Description

The Journal of Applied Physiology publishes original papers that deal with diverse areas of research in applied physiology, especially those emphasizing adaptive and integrative mechanisms. Adaptive physiology includes 1) inherent adaptations such as those related to development, aging, and pathophysiological conditions and 2) adaptations to the external environment such as those occurring with exercise, microgravity, hypoxia, hypo- and hyperbaria, and hypo- and hyperthermic conditions. Integrative physiology includes 1) horizontal integration across organ systems and 2) vertical integration from molecule to cell to organ. In all areas of applied physiology, the use of cutting-edge techniques including molecular and cellular biology is strongly encouraged.

Publisher details

American Physiological Society

Publications in this journal

• Short-term creatine supplementation decreases reactive oxygen species content with no changes in expression and activity of antioxidant enzymes in skeletal muscle

  Authors: Lucas Guimarães-Ferreira, Carlos Hermano J Pinheiro, Frederico Gerlinger-Romero, Kaio F Vitzel, Renato T Nachbar, Rui Curi, Maria Tereza Nunes

  Journal of Applied Physiology.

• Counterpoint: Exercise-induced intrapulmonary shunting is real.

  Authors: Andrew T Lovering, Marlowe W Eldridge, Michael K Stickland

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):994-7.

• Last Word on Point:Counterpoint: Exercise-induced intrapulmonary shunting is imaginary vs. real.

  Authors: Susan R Hopkins, I Mark Olfert, Peter D Wagner

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):1002.

• Estimating the diameter of airways susceptible for collapse using crackle sound.

  Authors: Arnab Majumdar, Zoltán Hantos, Jozsef Tolnai, Harikrishnan Parameswaran, Robert S Tepper, Bela Suki

  Journal of applied physiology (Bethesda, Md. : 1985).

  Airways that collapse during deflation generate a crackle sound when they reopen during subsequent reinflation. Since each crackle is associated with the reopening of a collapsed airway, theAirways that collapse during deflation generate a crackle sound when they reopen during subsequent reinflation. Since each crackle is associated with the reopening of a collapsed airway, the likelihood of an airway to be a crackle source is identical to its vulnerability to collapse. To investigate this vulnerability of airways to collapse, crackles were recorded during the first inflation of six excised rabbit lungs from the collapsed state, and subsequent reinflations from 5, 2, 1 and 0 cmH2O end-expiratory pressure (EEP) levels. We derived a relationship between the amplitude of a crackle sound at the trachea and the generation number (n) of the source airway where the crackle was generated. Using an asymmetrical tree model of the rabbit airways with elastic walls, airway vulnerability to collapse was also determined in terms of airway diameter D. During the reinflation from EEP=0 cmH2O, the most vulnerable airways were estimated to be centered at n=12 with a peak. Vulnerability in terms of D ranged between 0.1 and 1.3 mm with a peak at 0.3 mm. During the inflation from the collapsed state, however, vulnerability was much less localized to a particular n or D with maximum values of n=8 and D=0.75 mm. Numerical simulations using a tree model that incorporates airway opening and closing support these conclusions. Thus, our results indicate that there are airways of a given range of diameters which can become unstable during deflation and vulnerable to collapse and subsequent injury. Key words: p-v curve, inflation, trapped gas, avalanche.

• Cerebral blood flow during exercise; mechanisms of regulation.

  Authors: Shigehiko Ogoh, Philip N Ainslie

  Journal of applied physiology (Bethesda, Md. : 1985).

  The response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed, and is strongly regulated by cerebral autoregulation and the partialThe response of cerebral vasculature to exercise is different from other peripheral vasculature; it has a small vascular bed, and is strongly regulated by cerebral autoregulation and the partial pressure of arterial carbon dioxide (PaCO2). In contrast to other organs, the traditional thinking is that total cerebral blood flow (CBF) remains relatively constant and is largely unaffected by a variety of conditions, including those imposed during exercise. Recent research, however, indicates that cerebral neuronal activity and metabolism drives an increase in CBF during exercise. Increases in exercise intensity up to approximately 60% of maximal oxygen uptake produce elevations in CBF, after which CBF decreases towards baseline values because of lower PaCO2 via hyperventilation-induced cerebral vasoconstriction. This finding indicates that during heavy exercise CBF decreases despite the cerebral metabolic demand. In contrast, this reduced CBF during heavy exercise lowers cerebral oxygenation and therefore may act as an independent influence on central fatigue. In this review, we highlight methodological considerations relevant for the assessment of CBF, and then summarize the integrative mechanisms underlying the regulation of CBF at rest and during exercise. In addition, we examine how CBF regulation during exercise is altered by exercise training, hypoxia and aging, and suggest avenues for future research. Key words: Hypoxia, Cerebral autoregulation, Autonomic Nervous System, Carbon Dioxide Tension.

• Estrogen and HRT promote a pro-anabolic skeletal muscle environment in older women.

  Authors: Peter M Tiidus

  Journal of applied physiology (Bethesda, Md. : 1985).

  N/A Key words: Estrogen, skeletal muscle, Hormone replacement therapy.

• The Effect of Nandrolone Decanoate Administration on Recovery from Bupivacaine-induced Muscle Injury.

  Authors: James P White, Kristen A Baltgalvis, Shuichi Sato, L Britt Wilson, James A Carson

  Journal of applied physiology (Bethesda, Md. : 1985).

  Although testosterone administration elicits well documented anabolic effects on skeletal muscle mass, the enhancement of muscle regeneration after injury has not been widely examined. The purpose ofAlthough testosterone administration elicits well documented anabolic effects on skeletal muscle mass, the enhancement of muscle regeneration after injury has not been widely examined. The purpose of this study was to determine if anabolic steroid administration improves skeletal muscle regeneration from bupivacaine-induced injury. Male C57BL/6 mice were castrated 2 weeks prior to muscle injury induced by an intramuscular bupivacaine injection into the tibialis anterior (TA) muscle. Control mice received an intramuscular PBS injection. Anabolic steroid (nandrolone decanoate (ND), 6mg/kg) or sesame seed oil was administered at the time of initial injury and continued every 7 days for the study's duration. Mice were randomly assigned to one of 4 treatment groups for 5, 14 or 42 days of recovery as follows: 1) Control (uninjured); 2) nandrolone decanoate only (uninjured + ND); 3) Bupivacaine only (Injured); or 4) Bupivacaine + ND (Injured + ND). TA morphology, protein and gene expression was analyzed at 14 and 42 days after injury, protein expression was analyzed at 5 days after injury. After 14d of recovery the Injury and Injury + ND treatments induced small diameter myofiber incidence, and also decreased mean myofiber area. The increase in small myofiber incidence was 65% greater in Injury + ND muscle when compared to Injury alone. At 14d, Injury + ND induced a 5-fold increased in muscle IGF-1 mRNA expression, which was greater than injury alone. Muscle Akt activity and GSK3beta activity were also induced by Injury + ND at 14d of recovery, but not by Injury alone. ND had a main effect for increasing muscle MyoD and Cyclin D1 mRNA expression at 14d. After 42d of recovery, Injury + ND increased large diameter myofiber incidence compared to Injury only. Nandrolone decanoate administration can enhance castrated mouse muscle regeneration during the recovery from bupivacaine-induced injury. Key words: Muscle Regeneration, Anabolic Steroids, Myotoxin, hypertrophy.

• Pulmonary responses to subacute ozone exposure in obese versus lean mice.

  Authors: Stephanie A Shore, Jason E Lang, David I Kasahara, Frank L Lu, Norah G Verbout, Huiqing Si, Erin S Williams, Raya D Terry, Anna Lee, Richard A Johnston

  Journal of applied physiology (Bethesda, Md. : 1985).

  The purpose of this study was to determine whether obesity affects pulmonary responses following a three day ozone exposure. Obese db/db and lean wildtype mice were exposed to ozone (0.3 ppm) for 72The purpose of this study was to determine whether obesity affects pulmonary responses following a three day ozone exposure. Obese db/db and lean wildtype mice were exposed to ozone (0.3 ppm) for 72 h. In wildtype mice, ozone exposure caused pulmonary injury and inflammation and these events were associated with reduced pulmonary compliance. In db/db mice, ozone-induced neutrophil recruitment to the lung was reduced and no reduction in compliance was observed. Similar results were obtained in obese Cpe(fat) mice, indicating that loss of leptin signaling in db/db mice does not account for these obesity-related changes. To examine the role of interleukin (IL)-6 in this obesity-related difference in ozone responsiveness, wildtype and IL-6 deficient mice were raised on 10% or 60% fat diets. Compared to 10% fat-fed mice, wildtype 60% fat-fed mice were obese, and had reduced neutrophil recruitment following ozone. IL-6 deficiency reduced ozone-induced neutrophil recruitment in 10% fat-fed mice. In contrast, in obese mice, no effect of IL-6 deficiency on neutrophil recruitment was observed. Obesity-related differences in the effect of ozone on compliance were observed in both wildtype and IL-6 deficient mice. Obesity-related differences in serum IL-6 were observed and may account for obesity-related differences in the effect of IL-6 deficiency on neutrophil recruitment. In summary, the neutrophilic inflammation induced by prolonged low level ozone exposure was attenuated in obese mice and appeared to result from an absence of IL-6 dependent neutrophil recruitment in the obese mice. Key words: neutrophil, marophage, sTNFR1, dynamic compliance.

• Synergistic and antagonistic interactions in the rat forelimb: acute effects of coactivation.

  Authors: Huub Maas, Peter A Huijing

  Journal of applied physiology (Bethesda, Md. : 1985).

  The goals of the present study were (a) to assess effects of antagonist coactivation on interactions between synergistic muscles and (b) to quantify the extent of epimuscular myofascial forceThe goals of the present study were (a) to assess effects of antagonist coactivation on interactions between synergistic muscles and (b) to quantify the extent of epimuscular myofascial force transmission between synergistic and antagonistic muscles in the rat forelimb. Connective tissues enveloping the muscle bellies in the antebrachium were left intact. Forces exerted at the distal tendons of flexor carpi ulnaris (FCU), palmaris longus (PL) and extensor carpi ulnaris (ECU) muscles were measured at various FCU lengths for two different stimulation protocols: (i) simultaneous stimulation of ulnar/median nerve complex (exciting all wrist flexors, including synergistic FCU and PL) and radial nerve (exciting all wrist extensors, including antagonistic ECU) and (ii) stimulation of the ulnar/median nerve exclusively. PL and ECU were kept at a constant length. In addition, muscle forces were measured during stimulation of one of the indicated nerves with later addition of stimulation of the second nerve during the maintained tetanic contraction. Coactivation of antagonistic muscles increased FCU isometric forces (on average by 10% of optimal force) and PL forces (on average by 13% of maximal force), but mechanical interaction between FCU and PL was unchanged. Changing the length and relative position of FCU significantly affected PL (by 20%) as well as ECU forces (by 8%). In addition, distal tetanic force of FCU kept at a constant high length was determined by the order of nerve stimulation onset. These results indicate effects of myofascial pathways between synergistic and antagonistic muscles in the rat forelimb. Coactivation may enhance the stiffness of connective tissues between muscles, but the present data suggest that activation of all wrist flexors already preloaded the myofascial pathways to the greatest extent. The stimulation order effects were explained by dynamic features of muscle and connective tissues (i.e., length-history dependence and viscoelasticity). Key words: force transmission, skeletal muscle, connective tissue, sarcomere length distribution.

• EFFECTS OF THE MOLECULAR WEIGHT OF TENSE-STATE POLYMERIZED BOVINE HEMOGLOBIN ON BLOOD PRESSURE AND VASOCONSTRICTION.

  Authors: Pedro Cabrales, Guoyong Sun, Yipin Zhou, David R Harris, Amy G Tsai, Marcos Intaglietta, Andre F Palmer

  Journal of applied physiology (Bethesda, Md. : 1985).

  Despite recent advances in the design of hemoglobin (Hb)-based oxygen carriers (HBOCs), vasoconstriction, presumably caused by nitric oxide (NO) scavenging, vessel wall hyperoxygenation and/orDespite recent advances in the design of hemoglobin (Hb)-based oxygen carriers (HBOCs), vasoconstriction, presumably caused by nitric oxide (NO) scavenging, vessel wall hyperoxygenation and/or extravasation, has been identified as the principal road block hampering commercial development of HBOCs. This study was designed to analyze systemic and microvascular responses to the molecular weight (MW) and plasma concentration of tense (T)-state polymerized bovine Hb (PolybHb) solutions. Experiments were performed using the hamster window chamber model subjected to successive hypervolemic infusions of T-state PolybHb solutions. PolybHb plasma concentrations were evaluated, namely: 0.5, 1.0 and 1.5 g/dl, respectively. Infusion of PolybHb solutions with MWs above 500 kDa elicited hypertension and vasoconstriction proportional to the plasma concentration and inversely proportional to the PolybHb cross-link density. However, two high MW PolybHb solutions PolybHb(40:1)high PolybHb(50:1)high did not elicit vasoconstriction at all concentrations studied, while PolybHb(50:1)high only elicited moderate hypertension at the highest concentration studied. In contrast, infusion of PolybHb solutions with MWs below 500 kDa elicited significant hypertension and vasoconstriction compared to PolybHb solutions with MWs above 500 kDa that was proportional to the plasma concentration, and inversely proportional to the PolybHb cross-link density. We present promising results for highly cross-linked T-state PolybHb solutions with MWs above 500 kDa (PolybHb(40:1)high PolybHb(50:1)high), which supports the concept that HBOC size/molecular weight influences its proximity to the vascular endothelium and molecular diffusivity. The hemodynamics of HBOC within the plasma layer surrounding the abluminal side endothelium regulates NO production and consumption, vessel oxygen flux and extravasation. Although mechanistically attractive, neither of these hypotheses can be directly tested in vivo, and will require further investigation. Key words: Microcirculation, polymerized hemoglobin, hemoglobin-based oxygen carrier, vasoconstriction.

• Protective mechanical ventilation does not exacerbate lung function impairment or lung inflammation following influenza A infection.

  Authors: Graeme R Zosky, Vincenzo Cannizzaro, Zoltán Hantos, Peter D Sly

  Journal of applied physiology (Bethesda, Md. : 1985).

  The degree to which mechanical ventilation induces ventilator associated lung injury (VALI) is dependent on the initial acute lung injury (ALI). Viral induced ALI is poorly studied and this studyThe degree to which mechanical ventilation induces ventilator associated lung injury (VALI) is dependent on the initial acute lung injury (ALI). Viral induced ALI is poorly studied and this study aimed to determine if ALI induced by a clinically relevant infection is exacerbated by protective mechanical ventilation. Adult female BALB/c mice were inoculated with 10(4.5) pfu of Influenza A/Mem71 in 50 microL of media or media alone. Mice were anaesthetised, tracheostomised and mechanically ventilated for 2 hours with a protective ventilation strategy. Lung mechanics were measured periodically throughout the ventilation period using a modification of the forced oscillation technique to obtain measures of airway resistance (Raw) and coefficients of tissue damping (G) and tissue elastance (H). Thoracic gas volume (TGV) was measured and used to obtain specific Raw, G and H. At the end of the ventilation period a bronchoalveolar lavage sample was collected to measure inflammatory cells, MIP-2, IL-6, TNF-alpha and protein leak. Influenza infection caused significant increases in inflammatory cells, protein leak and deterioration in lung mechanics that were not exacerbated by mechanical ventilation in contrast to previous studies using bacterial and mouse specific viral infection. This study highlighted the importance of type and severity of lung injury in determining outcome following mechanical ventilation. Key words: ventilator associated lung injury, viral infection, BALB/c.

• Point: Counterpoint - Afferent feedback from fatigued locomotor muscles is / is not an important determinant of endurance exercise performance.

  Authors: Markus Amann, Niels Henry Secher, Samuele Maria Marcora

  Journal of applied physiology (Bethesda, Md. : 1985).

  None.

• Insulin Resistance without Elevated Mammalian Target of Rapamycin Complex 1 Activity in Muscles of Mice Fed a High Fat Diet.

  Authors: Thomas H Reynolds, Nicholas Cinquino, Marcus Anthony, Charles B Phelps, Eli Zachary Berk

  Journal of applied physiology (Bethesda, Md. : 1985).

  The mammalian target of rapamycin complex 1 (mTORC1) appears to mediate the development of insulin resistance in cultured cells. We studied in vivo insulin action and mTORC1 signaling in skeletalThe mammalian target of rapamycin complex 1 (mTORC1) appears to mediate the development of insulin resistance in cultured cells. We studied in vivo insulin action and mTORC1 signaling in skeletal muscles of mice fed a normal chow diet (CON) or a high fat diet (HFD) for 16 weeks. In vivo insulin action was assessed by measuring glucose tolerance (GT), insulin tolerance (IT), and insulin-assisted GT (IAGT). Although glucose GT was not altered, the HFD significantly reduced IT and IAGT. Acute treatment with rapamycin, a highly specific inhibitor of mTORC1, did not improve GT, IT, or IAGT in mice fed a CON or HFD. The phosphorylation of S6K on Thr(389), a surrogate measure of mTORC1 kinase activity, was assessed in skeletal muscles of mice 15 min following an intraperitoneal injection of insulin or saline. In the basal state and following insulin stimulation, the phosphorylation of S6K on Thr(389) was similar in muscles of mice fed a HFD compared to mice fed a CON diet, indicating that mTORC1 activity is not elevated. Furthermore, the phosphorylation of insulin receptor substrate 1 (IRS1) on Ser(636), a site phosphorylated by the mTORC1, was similar in muscles of mice fed a HFD compared to a CON diet. Taken together, these findings indicate that in vivo insulin resistance can occur without an increase in mTORC1 activity in skeletal muscle and that inhibiting mTORC1 with rapamycin does not improve insulin action. Key words: signal transduction, type 2 diabetes, obesity.

• Non-invasive quantification of heterogeneous lung growth following extensive lung resection by high resolution computed tomography.

  Authors: Cuneyt Yilmaz, Priya Ravikumar, D Merrill Dane, Dennis J Bellotto, Robert L Johnson, Connie C W Hsia

  Journal of applied physiology (Bethesda, Md. : 1985).

  To quantify the in vivo magnitude and distribution of regional compensatory lung growth following extensive lung resection, we performed high-resolution computed tomography (HRCT) at 15 and 30cmH2OTo quantify the in vivo magnitude and distribution of regional compensatory lung growth following extensive lung resection, we performed high-resolution computed tomography (HRCT) at 15 and 30cmH2O transpulmonary pressures and measured air and tissue (including microvascular blood) volumes within and among lobes in 6 adult male foxhounds before and after balanced 65% lung resection (~32% removed from each side). Each lobe was identified from lobar fissures. Intra-lobar gradients in air and tissue volumes were expressed along standardized x,y,z-coordinate axes. Fractional tissue volume (FTV) was calculated as the volume ratio of tissue/(tissue+air). Following resection compared to before, lobar air and tissue volumes increased 1.8 to 3.5 fold, and whole lung air and tissue volumes were 67% and 90% of normal, respectively. Lobar specific compliance doubled post-resection and whole lung specific compliance normalized. These results are consistent with vigorous compensatory growth in all remaining lobes. Compared to pre-resection, post-resection inter-lobar heterogeneity of FTV, assessed from the coefficient of variation (CV), decreased at submaximal inflation but was unchanged at maximal inflation. The CV of intra-lobar FTV gradients changed variably due to the patchy development of thickened pleura and alveolar septa, with elevated alveolar septal density and connective tissue content in posterior-caudal and peripheral regions of the remaining lobes; these areas likely experienced disproportional mechanical stress. We conclude that HRCT can non-invasively and quantitatively assess the magnitude and spatial heterogeneity of compensatory lung growth. Following extensive resection, heterogeneous regional mechanical lung strain may exceed the level that could be sustained solely by existing connective tissue elements. Key words: Lung air volume, lung tissue volume, specific lung compliance, pneumonectomy.

• Comments on Point:Counterpoint: Exercise-induced intrapulmonary shunting is imaginary vs. real.

  Authors: Richard L Jones, A William Sheel, Robert Naeije, J Michael B Hughes, Melissa L Bates

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):999-1001.

• Last Word on Point:Counterpoint: Exercise-induced intrapulmonary shunting is imaginary vs. real.

  Authors: Andrew T Lovering, Marlowe W Eldridge, Michael K Stickland

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):1003.

• Surround inhibition depends on the force exerted and abnormalities in focal hand dystonia.

  Authors: Sandra Beck, Martin Schubert, Sarah Pirio Richardson, Mark Hallett

  Journal of applied physiology (Bethesda, Md. : 1985).

  There is evidence that surround inhibition (SI), a neural mechanism to enhance contrast between signals, may play a role in primary motor cortex (M1) during movement initiation, while it is deficientThere is evidence that surround inhibition (SI), a neural mechanism to enhance contrast between signals, may play a role in primary motor cortex (M1) during movement initiation, while it is deficient in patients with focal hand dystonia (FHD). To further characterize SI with respect to different force levels, single and paired pulse transcranial magnetic stimulation (TMS) was applied at rest and during index finger movement to evoke potentials in the non-synergistic, abductor policis muscle (APB). In Experiment 1, in nineteen healthy volunteers, SI was tested using single pulse TMS. Motor evoked potentials (MEPs) at rest were compared to those during contraction using four different force levels (5%, 10%, 20% and 40% of maximum force (Fmax)). In Experiment 2 and 3, SI and short intracortical inhibition (SICI) were tested, respectively, in sixteen patients with FHD and twenty age-matched controls for the 10% and 20% Fmax level. The results show that SI was most pronounced for 10% Fmax and abolished for the 40% Fmax level in controls, while FHD patients had no SI at all. In contrast, a loss of SICI was observed in FHD patients, which was more pronounced for 10% Fmax than for 20% Fmax. The current findings suggest that SI is involved in the generation of fine finger movements with low force levels. The greater loss of SICI for the 10% Fmax level in patients with FHD compared to 20% Fmax indicates that this inhibitory mechanism is more abnormal at lower levels of force. Key words: transcranial magnetic stimulation, fine finger movement, movement selection, short intracortical inhibition.

• Calpain and caspase-3 are required for sepsis-induced diaphragmatic weakness.

  Authors: Scott K Powers

  Journal of applied physiology (Bethesda, Md. : 1985).

  NA Key words: diaphragm, weakness, protease, calpain.

• Evidence against a 40{degrees}C core temperature threshold for fatigue in humans.

  Authors: Brett R Ely, Matthew R Ely, Samuel N Cheuvront, Robert W Kenefick, David W DeGroot, Scott J Montain

  Journal of applied physiology (Bethesda, Md. : 1985).

  There is experimental evidence that core temperatures of ~40 degrees C can induce fatigue, but this observation may be confounded by coincident elevations in skin temperatures and maximalThere is experimental evidence that core temperatures of ~40 degrees C can induce fatigue, but this observation may be confounded by coincident elevations in skin temperatures and maximal cardiovascular strain. An observational field study provided the opportunity to examine the validity of a core temperature threshold for fatigue. PURPOSE: To determine if running performance is impaired with attainment of a rectal temperature >40 degrees C when skin temperatures remain modest. METHODS: Seventeen competitive runners (7 women, 8km best 1759+/-78s; 10 men, 8km best 1531+/-60s) completed an 8km track time trial in COOL (WBGT~13 degrees C, n=6), WARM conditions (WBGT~27 degrees C, n=4), or both (n=7). Rectal temperature (Tre), chest skin temperature (Tsk), and heart rate (HR) were logged continuously during the time trial while elapsed time was recorded every 200m. Running velocity when Tre>40 degrees C was compared to running velocity when Tre<40 degrees C for each runner. Additionally, change in running velocity over the last 600m were compared between runners with Tre>40 degrees C and Tre<40 degrees C RESULTS: Twelve runners achieved Tre>40.0 degrees C (n=3 COOL; n=9 WARM) with >/=600m remaining (range: 600-3400m). Average running velocity while Tre<40 degrees C (282+/-27m(.)min(-1)) was not different than when Tre>40 degrees C (279+/-28m(.)min(-1); p=0.82). There were no differences in running velocity during the final 600m between runners with a final Tre>40 degrees C or Tre<40 degrees C (p=0.16). Chest skin temperature ranged from 30-34 degrees C while HR was >95% of age-predicted maximum. CONCLUSION: The observation that runners were able to sustain running velocity despite Tre>40 degrees C is evidence against the idea that 40 degrees C represents a 'critical' core temperature limit to performance. Key words: Pacing, Performance, Body temperature, Ambient temperature.

• Pathophysiological insight into shunted bubbles.

  Authors: Robert Naeije, Vitalie Faoro

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):999-1000; discussion 997-8, 998.

• A potential role for intrapulmonary shunt pathways in pathology.

  Authors: Melissa L Bates

  Journal of applied physiology (Bethesda, Md. : 1985). 107(3):1000-1; discussion 997-8, 998.

• NOS inhibition blunts and delays the compensatory dilation in hypoperfused contracting human muscles.

  Authors: Darren P Casey, Michael J Joyner

  Journal of applied physiology (Bethesda, Md. : 1985).

  We previously demonstrated that skeletal muscle blood flow is restored in the exercising forearm during experimental hypoperfusion via local dilator and/or myogenic mechanisms. This study examinedWe previously demonstrated that skeletal muscle blood flow is restored in the exercising forearm during experimental hypoperfusion via local dilator and/or myogenic mechanisms. This study examined the role of nitric oxide (NO) in the restoration of blood flow to the active muscles during hypoperfusion. Eleven healthy subjects (10M/1F; 25 +/- 1 yrs) performed rhythmic forearm exercise (10% and 20% of maximum) while hypoperfusion was evoked by balloon inflation in the brachial artery above the elbow. Each trial included; baseline, exercise, exercise with inflation, and exercise after deflation (3 min each). FBF (ultrasound), local (brachial artery catheter pressure, BAP), and systemic arterial pressure (MAP; Finometer) were measured. The exercise bouts were repeated during N(G)-monomethyl-L-arginine (L-NMMA) infusion (NO synthase inhibition). Forearm vascular conductance (FVC; ml/min/100mmHg) was calculated from BF (ml/min) and BAP (mmHg). FBF and FVC fell acutely with balloon inflation during all trials (P < 0.01). Recovery of FBF and FVC (inflation - nadir/steady state exercise-nadir) with L-NMMA administration was reduced during 20% exercise (FBF = 77 +/- 7% vs. 88 +/- 8%; FVC = 71 +/- 8% vs. 90 +/- 9%; P < 0.01) but not 10% exercise (FBF = 83 +/- 4% vs. 81 +/- 5%, P = 0.37; FVC = 75 +/- 10% vs. 76 +/- 7%; P = 0.44) compared to the respective control trial. The time to steady state vasodilator response was substantially longer during the L-NMMA trials (10% = 74 +/- 4s vs. 61 +/- 6s; 20% = 53 +/- 4s vs. 41 +/- 4s; P < 0.05). Thus the magnitude and timing of the NO contribution to compensatory dilation during forearm exercise with hypoperfusion is dependent on exercise intensity. These observations suggest that NO is released by contracting muscles or that a portion of the dilation caused by ischemic metabolites is NO dependent. Key words: exercise hyperemia, nitric oxide, vasodilation, hypoperfusion.

• Discerning aortic waves during intra-aortic balloon pumping and their relation to benefits of counterpulsation in humans.

  Authors: Christina Kolyva, George M Pantalos, Guruprasad A Giridharan, John R Pepper, Ashraf W Khir

  Journal of applied physiology (Bethesda, Md. : 1985).

  An explanation of the mechanisms leading to the beneficial hemodynamic effects of the intra-aortic balloon pump (IABP) is lacking. We hypothesized that inflation and deflation of the balloon wouldAn explanation of the mechanisms leading to the beneficial hemodynamic effects of the intra-aortic balloon pump (IABP) is lacking. We hypothesized that inflation and deflation of the balloon would generate a compression (BCW) and an expansion (BEW) wave, respectively, which, when analyzed with wave intensity analysis, could be used to explain the hemodynamic benefits of IABP support. Simultaneous ascending aortic pressure (Pao) and flow rate (Qao) were recorded in 25 patients during control conditions and with IABP support of 1:1 and 1:2. Diastolic aortic pressure augmentation (Paug) and end-diastolic aortic pressure (ED Pao) reduction were calculated from Pao. Energies of the BCW and BEW were obtained by integrating the wave intensity contour over time. Paug was 19.1 mmHg (SD 13.6) during 1:2 support. During 1:1 support significantly higher Paug of 21.1 mmHg (SD 13.4) was achieved (P<0.001). ED Pao decreased from 50.9 mmHg (SD 15.1) to 43.9 mmHg (SD 15.7) (P<0.0001) during 1:1 assistance and the decrease was not statistically different with 1:2. During 1:1 support the energy of BCW was correlated positively to Paug (r = 0.83, P<0.0001) and energy of the BEW correlated negatively to ED Pao (r = 0.78, P<0.005); these relationships were not statistically different during 1:2. In conclusion, the energies of the BCW and BEW are directly related to Paug and ED Pao, which are the conventional hemodynamic parameters indicating IABP benefits. These findings imply a 'cause and effect' mechanism between the energies of BCW and BEW, and IABP hemodynamic effects. Key words: counterpulsation, waves, aortic pressure, aortic flow.

• IMPACT FACTOR AND ITS ROLE IN ACADEMIC PROMOTION: A statement adopted by the International Respiratory Journal Editors Roundtable.

  Authors: Jerome A Dempsey

  Journal of applied physiology (Bethesda, Md. : 1985).

  N/A.

• Aging Affects the Cardiovascular Responses to Cold Stress in Humans.

  Authors: Kari L Hess, Thad E Wilson, Charity L Sauder, Zhaohui Gao, Chester A Ray, Kevin D Monahan

  Journal of applied physiology (Bethesda, Md. : 1985).

  Cardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure mayCardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure may contribute to these associations. To determine if the blood pressure raising effect (pressor response) of acute non-hypothermic cold stress is greater with age we measured physiological responses to 20 minutes of skin surface cooling, via water-perfused suit, in 12 young (25+/-1 years old, mean+/-SE) and 12 older (65+/-2) adults. We found that skin surface cooling elicited a pressor response (P<0.05) in both young and older adults although this response (systolic and mean blood pressure) was greater than 2-fold higher in older adults (P<0.05 compared to young). The magnitude of the pressor response was similar at peripheral (brachial) and central (estimated in the aorta) measurement sites. Regression analysis revealed that aortic pulse wave velocity, a measure of central arterial stiffness, obtained before cooling was the best predictor of the increased pressor response to skin surface cooling in older adults, explaining ~63% of its variability. These results indicate that there is a greater pressor response to acute non-hypothermic cold stress with age in humans, which may be mediated by increased central arterial stiffness. Key words: Age, pulse wave velocity.

Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.