bluuebunny/crossref_metadata_2025 huggingface dataset:
Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading
Authors: Goforth Harold W. , Arnall Jr., David A. , Bennett Brad L. , Law Patricia G.
Published: December 2017

Goforth, Jr., Harold W., David A. Arnall, Brad L. Bennett, and Patricia G. Law. Persistence of supercompensated muscle glycogen in trained subjects after carbohydrate loading. J. Appl. Physiol. 82(1): 342–347, 1997.—Several carbohydrate (CHO)-loading protocols have been used to achieve muscle glycogen supercompensation and prolong endurance performance. This study assessed the persistence of muscle glycogen supercompensation over the 3 days after the supercompensation protocol. Trained male athletes completed a 6-day CHO-loading protocol that included cycle ergometer exercise and dietary manipulations. The 3-day depletion phase began with 115 min of cycling at 75% peak oxygen uptake followed by 3 × 60-s sprints and included the subjects consuming a low-CHO/high-protein/high-fat (10:41:49%) diet. Subjects cycled 40 min at the same intensity for the next 2 days. During the 3-day repletion phase, subjects rested and consumed a high-CHO/low-protein/low-fat (85:08:07%) diet, including a glucose-polymer beverage. A 3-day postloading phase followed, which involved a moderately high CHO diet (60%) and no exercise. Glycogen values for vastus lateralis biopsies at baseline and postloading days 1–3 were 408 ± 168 (SD), 729 ± 222, 648 ± 186, and 714 ± 196 mmol/kg dry wt, respectively. The CHO-loading protocol increased muscle glycogen by 1.79 times baseline, and muscle glycogen remained near this level during the 3-day postloading period. Results indicate that supercompensated muscle glycogen levels can be maintained for at least 3 days in a resting athlete when a moderate-CHO diet is consumed.
Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women
Authors: De Crée Carl , Ball Peter , Seidlitz Bärbel , Van Kranenburg Gerrit , Geurten Peter , Keizer Hans A.
Published: December 2017

De Crée, Carl, Peter Ball, Bärbel Seidlitz, Gerrit Van Kranenburg, Peter Geurten, and Hans A. Keizer. Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women. J. Appl. Physiol. 82(1): 364–370, 1997.—Exercise-induced menstrual problems are accompanied by an increase in catecholestrogen (CE) formation. It has been hypothesized that hypoestrogenemia may be secondary to an increased turnover from estrogens to CE, which then may disrupt luteinizing hormone release. In addition, the strong affinity of CE for the catecholamine-deactivating enzyme catechol- O-methyltransferase (COMT) has led to speculations about their possible role in safeguarding norepinephrine from premature decomposition during exercise. We investigated whether acute exercise on a cycle ergometer produces any changes in CE homeostasis. Nine untrained eumenorrheic women (body fat, 24.8 ± 3.1%) volunteered for this study. Baseline plasma CE averages for total 2-hydroxyestrogens (2-OHE) were 218 ± 29 (SE) pg/ml during the follicular phase (FPh) and 420 ± 58 pg/ml during the luteal phase (LPh). 2-Methoxyestrogens (2-MeOE) measured 257 ± 17 pg/ml in the FPh and 339 ± 39 pg/ml in the LPh. During incremental exercise, total estrogens (E) increased, but 2-OHE and 2-MeOE levels did not significantly change in either phase. The 2-OHE/E ratio (measure of CE turnover) decreased during exercise in both menstrual phases, whereas the 2-MeOE/2-OHE ratio (correlates with COMT activity) did not significantly change. These findings suggest that there is insufficient evidence to conclude that brief incremental exercise in untrained eumenorrheic females acutely produces increased CE formation.
Dirofilaria immitis: heartworm infection alters pulmonary artery endothelial cell behavior
Authors: Mupanomunda Maria , Williams Jeffrey F. , Mackenzie Charles D. , Kaiser Lana
Published: December 2017

Mupanomunda, Maria, Jeffrey F. Williams, Charles D. Mackenzie, and Lana Kaiser. Dirofilaria immitis:heartworm infection alters pulmonary artery endothelial cell behavior. J. Appl. Physiol. 82(2): 389–398, 1997.—The pathogenesis of filariasis has generally been attributed to either physical presence of the adult parasites or the host’s immune response to the parasites. However, the spectrum of filariasis cannot be entirely explained by these causes, and other mechanisms must be operative. It is now evident that factors released by filarial parasites likely contribute to the pathogenesis of filarial diseases. Adult heartworms ( Dirofilaria immitis) reside in the right heart and pulmonary artery, so the pulmonary artery should be exposed to the highest concentration of filarial factors. We tested the hypothesis that endothelium-dependent relaxation is altered in the in vitro pulmonary artery from heartworm-infected dogs. Relaxation responses to endothelium-dependent vasodilators (methacholine, bradykinin, substance P, and A-23187) and the non-endothelium-dependent vasodilator nitroglycerin and contractile responses were measured in rings of pulmonary artery from control and heartworm-infected dogs. Endothelium-dependent relaxation was assessed in the presence and absence of inhibitors of nitric oxide synthase, cyclooxygenase, and guanylate cyclase. Responses to methacholine, substance P, and A-23187, but not to bradykinin, nitroglycerin, norepinephrine, or KCl, were depressed in pulmonary artery from heartworm-infected dogs when compared with control, suggesting that changes in endothelial cell and not vascular smooth muscle behavior are involved in altered relaxation. The mechanism of endothelium-dependent relaxation in control pulmonary artery appears to involve nitric oxide in the case of methacholine and both nitric oxide and a cyclooxygenase product in the case of bradykinin and A-23187. The mechanism of endothelium-dependent relaxation in pulmonary artery from heartworm-infected dogs was not clearly elucidated. These data provide no evidence that heartworm infection globally influences either endothelial cell receptor function or the vascular smooth muscle guanylate cyclase guanosine 3′,5′-cyclic monophosphate system, making it likely that changes in intracellular signaling are primarily responsible for the observed alteration of endothelium-mediated relaxation. Alteration of endothelial cell function by filarial parasites may be an important component in the pathology associated with filariasis.
Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia
Authors: Tansley J. G. , Clar C. , Pedersen M. E. F. , Robbins P. A.
Published: December 2017

Tansley, J. G., C. Clar, M. E. F. Pedersen, and P. A. Robbins. Human ventilatory response to acute hyperoxia during and after 8 h of both isocapnic and poikilocapnic hypoxia. J. Appl. Physiol. 82(2): 513–519, 1997.—During 8 h of either isocapnic or poikilocapnic hypoxia, there may be a rise in ventilation (V˙e) that cannot be rapidly reversed with a return to higher[Formula: see text] (L. S. G. E. Howard and P. A. Robbins. J. Appl. Physiol. 78: 1098–1107, 1995). To investigate this further, three protocols were compared: 1) 8-h isocapnic hypoxia [end-tidal[Formula: see text]([Formula: see text] ) held at prestudy value, end-tidal [Formula: see text]([Formula: see text]) = 55 Torr], followed by 8-h isocapnic euoxia[Formula: see text] = 100 Torr); 2) 8-h poikilocapnic hypoxia followed by 8-h poikilocapnic euoxia; and 3) 16-h air-breathing control. Before and at intervals throughout each protocol, theV˙e response to eucapnic hyperoxia [Formula: see text] held 1–2 Torr above prestudy value,[Formula: see text] = 300 Torr) was determined. There was a significant rise in hyperoxicV˙e over 8 h during both forms of hypoxia ( P < 0.05, analysis of variance) that persisted during the subsequent 8-h euoxic period ( P < 0.05, analysis of variance). These results support the notion that an 8-h period of hypoxia increases subsequent hyperoxic V˙e, even if acid-base changes have been minimized through maintenance of isocapnia during the hypoxic period.
Nociceptive atrophy of the rat soleus muscle induced by bone fracture: a morphometric study
Authors: Zachařová Gisela , Knotková-Urbancová Helena , Hník Pavel , Soukup Tomáš
Published: December 2017

Zachařová, Gisela, Helena Knotková-Urbancová, Pavel Hnı́k, and Tomáš Soukup. Nociceptive atrophy of the rat soleus muscle induced by bone fracture: a morphometric study. J. Appl. Physiol. 82(2): 552–557, 1997.—Reflex atrophy of the soleus muscle induced by ipsilateral metatarsal bone fracture in Sagatal-anesthetized adult male rats was studied by using two-dimensional stereological methods 7 days after the operation. When compared with contralateral solei, the wet weight of the experimental soleus muscles was decreased by ∼24% and the area of the entire muscle section by ∼29%. In atrophied solei, the number of type 1 fibers was lower by ∼8%, resulting in lower total number of fibers (by ∼6%). This indicates that slow motor units might be more sensitive to nociceptive stimulation. However, with respect to the fiber area, the reflex atrophy induced by metatarsal bone fracture in the rat soleus muscle resembles simple atrophy after 7 days, as the mean muscle fiber area was decreased by ∼26% with no significant difference between atrophy in type 1 and type 2a fibers (by 27.3 and 23.0%, respectively).
Adaptation of the doubly labeled water method for subjects consuming isotopically enriched water
Authors: Gretebeck Randall J. , Schoeller Dale A. , Socki Rick A. , Davis-Street Janis , Gibson Everett K. , Schulz Leslie O. , Lane Helen W.
Published: December 2017

Gretebeck, Randall J., Dale A. Schoeller, Rick A. Socki, Janis Davis-Street, Everett K. Gibson, Leslie O. Schulz, and Helen W. Lane. Adaptation of the doubly labeled water method for subjects consuming isotopically enriched water. J. Appl. Physiol. 82(2): 563–570, 1997.—The use of doubly labeled water (DLW) to measure energy expenditure is subject to error if the background abundance of the oxygen and hydrogen isotope tracers changes during the test period. This study evaluated the accuracy and precision of different methods by which such background isotope changes can be corrected, including a modified method that allows prediction of the baseline that would be achieved if subjects were to consume water from a given source indefinitely. Subjects in this study were eight women (4 test subjects and 4 control subjects) who consumed for 28 days water enriched to resemble drinking water aboard the United States space shuttle. Test subjects and control subjects were given a DLW dose on days 1 and 15, respectively. The change to an enriched water source produced a bias in expenditure calculations that exceeded 2.9 MJ/day (35%), relative to calculations from intake-balance. The proposed correction based on the predicted final abundance of18O and deuterium after equilibration to the new water source eliminated this bias, as did the traditional use of a control group. This new modified correction method is advantageous under field conditions when subject numbers are limited.
Thromboxane A2mediates increased pulmonary microvascular permeability after intestinal reperfusion
Authors: Turnage Richard H. , Lanoue John L. , Kadesky Kevin M. , Meng Yan , Myers Stuart I.
Published: December 2017

Turnage, Richard H., John L. LaNoue, Kevin M. Kadesky, Yan Meng, and Stuart I. Myers. Thromboxane A2mediates increased pulmonary microvascular permeability after intestinal reperfusion. J. Appl. Physiol. 82(2): 592–598, 1997.—This study examines the hypothesis that intestinal reperfusion (IR)-induced pulmonary thromboxane A2(TxA2) release increases local microvascular permeability and induces pulmonary vasoconstriction. Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of IR. Sham-operated animals (Sham) served as controls. After IR or Sham, the pulmonary vessels were cannulated, and the lungs were perfused in vitro with Krebs buffer. Microvascular permeability was quantitated by determining the filtration coefficient ( Kf), and pulmonary arterial (Ppa), venous (Ppv), and capillary (Ppc) pressures were measured to calculate vascular resistance (Rt). After baseline measurements, imidazole (TxA2synthase inhibitor) or SQ-29,548 (TxA2-receptor antagonist) was added to the perfusate; then Kf, Ppa, Ppv, and Ppc were again measured. The Kfof lungs from IR animals was four times greater than that of Sham ( P = 0.001), and Rt was 63% greater in the injured group ( P = 0.01). Pc of IR lungs was twice that of controls (5.4 ± 1.0 vs. 2.83 ± 0.3 mmHg, IR vs. Sham, respectively; P < 0.05). Imidazole or SQ-29,548 returned Kfto baseline measurements ( P < 0.05) and reduced Rt by 23 and 17%, respectively ( P < 0.05). IR-induced increases in Pc were only slightly reduced by 500 μg/ml imidazole (14%; P = 0.05) but unaffected by lower doses of imidazole (5 or 50 μg/ml) or SQ-29,548. These data suggest that IR-induced pulmonary edema is caused by both increased microvascular permeability and increased hydrostatic pressure and that these changes are due, at least in part, to the ongoing release of TxA2.
Effect of pulmonary emphysema on diaphragm capillary geometry
Authors: Poole David C. , Mathieu-Costello Odile
Published: December 2017

Poole, David C., and Odile Mathieu-Costello. Effect of pulmonary emphysema on diaphragm capillary geometry. J. Appl. Physiol. 82(2): 599–606, 1997.—In emphysema, the diaphragm shortens by losing sarcomeres. We hypothesized that unless capillaries undergo a similar shortening, capillary geometry must be altered. Without quantifying this geometry, capillary length and surface area per fiber volume, which are critical measurements of the structural potential for blood-tissue exchange, cannot be resolved. Five months after intratracheal elastase (E) or saline (control; C) instillation, diaphragms from male Syrian golden hamsters were glutaraldehyde perfusion fixed in situ at reference lung positions (residual volume, functional residual capacity, total lung capacity) to provide diaphragms fixed over a range of sarcomere lengths. Subsequently, diaphragms were processed for electron microscopy and analyzed morphometrically. Emphysema increased lung volume changes from −20 to 25 cmH2O airway pressure (i.e., passive vital capacity) and excised lung volume (both P < 0.001). In each region of the costal diaphragm (i.e., ventral, medial, dorsal), sarcomere number was reduced (all P < 0.05). Capillary-to-fiber ratio increased (C = 2.2 ± 0.1, E = 2.8 ± 0.1; P < 0.01) and fibers hypertrophied (C = 815 ± 35, E = 987 ± 67 μm2; P < 0.05; both values at 2.5 μm sarcomere length). Capillary geometry was markedly altered by the loss of sarcomeres in series. Specifically, the additional capillary length derived from capillary tortuosity and branching was increased by 183% at 2.5 μm sarcomere length compared with C values (C, 359 ± 43; E, 1,020 ± 158 mm−2, P < 0.01). This significantly increased total capillary length (C, 3,115 ± 173; E, 3,851 ± 219 mm−2 at 2.5 μm, P < 0.05) and surface area (C, 456 ± 13; E, 519 ± 24 cm−1, P < 0.05) per fiber volume. Thus emphysema substantially alters diaphragm capillary geometry and augments the capillary length and surface area available for blood-tissue exchange.
Periodic breathing induced on demand in awake newborn lamb
Authors: Canet Emmanuel , Praud Jean-Paul , Bureau Michel A.
Published: December 2017

Canet, Emmanuel, Jean-Paul Praud, and Michel A. Bureau.Periodic breathing induced on demand in awake newborn lamb. J. Appl. Physiol. 82(2): 607–612, 1997.—Spontaneous periodic breathing, although a common feature in fullterm and preterm human infants, is scarce in other newborn mammals. The aim of this study was to induce periodic breathing in lambs. Four 10-day-old and two <48-h-old awake lambs were instrumented with jugular catheters connected to an extracorporeal membrane lung aimed at controlling arterial [Formula: see text]([Formula: see text]). Arterial[Formula: see text]([Formula: see text]) was set and maintained at the desired level by changing inspired O2fraction and providing O2through a small catheter into the “apneic” lung. At a critical[Formula: see text]/[Formula: see text]combination, the four 10-day-old lambs exhibited periodic breathing that could be initiated, terminated, and reinitiated on demand. In the 2-day-old lambs with low chemoreceptor gain, periodic breathing was hardly seen, regardless of the trials done to find the critical[Formula: see text]/[Formula: see text]combination. We conclude that periodic breathing can be induced in lambs and depends on critical[Formula: see text]/[Formula: see text]combinations and maturity of the chemoreceptors.
H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin
Authors: Wells U. M. , Duneclift S. , Widdicombe J. G.
Published: December 2017

Wells, U. M., S. Duneclift, and J. G. Widdicombe.H2O2increases sheep tracheal blood flow, permeability, and vascular response to luminal capsaicin. J. Appl. Physiol. 82(2): 621–631, 1997.—Exogenous hydrogen peroxide (H2O2) causes airway epithelial damage in vitro. We have studied the effects of luminal H2O2in the sheep trachea in vivo on tracheal permeability to low-molecular-weight hydrophilic (technetium-99m-labeled diethylenetriamine pentaacetic acid;99mTc-DTPA) and lipophilic ([14C]antipyrine; [14C]AP) tracers and on the tracheal vascular response to luminal capsaicin, which stimulates afferent nerve endings. A tracheal artery was perfused, and tracheal venous blood was collected. H2O2exposure (10 mM) reduced tracheal potential difference (−42.0 ± 6.4 mV) to zero. It increased arterial and venous flows (56.7 ± 6.1 and 57.3 ± 10.0%, respectively; n = 5, P < 0.01, paired t-test) but not tracheal lymph flow (unstimulated flow 5.0 ± 1.2 μl ⋅ min−1⋅ cm−1, n = 4). During H2O2exposure, permeability to99mTc-DTPA increased from −2.6 to −89.7 × 10−7cm/s ( n = 5, P < 0.05), whereas permeability to [14C]AP (−3,312.6 × 10−7cm/s, n = 4) was not altered significantly (−2,565 × 10−7cm/s). Luminal capsaicin (10 μM) increased tracheal blood flow (10.1 ± 4.1%, n = 5) and decreased venous99mTc-DTPA concentration (−19.7 ± 4.0, P < 0.01), and these effects were significantly greater after epithelial damage (28.1 ± 6.0 and −45.7 ± 4.3%, respectively, P < 0.05, unpaired t-test). Thus H2O2increases the penetration of a hydrophilic tracer into tracheal blood and lymph but has less effect on a lipophilic tracer. It also enhances the effects of luminal capsaicin on blood flow and tracer uptake.
Blood pressure risk factors in healthy postmenopausal women: physical activity and hormone replacement
Authors: Stevenson Edith T. , Davy Kevin P. , Jones Pamela P. , Desouza Christopher A. , Seals and Douglas R. ,   (With the Technical Assistance of Mary Jo Reiling)
Published: December 2017

Stevenson, Edith T., Kevin P. Davy, Pamela P. Jones, Christopher A. Desouza, and Douglas R. Seals. Blood pressure risk factors in healthy postmenopausal women: physical activity and hormone replacement. J. Appl. Physiol. 82(2): 652–660, 1997.—The prevalence of cardiovascular disease (CVD) increases with advancing age in women, particularly after menopause. CVD risk is lower in physically active women relative to their sedentary peers, but the responsible mechanisms are not well understood. The aims of this study were to test the hypotheses that 1) physically active postmenopausal women demonstrate more favorable blood pressure (BP)-related risk factors for CVD than do sedentary healthy women and 2) women on hormone replacement therapy (HRT) also have more favorable levels of these CVD risk factors. BP-related CVD risk factors were measured in physically active women ( n = 18; age 55 ± 1 yr; n = 8 on HRT) and in healthy less-active controls ( n = 34; age 59 ± 1 yr; n = 17 on HRT). Maximal oxygen consumption was higher in the active group, whereas waist-to-hip ratio and waist circumference were lower (all P < 0.005). The active women demonstrated marginally lower (5–8 mmHg; P ≤ 0.10) levels of casual, 24-h, and daytime systolic BP (SBP). They also tended to have lower ( P = 0.11) daytime SBP loads (percentage of BP recordings >140/90 mmHg) and lower daytime and nighttime BP variabilities ( P = 0.04) and a reduced ( P < 0.007) SBP response to submaximal exercise. Women on HRT tended to have lower (3–4 mmHg; P = 0.07) levels of 24-h and nighttime diastolic BP (DBP) relative to the nonusers and smaller ( P < 0.04) daytime and 24-h DBP loads. Stepwise multiple regression indicated that waist circumference was the primary predictor of most of the SBP-related CVD risk factors while HRT use was the best predictor for DBP loads. These findings indicate that, in general, physically active postmenopausal women demonstrate more favorable SBP-related CVD risk factors relative to their less-active healthy peers, which may be mediated, in part, by their lower levels of abdominal adiposity. In addition, HRT use tends to be associated with lower levels of DBP-related CVD risk factors.
Decompression comparison of helium and hydrogen in rats
Authors: Lillo R. S. , Parker E. C. , Porter W. R.
Published: December 2017

Lillo, R. S., E. C. Parker, and W. R. Porter.Decompression comparison of helium and hydrogen in rats. J. Appl. Physiol. 82(3): 892–901, 1997.—The hypothesis that there are differences in decompression risk between He and H2 was examined in 1,607 unanesthetized male albino rats subjected to dives on 2% O2-balance He or 2% O2-balance H2 (depths ≤ 50 ATA, bottom times ≤ 60 min). The animals were decompressed to 10.8 ATA with profiles varying from rapid to slow, with up to four decompression stops of up to 60 min each. Maximum likelihood analysis was used to estimate the relative decompression risk on a per unit pressure basis (termed “potency”) and the rate of gas uptake and elimination, both factors affecting the decompression sickness risk, from a specific dive profile. H2 potency for causing decompression sickness was found to be up to 35% greater than that for He. Uptake rates were unresolvable between the two gases with the time constant (TC) estimated at ∼2–3 min, leading to saturation in both cases in <15 min. Washout of both gases was significantly slower than uptake, with He washout (TC ∼1.5–3 h) substantially slower than H2 washout (TC ∼0.5 h). It is unknown whether the decompression advantage of the faster washout of H2 or the disadvantage of its increased potency, observed in the rat, would be important for human diving.
Determination of production of nitric oxide by lower airways of humans—theory
Authors: Hyde Richard W. , Geigel Edgar J. , Olszowka Albert J. , Krasney John A. , Forster Robert E. , Utell Mark J. , Frampton Mark W.
Published: December 2017

Hyde, Richard W., Edgar J. Geigel, Albert J. Olszowka, John A. Krasney, Robert E. Forster II, Mark J. Utell, and Mark W. Frampton.Determination of production of nitric oxide by the lower airways of humans—theory. J. Appl. Physiol.82(4): 1290–1296, 1997.—Exercise and inflammatory lung disorders such as asthma and acute lung injury increase exhaled nitric oxide (NO). This finding is interpreted as a rise in production of NO by the lungs (V˙no) but fails to take into account the diffusing capacity for NO (Dno) that carries NO into the pulmonary capillary blood. We have derived equations to measureV˙no from the following rates, which determine NO tension in the lungs (Pl) at any moment from 1) production (V˙no); 2) diffusion, where Dno(Pl) = rate of removal by lung capillary blood; and 3) ventilation, whereV˙a(Pl)/(Pb− 47) = the rate of NO removal by alveolar ventilation (V˙a) and Pb is barometric pressure. During open-circuit breathing when Pl is not in equilibrium, d/d tPl[Vl/ (Pb − 47)] (where Vlis volume of NO in the lower airways) =V˙no− Dno(Pl) −V˙a(Pl)/(Pb− 47). When Pl reaches a steady state so that d/d t = 0 andV˙a is eliminated by rebreathing or breath holding, then Pl =V˙no/Dno. Pl can be interpreted as NO production per unit of Dno. This equation predicts that diseases that diminish Dno but do not alterV˙no will increase expired NO levels. These equations permit precise measurements of V˙no that can be applied to determining factors controlling NO production by the lungs.
Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects
Authors: Isono Shiroh , Remmers John E. , Tanaka Atsuko , Sho Yasuhide , Sato Jiro , Nishino Takashi
Published: December 2017

Isono, Shiroh, John E Remmers, Atsuko Tanaka, Yasuhide Sho, Jiro Sato, and Takashi Nishino. Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects. J. Appl. Physiol. 82(4): 1319–1326, 1997.—Anatomic abnormalities of the pharynx are thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but their contribution has never been conclusively proven. The present study tested this anatomic hypothesis by comparing the mechanics of the paralyzed pharynx in OSA patients and in normal subjects. According to evaluation of sleep-disordered breathing (SDB) by nocturnal oximetry, subjects were divided into three groups: normal group ( n = 17), SDB-1 ( n = 18), and SDB-2 ( n = 22). The static pressure-area relationship of the passive pharynx was quantified under general anesthesia with complete paralysis. Age and body mass index were matched among the three groups. The site of the primary closure was the velopharynx in 49 subjects and the oropharynx in only 8 subjects. Distribution of the location of the primary closure did not differ among the groups. Closing pressure (Pc) of the velopharynx for SDB-1 and SDB-2 groups (0.90 ± 1.34 and 2.78 ± 2.78 cmH2O, respectively) was significantly higher than that for the normal group (−3.77 ± 3.44 cmH2O; P < 0.01). Maximal velopharyngeal area for the normal group (2.10 ± 0.85 cm2) was significantly greater than for SDB-1 and SDB-2 groups (1.15 ± 0.46 and 1.06 ± 0.75 cm2, respectively). The shape of the pressure-area curve for the velopharynx differed between normal subjects and patients with SDB, being steeper in slope near Pc in patients with SDB. Multivariate analysis of mechanical parameters and oxygen desaturation index (ODI) revealed that velopharyngeal Pc was the only variable highly correlated with ODI. Velopharyngeal Pc was associated with oropharyngeal Pc, suggesting mechanical interdependence of these segments. We conclude that the passive pharynx is more narrow and collapsible in sleep-apneic patients than in matched controls and that velopharyngeal Pc is the principal correlate of the frequency of nocturnal desaturations.
Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function
Authors: Watchko Jon F. , Daood Monica J. , Sieck Gary C. , Labella John J. , Ameredes Bill T. , Koretsky Alan P. , Wieringa Be
Published: December 2017

Watchko, Jon F., Monica J. Daood, Gary C. Sieck, John J. LaBella, Bill T. Ameredes, Alan P. Koretsky, and Be Wieringa. Combined myofibrillar and mitochondrial creatine kinase deficiency impairs mouse diaphragm isotonic function. J. Appl. Physiol. 82(5): 1416–1423, 1997.—Creatine kinase (CK) is an enzyme central to cellular high-energy phosphate metabolism in muscle. To characterize the physiological role of CK in respiratory muscle during dynamic contractions, we compared the force-velocity relationships, power, and work output characteristics of the diaphragm (Dia) from mice with combined myofibrillar and sarcomeric mitochondrial CK deficiency (CK[−/−]) with CK-sufficient controls (Ctl). Maximum velocity of shortening was significantly lower in CK[−/−] Dia (14.1 ± 0.9 Lo/s, where Lois optimal fiber length) compared with Ctl Dia (17.5 ± 1.1 Lo/s) ( P < 0.01). Maximum power was obtained at 0.4–0.5 tetanic force in both groups; absolute maximum power (2,293 ± 138 W/m2) and work (201 ± 9 J/m2) were lower in CK[−/−] Dia compared with Ctl Dia (2,744 ± 146 W/m2and 284 ± 26 J/m2, respectively) ( P < 0.05). The ability of CK[−/−] Dia to sustain shortening during repetitive isotonic activation (75 Hz, 330-ms duration repeated each second at 0.4 tetanic force load) was markedly impaired, with CK[−/−] Dia power and work declining to zero by 37 ± 4 s, compared with 61 ± 5 s in Ctl Dia. We conclude that combined myofibrillar and sarcomeric mitochondrial CK deficiency profoundly impairs Dia power and work output, underscoring the functional importance of CK during dynamic contractions in skeletal muscle.
Release of glutathione from erythrocytes and other markers of oxidative stress in carbon monoxide poisoning
Authors: Thom Stephen R. , Kang Melissa , Fisher Donald , Ischiropoulos Harry
Published: December 2017

Thom, Stephen R., Melissa Kang, Donald Fisher, and Harry Ischiropoulos. Release of glutathione from erythrocytes and other markers of oxidative stress in carbon monoxide poisoning. J. Appl. Physiol. 82(5): 1424–1432, 1997.—Rats exposed to CO in a manner known to cause oxidative stress in brain exhibited a twofold increase in plasma levels of oxidized proteins, thiobarbituric acid-reactive substances (TBARS), oxidized glutathione (GSSG), and reduced glutathione (GSH). Changes were neither directly related to hypoxic stress from carboxyhemoglobin nor significantly influenced by circulating platelets or neutrophils. Treatment with the nitric oxide synthase inhibitor Nω-nitro-l-arginine methyl ester inhibited elevations in GSH and GSSG but not changes in oxidized proteins or TBARS, suggesting that two oxidative mechanisms may be operating in this model and that GSH and GSSG elevations involved nitric oxide-derived oxidants. Elevations of blood GSH and GSSG occurred at different anatomic sites, indicating that no single organ was the source of the increased peptides. Animals that underwent exchange transfusion with a hemoglobin-containing saline solution did not exhibit elevations in GSH and GSSG, suggesting that blood-borne cells released these peptides in response to oxidative stress. In in vitro studies, erythrocytes, but not platelets and leukocytes, responded to oxidative stress from peroxynitrite by releasing GSH, whereas no release was observed in response to nitric oxide or superoxide. Glucose, maltose, and cytochalasin B, agents that protect extracellular components of the hexose transport protein complex from oxidative stress, prevented GSH release. The data indicate that nitric oxide-derived oxidants are involved in CO-mediated oxidative stress within the vascular compartment and that elevations of several compounds may be useful for identifying exposures to CO likely to precipitate brain injury.
Effects of electrically induced fatigue on the twitch and tetanus of paralyzed soleus muscle in humans
Authors: Shields Richard K. , Law Laura Frey , Reiling Brenda , Sass Kelly , Wilwert Jason
Published: December 2017

Shields, Richard K., Laura Frey Law, Brenda Reiling, Kelly Sass, and Jason Wilwert. Effects of electrically induced fatigue on the twitch and tetanus of paralyzed soleus muscle in humans. J. Appl. Physiol. 82(5): 1499–1507, 1997.—We analyzed the twitch and summated torque (tetanus) during repetitive activation and recovery of the human soleus muscle in individuals with spinal cord injury. Thirteen individuals with complete paralysis (9 chronic, 4 acute) had the tibial nerve activated every 1,500 ms with a 20-Hz train (7 stimuli) for 300 ms and a single pulse at 1,100 ms. The stimulation protocol lasted 3 min and included 120 twitches and 120 tetani. Minimal changes were found for the acute group. The chronic group showed a significant reduction in the torque and a significant slowing of the contractile speeds of both the twitch and tetanus. The decrease in the peak twitch torque was significantly greater than the decrease in the peak tetanus torque early during the fatigue protocol for the chronic group. The twitch time to peak and half relaxation time were prolonged during fatigue, which was associated with improved fusion of the tetanus torque. At the end of the fatigue protocol, the decrease in the peak twitch torque was not significantly different from the decrease in the peak tetanus torque. After 5 min of rest, the contractile speeds recovered causing the tetanus to become unfused, but the tetanus torque became less depressed than the twitch torque. The differential responses for the twitch and the tetanus suggest an interplay between optimal fusion created from contractile speed slowing and excitation contraction coupling compromise. These issues make the optimal design of functional electrical stimulation systems a formidable task.
Dynamic resistance exercise and resting blood pressure in adults: a meta-analysis
Authors: Kelley George
Published: December 2017

George, Kelley. Dynamic resistance exercise and resting blood pressure in adults: a meta-analysis. J. Appl. Physiol. 82(5): 1559–1565, 1997.—With the use of the meta-analytic approach, the purpose of this study was to examine the effects of dynamic resistance exercise, i.e., weight training, on resting systolic and diastolic blood pressure in adults. A total of nine studies consisting of 259 subjects (144 exercise, 115 control) and 18 groups (9 exercise, 9 control) were included in this analysis. With the use of the bootstrap technique (10,000 samples), significant treatment effect (Δ3) reductions were found across all designs and categories for both systolic and diastolic blood pressure [systolic, mean ± SD = −4.55 ± 1.75 mmHg, 95% confidence interval (CI) = −1.56 to −8.56; diastolic, mean ± SD = −3.79 + 1.12 mmHg, 95% confidence interval CI = −1.89 to −6.33]. Δ3 changes corresponded with relative decreases of ∼3 and 4% in resting systolic and diastolic blood pressure, respectively. In conclusion, meta-analytic review of included studies suggests that dynamic resistance exercise reduces resting systolic and diastolic blood pressure in adults. However, it is premature to form strong conclusions regarding the effects of dynamic resistance exercise on resting blood pressure. A need exists for additional, well-designed studies on this topic before a recommendation can be made regarding the efficacy of dynamic resistance exercise as a nonpharmacological therapy for reducing resting blood pressure in adults, especially in hypertensive adults.
Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses
Authors: Birks Eric K. , Mathieu-Costello Odile , Fu Zhenxing , Tyler Walter S. , West John B.
Published: December 2017

Birks, Eric K., Odile Mathieu-Costello, Zhenxing Fu, Walter S. Tyler, and John B. West. Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses. J. Appl. Physiol. 82(5): 1584–1592, 1997.—Thoroughbred horses develop extremely high pulmonary vascular pressures during galloping, all horses in training develop exercise-induced pulmonary hemorrhage, and we have shown that this is caused by stress failure of pulmonary capillaries. It is known that the capillary transmural pressure (Ptm) necessary for stress failure is higher in dogs than in rabbits. The present study was designed to determine this value in horses. The lungs from 15 Thoroughbred horses were perfused with autologous blood at Ptm values (midlung) of 25, 50, 75, 100 and 150 mmHg, and then perfusion fixed, and samples (dorsal and ventral, from caudal region) were examined by electron microscopy. Few disruptions of capillary endothelium were observed at Ptm ≤ 75 mmHg, and 5.3 ± 2.2 and 4.3 ± 0.7 breaks/mm endothelium were found at 100 and 150 mmHg Ptm, respectively. Blood-gas barrier thickness did not change with Ptm. At low Ptm, interstitial thickness was greater than previously found in rabbits but not in dogs. We conclude that the Ptm required to cause stress failure of pulmonary capillaries is between 75 and 100 mmHg and is greater in Thoroughbred horses than in both rabbits and dogs.
Regression of hypoxic hypertension-induced changes in the elastic laminae of rat pulmonary arteries
Authors: Liu S. Q.
Published: December 2017

Liu, S. Q. Regression of hypoxic hypertension-induced changes in the elastic laminae of rat pulmonary arteries. J. Appl. Physiol. 82(5): 1677–1684, 1997.—The elastic laminae of the pulmonary arteries (PAs) undergo a progressive structural change in hypoxic hypertension. This study focused on the reversibility of altered PA elastic laminae of the rat due to hypoxic hypertension. The structure and cross-sectional area of the PA medial elastic laminae were examined by using electron-microscopic and image-analytic approaches during recovery from 12 h and 10 days of hypoxic hypertension. At 12 h of hypoxic hypertension, the elastic laminae, which appeared homogeneous in normal control animals, were reorganized into structures composed of randomly oriented filaments, with an increase in the cross-sectional area of 70%. At 10 days of hypoxic hypertension, the elastic laminae appeared homogeneous in structure and normal in cross-sectional area despite continuous exposure to hypoxia. During recovery from 12 h of hypoxic hypertension, the medial elastic laminae regained their homogeneous structure and normal cross-sectional area after day 2. During recovery from 10 days of hypoxic hypertension, the medial elastic laminae changed from homogeneous to filamentous structures, with a progressively altered cross-sectional area that increased by 89% from recovery day 0 to day 10 and returned to the normal level on day 30. These changes were associated with alterations in the PA wall tensile stress. These results indicated that structural changes in the PA elastic laminae were reversible and that the regression process depended on the duration of exposure to hypoxia, the state of the elastic laminae, and possibly the tensile stress level in the PA wall.
Weight loss and wrestling training: effects on growth-related hormones
Authors: Roemmich James N. , Sinning Wayne E.
Published: December 2017

Roemmich, James N., and Wayne E. Sinning. Weight loss and wrestling training: effects on growth-related hormones. J. Appl. Physiol. 82(6): 1760–1764, 1997.—Adolescent wrestlers ( n = 9, 15.4 yr) and recreationally active control males ( n = 7, 15.7 yr) were measured before, at the end of, and 3.5–4 mo after a competitive wrestling season to assess the influence of dietary restriction on growth-related hormones. Wrestlers had significant elevations preseason to late season for morning serum concentrations (mean of 8 serial samples) of growth hormone (GH; 2.9 ± 0.7 vs. 6.5 ± 1.4 ng/ml) and sex hormone-binding globulin (SHBG; 16.1 ± 2.3 vs. 27.9 ± 6.9 nmol/l) and significant reductions in GH-binding protein (GHBP; 178 ± 19 vs. 109 ± 17 pmol/l), insulin-like growth factor I (IGF-I; 332 ± 30 vs. 267 ± 34 ng/ml), testosterone (T; 4.9 ± 0.4 vs. 3.6 ± 0.4 ng/ml), and free testosterone (Free-T; 22.4 ± 3.6 vs. 15.7 ± 2.8 pg/ml). Wrestlers had significant postseason reductions in GH (3.44 ± 1.30 ng/ml) and SHBG (10.43 ± 4.13 nmol/l) but elevations in GHBP (66.7 ± 23.8 pmol/l), IGF-I (72.9 ± 25.1 ng/ml), T (2.10 ± 0.46 ng/ml), and Free-T (9.76 ± 3.01 pg/ml). Concentrations of luteinizing hormone (LH), estradiol, prolactin, cortisol, insulin, and thyroid hormones did not differ because of exercise-dietary practices of wrestlers. In-season elevations in GH, with concomitant reductions in GHBP and IGF-I, that were reversed during the postseason suggest a reduction in GH receptor number and partial GH resistance during the season. Nonelevated LH with reduced T levels suggests a central hypothalamic-pituitary-gonadal (H-P-G) axis impairment. In conclusion, undernutrition may lead to altered H-P-G and GH-IGF-I axes function in adolescent wrestlers. However, only the wrestlers’ late-season Free-T concentrations were outside the normal range, and the hormone axis impairments were quickly reversed. The present data do not address hormonal axis responses to several years of wrestling and weight loss.
Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m
Authors: Robach Paul , Biou Daniel , Herry Jean-Pierre , Deberne Denis , Letournel Murielle , Vaysse Jenny , Richalet Jean-Paul
Published: December 2017

Robach, Paul, Daniel Biou, Jean-Pierre Herry, Denis Deberne, Murielle Letournel, Jenny Vaysse, and Jean-Paul Richalet. Recovery processes after repeated supramaximal exercise at the altitude of 4,350 m. J. Appl. Physiol. 82(6): 1897–1904, 1997.—We tested the hypothesis that prolonged exposure to high altitude would impair the restoration of muscle power during repeated sprints. Seven subjects performed two 20-s Wingate tests (WT1 and WT2) separated by 5 min of recovery, at sea level (N) and after 5–6 days at 4,350 m (H). Mean power output (MPO) and O2 deficit were measured during WT. O2 uptake (V˙o 2) and ventilation (V˙e) were measured continuously. Blood velocity in the femoral artery (FBV) was recorded by Doppler ultrasound during recovery. Arterialized blood pH and concentrations of bicarbonate ([[Formula: see text]]), venous plasma lactate ([La−]), norepinephrine ([NE]), and epinephrine ([Epi]) were measured before and after WT1 and WT2. MPO decreased between WT1 and WT2 by 6.9% in N ( P < 0.05) and by 10.7% in H ( P < 0.01). H did not further decrease MPO. O2 deficit decreased between WT1 and WT2 in H only ( P < 0.01). PeakV˙o 2 after WT was reduced by 30–40% in H ( P < 0.01), but excess postexercise O2 consumption was not significantly lowered in H. During recovery in H compared with N, V˙e, exercise-induced acidosis, and [NE] were higher, [Epi] tended to be higher, [La−] was not altered, and [[Formula: see text]] and FBV were lower. The similar [La−] accumulation was associated with a higher exercise-induced acidosis and a larger increase in [NE] in H. We concluded from this study that prolonged exposure to high altitude did not significantly impair the restoration of muscle power during repeated sprints, despite a limitation of aerobic processes during early recovery.
Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients
Authors: Grassi Bruno , Marconi Claudio , Meyer Michael , Rieu Michel , Cerretelli Paolo
Published: December 2017

Grassi, Bruno, Claudio Marconi, Michael Meyer, Michel Rieu, and Paolo Cerretelli. Gas exchange and cardiovascular kinetics with different exercise protocols in heart transplant recipients. J. Appl. Physiol. 82(6): 1952–1962, 1997.—Metabolic and cardiovascular adjustments to various submaximal exercises were evaluated in 82 heart transplant recipients (HTR) and in 35 control subjects (C). HTR were tested 21.5 ± 25.3 (SD) mo (range 1.0–137.1 mo) posttransplantation. Three protocols were used: protocol A consisted of 5 min of rectangular 50-W load repeated twice, 5 min apart [5 min rest, 5 min 50 W ( Ex 1), 5 min recovery, 5 min 50 W ( Ex 2)]; protocol B consisted of 5 min of rectangular load at 25, 50, or 75 W; protocol Cconsisted of 15 min of rectangular load at 25 W. Breath-by-breath pulmonary ventilation (V˙e), O2 uptake (V˙o 2), and CO2 output (V˙co 2) were determined. During protocol A, beat-by-beat cardiac output (Q˙) was estimated by impedance cardiography. The half times ( t 1/2) of the on- and off-kinetics of the variables were calculated. In all protocols, t 1/2 values forV˙o 2 on-,V˙e on-, andV˙co 2 on-kinetics were higher (i.e., the kinetics were slower) in HTR than in C, independently of workload and of the time posttransplantation. Also, t 1/2 Q˙ on- was higher in HTR than in C. In protocol A, no significant difference of t 1/2 V˙o 2on- was observed in HTR between Ex 1 (48 ± 9 s) and Ex 2 (46 ± 8 s), whereas t 1/2Q˙ on- was higher during Ex 1 (55 ± 24 s) than during Ex 2 (47 ± 15 s). In all protocols and for all variables, the t 1/2 off-values were higher in HTR than in C. In protocol C, no differences of steady-stateV˙e,V˙o 2, andV˙co 2 were observed in both groups between 5, 10, and 15 min of exercise. We conclude that 1) in HTR, a “priming” exercise, while effective in speeding up the adjustment of convective O2 flow to muscle fibers during a second on-transition, did not affect theV˙o 2 on-kinetics, suggesting that the slower V˙o 2 on- in HTR was attributable to peripheral (muscular) factors; 2) the dissociation between Q˙ on- andV˙o 2 on-kinetics in HTR indicates that an inertia of muscle metabolic machinery is the main factor dictating theV˙o 2on-kinetics; and 3) theV˙o 2 off-kinetics was slower in HTR than in C, indicating a greater alactic O2 deficit in HTR and, therefore, a sluggish muscleV˙o 2 adjustment.
Lung parenchymal shear modulus, airway wall remodeling, and bronchial hyperresponsiveness
Authors: Lambert Rodney K. , Paré Peter D.
Published: December 2017

Lambert, Rodney K., and Peter D. Paré. Lung parenchymal shear modulus, airway wall remodeling, and bronchial hyperresponsiveness. J. Appl. Physiol.83(1): 140–147, 1997.—When airways narrow, either through the action of smooth muscle shortening or during forced expiration, the lung parenchyma is locally distorted and provides an increased peribronchial stress that resists the narrowing. Although this interdependence has been well studied, the quantitative significance of airway remodeling to interdependence has not been elucidated. We have used an improved computational model of the bronchial response to smooth muscle agonists to investigate the relationships between airway narrowing (as indicated by airway resistance), parenchymal shear modulus, adventitial thickening, and inner wall thickening at lung recoil pressures of 4, 5, and 8 cmH2O. We have found that, at low recoil pressures, decreases in parenchymal shear modulus have a significant effect that is comparable to that of moderate thickening of the airway wall. At higher lung recoil pressures, the effect is negligible.
When does the lung die?K fc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung
Authors: Jones David R. , Becker Randy M. , Hoffmann Steve C. , Lemasters John J. , Egan Thomas M.
Published: December 2017

Jones, David R., Randy M. Becker, Steve C. Hoffmann, John J. Lemasters, and Thomas M. Egan. When does the lung die? K fc, cell viability, and adenine nucleotide changes in the circulation-arrested rat lung. J. Appl. Physiol. 83(1): 247–252, 1997.—Lungs harvested from cadaveric circulation-arrested donors may increase the donor pool for lung transplantation. To determine the degree and time course of ischemia-reperfusion injury, we evaluated the effect of O2 ventilation on capillary permeability [capillary filtration coefficient ( K fc)], cell viability, and total adenine nucleotide (TAN) levels in in situ circulation-arrested rat lungs. K fc increased with increasing postmortem ischemic time ( r = 0.88). Lungs ventilated with O2 1 h postmortem had similar K fc and wet-to-dry ratios as controls. Nonventilated lungs had threefold ( P < 0.05) and sevenfold ( P < 0.0001) increases in K fc at 30 and 60 min postmortem compared with controls. Cell viability decreased in all groups except for 30-min postmortem O2-ventilated lungs. TAN levels decreased with increasing ischemic time, particularly in nonventilated lungs. Loss of adenine nucleotides correlated with increasing K fc values ( r = 0.76). This study indicates that lungs retrieved 1 h postmortem may have normal K fc with preharvest O2 ventilation. The relationship between K fc and TAN suggests that vascular permeability may be related to lung TAN levels.