bluuebunny/crossref_metadata_2025 huggingface dataset:
Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans
Authors: Dietz Niki M. , Halliwill John R. , Spielmann John M. , Lawler Lori A. , Papouchado Bettina G. , Eickhoff Tamara J. , Joyner Michael J.
Published: December 2017

Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans. J. Appl. Physiol. 82(6): 1785–1793, 1997.—Our aim was to determine whether sympathetic withdrawal alone can account for the profound forearm vasodilation that occurs during syncope in humans. We also determined whether either vasodilating β2-adrenergic receptors or nitric oxide (NO) contributes to this dilation. Forearm blood flow was measured bilaterally in healthy volunteers ( n = 10) by using plethysmography during two bouts of graded lower body negative pressure (LBNP) to syncope. In one forearm, drugs were infused via a brachial artery catheter while the other forearm served as a control. In the control arm, forearm vascular resistance (FVR) increased from 77 ± 7 units at baseline to 191 ± 36 units with −40 mmHg of LBNP ( P < 0.05). Mean arterial pressure fell from 94 ± 2 to 47 ± 4 mmHg just before syncope, and all subjects demonstrated sudden bradycardia at the time of syncope. At the onset of syncope, there was sudden vasodilation and FVR fell to 26 ± 6 units ( P < 0.05 vs. baseline). When the experimental forearm was treated with bretylium, phentolamine, and propranolol, baseline FVR fell to 26 ± 2 units, the vasoconstriction during LBNP was absent, and FVR fell further to 16 ± 1 units at syncope ( P < 0.05 vs. baseline). During the second trial of LBNP, mean arterial pressure again fell to 47 ± 4 mmHg and bradycardia was again observed. Treatment of the experimental forearm with the NO synthase inhibitor NG-monomethyl-l-arginine in addition to bretylium, phentolamine, and propranolol significantly increased baseline FVR to 65 ± 5 units but did not prevent the marked forearm vasodilation during syncope (FVR = 24 ± 4 vs. 29 ± 8 units in the control forearm). These data suggest that the profound vasodilation observed in the human forearm during syncope is not mediated solely by sympathetic withdrawal and also suggest that neither β2-adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.
Liposome encapsulation attenuates hemoglobin-induced vasoconstriction in rabbit arterial segments
Authors: Rudolph Alan S. , Sulpizio Anthony , Hieble Paul , Macdonald Victor , Chavez Mark , Feuerstein Giora
Published: December 2017

Rudolph, Alan S., Anthony Sulpizio, Paul Hieble, Victor Macdonald, Mark Chavez, and Giora Feuerstein. Liposome encapsulation attenuates hemoglobin-induced vasoconstriction in rabbit arterial segments. J. Appl. Physiol.82(6): 1826–1835, 1997.—Free hemoglobin (Hb) induces a potent vasoconstrictor response that may limit its therapeutic application as a red blood cell replacement. We have investigated whether encapsulation of stroma-free Hb (SFHb) or cross-linked Hb (αα-Hb) in liposomes modulates Hb vasoactivity in isolated blood vessels. Relaxation of rabbit thoracic vessels was measured before and after exposure to acellular SFHb, αα-Hb, and liposome-encapsulated SFHb or αα-Hb. SFHb and αα-Hb caused significant inhibition of carbachol-induced relaxation at 0.5 mg/dl, whereas encapsulation inhibited vessel relaxation at 30- to 60-fold higher Hb concentrations. The contractile response of rabbit ear arterial segments to electrical stimulation in the presence of acellular αα-Hb resulted in a 150% increase (EC150) in contractile amplitude at 0.23 mg/dl, whereas the EC150for encapsulated αα-Hb was 13.7 mg/dl. Mechanistic studies of the vasoconstrictor activity of Hb demonstrated that acellular αα-Hb had no effect on norepinephrine release in the rabbit ear artery. In addition, neither acellular nor encapsulated αα-Hb preparations inhibited endothelial nitric oxide (NO) synthase activity isolated from bovine pulmonary artery. However, inhibition of vessel relaxation by acellular or encapsulated αα-Hb was reversed by the NO donor S-nitrosylpenacillamine, implicating Hb-NO binding as a possible mechanism for the vasoconstrictor response. In vitro stopped-flow kinetic studies of Hb-NO binding showed similar rates of reaction for conversion of oxyhemoglobin to methemoglobin (metHb; <2 ms), followed by rapid conversion of metHb to NO-Hb (300 ms) for both acellular and encapsulated αα-Hb, demonstrating that liposome encapsulation does not retard NO-Hb binding. The attenuated vasoactivity of encapsulated Hb may, therefore, result from the limited access of encapsulated Hb to NO imposed by the physical size of the liposome and reduced penetration of Hb across the vascular endothelium.
Muscle adaptations to hindlimb suspension in mature and old Fischer 344 rats
Authors: Stump Craig S. , Tipton Charles M. , Henriksen Erik J.
Published: December 2017

Stump, Craig S., Charles M. Tipton, and Erik J. Henriksen.Muscle adaptations to hindlimb suspension in mature and old Fischer 344 rats. J. Appl. Physiol.82(6): 1875–1881, 1997.—We examined skeletal and cardiac muscle responses of mature (8 mo) and old (23 mo) male Fischer 344 rats to 14 days of hindlimb suspension. Hexokinase (HK) and citrate synthase (CS) activities and GLUT-4 glucose transporter protein level, which are coregulated in many instances of altered neuromuscular activity, were analyzed in soleus (Sol), plantaris (Pl), tibialis anterior (TA), extensor digitorum longus (EDL), and left ventricle. Protein content was significantly ( P < 0.05) lower in all four hindlimb muscles after suspension compared with controls in both mature (21–44%) and old (17–43%) rats. Old rats exhibited significantly lower CS activities than mature rats for the Sol, Pl, and TA. HK activities were significantly lower in the old rats for the Pl (19%) and TA (33%), and GLUT-4 levels were lower in the old rats for the TA (38%) and EDL (24%) compared with the mature rats. Old age was also associated with a decrease in CS activity (12%) and an increase in HK activity (14%) in cardiac muscle. CS activities were lower in the Sol (20%) and EDL (18%) muscles from mature suspended rats and in the Sol (25%), Pl (27%), and EDL (25%) muscles from old suspended rats compared with corresponding controls. However, suspension was associated with significantly higher HK activities for all four hindlimb muscles examined, in both old (16–57%) and mature (10–43%) rats, and higher GLUT-4 concentrations in the TA muscles of the old rats (68%) but not the mature rats. These results indicate that old age is associated with decreased CS and HK activities and GLUT-4 protein concentration for several rat hindlimb muscles, and these variables are not coregulated during suspension. Finally, old rat skeletal muscle appears to respond to suspension to a similar or greater degree than mature rat muscle responds.
Improved fatigue resistance not associated with maximum oxygen consumption in creatine-depleted rats
Authors: Tanaka T. , Ohira Y. , Danda M. , Hatta H. , Nishi I.
Published: December 2017

Tanaka, T., Y. Ohira, M. Danda, H. Hatta, and I. Nishi.Improved fatigue resistance not associated with maximum oxygen consumption in creatine-depleted rats. J. Appl. Physiol. 82 (6): 1911–1917, 1997.—Effects of feeding of either creatine or its analog β-guanidinopropionic acid (β-GPA) on endurance work capacity and oxygen consumption were studied in rats. Resting high-energy phosphate contents in hindlimb muscles were lower in the β-GPA group and higher in the creatine group than in controls. The glycogen contents in resting hindlimb muscles of rats fed β-GPA were significantly higher than those in controls. The endurance run and swimming times to exhaustion were significantly greater (32–70%) in the β-GPA group than in the control and creatine groups. However, there were no beneficial effects on the maximum oxygen consumption (V˙o2 max) and oxygen transport capacity of blood by the feeding of β-GPA. None of these parameters were significantly influenced by creatine supply. Both maximum exercise time andV˙o2 maxin the β-GPA group were not changed by normalization of glycogen levels. The activities of mitochondrial enzymes in skeletal muscles were higher in the β-GPA group than in the controls. Thus endurance capacity is improved if the respiratory capacity of muscles is increased, even when the contents of high-energy phosphates in muscles are lower. Increased endurance capacity was not directly associated with the elevated levels of muscle glycogen, oxygen transport capacity of blood, orV˙o2 max.
Marked differences in functioning of the hypothalamicpituitary-adrenal axis between groups of men
Authors: Petrides John S. , Gold Philip W. , Mueller Gregory P. , Singh Anita , Stratakis Costas , Chrousos George P. , Deuster Patricia A.
Published: December 2017

Petrides, John S., Philip W. Gold, Gregory P. Mueller, Anita Singh, Costas Stratakis, George P. Chrousos, and Patricia A. Deuster.Marked differences in functioning of the hypothalamic-pituitary-adrenal axis between groups of men. J. Appl. Physiol. 82(6): 1979–1988, 1997.—To compare profiles of hypothalamic-pituitary-adrenal (HPA) responsiveness, healthy, moderately trained men ( n = 15) were classified as high ( n = 7) or low responders ( n = 8) on the basis of plasma adrenocorticotropic hormone (ACTH) responses to strenuous treadmill exercise 4 h after 4 mg of dexamethasone (Dex). These groups were then evaluated to compare 1) HPA and growth hormone responses to exercise at 90% maximal oxygen uptake 4 h after placebo, Dex (4 mg), and hydrocortisone (100 mg); 2) pituitary-adrenal responses to infusion of arginine vasopressin (AVP); 3) plasma cortisol after a Dex suppression test (1 mg); and 4) behavioral characteristics. In comparison to low responders, high responders exhibited significantly 1) higher plasma ACTH responses to exercise after placebo and Dex; 2) higher plasma AVP secretion with exercise after placebo and marked Dex- and hydrocortisone-induced enhancement of exercise-induced AVP secretion; 3) lower Dex-induced increases in basal and stimulated growth hormone secretion; 4) higher plasma ACTH responses to infusion of AVP; and 5) a trend ( P = 0.09) for higher trait anxiety ratings. Similar suppression of plasma cortisol was noted after 1 mg Dex. We conclude that subgroups of healthy male volunteers exhibit unique profiles of HPA responsiveness. We also believe that glucocorticoid pretreatment combined with strenuous exercise allows functional HPA responsiveness to be distinguished between subgroups of healthy controls and may be useful in the determination of susceptibility to disorders characterized by hyper- and hypo-HPA activation.
Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis
Authors: Ksenzenko Sergey M. , Davidson Scott B. , Saba Amer A. , Franko Alexander P. , Raafat Aml M. , Diebel Lawrence N. , Dulchavsky Scott A.
Published: December 2017

Ksenzenko, Sergey M., Scott B. Davidson, Amer A. Saba, Alexander P. Franko, Aml M. Raafat, Lawrence N. Diebel, and Scott A. Dulchavsky. Effect of triiodothyronine augmentation on rat lung surfactant phospholipids during sepsis. J. Appl. Physiol. 82(6): 2020–2027, 1997.—Surfactant functional effectiveness is dependent on phospholipid compositional integrity; sepsis decreases this through an undefined mechanism. Sepsis-induced hypothyroidism is commensurate and may be related. This study examines the effect of 3,3′,5-triiodo-l-thyronine (T3) supplementation on surfactant composition and function during sepsis. Male Sprague-Dawley rats underwent sham laparotomy (Sham) or cecal ligation and puncture (CLP) with or without T3supplementation [CLP/T3(3 ng/h)]. After 6, 12, or 24 h, surfactant was obtained by lavage. Function was assessed by a pulsating bubble surfactometer and in vivo compliance studies. Sepsis produced a decrease in surfactant phosphatidylglycerol and phosphatidic acid, with an increase in lesser surface-active lipids phosphatidylserine and phosphatidylinositol. Phosphatidylcholine content was not significantly changed. Sepsis caused an alteration in the fatty acid composition and an increase in saturation in most phospholipids. Hormonal replacement attenuated these changes. Lung compliance and surfactant adsorption were reduced by sepsis and maintained by T3treatment. Thyroid hormone may have an active role in lung functional preservation through maintenance of surfactant homeostasis during sepsis.
Excess postexercise oxygen consumption and recovery rate in trained and untrained subjects
Authors: Short Kevin R. , Sedlock Darlene A.
Published: December 2017

Short, Kevin R., and Darlene A. Sedlock. Excess postexercise oxygen consumption and recovery rate in trained and untrained subjects. J. Appl. Physiol.83(1): 153–159, 1997.—The purpose of this study was to determine whether aerobic fitness level would influence measurements of excess postexercise oxygen consumption (EPOC) and initial rate of recovery. Twelve trained [Tr; peak oxygen consumption (V˙o 2 peak) = 53.3 ± 6.4 ml ⋅ kg−1 ⋅ min−1] and ten untrained (UT;V˙o 2 peak = 37.4 ± 3.2 ml ⋅ kg−1 ⋅ min−1) subjects completed two 30-min cycle ergometer tests on separate days in the morning, after a 12-h fast and an abstinence from vigorous activity of 24 h. Baseline metabolic rate was established during the last 10 min of a 30-min seated preexercise rest period. Exercise workloads were manipulated so that they elicited the same relative, 70%V˙o 2 peak (W70%), or the same absolute, 1.5 l/min oxygen uptake (V˙o 2) (W1.5), intensity for all subjects, respectively. RecoveryV˙o 2, heart rate (HR), and respiratory exchange ratio (RER) were monitored in a seated position until baseline V˙o 2 was reestablished. Under both exercise conditions, Tr had shorter EPOC duration (W70% = 40 ± 15 min, W1.5 = 21 ± 9 min) than UT (W70% = 50 ± 14 min; W1.5 = 39 ± 14 min), but EPOC magnitude (Tr: W70% = 3.2 ± 1.0 liters O2, W1.5 = 1.5 ± 0.6 liters O2; UT: W70% = 3.5 ± 0.9 liters O2, W1.5 = 2.4 ± 0.6 liters O2) was not different between groups. The similarity of Tr and UT EPOC accumulation in the W70% trial is attributed to the parallel decline in absolute V˙o 2 during most of the initial recovery period. Tr subjects had faster relative decline during the fast-recovery phase, however, when a correction for their higher exerciseV˙o 2 was taken. Postexercise V˙o 2 was lower for Tr group for nearly all of the W1.5 trial and particularly during the fast phase. Recovery HR kinetics were remarkably similar for both groups in W70%, but recovery was faster for Tr during W1.5. RER values were at or below baseline throughout much of the recovery period in both groups, with UT experiencing larger changes than Tr in both trials. These findings indicate that Tr individuals have faster regulation of postexercise metabolism when exercising at either the same relative or same absolute work rate.
Ventilatory and metabolic responses to ambient hypoxia or hypercapnia in rats exposed to CO hypoxia
Authors: Gautier Henry , Murariu Cristina , Bonora Monique
Published: December 2017

Gautier, Henry, Cristina Murariu, and Monique Bonora.Ventilatory and metabolic responses to ambient hypoxia or hypercapnia in rats exposed to CO hypoxia. J. Appl. Physiol.83(1): 253–261, 1997.—We have investigated at ambient temperatures (Tam) of 25 and 5°C the effects of ambient hypoxia (Hxam; fractional inspired O2 = 0.14) and hypercapnia (fractional inspired CO2 = 0.04) on ventilation (V˙), O2 uptake (V˙o 2), and colonic temperature (Tc) in 12 conscious rats before and after carotid body denervation (CBD). The rats were concomitantly exposed to CO hypoxia (HxCO; fractional inspired CO = 0.03–0.05%), which decreases arterial O2 saturation by ∼25–40%. The results demonstrate the following. 1) At Tam of 5°C, in both intact and CBD rats,V˙/V˙o 2 is larger when Hxam or CO2 is associated with HxCO than with normoxia. At Tam of 25°C, this is also the case except for CO2 in CBD rats. 2) At Tam of 5°C, the changes inV˙o 2 and Tc seem to result from additive effects of the separate changes induced by Hxam, CO2, and HxCO. It is concluded that, in conscious rats, central hypoxia does not depress respiratory activity. On the contrary, particularly whenV˙o 2 is augmented during a cold stress, bothV˙/V˙o 2during HxCO and the ventilatory responses to Hxam and CO2 are increased. The mechanisms involved in this relative hyperventilation are likely to involve diencephalic integrative structures.
Functional deficits in medial gastrocnemius grafts in rats: relation to muscle metabolism and β-AR regulation
Authors: Larkin Lisa M. , Faulkner John A. , Hinkle Richard T. , Hassett Cheryl A. , Supiano Mark A. , Halter Jeffrey B.
Published: December 2017

Larkin, Lisa M., John A. Faulkner, Richard T. Hinkle, Cheryl A. Hassett, Mark A. Supiano, and Jeffrey B. Halter.Functional deficits in medial gastrocnemius grafts in rats: relation to muscle metabolism and β-AR regulation. J. Appl. Physiol. 83(1): 67–73, 1997.—This study tested the hypothesis that alterations in the metabolic integrity of grafted muscle contribute to its diminished ability to sustain power. Compared with control muscles, muscles studied 120 days after the grafting procedure had lower specific force and sustained power. The sustained power protocol resulted in a depletion of muscle glycogen in control (83%) and grafted (85%) animals. Grafts had lower pre- and poststimulation glycogen, diminished citrate synthase activity, and greater hexokinase activity. No differences were observed in phosphofructokinase activity, glucose transporter GLUT-4 content, fiber type, β-adrenergic-receptor (β-AR) density, or binding affinity. Isoproterenol-stimulated adenylyl cyclase activity was lower in grafted vs. control muscle, suggesting an uncoupling of the β-AR-effector complex. Thus the diminished ability of the grafted muscle to sustain power may be explained, in part, by a decrease in energy available from glycogen stores and/or a decrease in oxidative capacity.
Cerebellar modulation of cough motor pattern in cats
Authors: Xu Fadi , Frazier Donald T. , Zhang Zhong , Baekey David M. , Shannon Roger
Published: December 2017

Xu, Fadi, Donald T. Frazier, Zhong Zhang, David M. Baekey, and Roger Shannon. Cerebellar modulation of cough motor pattern in cats. J. Appl. Physiol. 83(2): 391–397, 1997.—The cerebellum modulates respiratory muscle activity in part via its influence on the central respiratory pattern generator. Because coughing requires well-coordinated respiratory muscle activity, studies were conducted to determine whether the cerebellum influences the centrally generated cough motor pattern. Integrated phrenic and lumbar efferent neurograms ([Formula: see text]PN and [Formula: see text]LN, respectively) were monitored in decerebrated, paralyzed, and ventilated cats. Mechanical probing of the intrathoracic trachea was used to evoke fictive coughs; i.e., large increases in[Formula: see text]PN and [Formula: see text]LN amplitudes. Cerebellectomy resulted in a decrease in the number of coughs per trial (cough frequency) and [Formula: see text]LN peak amplitudes without any consistent change in[Formula: see text]PN peak amplitudes. Cerebellar nuclei [the rostral interposed nucleus (INr) and the rostral fastigial nucleus (FNr)] known to be involved in respiratory control were ablated to determine their potential role in the cough response. Control (eupneic) respiratory frequency was not affected by cerebellectomy or INr/FNr lesions. Cough frequency was depressed by lesion of the INr but not by ablation of the FNr. No significant changes in[Formula: see text]PN and [Formula: see text]LN amplitudes were observed after lesion of either the INr or FNr. These results suggest that the cerebellum, specifically the INr, is involved in modulation of the frequency of centrally generated coughing.
Contractile responsiveness of coronary arteries from exercise-trained rats
Authors: Parker Janet L. , Mattox Mildred L. , Laughlin M. Harold
Published: December 2017

Parker, Janet L., Mildred L. Mattox, and M. Harold Laughlin.Contractile responsiveness of coronary arteries from exercise trained rats. J. Appl. Physiol. 83(2): 434–443, 1997.—The purpose of this study was to determine whether exercise training alters vasomotor reactivity of rat coronary arteries. In vitro isometric microvessel techniques were used to evaluate vasomotor properties of proximal left anterior artery rings (1 ring per animal) from exercise-trained rats (ET; n = 10) subjected to a 12-wk treadmill training protocol (32 m/min, 15% incline, 1 h/day, 5 days/wk) and control rats (C; n = 6) restricted to cage activity. No differences in passive length-tension characteristics or internal diameter (158 ± 9 and 166 ± 9 μm) were observed between vessesls of C and ET rats. Concentration-response curves to K+ (5–100 mM), prostaglandin F2α(10−8–10−4M), and norepinephrine (10−8–10−4) were unaltered ( P > 0.05) in coronary rings from ET rats compared with C rats; however, lower values of the concentration producing 50% of the maximal contractile response in rings from ET rats ( P = 0.05) suggest that contractile sensitivity to norepinephrine was enhanced. Vasorelaxation responses to sodium nitroprusside (10−9-10−4M) and adenosine (10−9-10−4M) were not different ( P > 0.05) between vessels of C and ET rats. However, relaxation responses to the endothelium-dependent vasodilator acetylcholine (ACh; 10−10-10−4M) were significantly blunted ( P < 0.001) in coronary rings from ET animals; maximal ACh relaxation averaged 90 ± 5 and 46 ± 12%, respectively, in vessels of C and ET groups. In additional experiments, two coronary rings (proximal and distal) were isolated from each C ( n = 7) and ET ( n = 7) animal. Proximal coronary artery rings from ET animals demonstrated decreased relaxation responses to ACh; however, ACh-mediated relaxation of distal coronary rings was not different between C and ET groups. N G-monomethyl-l-arginine (inhibitor of nitric oxide synthase) blocked ACh relaxation of all rings. l-Arginine (substrate for nitric oxide synthase) did not improve the blunted ACh relaxation in proximal coronary artery rings from ET rats. These studies suggest that exercise-training selectively decreases endothelium-dependent (ACh) but not endothelium-independent (sodium nitroprusside) relaxation responses of rat proximal coronary arteries; endothelium-dependent relaxation of distal coronary arteries is unaltered by training.
Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans
Authors: Beaumont Maurice , Lejeune Damien , Marotte Henri , Harf Alain , Lofaso Frédéric
Published: December 2017

Beaumont, Maurice, Damien Lejeune, Henri Marotte, Alain Harf, and Frédéric Lofaso. Effects of chest wall counterpressures on lung mechanics under high levels of CPAP in humans. J. Appl. Physiol. 83(2): 591–598, 1997.—We assessed the respective effects of thoracic (TCP) and abdominal/lower limb (ACP) counterpressures on end-expiratory volume (EEV) and respiratory muscle activity in humans breathing at 40 cmH2O of continuous positive airway pressure (CPAP). Expiratory activity was evaluated on the basis of the inspiratory drop in gastric pressure (ΔPga) from its maximal end-expiratory level, whereas inspiratory activity was evaluated on the basis of the transdiaphragmatic pressure-time product (PTPdi). CPAP induced hyperventilation (+320%) and only a 28% increase in EEV because of a high level of expiratory activity (ΔPga = 24 ± 5 cmH2O), contrasting with a reduction in PTPdi from 17 ± 2 to 9 ± 7 cmH2O ⋅ s−1 ⋅ cycle−1during 0 and 40 cmH2O of CPAP, respectively. When ACP, TCP, or both were added, hyperventilation decreased and PTPdi increased (19 ± 5, 21 ± 5, and 35 ± 7 cmH2O ⋅ s−1 ⋅ cycle−1, respectively), whereas ΔPga decreased (19 ± 6, 9 ± 4, and 2 ± 2 cmH2O, respectively). We concluded that during high-level CPAP, TCP and ACP limit lung hyperinflation and expiratory muscle activity and restore diaphragmatic activity.
Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans
Authors: Nóbrega Antonio C. L. , Williamson Jon W. , Garcia Jorge A. , Mitchell Jere H.
Published: December 2017

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712–717, 1997.—Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118–136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55–38 ml) mediated the increase in SV.
Effect of convective stretching and folding on aerosol mixing deep in the lung, assessed by approximate entropy
Authors: Butler J. P. , Tsuda A.
Published: December 2017

Butler, J. P., and A. Tsuda. Effect of convective stretching and folding on aerosol mixing deep in the lung, assessed by approximate entropy. J. Appl. Physiol. 83(3): 800–809, 1997.—There is a surprisingly substantial amount of aerosol mixing and deposition deep in the lung, which cannot be explained by classic transport mechanisms such as streamline crossing, inertial impaction, or gravitational sedimentation with reversible acinar flow. Mixing associated with “stretch and fold” convective flow patterns can, however, be a potent source of transport. We show such patterns in experimental preparations using rat lungs and in the theoretical Baker Transform. In both cases, mixing is associated with the temporal evolution of two length scales. The first is the slowly increasing diffusive length scale. The second is the rapidly decreasing lateral length scale, due to “stretching and folding,” over which diffusion must take place. This interaction leads to aerosol mixing in much shorter times than previously appreciated. Finally, we propose a new method by which to quantify the state of mixing, using an approximation to the entropy of the aerosol concentration distribution. The results of the analysis suggest that stretching and folding may be a key feature underlying peripheral aerosol transport.
Hyperhydration: thermoregulatory effects during compensable exercise-heat stress
Authors: Latzka William A. , Sawka Michael N. , Montain Scott J. , Skrinar Gary S. , Fielding Roger A. , Matott Ralph P. , Pandolf Kent B.
Published: December 2017

Latzka, William A., Michael N. Sawka, Scott J. Montain, Gary S. Skrinar, Roger A. Fielding, Ralph P. Matott, and Kent B. Pandolf.Hyperhydration: thermoregulatory effects during compensable exercise-heat stress. J. Appl. Physiol. 83(3): 860–866, 1997.—This study examined the effects of hyperhydration on thermoregulatory responses during compensable exercise-heat stress. The general approach was to determine whether 1-h preexercise hyperhydration [29.1 ml/kg lean body mass; with or without glycerol (1.2 g/kg lean body mass)] would improve sweating responses and reduce core temperature during exercise. During these experiments, the evaporative heat loss required (Ereq = 293 W/m2) to maintain steady-state core temperature was less than the maximal capacity (Emax = 462 W/m2) of the climate for evaporative heat loss (Ereq/Emax= 63%). Eight heat-acclimated men completed five trials: euhydration, glycerol hyperhydration, and water hyperhydration both with and without rehydration (replace sweat loss during exercise). During exercise in the heat (35°C, 45% relative humidity), there was no difference between hyperhydration methods for increasing total body water (∼1.5 liters). Compared with euhydration, hyperhydration did not alter core temperature, skin temperature, whole body sweating rate, local sweating rate, sweating threshold temperature, sweating sensitivity, or heart rate responses. Similarly, no difference was found between water and glycerol hyperhydration for these physiological responses. These data demonstrate that hyperhydration provides no thermoregulatory advantage over the maintenance of euhydration during compensable exercise-heat stress.
Measurement of magnetic resonance T2 for physiological experiments
Authors: Hardy Peter A. , Yue Guang
Published: December 2017

Hardy, Peter A., and Guang Yue. Measurement of magnetic resonance T2 for physiological experiments. J. Appl. Physiol. 83(3): 904–911, 1997.—The proton transverse relaxation time (T2) of human skeletal muscles has been increasingly used in magnetic resonance imaging experiments to examine muscle physiology and neuromuscular control. However, little attention has been paid to the experimental factors affecting the accuracy or sensitivity of the T2 measurement. We have explored theoretically and experimentally the structure of several magnetic resonance pulse sequences for measuring T2 of the first dorsal interosseous muscle and found that a multiecho imaging technique using non-slice-selective refocusing pulses (MENSS) produces more accurate T2 estimates than multiecho slice-selective (MESS) imaging methods that are commonly used. Using either technique we acquired four 5-mm-thick transverse images of the first dorsal interosseous muscle with a spatial resolution of 0.6 mm within 5 min. The T2 measured by the MENSS method was closer to the true T2 than was the T2 estimated by the MESS method. After a given amount of exercise, the MENSS technique revealed an average 28 ± 10% increase in T2 compared with a 13 ± 3% increase measured with an equivalent MESS technique. We conclude that the MENSS method is a more accurate and sensitive procedure for studying neuromuscular physiology compared with the more commonly used MESS method.
Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans
Authors: Kayser Bengt , Sliwinski Pawel , Yan Sheng , Tobiasz Mirek , Macklem Peter T.
Published: December 2017

Kayser, Bengt, Pawel Sliwinski, Sheng Yan, Mirek Tobiasz, and Peter T. Macklem. Respiratory effort sensation during exercise with induced expiratory-flow limitation in healthy humans. J. Appl. Physiol. 83(3): 936–947, 1997.—Nine healthy subjects (age 31 ± 4 yr) exercised with and without expiratory-flow limitation (maximal flow ∼1 l/s). We monitored flow, end-tidal [Formula: see text], esophageal (Pes) and gastric pressures, changes in end-expiratory lung volume, and perception (sensation) of difficulty in breathing. Subjects cycled at increasing intensity (+25 W/30 s) until symptom limitation. During the flow-limited run, exercise performance was limited in all subjects by maximum sensation. Sensation was equally determined by inspiratory and expiratory pressure changes. In both runs, 90% of the variance in sensation could be explained by the Pes swings (difference between peak inspiratory and peak expiratory Pes). End-tidal[Formula: see text] did not explain any variance in sensation in the control run and added only 3% to the explained variance in the flow-limited run. We conclude that in healthy subjects, during normal as well as expiratory flow-limited exercise, the pleural pressure generation of the expiratory muscles is equally related to the perception of difficulty in breathing as that of the inspiratory muscles.
Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase
Authors: Rasmussen B. B. , Winder W. W.
Published: December 2017

Rasmussen, B. B., and W. W. Winder. Effect of exercise intensity on skeletal muscle malonyl-CoA and acetyl-CoA carboxylase. J. Appl. Physiol. 83(4): 1104–1109, 1997.—Malonyl-CoA is synthesized by acetyl-CoA carboxylase (ACC) and is an inhibitor of fatty acid oxidation. Exercise induces a decline in skeletal muscle malonyl-CoA, which is accompanied by inactivation of ACC and increased activity of AMP-activated protein kinase (AMPK). This study was designed to determine the effect of exercise intensity on the enzyme kinetics of ACC, malonyl-CoA levels, and AMPK activity in skeletal muscle. Male Sprague-Dawley rats were killed (pentobarbital sodium anesthesia) at rest or after 5 min of exercise (10, 20, 30, or 40 m/min at 5% grade). The fast-twitch red and white regions of the quadriceps muscle were excised and frozen in liquid nitrogen. A progressive decrease in red quadriceps ACC maximal velocity (from 28.6 ± 1.5 to 14.3 ± 0.7 nmol ⋅ g−1⋅ min−1, P < 0.05), an increase in activation constant for citrate, and a decrease in malonyl-CoA (from 1.9 ± 0.2 to 0.9 ± 0.1 nmol/g, P < 0.05) were seen with the increase in exercise intensity from rest to 40 m/min. AMPK activity increased more than twofold. White quadriceps ACC activity decreased only during intense exercise. We conclude that the extent of ACC inactivation during short-term exercise is dependent on exercise intensity.
Effects of nitric oxide on blood flow distribution and O2extraction capabilities during endotoxic shock
Authors: Zhang Haibo , Rogiers Peter , Smail Nadia , Cabral Ana , Preiser Jean-Charles , Peny Marie-Odile , Vincent Jean-Louis
Published: December 2017

Zhang, Haibo, Peter Rogiers, Nadia Smail, Ana Cabral, Jean-Charles Preiser, Marie-Odile Peny, and Jean-Louis Vincent.Effects of nitric oxide on blood flow distribution and O2extraction capabilities during endotoxic shock. J. Appl. Physiol.83(4): 1164–1173, 1997.—The effects of the nitric oxide (NO) synthase inhibitor NG-monomethyl-l-arginine (l-NMMA) and the NO donor 3-morpholinosydnonimine (SIN-1) were tested in 18 endotoxic dogs. l-NMMA infusion (10 mg ⋅ kg−1⋅ h−1) increased arterial and pulmonary artery pressures and systemic and pulmonary vascular resistances but decreased cardiac index, left ventricular stroke work index, and blood flow to the hepatic, portal, mesenteric, and renal beds. SIN-1 infusion (2 μg ⋅ kg−1⋅ min−1) increased cardiac index; left ventricular stroke work index; and hepatic, portal, and mesenteric blood flow. It did not significantly influence arterial and pulmonary artery pressures but decreased renal blood flow. The critical O2delivery was similar in thel-NMMA group and in the control group (13.3 ± 1.6 vs. 12.8 ± 3.3 ml ⋅ kg−1⋅ min−1) but lower in the SIN-1 group (9.1 ± 1.8 ml ⋅ kg−1⋅ min−1, both P < 0.05). The critical O2extraction ratio was also higher in the SIN-1 group than in the other groups (58.7 ± 10.6 vs. 42.2 ± 7.6% in controls, P < 0.05; 43.0 ± 15.5% inl-NMMA group, P = not significant). We conclude that NO is not implicated in the alterations in O2extraction capabilities observed early after endotoxin administration.
Acceleration of V˙o 2kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise
Authors: Macdonald Maureen , Pedersen Preben K. , Hughson Richard L.
Published: December 2017

MacDonald, Maureen, Preben K. Pedersen, and Richard L. Hughson. Acceleration ofV˙o 2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J. Appl. Physiol. 83(4): 1318–1325, 1997.—We examined the hypothesis that O2 uptake (V˙o 2) would change more rapidly at the onset of step work rate transitions in exercise with hyperoxic gas breathing and after prior high-intensity exercise. The kinetics ofV˙o 2 were determined from the mean response time (MRT; time to 63% of total change inV˙o 2) and calculations of O2 deficit and slow component during normoxic and hyperoxic gas breathing in one group of seven subjects during exercise below and above ventilatory threshold (VT) and in another group of seven subjects during exercise above VT with and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of V˙o 2 at the onset or end of exercise. At work rates above VT, hyperoxic gas breathing accelerated both the on- and off-transient MRT, reduced the O2 deficit, and decreased theV˙o 2 slow component from minute 3 to minute 6 of exercise, compared with normoxia. Prior exercise above VT accelerated the on-transient MRT and reduced theV˙o 2 slow component from minute 3 to minute 6 of exercise in a second bout of exercise with both normoxic and hyperoxic gas breathing. However, the summated O2 deficit in the second normoxic and hyperoxic steps was not different from that of the first steps in the same gas condition. Faster on-transient responses in exercise above, but not below, VT with hyperoxia and, to a lesser degree, after prior high-intensity exercise above VT support the theory of an O2 transport limitation at the onset of exercise for workloads >VT.
Vascular tree structure affects lung blood flow heterogeneity simulated in three dimensions
Authors: Parker James C. , Cave Chris B. , Ardell Jeffrey L. , Hamm Charles R. , Williams Susan G.
Published: December 2017

Parker, James C., Chris B. Cave, Jeffrey L. Ardell, Charles R. Hamm, and Susan G. Williams. Vascular tree structure affects lung blood flow heterogeneity simulated in three dimensions. J. Appl. Physiol. 83(4): 1370–1382, 1997.—Pulmonary arterial tree structures related to blood flow heterogeneity were simulated by using a symmetrical, bifurcating model in three-dimensional space. The branch angle (Θ), daughter-parent length ratio ( rL ), branch rotation angle (φ), and branch fraction of parent flow (γ) for a single bifurcation were defined and repeated sequentially through 11 generations. With φ fixed at 90°, tree structures were generated with Θ between 60 and 90°, rL between 0.65 and 0.85, and an initial segment length of 5.6 cm and sectioned into 1-cm3 samples for analysis. Blood flow relative dispersions (RD%) between 52 and 42% and fractal dimensions ( D s) between 1.20 and 1.15 in 1-cm3samples were observed even with equal branch flows. When γ ≠ 0.5, RD% increased, but D s either decreased with gravity bias of higher branch flows or increased with random assignment of higher flows. Blood flow gradients along gravity and centripetal vectors increased with biased flow assignment of higher flows, and blood flows correlated negatively with distance only when γ ≠ 0.5. Thus a recursive branching vascular tree structure simulated D s and RD% values for blood flow heterogeneity similar to those observed experimentally in the pulmonary circulation due to differences in the number of terminal arterioles per 1-cm3 sample, but blood flow gradients and a negative correlation of flows with distance required unequal partitioning of blood flows at branch points.
Exercise, alveolar macrophage function, and susceptibility to respiratory infection
Authors: Davis J. M. , Kohut M. L. , Colbert L. H. , Jackson D. A. , Ghaffar A. , Mayer E. P.
Published: December 2017

Davis, J. M., M. L. Kohut, L. H. Colbert, D. A. Jackson, A. Ghaffar, and E. P. Mayer. Exercise, alveolar macrophage function, and susceptibility to respiratory infection. J. Appl. Physiol. 83(5): 1461–1466, 1997.—The effects of exercise on susceptibility to respiratory infection were determined by using a murine model of intranasal challenge with herpes simplex type 1 virus (HSV-1). Two doses of treadmill exercise were assessed: moderate short-term (30 min) exercise and prolonged strenuous exercise to voluntary fatigue (2.5–3.5 h). Morbidity and mortality among exercised and control mice were compared after intranasal challenge with HSV-1. We also assessed the ability of alveolar macrophages to restrict HSV-1 viral replication (intrinsic resistance) among exercise and control groups of mice at several time points postexercise. Exercise to fatigue followed by exposure to viral infection resulted in greater morbidity and mortality than either no exercise or short-term moderate exercise. In addition, antiviral resistance of macrophages obtained from the lungs of both exercised groups was suppressed, albeit for a longer duration in the fatigued group. These data are particularly important in that they identify an exercise-induced decrease in antiviral resistance of a specific component of the immune system within the lungs, in conjunction with increased susceptibility to respiratory infection in vivo. The specific mechanism of decreased antiviral resistance of alveolar macrophages and its role in respiratory infection after exercise remains to be determined.
Growth hormone, IGF-I, and exercise effects on non-weightbearing fast muscles of hypophysectomized rats
Authors: Grossman Elena J. , Grindeland Richard E. , Roy Roland R. , Talmadge Robert J. , Evans Juliann , Edgerton V. Reggie
Published: December 2017

Grossman, Elena J., Richard E. Grindeland, Roland R. Roy, Robert J. Talmadge, Juliann Evans, and V. Reggie Edgerton. Growth hormone, IGF-I, and exercise effects on non-weight-bearing fast muscles of hypophysectomized rats. J. Appl. Physiol. 83(5): 1522–1530, 1997.—The effects of growth hormone (GH) or insulin-like growth factor I (IGF-I) with or without exercise (ladder climbing) in countering the effects of unweighting on fast muscles of hypophysectomized rats during 10 days of hindlimb suspension were determined. Compared with untreated suspended rats, muscle weights were 16–29% larger in GH-treated and 5–15% larger in IGF-I-treated suspended rats. Exercise alone had no effect on muscle weights. Compared with ambulatory control, the medial gastrocnemius weight in suspended, exercised rats was larger after GH treatment and maintained with IGF-I treatment. The combination of GH or IGF-I plus exercise in suspended rats resulted in an increase in the size of each predominant fiber type, i.e., types I, I+IIa and IIa+IIx, in the medial gastrocnemius compared with untreated suspended rats. Normal ambulation or exercise during suspension increased the proportion of fibers expressing embryonic myosin heavy chain in hypophysectomized rats. The phenotype of the medial gastrocnemius was minimally affected by GH, IGF-I, and/or exercise. These results show that there is an IGF-I, as well as a GH, and exercise interactive effect in maintaining medial gastrocnemius fiber size in suspended hypophysectomized rats.
Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits
Authors: Losser Marie-Reine , Bernard Catherine , Beaudeux Jean-Louis , Pison Christophe , Payen Didier
Published: December 2017

Losser, Marie-Reine, Catherine Bernard, Jean-Louis Beaudeux, Christophe Pison, and Didier Payen. Glucose modulates hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide in rabbits. J. Appl. Physiol. 83(5): 1566–1574, 1997.—Glucose is important for vascular and immunocompetent cell functions. We hypothesized that modifications in glucose metabolism (normal feeding, 24-h fasting, glucose loading) may influence the hemodynamic, metabolic, and inflammatory responses to lipopolysaccharide administration (LPS; 600 μg/kg iv) in rabbits. Aortic (ABFV), hepatic artery (HABFV), and portal vein blood flow velocities (PVBFV) (pulsed Doppler), plasma tumor necrosis factor (TNF) and nitrites were measured. Fasting depleted hepatic glycogen content, and intraportal glucose load (2 g/kg) partially restored it. LPS induced a similar hypotension (−20%, P < 0.05) in three groups of animals. In fed animals, systemic vasoconstriction occured with low ABFV and PVBFV (−40%, P < 0.05), together with lactacidemia and hyperglycemia. In fasted animals, ABFV and PVBFV were maintained, without metabolic acidosis or hyperglycemia. Glucose loading induced hemodynamic and metabolic patterns comparable to those observed in fed animals, although significantly more severe. TNF release was amplified fourfold by glucose loading, with no impact on nitrite levels. In conclusion, glucose metabolism interferes with hemodynamic, metabolic, and inflammatory responses to LPS.
Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise
Authors: Buckwalter John B. , Mueller Patrick J. , Clifford Philip S.
Published: December 2017

Buckwalter, John B., Patrick J. Mueller, and Philip S. Clifford. Sympathetic vasoconstriction in active skeletal muscles during dynamic exercise. J. Appl. Physiol. 83(5): 1575–1580, 1997.—Studies utilizing systemic administration of α-adrenergic antagonists have failed to demonstrate sympathetic vasoconstriction in working muscles during dynamic exercise. The purpose of this study was to examine the existence of active sympathetic vasoconstriction in working skeletal muscles by using selective intra-arterial blockade. Six mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and with a catheter in one femoral artery. All dogs ran on a motorized treadmill at three intensities on separate days. After 2 min, the selective α1-adrenergic antagonist prazosin (0.1 mg) was infused as a bolus into the femoral artery catheter. At mild, moderate, and heavy workloads, there were immediate increases in iliac conductance of 76 ± 7, 54 ± 11, and 22 ± 6% (mean ± SE), respectively. Systemic blood pressure and blood flow in the contralateral iliac artery were unaffected. These results demonstrate that there is sympathetic vasoconstriction in active skeletal muscles even at high exercise intensities.
Vagal stimulation induces expiratory lengthening in the in vitro neonate rat
Authors: Mellen Nicholas M. , Feldman Jack L.
Published: December 2017

Mellen, Nicholas M., and Jack L. Feldman.Vagal stimulation induces expiratory lengthening in the in vitro neonate rat. J. Appl. Physiol. 83(5): 1607–1611, 1997.—Respiration is modulated by lung mechanoreceptor feedback in vivo on a cycle-to-cycle basis. We replicated this modulation in vitro and tested four stimulus protocols to identify which of these most closely replicated in vivo responses to lung mechanoreceptor activation in mammals. We activated pulmonary vagal afferent pathways by electrical stimulation or by lung inflation, applied during expiration, which produces expiratory lengthening in vivo. In each modality, transient and tonic stimuli were applied. Stimuli were applied over a range of delays following inspiratory termination. Tonic stimuli were maintained until subsequent inspiratory onset. All stimulus modalities prolonged expiration ( P < 0.05). These results indicate that the neural circuitry mediating pulmonary afferent modulation of expiratory duration is retained in vitro.
Partial liquid ventilation protects lung during resuscitation from shock
Authors: Younger John G. , Taqi Ali S. , Till Gerd O. , Hirschl Ronald B.
Published: December 2017

Younger, John G., Ali S. Taqi, Gerd O. Till, and Ronald B. Hirschl. Partial liquid ventilation protects lung during resuscitation from shock. J. Appl. Physiol. 83(5): 1666–1670, 1997.—Preliminary animal experience with partial liquid ventilation (PLV) suggests that this therapy may diminish neutrophil invasion and capillary leak during acute lung injury. We sought to confirm these findings in a model of shock-induced lung injury. Sixty anesthetized rats were studied. After hemorrhage to an arterial pressure of 25 mmHg for 45 min, animals were resuscitated with blood and saline and treated with gas ventilation alone or with 5 ml/kg of intratracheally administered perflubron. Myeloperoxidase activity was used to measure lung neutrophil content. A permeability index (the bronchoalveolar-to-blood ratio of125I-labeled albumin activity) quantified alveolar leak. Injury caused an increase in myeloperoxidase that was reversed by PLV (injury = 0.837 ± 0.452, PLV = 0.257 ± 0.165; P < 0.01). Capillary permeability also increased with hemorrhage, with a strong trend toward improvement in the PLV group (permeability indexes: injury = 0.094 ± 0.102, PLV = 0.045 ± 0.045; 95% confidence interval for injury − PLV: −0.024, 0.1219). We conclude that PLV is associated with a decrease in pulmonary neutrophil accumulation and a trend toward decreased capillary leak after hemorrhagic shock.