated with five 1-min sprints. Subjects ate 10 g carbohydrate ⋅ kg−1⋅ day−1for 48–72 h postexercise. Muscle glycogen accumulation averaged 71 ± 9 (SE) mmol/kg (Trn) and 31 ± 9 mmol/kg (UT) during the first 6 h postexercise ( P < 0.01) and 79 ± 22 mmol/kg (Trn) and 60 ± 9 mmol/kg (UT) between 6 and 48 or 72 h postexercise (not significant). Muscle glycogen concentration was 164 ± 21 mmol/kg (Trn) and 99 ± 16 mmol/kg (UT) 48–72 h postexercise ( P < 0.05). Muscle GLUT-4 content immediately postexercise was threefold higher in Trn than in UT ( P < 0.05) and correlated with glycogen accumulation rates ( r = 0.66, P < 0.05). Glycogen synthase in the active I form was 2.5 ± 0.5, 3.3 ± 0.5, and 1.0 ± 0.3 μmol ⋅ g−1⋅ min−1in Trn at 0, 6, and 48 or 72 h postexercise, respectively; corresponding values were 1.2 ± 0.3, 2.7 ± 0.5, and 1.6 ± 0.3 μmol ⋅ g−1⋅ min−1in UT ( P < 0.05 at 0 h). Plasma insulin and plasma C-peptide area under the curve were lower in Trn than in UT over the first 6 h postexercise ( P < 0.05). Plasma creatine kinase concentrations were 125 ± 25 IU/l (Trn) and 91 ± 9 IU/l (UT) preexercise and 112 ± 14 IU/l (Trn) and 144 ± 22 IU/l (UT; P < 0.05 vs. preexercise) at 48–72 h postexercise (normal: 30–200 IU/l). We conclude that endurance exercise training results in an increased ability to accumulate muscle glycogen after exercise.
Relationship between cold tolerance and generation of suppressor macrophages during acute cold stress
Authors: Kizaki Takako , Ookawara Tomomi , Izawa Tetsuya , Nagasawa Junichi , Haga Shukoh , Radák Zsolt , Ohno Hideki
Published: December 2017

Kizaki, Takako, Tomomi Ookawara, Tetsuya Izawa, Junichi Nagasawa, Shukoh Haga, Zsolt Radák, and Hideki Ohno.Relationship between cold tolerance and generation of suppressor macrophages during acute cold stress. J. Appl. Physiol. 83(4): 1116–1122, 1997.—Acute cold stress induces suppressor macrophages expressing large numbers of receptors to the crystallizable fragment (Fc) portion of immunoglobulin G (MAC-1+FcγRII/IIIbrightcells), resulting in the immunosuppression of splenocyte mitogenesis. The generation of MAC-1+FcγRII/IIIbrightcells is mediated by the action of glucocorticoids (GCs) through the GC-receptor. In the present study, the generation of MAC-1+FcγRII/IIIbrightcells in peritoneal exudate cells was closely related to the decrease of rectal temperature during 3-day exposure to 5°C. We next investigated the effects of improved cold tolerance on the generation of MAC-1+FcγRII/IIIbrightcells during acute cold stress. Mice were adapted to cold by exposure to 5°C for 3 wk (cold-acclimated mice) and then reexposed to 5°C for 3 h (acute cold stress) after living at 25°C for 24 h. The rectal temperature of cold-acclimated mice was not decreased by the acute cold stress. In addition, the proportion of MAC-1+FcγRII/IIIbrightcells in peritoneal exudate cell population from cold-acclimated mice was unaffected by the acute cold stress. The cold acclimation significantly attenuated the increases in serum corticosterone levels and the expression of the GC-receptor mRNA on peritoneal exudate cells in response to acute cold stress. These results suggest that the altered GC response to acute cold stress by the improvement of cold tolerance inhibits the generation of suppressor macrophages during acute cold stress.