bluuebunny/crossref_metadata_2025 huggingface dataset:
A moderate glycemic meal before endurance exercise can enhance performance
Authors: Kirwan John P. , O’Gorman Donal , Evans William J.
Published: December 2017

Kirwan, John P., Donal O’Gorman, and William J. Evans.A moderate glycemic meal before endurance exercise can enhance performance. J. Appl. Physiol. 84(1): 53–59, 1998.—The purpose of this study was to determine whether presweetened breakfast cereals with various fiber contents and a moderate glycemic index optimize glucose availability and improve endurance exercise performance. Six recreationally active women ate 75 g of available carbohydrate in the form of breakfast cereals: sweetened whole-grain rolled oats (SRO, 7 g of dietary fiber) or sweetened whole-oat flour (SOF, 3 g of dietary fiber) and 300 ml of water or water alone (Con). The meals were provided 45 min before semirecumbent cycle ergometer exercise to exhaustion at 60% of peak O2consumption (V˙o2 peak). Diet and physical activity were controlled by having the subjects reside in the General Clinical Research Center for 2 days before each trial. Blood samples were drawn from an antecubital vein for glucose, free fatty acid (FFA), glycerol, insulin, epinephrine, and norepinephrine determination. Breath samples were obtained at 15-min intervals after meal ingestion and at 30-min intervals during exercise. Muscle glycogen concentration was determined from biopsies taken from the vastus lateralis muscle before the meal and immediately after exercise. Plasma FFA concentrations were lower ( P < 0.05) during the SRO and SOF trials for the first 60 and 90 min of exercise, respectively, than during the Con trial. Respiratory exchange ratios were higher ( P < 0.05) at 90 and 120 min of exercise for the SRO and SOF trials, respectively, than for the Con trial. At exhaustion, glucose, insulin, FFA, glycerol, epinephrine, and norepinephrine concentrations, respiratory exchange ratio, and muscle glycogen use in the vastus lateralis muscle were similar for all trials. Exercise time to exhaustion was 16% longer ( P < 0.05) during the SRO than during the Con trial: 266.5 ± 13 and 225.1 ± 8 min, respectively. There was no difference in exercise time for the SOF (250.8 ± 12) and Con trials. We conclude that eating a meal with a high dietary fiber content and moderate glycemic index 45 min before prolonged moderately intense exercise significantly enhances exercise capacity.
Importance of the lactate anion in control of breathing
Authors: Hardarson Thorir , Skarphedinsson Jon O. , Sveinsson Torarinn
Published: December 2017

Hardarson, Thorir, Jon O. Skarphedinsson, and Torarinn Sveinsson. Importance of the lactate anion in control of breathing. J. Appl. Physiol. 84(2): 411–416, 1998.—The purpose of this study was to examine the effects of raising the arterial La− and K+ levels on minute ventilation (V˙e) in rats. Either La− or KCl solutions were infused in anesthetized spontaneously breathing Wistar rats to raise the respective ion arterial concentration ([La−] and [K+]) gradually to levels similar to those observed during strenuous exercise.V˙e, blood pressure, and heart rate were recorded continuously, and arterial [La−], [K+], pH, and blood gases were repeatedly measured from blood samples. To prevent changes in pH during the La−infusions, a solution of sodium lactate and lactic acid was used. Raising [La−] to 13.2 ± 0.6 (SE) mM induced a 47.0 ± 4.0% increase inV˙e without any concomitant changes in either pH or [Formula: see text]. Raising [K+] to 7.8 ± 0.11 mM resulted in a 20.3 ± 5.28% increase inV˙e without changes in pH. Thus our results show that La−itself, apart from lactic acidosis, may be important in increasingV˙e during strenuous exercise, and we confirm earlier results regarding the role of arterial [K+] in the control ofV˙e during exercise.
Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression
Authors: Harridge S. D. R. , Bottinelli R. , Canepari M. , Pellegrino M. , Reggiani C. , Esbjörnsson M. , Balsom P. D. , Saltin B.
Published: December 2017

Harridge, S. D. R., R. Bottinelli, M. Canepari, M. Pellegrino, C. Reggiani, M. Esbjörnsson, P. D. Balsom, and B. Saltin. Sprint training, in vitro and in vivo muscle function, and myosin heavy chain expression. J. Appl. Physiol. 84(2): 442–449, 1998.—Sprint training represents the condition in which increases in muscle shortening speed, as well as in strength, might play a significant role in improving power generation. This study therefore aimed to determine the effects of sprint training on 1) the coupling between myosin heavy chain (MHC) isoform expression and function in single fibers, 2) the distribution of MHC isoforms across a whole muscle, and 3) in vivo muscle function. Seven young male subjects completed 6 wk of training (3-s sprints) on a cycle ergometer. Training was without effect on maximum shortening velocity in single fibers or in the relative distribution of MHC isoforms in either the soleus or the vastus lateralis muscles. Electrically evoked and voluntary isometric torque generation increased ( P < 0.05) after training in both the plantar flexors (+8% at 50 Hz and +16% maximal voluntary contraction) and knee extensors (+8% at 50 Hz and +7% maximal voluntary contraction). With the shortening potential of the muscles apparently unchanged, the increased strength of the major lower limb muscles is likely to have contributed to the 7% increase ( P < 0.05) in peak pedal frequency during cycling.
Similar hypoxic ventilatory responses in sea-level natives and high-altitude Andean natives living at sea level
Authors: Vargas Manuel , León-Velarde Fabiola , Monge-C. Carlos , Palacios José-Antonio , Robbins Peter A.
Published: December 2017

High-altitude (HA) natives have blunted ventilatory sensitivities to hypoxia, and it is uncertain whether this blunting is reversible on migration to sea level (SL). To study this, the ventilatory sensitivities to hypoxia of HA natives residing near SL were compared with those of SL natives. Two studies were performed. In study A, 24 HA subjects who had lived above 3,000 m for an average of 14 yr and had been resident at SL for an average of 23 yr were compared with 23 SL controls. In study B, 25 HA subjects who had lived above 3,500 m for at least 20 yr and had been resident at SL for no more than 5 yr were compared with 25 SL controls. Hypoxic sensitivities were assessed by breathing seven progressively more hypoxic gas mixtures that contained progressively more CO2 in an attempt to maintain isocapnia throughout. The ventilatory sensitivities to hypoxia (l ⋅ min−1 ⋅ %−1 ⋅ m−2) did not differ significantly (by analysis of variance) between HA and SL natives in either study A(−0.51 ± 0.25, mean ± SD) or study B (−0.34 ± 0.15), but the ventilatory sensitivities did differ significantly between the two studies for reasons which are not entirely clear. We conclude that HA natives residing at SL, even if previously at HA for >20 yr, do not maintain the severely blunted hypoxic responses that have been reported in such individuals.
Pulmonary fluid extraction and osmotic conductance, ςK, measured in vivo
Authors: Karch Joseph M. , Lee Jen-Shih
Published: December 2017

The change in aortic blood density in an in vivo rabbit preparation was measured to assess fluid movement at the pulmonary capillaries caused by infusion of hypertonic solution (NaCl, urea, glucose, sucrose, or raffinose in isotonic saline) into the vena cava over 20 s. The hypertonic disturbance increased the plasma osmotic pressure by ≤30 mosmol/l. The density change indicates that the fluid extraction from the lung tissue was completed within 10 s. It was followed by a fluid filtration into the lung tissue and then an extraction and filtration from peripheral organs. An exchange model with flow dispersion yields two equations to estimate the osmotic conductance (ς K; where ς is the reflection coefficient of the test solute and K is the filtration coefficient including the total capillary surface area), and the tissue fluid volume from the area and first moment of the measured density change over the extraction phase. The values of ς K are 1.40 ± 0.11, 1.00 ± 0.10, 1.71 ± 0.10, 2.60 ± 0.23, and 3.73 ± 0.34 (SE) ml ⋅ h−1⋅ mosmol−1⋅ l ⋅ g−1for NaCl, urea, glucose, sucrose, and raffinose, respectively. Consistent with the model prediction, the tissue fluid volume (0.28 ± 0.04 ml/g wet lung tissue) was independent of the solute used. This value suggests that all fluid spaces in the alveolar septa participate in the process of fluid extraction due to an increase in plasma osmotic pressure.
Protective effects of intravascular pressure and nitric oxide in ischemic lung injury
Authors: Becker Patrice M. , Buchanan Wendy , Sylvester J. T.
Published: December 2017

Cessation of blood flow during ischemia will decrease both distending and shear forces exerted on endothelium and may worsen ischemic lung injury by decreasing production of nitric oxide (NO), which influences vascular barrier function. We hypothesized that increased intravascular pressure (Piv) during ventilated ischemia might maintain NO production by increasing endothelial stretch or shear forces, thereby attenuating ischemic lung injury. Injury was assessed by measuring the filtration coefficient ( Kf) and the osmotic reflection coefficient for albumin (ςalb) after 3 h of ventilated (95% O2-5% CO2; expiratory pressure 3 mmHg) ischemia. Lungs were flushed with physiological salt solution, and then Piv was adjusted to achieve High Piv (mean 6.7 ± 0.4 mmHg, n = 15) or Low Piv (mean 0.83 ± 0.4 mmHg, n = 10). NG-nitro-l-arginine methyl ester (l-NAME; 10−5M, n = 10), NG-nitro-d-arginine methyl ester (d-NAME; 10−5M, n = 11), orl-NAME (10−5M)+l-arginine (5 × 10−4M, n = 6) was added at the start of ischemia in three additional groups of lungs with High Piv. High Piv attenuated ischemic injury compared with Low Piv (ςalb0.67 ± 0.04 vs. 0.35 ± 0.04, P < 0.05). The protective effect of High Piv was abolished byl-NAME (ςalb0.37 ± 0.04, P < 0.05) but not byd-NAME (ςalb0.63 ± 0.07). The effects of l-NAME were overcome by an excess of l-arginine (ςalb0.56 ± 0.05, P < 0.05). Kfdid not differ significantly among groups. These results suggest that Piv modulates ischemia-induced barrier dysfunction in the lung, and these effects may be mediated by NO.
Depressed ventilatory response to hypoxia in hypothermic newborn piglets: role of glutamate
Authors: McCormick Annette , Suguihara Cleide , Huang Jian , Devia Carlos , Hehre Dorothy , Bruce Jocelyn H. , Bancalari Eduardo
Published: December 2017

To evaluate whether changes in extracellular glutamate (Glu) levels in the central nervous system could explain the depressed hypoxic ventilatory response in hypothermic neonates, 12 anesthetized, paralyzed, and mechanically ventilated piglets <7 days old were studied. The Glu levels in the nucleus tractus solitarius obtained by microdialysis, minute phrenic output (MPO), O2consumption, arterial blood pressure, heart rate, and arterial blood gases were measured in room air and during 15 min of isocapnic hypoxia (inspired O2fraction = 0.10) at brain temperatures of 39.0 ± 0.5°C [normothermia (NT)] and 35.0 ± 0.5°C [hypothermia (HT)]. During NT, MPO increased significantly during hypoxia and remained above baseline. However, during HT, there was a marked decrease in MPO during hypoxia (NT vs. HT, P < 0.03). Glu levels increased significantly in hypoxia during NT; however, this increase was eliminated during HT ( P < 0.02). A significant linear correlation was observed between the changes in MPO and Glu levels during hypoxia ( r = 0.61, P < 0.0001). Changes in pH, arterial[Formula: see text], O2consumption, arterial blood pressure, and heart rate during hypoxia were not different between the NT and HT groups. These results suggest that the depressed ventilatory response to hypoxia observed during HT is centrally mediated and in part related to a decrease in Glu concentration in the nucleus tractus solitarius.
Does an acute COPD crisis modify the cardiorespiratory and ventilatory adjustments to exercise in horses?
Authors: Art T. , Duvivier D. H. , Votion D. , Anciaux N. , Vandenput S. , Bayly W. M. , Lekeux P.
Published: December 2017

The present study was conducted to understand better the mechanisms leading to the decrease in exercise capacity observed in horses suffering from chronic obstructive pulmonary disease (COPD). Five COPD horses were submitted to a standardized submaximal treadmill exercise test while they were in clinical remission or in acute crisis. Respiratory airflow, O2and CO2fractions in the respired gas, pleural pressure changes and heart rate were recorded, and arterial and mixed venous blood were analyzed for gas tensions, hemoglobin, and plasma lactate concentrations. O2consumption, CO2production, expired minute ventilation, tidal volume, alveolar ventilation, cardiac output, total pulmonary resistance, and mechanical work of breathing were calculated. The results showed that, when submaximally exercised, COPD horses in crisis were significantly more hypoxemic and hypercapnic and that their total pulmonary resistance and mechanical work of breathing were significantly higher and their expired minute ventilation significantly lower than when they were in remission. However, their O2consumption remained unchanged, which was probably due to the occurrence of compensatory mechanisms, i.e., higher heart rate, cardiac output, and hemoglobin concentration. Last, their net anaerobic metabolism seemed to be more important.
Metabolic effects of low cortisol during exercise in humans
Authors: Del Corral Pedro , Howley Edward T. , Hartsell Mike , Ashraf Muhammad , Younger Mary Sue
Published: December 2017

This study examined the physiological effect of reduced plasma cortisol (C) during prolonged exercise in humans. The effects of normal C (NC) were compared with metyrapone-induced low C (LC) on plasma substrate availability and the respiratory exchange ratio during 2 h of exercise at ∼60% peak O2consumption in nine subjects. The C responses were compared with preexercise (Pre) levels and with a rest day (Con). At rest, C was attenuated by ∼70% for LC compared with NC. At rest, plasma glucose, lactate, glycerol, β-hydroxybutyrate, alanine, branched-chain amino acids, insulin, glucagon, growth hormone, epinephrine, and norepinephrine were similar under LC and NC ( P > 0.05). During exercise under NC, plasma C increased compared with Pre, whereas it remained unchanged during LC. During NC, plasma C was elevated at 90 min (compared with Con) and at 120 min (compared with Con and Pre). During exercise, plasma glucose decreased to the same extent and lactate was similar under both conditions, whereas plasma glycerol, β-hydroxybutyrate, alanine, and branched-chain amino acids were higher ( P < 0.01) under NC. Plasma insulin declined ( P = 0.01) to a greater extent under LC, whereas growth hormone, epinephrine, and norepinephrine tended to be higher (0.05 ≤ P ≤ 0.10). Plasma glucagon increased under both conditions ( P < 0.01). The respiratory exchange ratio did not differ between conditions. We conclude that, during exercise, 1) C accelerates lipolysis, ketogenesis, and proteolysis; 2) under LC, glucoregulatory hormone adjustments maintain glucose homeostasis; and 3) LC does not alter whole body substrate utilization or the ability to complete 2 h of moderate exercise.
Pulmonary blood flow redistribution by increased gravitational force
Authors: Hlastala Michael P. , Chornuk Myron A. , Self David A. , Kallas Harry J. , Burns John W. , Bernard Susan , Polissar Nayak L. , Glenny Robb W.
Published: December 2017

This study was undertaken to assess the influence of gravity on the distribution of pulmonary blood flow (PBF) using increased inertial force as a perturbation. PBF was studied in unanesthetized swine exposed to −G x (dorsal-to-ventral direction, prone position), where G is the magnitude of the force of gravity at the surface of the Earth, on the Armstrong Laboratory Centrifuge at Brooks Air Force Base. PBF was measured using 15-μm fluorescent microspheres, a method with markedly enhanced spatial resolution. Each animal was exposed randomly to −1, −2, and −3 G x . Pulmonary vascular pressures, cardiac output, heart rate, arterial blood gases, and PBF distribution were measured at each G level. Heterogeneity of PBF distribution as measured by the coefficient of variation of PBF distribution increased from 0.38 ± 0.05 to 0.55 ± 0.11 to 0.72 ± 0.16 at −1, −2, and −3 G x , respectively. At −1 G x , PBF was greatest in the ventral and cranial and lowest in the dorsal and caudal regions of the lung. With increased −G x , this gradient was augmented in both directions. Extrapolation of these values to 0 G predicts a slight dorsal (nondependent) region dominance of PBF and a coefficient of variation of 0.22 in microgravity. Analysis of variance revealed that a fixed component (vascular structure) accounted for 81% and nonstructure components (including gravity) accounted for the remaining 19% of the PBF variance across the entire experiment (all 3 gravitational levels). The results are inconsistent with the predictions of the zone model.
Aerobic exercise maintains regional bone mineral density during weight loss in postmenopausal women
Authors: Ryan Alice S. , Nicklas Barbara J. , Dennis Karen E.
Published: December 2017

This study examines the effects of weight loss by caloric restriction (WL) and aerobic exercise plus weight loss (AEx+WL) on total and regional bone mineral density (BMD) in older women. Healthy, postmenopausal women [age 63 ± 1 (SE) yr] not on hormone-replacement therapy underwent 6 mo of WL ( n = 15) consisting of dietary counseling one time per week with a caloric deficit (250–350 kcal/day) or AEx+WL ( n = 15) consisting of treadmill exercise three times per week in addition to the weight loss. Maximal aerobic capacity increased only in the AEx+WL group ( P < 0.001). Body weight, percent fat, and fat mass decreased similarly in both groups ( P < 0.005), with no changes in fat-free mass. Total body BMD (by dual-energy X-ray absorptiometry) decreased in both groups ( P < 0.05). Femoral neck, Ward’s triangle, and greater trochanter BMD decreased in the WL group ( P ≤ 0.05) but were not significantly different after AEx+WL. L2–L4BMD did not significantly change in either group. Thus WL and AEx+WL both result in losses of total body BMD; however, AEx+WL appears to prevent the loss in regional BMD seen with WL alone in healthy, older women. This suggests that the addition of exercise to weight-loss programs may reduce the risk for bone loss.
Improved oxygenation with prostaglandin F2α with and without inhaled nitric oxide in dogs
Authors: Marshall Bryan E. , Chen Linda , Frasch H. Fred , Hanson C. William , Marshall Carol
Published: December 2017

Dogs of mixed breed ( n = 7) were anesthetized, right lung atelectasis was established, and the cyclooxygenase pathway was blocked with ibuprofen. Measurements of pulmonary gas exchange were performed (fractional concentration of inspired O2 = 0.95) after infusions of prostaglandin F2α(PGF2α; 2 μg ⋅ kg−1 ⋅ min−1), ventilation with nitric oxide (NO; 40 ppm), or both (PGF2α + NO) in random order. The arterial [Formula: see text]([Formula: see text]) under control conditions was 117 ± 16 Torr (shunt = 33 ± 2.5%), was unchanged with NO alone ([Formula: see text] = 114 ± 17 Torr; shunt = 35.7 ± 3.1%), but was significantly improved with PGF2α alone ([Formula: see text] = 180 ± 28 Torr; shunt = 23.2 ± 2.8%) and with the combination of PGF2α + NO ([Formula: see text]= 202 ± 30 Torr; shunt = 20.9 ± 2.5%). The addition of NO did not significantly enhance the effectiveness of the PGF2α on[Formula: see text]. Simulation of these data in a computer model, combining pulmonary gas exchange and pulmonary blood flow, reproduced the results on the basis that vasoconstriction with PGF2αwas maximal under hypoxia in the atelectatic lung and reduced by hyperoxia in the ventilated lung, consistent with the hypothesis of O2 dependence of PGF2α vasoconstriction.
Effect of increased blood glucose availability on glucose kinetics during exercise
Authors: Howlett Kirsten , Angus Damien , Proietto Joseph , Hargreaves Mark
Published: December 2017

This study examined the effect of increased blood glucose availability on glucose kinetics during exercise. Five trained men cycled for 40 min at 77 ± 1% peak oxygen uptake on two occasions. During the second trial (Glu), glucose was infused at a rate equal to the average hepatic glucose production (HGP) measured during exercise in the control trial (Con). Glucose kinetics were measured by a primed continuous infusion ofd-[3-3H]glucose. Plasma glucose increased during exercise in both trials and was significantly higher in Glu. HGP was similar at rest (Con, 11.4 ± 1.2; Glu, 10.6 ± 0.6 μmol ⋅ kg−1 ⋅ min−1). After 40 min of exercise, HGP reached a peak of 40.2 ± 5.5 μmol ⋅ kg−1 ⋅ min−1in Con; however, in Glu, there was complete inhibition of the increase in HGP during exercise that never rose above the preexercise level. The rate of glucose disappearance was greater ( P < 0.05) during the last 15 min of exercise in Glu. These results indicate that an increase in glucose availability inhibits the rise in HGP during exercise, suggesting that metabolic feedback signals can override feed-forward activation of HGP during strenuous exercise.
Free mobilization and low- to high-intensity exercise in immobilization-induced muscle atrophy
Authors: Kannus Pekka , Jozsa Laszlo , Järvinen Teppo L. N. , Kvist Martti , Vieno Toini , Järvinen Tero A. H. , Natri Antero , Järvinen Markku
Published: December 2017

After 3 wk of immobilization, the effects of free cage activity and low- and high-intensity treadmill running (8 wk) on the morphology and histochemistry of the soleus and gastrocnemius muscles in male Sprague-Dawley rats were investigated. In both muscles, immobilization produced a significant ( P < 0.001) increase in the mean percent area of intramuscular connective tissue (soleus: 18.9% in immobilized left hindlimb vs. 3.6% in nonimmobilized right hindlimb) and in the relative number of muscle fibers with pathological alterations (soleus: 66% in immobilized hindlimb vs. 6% in control), with a simultaneous significant ( P < 0.001) decrease in the intramuscular capillary density (soleus: mean capillary density in the immobilized hindlimb only 63% of that in the nonimmobilized hindlimb) and muscle fiber size (soleus type I fibers: mean fiber size in the immobilized hindlimb only 69% of that in the nonimmobilized hindlimb). Many of these changes could not be corrected by free remobilization, whereas low- and high-intensity treadmill running clearly restored the changes toward control levels, the effect being most complete in the high-intensity running group. Collectively, these findings indicate that immobilization-induced pathological structural and histochemical alterations in rat calf muscles are, to a great extent, reversible phenomena if remobilization is intensified by physical training. In this respect, high-intensity exercise seems more beneficial than low-intensity exercise.
Skeletal muscle afferent regulation of bioassayable growth hormone in the rat pituitary
Authors: Gosselink K. L. , Grindeland R. E. , Roy R. R. , Zhong H. , Bigbee A. J. , Grossman E. J. , Edgerton V. R.
Published: December 2017

There are forms of growth hormone (GH) in the plasma and pituitary of the rat and in the plasma of humans that are undetected by presently available immunoassays (iGH) but can be measured by bioassay (bGH). Although the regulation of iGH release is well documented, the mechanism(s) of bGH release is unclear. On the basis of changes in bGH and iGH secretion in rats that had been exposed to microgravity conditions, we hypothesized that neural afferents play a role in regulating the release of these hormones. To examine whether bGH secretion can be modulated by afferent input from skeletal muscle, the proximal or distal ends of severed hindlimb fast muscle nerves were stimulated (∼2 times threshold) in anesthetized rats. Plasma bGH increased ∼250%, and pituitary bGH decreased ∼60% after proximal nerve trunk stimulation. The bGH response was independent of muscle mass or whether the muscles were flexors or extensors. Distal nerve stimulation had little or no effect on plasma or pituitary bGH. Plasma iGH concentrations were unchanged after proximal nerve stimulation. Although there may be multiple regulatory mechanisms of bGH, the present results demonstrate that the activation of low-threshold afferents from fast skeletal muscles can play a regulatory role in the release of bGH, but not iGH, from the pituitary in anesthetized rats.
Inhibition of nitric oxide synthase slows heart rate recovery from cholinergic activation
Authors: Sears Claire E. , Choate Julia K. , Paterson David J.
Published: December 2017

The role of nitric oxide (NO) in the cholinergic regulation of heart rate (HR) recovery from an aspect of simulated exercise was investigated in atria isolated from guinea pig to test the hypothesis that NO may be involved in the cholinergic antagonism of the positive chronotropic response to adrenergic stimulation. Inhibition of NO synthesis with NG-monomethyl-l-arginine (l-NMMA, 100 μM) significantly slowed the time course of the reduction in HR without affecting the magnitude of the response elicited by bath-applied ACh (100 nM) or vagal nerve stimulation (2 Hz). The half-times ( t1/2) of responses were 3.99 ± 0.41 s in control vs. 7.49 ± 0.68 s inl-NMMA ( P < 0.05). This was dependent on prior adrenergic stimulation (norepinephrine, 1 μM). The effect ofl-NMMA was reversed byl-arginine (1 mM; t1/24.62 ± 0.39 s). The calcium-channel antagonist nifedipine (0.2 μM) also slowed the kinetics of the reduction in HR caused by vagal nerve stimulation. However, the t1/2for the reduction in HR with antagonists (2 mM Cs+and 1 μM ZD-7288) of the hyperpolarization-activated current were significantly faster compared with control. There was no additional effect ofl-NMMA orl-NMMA+l-arginine on vagal stimulation in groups treated with nifedipine, Cs+, or ZD-7288. We conclude that NO contributes to the cholinergic antagonism of the positive cardiac chronotropic effects of adrenergic stimulation by accelerating the HR response to vagal stimulation. This may involve an interplay between two pacemaking currents (L-type calcium channel current and hyperpolarization-activated current). Whether NO modulates the vagal control of HR recovery from actual exercise remains to be determined.
Patent foramen ovale and decompression sickness in sports divers
Authors: Germonpré P. , Dendale P. , Unger P. , Balestra C.
Published: December 2017

Patency of the foramen ovale (PFO) may be a cause of unexplained decompression sickness (DCS) in sports divers. To assess the relationship between PFO and DCS, a case-control study was undertaken in a population of Belgian sports divers. Thirty-seven divers who suffered from neurological DCS were compared with matched control divers who never had DCS. All divers were investigated with transesophageal contrast echocardiography for the presence of PFO. PFO size was semiquantified on the basis of the amount of contrast passage. Divers with DCS with lesions localized in the high cervical spinal cord, cerebellum, inner ear organs, or cerebrum had a significantly higher prevalence of PFO than divers with DCS localizations in the lower spinal cord. For unexplained DCS (DCS without commission of any diving procedural errors), this difference was significant for large PFOs only. We conclude that PFO plays a significant role in the occurrence of unexplained cerebral DCS, but not of spinal DCS. We further stress the importance of standardization and semiquantification of future PFO studies that use transesophageal contrast echocardiography.
Hypoproteinemia, strong-ion difference, and acid-base status in critically ill patients
Authors: Wilkes Peter
Published: December 2017

The present study was a prospective, nonrandomized, observational examination of the relationship among hypoproteinemia and electrolyte and acid-base status in a critical care population of patients. A total of 219 arterial blood samples reviewed from 91 patients was analyzed for arterial blood gas, electrolytes, lactate, and total protein. Plasma strong-ion difference ([SID]) was calculated from [Na+] + [K+] − [Cl−] − [La−]. Total protein concentration was used to derive the total concentration of weak acid ([A]tot). [A]tot encompassed a range of 18.7 to 9.0 meq/l, whereas [SID] varied from 48.1 to 26.6 meq/l and was directly correlated with [A]tot. The decline in [SID] was primarily attributable to an increase in [Cl−]. A direct correlation was also noted between[Formula: see text] and [SID], but not between [Formula: see text] and [A]tot. The decrease in [SID] and [Formula: see text] was such that neither [H+] nor [[Formula: see text]] changed significantly with [A]tot.
Head-down-tilt bed rest alters forearm vasodilator and vasoconstrictor responses
Authors: Shoemaker J. Kevin , Hogeman Cindy S. , Silber David H. , Gray Kristen , Herr Michael , Sinoway Lawrence I.
Published: December 2017

To test the hypothesis that head-down-tilt bed rest (HDBR) for 14 days alters vascular reactivity to vasodilatory and vasoconstrictor stimuli, the reactive hyperemic forearm blood flow (RHBF, measured by venous occlusion plethysmography) and mean arterial pressure (MAP, measured by Finapres) responses after 10 min of circulatory arrest were measured in a control trial ( n = 20) and when sympathetic discharge was increased by a cold pressor test (RHBF + cold pressor test; n = 10). Vascular conductance (VC) was calculated (VC = RHBF/MAP). In the control trial, peak RHBF at 5 s after circulatory arrest (34.1 ± 2.5 vs. 48.9 ± 4.3 ml ⋅ 100 ml−1 ⋅ min−1) and VC (0.34 ± 0.02 vs. 0.53 ± 0.05 ml ⋅ 100 ml−1 ⋅ min−1 ⋅ mmHg−1) were reduced in the post- compared with the pre-HDBR tests ( P < 0.05). Total excess RHBF over 3 min was diminished in the post- compared with the pre-HDBR trial (84.8 vs. 117 ml/100 ml, P < 0.002). The ability of the cold pressor test to lower forearm blood flow was less in the post- than in the pre-HDBR test ( P < 0.05), despite similar increases in MAP. These data suggest that regulation of vascular dilation and the interaction between dilatory and constrictor influences were altered with bed rest.
Qualitative aspects of exertional dyspnea in patients with interstitial lung disease
Authors: O’Donnell Denis E. , Chau Laurence K. L. , Webb Katherine A.
Published: December 2017

We compared qualitative and quantitative aspects of perceived exertional dyspnea in patients with interstitial lung disease (ILD) and normal subjects and sought a physiological rationale for their differences. Twelve patients with ILD [forced vital capacity = 64 ± 4 (SE) %predicted] and 12 age-matched normal subjects performed symptom-limited incremental cycle exercise tests with measurements of dyspnea intensity (Borg scale), ventilation, breathing pattern, operational lung volumes, and esophageal pressures (Pes). Qualitative descriptors of dyspnea were selected at exercise cessation. Both groups described increased “work and/or effort” and “heaviness” of breathing; only patients with ILD described “unsatisfied inspiratory effort” (75%), “increased inspiratory difficulty” (67%), and “rapid breathing” (58%) ( P < 0.05 patients with ILD vs. normal subjects). Borg-O2 uptake (V˙o 2) and Borg-ventilation slopes were significantly greater during exercise in patients with ILD ( P < 0.01). At peak exercise, when dyspnea intensity and inspiratory effort (Pes-to-maximal inspiratory pressure ratio) were similar, the distinct qualitative perceptions of dyspnea in patients with ILD were attributed to differences in dynamic ventilatory mechancis, i.e., reduced inspiratory capacity, heightened Pes-to-tidal volume ratio, and tachypnea. Factors contributing to dyspnea intensity in both groups were also different: the best correlate of the Borg-V˙o 2slope in patients with ILD was the resting tidal volume-to-inspiratory capacity ratio ( r = 0.58, P < 0.05) and in normal subjects was the slope of Pes-to-maximal inspiratory pressure ratio overV˙o 2( r = 0.60, P < 0.05).
Hydration effects on physiological strain of horses during exercise-heat stress
Authors: Geor Raymond J. , McCutcheon Laura Jill
Published: December 2017

This study examined the effects of hyperhydration, exercise-induced dehydration, and oral fluid replacement on physiological strain of horses during exercise-heat stress. On three occasions, six horses completed a 90-min exercise protocol (50% maximal O2uptake, 34.5°C, 48% relative humidity) divided into two 45-min periods ( exercise I and exercise II) with a 15-min recovery between exercise bouts. In random order, horses received no fluid (NF), 10 liters of water (W), or a carbohydrate-electrolyte solution (CE) 2 h before exercise and between exercise bouts. Compared with NF, preexercise hyperhydration (W and CE) did not alter heart rate, cardiac output (Q˙), stroke volume (SV), core body temperature, sweating rate (SR), or sweating sensitivity during exercise I. In contrast, after exercise II, exercise-induced dehydration in NF (decrease in body mass: NF, 5.6 ± 0.8%; W, 1.1 ± 0.4%; CE, 1.0 ± 0.2%) resulted in greater heat storage, with core body temperature ∼1.0°C higher compared with W and CE. In exercise II, the greater thermal strain in NF was associated with significant ( P < 0.05) decreases inQ˙ (10 ± 2%), SV (9 ± 3%), SR, and sweating sensitivity. We concluded that 1) preexercise hyperhydration provided no thermoregulatory advantage; 2) maintenance of euhydration by oral fluid replacement (∼85% of sweat fluid loss) during exercise in the heat was reflected in higher Q˙, SV, and SR with decreased heat storage; and 3) W or an isotonic CE solution was equally effective in reducing physiological strain associated with exercise-induced dehydration and heat stress.
Spaceflight has compartment- and gene-specific effects on mRNA levels for bone matrix proteins in rat femur
Authors: Evans Glenda L. , Morey-Holton Emily , Turner Russell T.
Published: December 2017

In the present study, we evaluated the possibility that the abnormal bone matrix produced during spaceflight may be associated with reduced expression of bone matrix protein genes. To test this possibility, we investigated the effects of a 14-day spaceflight (SLS-2 experiment) on steady-state mRNA levels for glyceraldehyde-3-phosphate dehydrogenase (GAPDH), osteocalcin, osteonectin, and prepro-α(1) subunit of type I collagen in the major bone compartments of rat femur. There were pronounced site-specific differences in the steady-state levels of expression of the mRNAs for the three bone matrix proteins and GAPDH in normal weight-bearing rats, and these relationships were altered after spaceflight. Specifically, spaceflight resulted in decreases in mRNA levels for GAPDH (decreased in proximal metaphysis), osteocalcin (decreased in proximal metaphysis), osteonectin (decreased in proximal and distal metaphysis), and collagen (decreased in proximal and distal metaphysis) compared with ground controls. There were no changes in mRNA levels for matrix proteins or GAPDH in the shaft and distal epiphysis. These results demonstrate that spaceflight leads to site- and gene-specific decreases in mRNA levels for bone matrix proteins. These findings are consistent with the hypothesis that spaceflight-induced decreases in bone formation are caused by concomitant decreases in expression of genes for bone matrix proteins.
Cadaver validation of skeletal muscle measurement by magnetic resonance imaging and computerized tomography
Authors: Mitsiopoulos N. , Baumgartner R. N. , Heymsfield S. B. , Lyons W. , Gallagher D. , Ross R.
Published: December 2017

Magnetic resonance imaging (MRI) and computerized tomography (CT) are promising reference methods for quantifying whole body and regional skeletal muscle mass. Earlier MRI and CT validation studies used data-acquisition techniques and data-analysis procedures now outdated, evaluated anatomic rather than adipose tissue-free skeletal muscle (ATFSM), studied only the relatively large thigh, or found unduly large estimation errors. The aim of the present study was to compare arm and leg ATFSM cross-sectional area estimates (cm2) by using standard MRI and CT acquisition and image-analysis methods with corresponding cadaver estimates. A second objective was to validate MRI and CT measurements of adipose tissue embedded within muscle (interstitial adipose tissue) and surrounding muscle (subcutaneous adipose tissue). ATFSM area ( n = 119) by MRI [38.9 ± 22.3 (SD) cm2], CT (39.7 ± 22.8 cm2), and cadaver (39.5 ± 23.0 cm2) were not different ( P > 0.001), and both MRI and CT estimates of ATFSM were highly correlated with corresponding cadaver values [MRI: r = 0.99, SE of estimate (SEE) 3.9 cm2, P < 0.001; and CT: r = 0.99, SEE = 3.8 cm2, P < 0.001]. Similarly good results were observed between MRI- and CT-measured vs. cadaver-measured interstitial and subcutaneous adipose tissue. For MRI-ATFSM the intraobserver correlation for duplicate measurements in vivo was 0.99 [SEE = 8.7 cm2(2.9%), P < 0.001]. These findings strongly support the use of MRI and CT as reference methods for appendicular skeletal muscle, interstitial and subcutaneous adipose tissue measurement in vivo.
Potentiation of hypoxic ventilatory response by hyperoxia in the conscious rat: putative role of nitric oxide
Authors: Gozal David
Published: December 2017

In humans, the hypoxic ventilatory response (HVR) is augmented when preceded by a short hyperoxic exposure (Y. Honda, H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. J. Appl. Physiol. 81: 1627–1632, 1996). To examine whether neuronal nitric oxide synthase (nNOS) is involved in such hyperoxia-induced HVR potentiation, 17 male Sprague-Dawley adult rats underwent hypoxic challenges (10% O2-5% CO2-balance N2) preceded either by 10 min of room air (−O2) or of 100% O2(+O2). At least 48 h later, similar challenges were performed after the animals received the selective nNOS inhibitor 7-nitroindazole (25 mg/kg ip). In −O2runs, minute ventilation (V˙e) increased from 121.3 ± 20.5 (SD) ml/min in room air to 191.7 ± 23.8 ml/min in hypoxia ( P< 0.01). After +O2,V˙e increased from 114.1 ± 19.8 ml/min in room air to 218.4 ± 47.0 ml/min in hypoxia (+O2vs. −O2: P < 0.005, ANOVA). After 7-nitroindazole administration, HVR was not affected in the −O2treatment group withV˙e increasing from 113.7 ± 17.8 ml/min in room air to 185.8 ± 35.0 ml/min in hypoxia ( P < 0.01). However, HVR potentiation in +O2-exposed animals was abolished (111.8 ± 18.0 ml/min in room air to 184.1 ± 35.6 ml/min in hypoxia; +O2vs. −O2: P not significant). We conclude that in the conscious rat nNOS activation mediates essential components of the HVR potentiation elicited by a previous short hyperoxic exposure.
Rib cage muscle interaction in airway pressure generation
Authors: Legrand Alexandre , Wilson Theodore A. , De Troyer André
Published: December 2017

We have previously demonstrated in dogs that the change in airway opening pressure (ΔPao) produced by isolated maximum activation of the parasternal intercostal or triangularis sterni muscle in a single interspace, the sternomastoids, and the scalenes is proportional to the product of muscle mass and the fractional change in muscle length per unit volume increase of the relaxed chest wall. In the present study, we have assessed the interactions between these muscles by comparing the ΔPao obtained during simultaneous activation of a pair of muscles (measured ΔPao) to the sum of the ΔPao values obtained during their separate activation (predicted ΔPao). Measured and predicted ΔPao values were compared for the following pairs of muscles: the parasternal intercostals in two interspaces, the parasternal intercostals in one interspace and either the sternomastoids or the scalenes, two segments of the triangularis sterni, and the interosseous intercostals in two contiguous interspaces. For all these pairs, the measured ΔPao was within ∼10% of the predicted value. We therefore conclude that 1) the pressure changes generated by the rib cage muscles are essentially additive; and 2) measurements of the mass of a particular muscle and of its fractional change in length during passive inflation can be used to estimate the potential pressure-generating ability of the muscle during coordinated activity as well as during isolated activation.
Neuropeptide Y and Y1-receptor agonists increase blood flow through arteriovenous anastomoses in rat tail
Authors: Heath Martha E.
Published: December 2017

The purpose of this study was to characterize neuropeptide Y (NPY)-induced vasodilation in the rat tail. Sterile surgical technique was used (with pentobarbital sodium anesthesia) to equip rats with a jugular catheter and a blind-ended thermocouple reentrant tube next to the carotid artery. Tail skin and core temperature were measured with thermocouples during experiments. Tail skin blood flow was monitored with a laser Doppler flowmeter, and tail total blood flow and volume were measured with plethysmography. After baseline data were collected, saline, NPY (16, 32, 64, and 128 μg/kg), [Leu31Pro34]NPY (63.25 μg/kg), or NPY[13–36] (44.7 μg/kg) was administered intravenously. Tail total blood flow, volume, and tail skin temperature increased, whereas tail skin blood flow and core temperature decreased in response to both NPY- and the Y1-receptor agonist [Leu31Pro34]NPY but not in response to saline or NPY[13–36]. Studies conducted with the use of color microspheres demonstrated that arteriovenous anastomoses are involved in this NPY-induced vasodilation.
Differences in rat skeletal muscles after incline and decline running
Authors: Lynn R. , Talbot J. A. , Morgan D. L.
Published: December 2017

Rats were trained for 5 days by running on either an inclined or declined treadmill. Three days later, the rats were anesthetized, and angle-torque curves were plotted for the vastus intermedius muscles. The maximum active torque was generated at significantly greater muscle lengths for muscles from decline-trained rats compared with incline-trained rats. Sixteen muscles were then fixed and acid digested, and fiber lengths and sarcomere lengths were measured. The estimated average number of sarcomeres in series was greater in muscle fibers from decline-trained animals. Fourteen other muscles underwent a test series of lengthening contractions, all from the same knee angle. Torque fell less and the optimum angle shifted less for muscles from decline-trained animals, showing that the decline-trained muscles were more resistant to changes in mechanical parameters that indicate damage. These results support but do not prove the proposal that the lesser damage from a series of eccentric contractions seen in muscles trained by prior eccentric contractions is due to a greater number of sarcomeres in series.
Fast and slow components of cerebral blood flow response to step decreases in end-tidal P CO 2 in humans
Authors: Poulin Marc J. , Liang Pei-Ji , Robbins Peter A.
Published: December 2017

This study examined the dynamics of the middle cerebral artery (MCA) blood flow response to hypocapnia in humans ( n = 6) by using transcranial Doppler ultrasound. In a control protocol, end-tidal[Formula: see text]([Formula: see text]) was held near eucapnia (1.5 Torr above resting) for 40 min. In a hypocapnic protocol, [Formula: see text]was held near eucapnia for 10 min, then at 15 Torr below eucapnia for 20 min, and then near eucapnia for 10 min. During both protocols, subjects hyperventilated throughout and[Formula: see text] and end-tidal[Formula: see text] were controlled by using the dynamic end-tidal forcing technique. Beat-by-beat values were calculated for the intensity-weighted mean velocity ([Formula: see text] IWM), signal power ([Formula: see text]), and their instantaneous product ([Formula: see text] IWM). A simple model consisting of a delay, gain terms, time constants (τf,on, τf,off) and baseline levels of flow for the on- and off-transients, and a gain term (gs) and time constant (τs) for a second slower component was fitted to the hypocapnic protocol. The cerebral blood flow response to hypocapnia was characterized by a significant ( P < 0.001) slow progressive adaptation in[Formula: see text] IWM, with gs = 1.26 %/Torr and τs = 427 s, that persisted throughout the hypocapnic period. Finally, the responses at the onset and relief of hypocapnia were asymmetric ( P < 0.001), with τf,on (6.8 s) faster than τf,off (14.3 s).
Expanded blood volumes contribute to the increased cardiovascular performance of endurance-trained older men
Authors: Hagberg James M. , Goldberg Andrew P. , Lakatta Loretta , O’Connor Frances C. , Becker Lewis C. , Lakatta Edward G. , Fleg Jerome L.
Published: December 2017

To determine whether expanded intravascular volumes contribute to the older athlete’s higher exercise stroke volume and maximal oxygen consumption (V˙o 2 max), we measured peak upright cycle ergometry cardiac volumes (99mTc ventriculography) and plasma (125I-labeled albumin) and red cell (NaCr51) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athletes had ∼40% higherV˙o 2 max values than did the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (all P < 0.05). Athletes had larger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m2, P < 0.05) and 17% larger end-diastolic volume indexes. In the total group,V˙o 2 maxcorrelated with plasma, red cell, and total blood volumes ( r = 0.61–0.70, P < 0.01). Peak exercise stroke volume was correlated directly with the blood volume variables ( r = 0.59–0.67, P < 0.01). Multiple regression analyses showed that fat-free mass and plasma or total blood volume, but not red cell volume, were independent determinants ofV˙o 2 max and peak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest to peak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higher peak exercise left ventricular end-diastolic volume, stroke volume, and cardiac output and hence the higherV˙o 2 max in master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.
Glucose infusion partially attenuates glucose production and increases uptake during intense exercise
Authors: Manzon Anthony , Fisher Simon J. , Morais José A. , Lipscombe Lorraine , Guimond Marie-Claude , Nessim Sharon J. , Sigal Ronald J. , Halter Jeffrey B. , Vranic Mladen , Marliss Errol B.
Published: December 2017

Glucose infusion can prevent the increase in glucose production (Ra) and increase glucose uptake (Rd) during exercise of moderate intensity. We postulated that 1) because in postabsorptive intense exercise (>80% maximal O2 uptake) the eightfold increase in Ra may be mediated by catecholamines rather than by glucagon and insulin, exogenous glucose infusion would not prevent the Ra increment, and 2) such infusion would cause greater Rd. Fit young men were exercised at >85% maximal O2uptake for 14 min in the postabsorptive state [controls (Con), n = 12] or at minute 210 of a 285-min glucose infusion. In seven subjects, the infusion was constant (CI; 4 mg ⋅ kg−1 ⋅ min−1), and in seven subjects it was varied (VI) to mimic the exercise Ra response in Con. Although glucose suppressed Ra to zero (with glycemia ∼6 mM and insulin ∼150 pM), an endogenous Ra response to exercise occurred, to peak increments two-thirds those in Con, in both CI and VI. Glucagon was unchanged, and very small increases in the glucagon-to-insulin ratio occurred in all three groups. Catecholamine responses were similar in all three groups, and correlation coefficients of Ra with plasma norepinephrine and epinephrine were significant in all. In all CI and VI, Rd at rest was 2× Con, increased earlier in exercise, and was higher for the 1 h of recovery with glucose infusion. Thus the Ra response was only partly attenuated, and the catecholamines are likely to be the regulators. This suggests that an acute endogenous Ra rise is possible even in the postprandial state. Furthermore, the fact that more circulating glucose is used by muscle during exercise and early recovery suggests that muscle glycogen is spared.