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1.
  • Maksuti, Elira, et al. (författare)
  • Cardiac remodeling in aortic and mitral valve disease : a simulation study with clinical validation
  • 2019
  • Ingår i: Journal of Applied Physiology. - Stockholm : Karolinska Institutet, Dept of Physiology and Pharmacology. - 8750-7587 .- 1522-1601.
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Remodeling is an important long-term determinant of cardiac function throughout the progression of heart disease. Numerous biomolecular pathways for mechanosensing and transduction are involved. However, we hypothesize that biomechanical factors alone can explain changes in myocardial volume and chamber size in valve disease. Methods: A validated model of the human vasculature and the four cardiac chambers was used to simulate aortic stenosis, mitral regurgitation and aortic regurgitation. Remodeling was simulated with adaptive feedback preserving myocardial fiber stress and wall shear stress in all four cardiac chambers. Briefly, the model used myocardial fiber stress to determine wall thickness and cardiac chamber wall shear stress to determine chamber volume. Results: Aortic stenosis resulted in the development of concentric left ventricular hypertrophy. Aortic and mitral regurgitation resulted in eccentric remodeling and eccentric hypertrophy, with more pronounced hypertrophy for aortic regurgitation. Comparisons with published clinical data showed the same direction and similar magnitudes of changes in end-diastolic volume index and left ventricular diameters. Changes in myocardial wall volume and wall thickness were within a realistic range both in stenotic and regurgitant valvular disease. Conclusions: Simulations of remodeling in left-sided valvular disease support, in both a qualitative and quantitative manner, that left ventricular chamber size and hypertrophy are primarily determined by preservation of wall shear stress and myocardial fiber stress.
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2.
  • Ahlborg, G, et al. (författare)
  • Central and regional hemodynamic effects during infusion of Big endothelin-1 in healthy humans
  • 1996
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 80:6, s. 1921-1927
  • Tidskriftsartikel (refereegranskat)abstract
    • Big endothelin-1 (Big ET-1) was given intravenously to six healthy men to study uptakes and vascular effects. Blood samples were taken from systemic and pulmonary arterial and internal jugular and deep forearm venous catheters. Arterial Big ET-1-like immunoreactivity (Big ET-1-LI) increased from 5.43 +/- 0.60 to 756 +/- 27 pmol/l, and ET-1-LI increased from 4.67 +/- 0.08 to 6.67 +/- 0.52 pmol/l (P < 0.001). Skeletal muscle fractional extraction of Big ET-1-LI was 15 +/- 4%. ET-1-LI release did not increase in the studied vascular beds. Heart rate fell by 17% (P < 0.001), cardiac output fell by 26% (P < 0.001), and stroke volume fell by 11% (P < 0.05). Mean arterial blood pressure increased 18%, systemic vascular resistance increased 65%, and pulmonary vascular resistance increased 57% (P < 0.01-0.001). Pulmonary blood pressures, forearm blood flow, arterial pH, arterial PCO2, and systemic arterial-internal jugular venous O2 difference remained unchanged. No specific Big ET-1 receptors were found in human pulmonary membranes. The half-maximal inhibitory concentration for the receptor antagonist bosentan was 181 nM. In summary, circulating Big ET-1 elicits greater increases in mean arterial blood pressure and systemic vascular resistance and decreases in heart rate and cardiac output compared with an equimolar ET-1 infusion (26).
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3.
  • AHLBORG, G, et al. (författare)
  • Circulating endothelin-1 reduces splanchnic and renal blood flow and splanchnic glucose production in humans
  • 1995
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 79:1, s. 141-145
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of minimal changes in circulating plasma endothelin-1 (ET-1) was studied in 12 healthy subjects receiving either 60 min of ET-1 (0.2 pmol.kg-1.min-1) or physiological saline intravenously. Blood was drawn from arterial, renal, and central hepatic vein catheters. Arterial ET-1-like immunoreactivity (ET-1-LI) increased from 4.7 +/- 0.4 (SE) to 8.6 +/- 1.0 pmol/l during ET-1 infusion. After 10 min, plasma ET-1-LI had increased to 6.12 +/- 0.29 pmol/l. For comparison the plasma ET-1-LI level was 12.9 +/- 4.2 pmol/in five patients with sepsis syndrome. Mean arterial blood pressure rose from 92 +/- 3 to 99 +/- 4 mmHg. Estimated splanchnic and renal blood flows fell by 18 +/- 5 and 10 +/- 3%, respectively, and splanchnic glucose production fell by 42 +/- 6% within 10 min of the ET-1 infusion and differed compared with corresponding control values. Only estimated splanchnic blood flow had increased 60 min after the ET-1 infusion. No change in splanchnic uptake of lactate or glycerol was seen. In conclusion, we suggest that circulating ET-1 with small or no demonstrable change in plasma concentration interferes with vasoactivity and splanchnic glycogenolyses in health and possibly pathophysiological conditions.
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4.
  • Ahlborg, G, et al. (författare)
  • Insulin sensitivity and big ET-1 conversion to ET-1 after ETA- or ETB-receptor blockade in humans
  • 2002
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 93:6, s. 2112-2121
  • Tidskriftsartikel (refereegranskat)abstract
    • Cardiovascular diseases are characterized by insulin resistance and elevated endothelin (ET)-1 levels. Furthermore, ET-1 induces insulin resistance. To elucidate this mechanism, six healthy subjects were studied during a hyperinsulinemic euglycemic clamp during infusion of (the ET-1 precursor) big ET-1 alone or after ETA- or ETB-receptor blockade. Insulin levels rose after big ET-1 with or without the ETB antagonist BQ-788 ( P < 0.05) but were unchanged after the ETA antagonist BQ-123 + big ET-1. Infused glucose divided by insulin fell after big ET-1 with or without BQ-788 ( P < 0.05). Insulin and infused glucose divided by insulin values were normalized by ETA blockade. Mean arterial blood pressure rose during big ET-1 with or without BQ-788 ( P < 0.001) but was unchanged after BQ-123. Skeletal muscle, splanchnic, and renal blood flow responses to big ET-1 were abolished by BQ-123. ET-1 levels rose after big ET-1 ( P< 0.01) in a similar way after BQ-123 or BQ-788, despite higher elimination capacity after ETA blockade. In conclusion, ET-1-induced reduction in insulin sensitivity and clearance as well as splanchnic and renal vasoconstriction are ETA mediated. ETA-receptor stimulation seems to inhibit the conversion of big ET-1 to ET-1.
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5.
  • AHLBORG, G, et al. (författare)
  • Metabolic and vascular effects of circulating endothelin-1 during moderately heavy prolonged exercise
  • 1995
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 78:6, s. 2294-2300
  • Tidskriftsartikel (refereegranskat)abstract
    • The aims were to investigate 1) the effects of endothelin-1 (ET-1) during exercise and 2) the influence of exercise on arterial ET-1 levels. Six healthy subjects performed two exercises of 2 h duration at 50% of peak oxygen uptake preceded by intravenous infusion of physiological saline or ET-1 (4 pmol.kg-1.min-1). Blood specimens were taken from arterial and hepatic vein catheters. Arterial ET-1 rose 15-fold during the infusion. Splanchnic blood flow fell after ET-1 and remained lower than in control subjects during exercise (P < 0.001). Splanchnic glucose production was approximately 25% lower compared with control values during the whole exercise period (P < 0.01). Neither heart rate, arterial glucagon, insulin, catecholamines, renin, glucose, lactate, nor glycerol levels differed from control exercise values. The calculated gluconeogenesis from glycerol and lactate did not differ from the control values. ET-1 levels rose approximately twofold in the control exercise (P < 0.01) and in another group of seven subjects performing 1 h of exercise at 70% of peak oxygen uptake (P < 0.001). In conclusion, ET-1 levels increased during exercise without ET-1 administration. In addition, circulating ET-1 has a (direct or indirect) regulatory action on splanchnic blood flow and glucose metabolism during exercise (and possibly under pathophysiological conditions) in humans.
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6.
  • Ahlborg, G, et al. (författare)
  • Nitric oxide-endothelin-1 interaction in humans
  • 1997
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 82:5, s. 1593-1600
  • Tidskriftsartikel (refereegranskat)abstract
    • Ahlborg, Gunvor, and Jan M. Lundberg. Nitric oxide–endothelin-1 interaction in humans. J. Appl. Physiol. 82(5): 1593–1600, 1997.—Healthy men received NG-monomethyl-l-arginine (l-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1.l-NMMA effects were that heart rate (17%), cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean arterial blood pressure (6%), and systemic (28%) and pulmonary (40%) vascular resistances increased ( P < 0.05 to 0.001). Arterial ET-1 levels (21%) increased due to a pulmonary net ET-1 release ( P < 0.05 to 0.01). Splanchnic glucose output (SGO) fell (26%, P < 0.01). Arterial insulin and glucagon were unchanged. Subsequent ET-1 infusion caused no change in mean arterial pressure, heart rate, or cardiac output, as found in the present controls, or in splanchnic and renal blood flow or splanchnic glucose output as previously found with ET-1 infusion (G. Ahlborg, E. Weitzberg, and J. M. Lundberg. J. Appl. Physiol. 79: 141–145, 1995). In conclusion, l-NMMA like ET-1, induces prolonged cardiovascular effects and suppresses SGO.l-NMMA causes pulmonary ET-1 release and blocks responses to ET-1 infusion. The results indicate that nitric oxide inhibits ET-1 production and thereby interacts with ET-1 regarding increase in vascular tone and reduction of SGO in humans.
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7.
  • Ahmed, AS, et al. (författare)
  • Type 2 diabetes impairs tendon repair after injury in a rat model
  • 2012
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 113:11, s. 1784-1791
  • Tidskriftsartikel (refereegranskat)abstract
    • Type 2 diabetes adversely affects the properties of native connective tissue. The underlying mechanisms, however, by which diabetes alters connective tissue metabolism, especially tendon, are poorly defined. The aim of this study was to determine the effect of type 2 diabetes on the mechanical, histological, and molecular properties of the intact and healing Achilles tendon. The right Achilles tendon was transected in 11 male diabetic Goto-Kakizaki (GK) and 10 age- and sex-matched Wistar control rats, while the left Achilles tendon was left intact. At 2 wk postinjury the intact and injured tendons were assessed by biomechanical testing and histology. The gene expression of collagen I and III, biglycan, versican, MMP-13, and MMP-3 was measured by quantitative RT-PCR, and their protein distribution was studied by immunohistochemistry. Intact tendons exhibited only small differences between the groups. In injured tendons, however, a significantly smaller transverse area and lower stiffness was found in diabetic GK compared with Wistar control rats. This correlated with impaired structural organization of collagen fibers and a reduced expression of collagen I and III in the injured tendons of the diabetic GK compared with Wistar control. Moreover, MMP-3 gene expression was downregulated in the injured diabetic GK tendons compared with injured Wistar controls. Our results indicate that in a rat model of diabetes tendon healing is impaired mainly due to altered expression of collagen and MMPs reflecting decreased degradation of matrix proteins and impaired tissue remodeling. Further our data suggest that therapeutic modulation of collagens or MMPs might be targets for new regenerative approaches in operated, injured, or maybe also degenerative tendon diseases in diabetes.
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8.
  • Al-Mashat, Mariam, et al. (författare)
  • Increased pulmonary blood volume variation in patients with heart failure compared to healthy controls; a non-invasive, quantitative measure of heart failure
  • 2020
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 128:2, s. 324-337
  • Tidskriftsartikel (refereegranskat)abstract
    • Variation of the blood content of the pulmonary vascular bed during a heartbeat can be quantified by pulmonary blood volume variation (PBVV) using magnetic resonance imaging (MRI). The aim was to evaluate if PBVV differs in patients with heart failure compared to healthy controls and investigate the mechanisms behind the PBVV. Forty-six patients and 10 controls underwent MRI. PBVV was calculated from blood flow measurements in the main pulmonary artery and a pulmonary vein, defined as the maximum difference in cumulative PBV over one heartbeat. PBVV was indexed to stroke volume (SV) in the main pulmonary artery (PBVVSV). Patients displayed higher PBVVSV than controls (58±14% vs 43±7%, p<0.001). The change in PBVVSV could be explained by left ventricular (LV) longitudinal contribution to SV (R2=0.15, p=0.02) and the phase shift between in- and outflow (R2=0.31, p<0.001) in patients. Both variables contributed to the multiple regression analysis model and predicted PBVVSV (R2=0.38), however, the phase shift alone explained about ~30% of the variation in PBVVSV. No correlation was found between PBVVSV and large vessel area. In conclusion, PBVVSV was higher in patients compared to controls. Approximately 40% of the variation of PBVVSV in patients can be explained by the LV longitudinal contribution to SV and the phase shift between pulmonary in- and outflow, where the phase shift alone accounts for ~30%. The remaining variation, (60-70%), most likely occurs on small vessel level. Future studies are needed to show the clinical added value of PBVVSV compared to right heart catheterization.
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9.
  • Allen, DG, et al. (författare)
  • Impaired calcium release during fatigue
  • 2008
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 104:1, s. 296-305
  • Tidskriftsartikel (refereegranskat)abstract
    • Impaired calcium release from the sarcoplasmic reticulum (SR) has been identified as a contributor to fatigue in isolated skeletal muscle fibers. The functional importance of this phenomenon can be quantified by the use of agents, such as caffeine, which can increase SR Ca2+release during fatigue. A number of possible mechanisms for impaired calcium release have been proposed. These include reduction in the amplitude of the action potential, potentially caused by extracellular K+accumulation, which may reduce voltage sensor activation but is counteracted by a number of mechanisms in intact animals. Reduced effectiveness of SR Ca2+channel opening is caused by the fall in intracellular ATP and the rise in Mg2+concentrations that occur during fatigue. Reduced Ca2+available for release within the SR can occur if inorganic phosphate enters the SR and precipitates with Ca2+. Further progress requires the development of methods that can identify impaired SR Ca2+release in intact, blood-perfused muscles and that can distinguish between the various mechanisms proposed.
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10.
  • Allen, G, et al. (författare)
  • Transient mechanical benefits of a deep inflation in the injured mouse lung
  • 2002
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 93:5, s. 1709-1715
  • Tidskriftsartikel (refereegranskat)abstract
    • The lasting effects of a recruitment maneuver (RM) in the injured lung are not well characterized. We speculated that the reduction in respiratory elastance (H) after a deep inflation (DI) is transient in nature and should be sustained longer at higher positive end-expiratory pressure (PEEP). Thirteen ventilated mice were given 2 DIs at various levels of PEEP before and after saline lavage. Forced oscillations were used to measure H periodically over 7 min after the DIs. Time constants (tau) were estimated for the post-DI recovery in H. Values for tau before lavage (80-115 s) were reduced after lavage (13-30 s) at all levels of PEEP (P = 0.0001). PEEP did not significantly influence tau before or after lavage. The plateau level and total recovery in H after a DI were significantly influenced by PEEP and lavage (P < 0.0001). Our results suggest that for a DI to be beneficial in the injured mouse lung, it may have to be applied several times a minute.
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11.
  • Almlen, A, et al. (författare)
  • Surfactant proteins B and C are both necessary for alveolar stability at end expiration in premature rabbits with respiratory distress syndrome
  • 2008
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 104:4, s. 1101-1108
  • Tidskriftsartikel (refereegranskat)abstract
    • Modified natural surfactant preparations, used for treatment of respiratory distress syndrome in premature infants, contain phospholipids and the hydrophobic surfactant protein (SP)-B and SP-C. Herein, the individual and combined effects of SP-B and SP-C were evaluated in premature rabbit fetuses treated with airway instillation of surfactant and ventilated without positive end-expiratory pressure. Artificial surfactant preparations composed of synthetic phospholipids mixed with either 2% (wt/wt) of porcine SP-B, SP-C, or a synthetic poly-Leu analog of SP-C (SP-C33) did not stabilize the alveoli at the end of expiration, as measured by low lung gas volumes of ∼5 ml/kg after 30 min of ventilation. However, treatment with phospholipids containing both SP-B and SP-C/SP-C33 approximately doubled lung gas volumes. Doubling the SP-C33 content did not affect lung gas volumes. The tidal volumes were similar in all groups receiving surfactant. This shows that SP-B and SP-C exert different physiological effects, since both proteins are needed to establish alveolar stability at end expiration in this animal model of respiratory distress syndrome, and that an optimal synthetic surfactant probably requires the presence of mimics of both SP-B and SP-C.
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12.
  • Almstrand, Ann-Charlotte, et al. (författare)
  • Effect of Airway Opening on Production of Exhaled Particles.
  • 2010
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 108:3, s. 584-588
  • Tidskriftsartikel (refereegranskat)abstract
    • The technique of sampling exhaled air is attractive because it is non-invasive, and so allows repeated sampling with ease and no risk for the patient. Knowledge of the biomarkers' origin is important in order to correctly understand and interpret the data. Endogenous particles, formed in the airways, are exhaled and reflect chemical composition of the respiratory tract lining fluid. However, the formation mechanisms and formation sites of these particles are unknown. We hypothesize that airway opening following airway closure cause production of airborne particles that are exhaled. The objective of this study was to examine production of exhaled particles following varying degrees of airway closure. 10 healthy volunteers performed 3 different breathing manoeuvres in which the initial lung volume preceding an inspiration to total lung capacity was varied between functional residual capacity (FRC) and residual volume (RV). Exhaled particle number concentrations in the size interval 0.30-2.0 mum were recorded. Number concentrations of exhaled particles showed a 2-18 fold increase after exhalations to RV compared to exhalations where no airway closure was shown (8500 (810-28000) vs. 1300 (330-13000) particles/expired litre, p=0.012). The difference was most noticeable for the smaller size range of particles (<1 mum). There were significant correlations between particle concentrations for the different manoeuvres. Our results show that airway reopening following airway closure is an important mechanism for formation of endogenous exhaled particles and that these particles originate from the terminal bronchioles. Key words: exhaled particles, airway closure, breath.
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13.
  • Andersson, Erik P., 1984-, et al. (författare)
  • The effect of exercise hyperpnea on gross efficiency and anaerobic capacity estimates during a 3-min cycle time trial
  • 2023
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 134:2, s. 253-263
  • Tidskriftsartikel (refereegranskat)abstract
    • This study aimed to analyze the effect of exercise-induced hyperpnea on gross efficiency (GE) and anaerobic capacity estimates during a self-paced 3-min supramaximal cycle time trial (TT). Fourteen highly trained male cyclists performed 7 × 4-min submaximal stages, a 6-min passive rest, a 3-min TT, a 5-min passive rest, and a 6-min submaximal stage. Three models were based on the 7 × 4-min linear regression extrapolation method, using 1) the conventional model (7-YLIN); 2) the same 7-YLIN model but correcting for the additional ventilatory cost (i.e., hyperpnea) (7-YLIN-V-cor); and 3) accounting for linearly declining GE during the TT (7-YLIN-D). The other three models were based on GE from the last submaximal stage, using the conventional model (GELAST) and the same modifications as described for 7+YLIN, i.e., 1) GELAST, 2) GELAST-V-cor, and 3) GELAST-D. The GELAST model generated 18% higher values of anaerobic capacity than the 7-YLIN model (P < 0.05). During the TT, the hyperpnea-corrected model (i.e., 7-YLIN-V-cor or GELAST-V-cor) generated, compared with the respective conventional model (i.e., 7-YLIN or GELAST), ∼0.7 percentage points lower GE and ∼11% higher anaerobic capacity (all, P < 0.05). The post-TT GE was 1.9 percentage points lower (P < 0.001) and the 7-YLIN-D or GELAST-D model generated, compared with the respective conventional model, a lower GE (∼1.0 percentage points) and ∼17% higher anaerobic capacity during the TT (all, P < 0.05). In conclusion, the correction for a declining GE due to hyperpnea during a supramaximal TT resulted in an increased required total metabolic rate and anaerobic energy expenditure compared with the conventional models.NEW & NOTEWORTHY This study demonstrates that GE declines during a 3-min supramaximal cycle TT, which is possibly related to the hyperpneic response during supramaximal exercise. The finding from this study also provides novel insight into how the increased ventilatory energy cost from exercise-induced hyperpnea contributes to decreased GE, increased required total metabolic rate, and increased anaerobic energy expenditure during supramaximal exercise. Therefore, conventional linear models for estimating anaerobic capacity are likely to generate underestimated values.
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14.
  • Andersson, Johan, et al. (författare)
  • Cardiovascular and respiratory responses to apneas with and without face immersion in exercising humans
  • 2004
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 96:3, s. 1005-1010
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of the diving response on alveolar gas exchange was investigated in 15 subjects. During steady-state exercise (80 W) on a cycle ergometer, the subjects performed 40-s apneas in air and 40-s apneas with face immersion in cold (10degreesC) water. Heart rate decreased and blood pressure increased during apneas, and the responses were augmented by face immersion. Oxygen uptake from the lungs decreased during apnea in air (-22% compared with eupneic control) and was further reduced during apnea with face immersion (-25% compared with eupneic control). The plasma lactate concentration increased from control (11%) after apnea in air and even more after apnea with face immersion (20%), suggesting an increased anaerobic metabolism during apneas. The lung oxygen store was depleted more slowly during apnea with face immersion because of the augmented diving response, probably including a decrease in cardiac output. Venous oxygen stores were probably reduced by the cardiovascular responses. The turnover times of these gas stores would have been prolonged, reducing their effect on the oxygen uptake in the lungs. Thus the human diving response has an oxygen-conserving effect.
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15.
  • Andersson, Johan, et al. (författare)
  • Diving response and arterial oxygen saturation during apnea and exercise in breath-hold divers
  • 2002
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 93:3, s. 882-886
  • Tidskriftsartikel (refereegranskat)abstract
    • This study addressed the effects of apnea in air and apnea with face immersion in cold water (10°C) on the diving response and arterial oxygen saturation during dynamic exercise. Eight trained breath-hold divers performed steady-state exercise on a cycle ergometer at 100 W. During exercise, each subject performed 30-s apneas in air and 30-s apneas with face immersion. The heart rate and arterial oxygen saturation decreased and blood pressure increased during the apneas. Compared with apneas in air, apneas with face immersion augmented the heart rate reduction from 21 to 33% (P < 0.001) and the blood pressure increase from 34 to 42% (P < 0.05). The reduction in arterial oxygen saturation from eupneic control was 6.8% during apneas in air and 5.2% during apneas with face immersion (P < 0.05). The results indicate that augmentation of the diving response slows down the depletion of the lung oxygen store, possibly associated with a larger reduction in peripheral venous oxygen stores and increased anaerobiosis. This mechanism delays the fall in alveolar and arterial Po2 and, thereby, the development of hypoxia in vital organs. Accordingly, we conclude that the human diving response has an oxygen-conserving effect during exercise.
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16.
  • Andersson, Johan, et al. (författare)
  • Increased serum levels of the brain damage marker S100B after apnea in trained breath-hold divers: a study including respiratory and cardiovascular observations
  • 2009
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 107:3, s. 809-815
  • Tidskriftsartikel (refereegranskat)abstract
    • The concentration of the protein S100B in serum is used as a brain damage marker in various conditions. We wanted to investigate whether a voluntary, prolonged apnea in trained breath-hold divers resulted in an increase of S100B in serum. Nine trained breath-hold divers performed a protocol mimicking the procedures they use during breath-hold training and competition, including extensive preapneic hyperventilation and glossopharyngeal insufflation, in order to perform a maximum-duration apnea, i.e., "static apnea" (average: 335 s, range: 281–403 s). Arterial blood samples were collected and cardiovascular variables recorded. Arterial partial pressures of O2 and CO2 (PaO2 and PaCO2) were 128 Torr and 20 Torr, respectively, at the start of apnea. The degree of asphyxia at the end of apnea was considerable, with PaO2 and PaCO2 reaching 28 Torr and 45 Torr, respectively. The concentration of S100B in serum transiently increased from 0.066 µg/l at the start of apnea to 0.083 µg/l after the apnea (P < 0.05). The increase in S100B is attributed to the asphyxia or to other physiological responses to apnea, for example, increased blood pressure, and probably indicates a temporary opening of the blood-brain barrier. It is not possible to conclude that the observed increase in S100B levels in serum after a maximal-duration apnea reflects a serious injury to the brain, although the results raise concerns considering negative long-term effects. At the least, the results indicate that prolonged, voluntary apnea affects the integrity of the central nervous system and do not preclude cumulative effects.
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17.
  • Andersson, Therese, et al. (författare)
  • Low-level mechanical stimulation is sufficient to improve tendon healing in rats
  • 2012
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 113:9, s. 1398-1402
  • Tidskriftsartikel (refereegranskat)abstract
    • Treatment of tendon injuries often involves immobilization. However, immobilization might not prevent mild involuntary isometric muscle contraction. The effect of weak forces on tendon healing is therefore of clinical interest. Studies of tendon healing with various methods for load reduction in rat Achilles tendon models show a consistent reduction in tendon strength by at least half, compared with voluntary cage activity. Unloading was not complete in any of these models, and the healing tendon was therefore still exposed to mild mechanical stimulation. By reducing the forces acting on the tendon even further, we now studied the effects of this mild stimulation. Rat Achilles tendons were transected and allowed to heal spontaneously under four different loading conditions: 1) normal cage activity; 2) calf muscle paralysis induced by botulinum toxin A (Botox); 3) tail suspension; 4) Botox and tail suspension, combined, to eliminate even mild stimulation. Healing was evaluated by mechanical testing after 8 days. Botox alone and suspension alone both reduced tendon callus size (transverse area), thereby impairing its strength compared with normal cage activity. The combination of Botox and suspension did not further reduce tendon callus size but drastically impaired the material properties of the tendon callus compared with each treatment alone. The peak force was only a fifth of that in the normal cage activity group. The results indicate that also the mild loading that occurs with either Botox or suspension alone stimulates tendon healing. This stimulation appears to affect mainly tissue quality, whereas stronger stimulation also increases callus size.
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18.
  • Andersson, Therese, et al. (författare)
  • Tissue memory in healing tendons : short loading episodes stimulate healing
  • 2009
  • Ingår i: JOURNAL OF APPLIED PHYSIOLOGY. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 107:2, s. 417-421
  • Tidskriftsartikel (refereegranskat)abstract
    • Intact tendons adapt slowly to changes in mechanical loading, whereas in healing tendons the effect of mechanical loading or its absence is dramatic. The longevity of the response to a single loading episode is, however, unknown. We hypothesized that the tissue has a "memory" of loading episodes and that therefore short loadings are sufficient to elicit improved healing. The Achilles tendon of 70 female rats was transected and unloaded by tail suspension for 12 days (suspension started on day 2 after surgery). Each day, the rats were let down from suspension for short daily training episodes according to different regimes: 15 min of cage activity or treadmill running for 15, 30, 60, or 2 x 15 min. Rats with transected Achilles tendons and full-time cage activity served as controls. The results demonstrated that full-time cage activity increased the peak force over three times compared with unloading. Short daily loading episodes (treadmill running) increased the peak force about half as much as full-time activity. Prolongation of treadmill running above 15 min or dividing the daily training in two separate episodes had minimal further effect. This mechanical stimulation increased the cross-sectional area but had no effect on the mechanical properties of the repair tissue. The findings indicate that once the tissue had received information from a certain loading type and level, this is "memorized" and leads to a response lasting many hours. This suggests that patients might be allowed early short loading episodes following, e. g., an Achilles tendon rupture for a better outcome.
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19.
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20.
  • Arvidsson, Per Martin, et al. (författare)
  • Kinetic energy of left ventricular blood flow across heart failure phenotypes and in subclinical diastolic dysfunction
  • 2022
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 133:3, s. 697-709
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Kinetic energy (KE) of intracardiac blood flow reflects myocardial work spent on accelerating blood and provides a mechanistic window into diastolic filling dynamics. Diastolic dysfunction may represent an early stage in the development of heart failure (HF). Here we evaluated the hemodynamic effects of impaired diastolic function in subjects with and without HF, testing the hypothesis that left ventricular KE differs between controls, subjects with subclinical diastolic dysfunction (SDD), and HF patients.METHODS: We studied 77 subjects (16 controls, 20 subjects with SDD, 16 HFpEF, 9 HFmrEF, and 16 HFrEF patients, age- and sex-matched at the group level). Cardiac magnetic resonance at 1.5T included intracardiac 4D flow and cine imaging. Left ventricular KE was calculated as 0.5*m*v 2. RESULTS: Systolic KE was similar between groups (p>0.4), also after indexing to stroke volume (p=0.25), and was primarily driven by ventricular emptying rate (p<0.0001, R 2=0.52). Diastolic KE was higher in heart failure patients than controls (p<0.05) but similar between SDD and HFpEF (p>0.18), correlating with inflow conditions (E-wave velocity, p<0.0001, R 2=0.24) and end-diastolic volume (p=0.0003, R 2=0.17) but not with average e' (p=0.07). CONCLUSIONS: Diastolic KE differs between controls and heart failure, suggesting more work is spent filling the failing ventricle, while systolic KE does not differentiate between well-matched groups with normal ejection fraction even in the presence of relaxation abnormalities and heart failure. Mechanistically, KE reflects the acceleration imparted on the blood and is driven by variations in ventricular emptying and filling rates, volumes, and heart rate, regardless of underlying pathology.
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21.
  • Arvidsson, Per Martin, et al. (författare)
  • Quantification of left and right atrial kinetic energy using four-dimensional intracardiac magnetic resonance imaging flow measurements.
  • 2013
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 114:10, s. 1472-1481
  • Tidskriftsartikel (refereegranskat)abstract
    • Kinetic energy (KE) of atrial blood has been postulated as a possible contributor to ventricular filling. Therefore, we aimed to quantify the left and right atrial blood KE using cardiac magnetic resonance (CMR). Fifteen healthy volunteers underwent CMR at 3T, including a four-dimensional phase contrast flow sequence. Mean left atrial (LA) KE was lower than right atrial (RA) KE (1.1±0.1 mJ vs 1.7±0.1 mJ, P<0.01). Three KE peaks were seen in both atria; one in ventricular systole, one during early ventricular diastole, and one during atrial contraction. The systolic LA peak was significantly smaller than the RA peak (P<0.001), and the early diastolic LA peak was larger than the RA peak (P<0.05). Rotational flow contained 46 ± 7% of total KE, and conserved energy better than non-rotational flow did. The KE increase in early diastole was higher in the LA (P<0.001). Systolic KE correlated with the combination of atrial volume and systolic velocity of the atrioventricular plane displacement (R2=0.57 for LA and R2=0.64 for RA). Early diastolic KE of the LA correlated with LV mass (R2=0.28), however no such correlation was found in the right heart. This suggests that LA KE increases during early ventricular diastole due to LV elastic recoil, indicating that LV filling is dependent on diastolic suction. RV relaxation does not seem to contribute to atrial KE. Instead, atrial KE generated during ventricular systole may be conserved in a hydraulic "flywheel" and transferred to the RV through helical flow, which may contribute to RV filling.
  •  
22.
  • Aspenberg, Per, 1949- (författare)
  • Editorial: Is inflammation harmless to loaded tendons?
  • 2007
  • Ingår i: Journal of applied physiology. - : American Psychological Association (APA). - 8750-7587 .- 1522-1601. ; 102:1, s. 3-4
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
23.
  • Astrand, H., et al. (författare)
  • In vivo estimation of the contribution of elastin and collagen to the mechanical properties in the human abdominal aorta: effect of age and sex
  • 2011
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 110:1, s. 176-187
  • Tidskriftsartikel (refereegranskat)abstract
    • Astrand H, Stalhand J, Karlsson J, Karlsson M, Sonesson B, Lanne T. In vivo estimation of the contribution of elastin and collagen to the mechanical properties in the human abdominal aorta: effect of age and sex. J Appl Physiol 110: 176-187, 2011. First published November 11, 2010; doi:10.1152/japplphysiol.00579.2010.-The mechanical properties of the aorta affect cardiac function and are related to cardiovascular morbidity/mortality. This study was designed to evaluate the isotropic (mainly elastin, elastin(iso)) and anisotropic (mainly collagen, collagen(ani)) material parameters within the human aorta in vivo. Thirty healthy men and women in three different age categories (23-30, 41-54, and 67-72 yr) were included. A novel mechanical model was used to identify the mechanical properties and the strain field with aid of simultaneously recorded pressure and radius in the abdominal aorta. The magnitudes of the material parameters relating to both the stiffness of elastin(iso) and collagen(ani) were in agreement with earlier in vitro studies. The load-bearing fraction attributed to collagen(ani) oscillated from 10 to 30% between diastolic and systolic pressures during the cardiac cycle. With age, stiffness of elastin(iso) increased in men, despite the decrease in elastin content that has been found due to elastolysis. Furthermore, an increase in stiffness of collagen(ani) at high physiological pressure was found. This might be due to increased glycation, as well as changed isoforms of collagen in the aortic wall with age. A marked sex difference was observed, with a much less age-related effect, both on elastin(iso) and collagen(ani) stiffness in women. Possible factors of importance could be the effect of sex hormones, as well as differing collagen isoforms, between the sexes.
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24.
  • Ax, M, et al. (författare)
  • The influence of gravity on regional lung blood flow in humans: SPECT in the upright and head-down posture
  • 2017
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 122:6, s. 1445-1451
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous studies in humans have shown that gravity has little influence on the distribution of lung blood flow while changing posture from supine to prone. This study aimed to evaluate the maximal influence of posture by comparison of regional lung blood flow in the upright and head-down posture in 8 healthy volunteers, using a tilt table. Regional lung blood flow was marked by intravenous injection of macroaggregates of human albumin labeled with 99mTc or 113mIn, in the upright and head-down posture, respectively, during tidal breathing. Both radiotracers remain fixed in the lung after administration. The distribution of radioactivity was mapped using quantitative single photon emission computed tomography (SPECT) corrected for attenuation and scatter. All images were obtained supine during tidal breathing. A shift from upright to the head-down posture caused a clear redistribution of blood flow from basal to apical regions. We conclude that posture plays a role for the distribution of lung blood flow in upright humans, and that the influence of posture, and thereby gravity, is much greater in the upright and head-down posture than in horizontal postures. However, the results of the study demonstrate that lung structure is the main determinant of regional blood flow and gravity is a secondary contributor to the distribution of lung blood flow in the upright and head-down positions. NEW & NOTEWORTHY Using a dual-isotope quantitative SPECT method, we demonstrated that although a shift in posture redistributes blood flow in the direction of gravity, the results are also consistent with lung structure being a greater determinant of regional blood flow than gravity. To our knowledge, this is the first study to use modern imaging methods to quantify the shift in regional lung blood flow in humans at a change between the upright and head-down postures.
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25.
  • Axelson, Hans W (författare)
  • Signs of muscle thixotropy during human ballistic wrist joint movements
  • 2005
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 99:5, s. 1922-1929
  • Tidskriftsartikel (refereegranskat)abstract
    • A study was conducted on healthy subjects to determine whether voluntary ballistic wrist flexion movements are influenced by immediately preceding conditioning of the forearm muscles. Single rapid wrist flexion movements were made in response to an auditory "Go" signal. Rectified surface EMG was recorded from wrist flexors and extensors, and joint position was measured by a goniometer. The movements were preceded (2-3 s) by four different conditioning routines: 40-s rest (Rest), 10-s voluntary alternating wrist joint flexion and extension movements (Osc), and 10 s of 25 degrees weak isometric wrist extensor (Ext) or flexor contractions (Flex). When subjects made ballistic movements after Osc compared with Rest, peak velocity was higher (P = 0.02) and movement time shorter (P = 0.06), but there was no difference (P = 0.83) in motor reaction time (time between the onset of the first agonist burst and movement onset). If the movements were preceded by Ext compared with Flex, motor reaction time was longer (P = 0.01), indicating a longer electromechanical delay. There were no indications that postconditioning differences in agonist or antagonist muscle activity could explain the results. It was also demonstrated that, after Rest, peak velocity was lower (P < 0.01) for the first than for the second of a series of repetitive ballistic movements. The observations corresponded to results from passive experiments in which the median nerve was electrically stimulated. In conclusion, history-dependent (thixotropic) changes in skeletal muscle resistance seem to have implications for voluntary ballistic wrist movements. The study also provided evidence that muscle conditioning influences the central nervous reaction time preceding ballistic contractions.
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26.
  • Axelsson, J, et al. (författare)
  • Hormonal changes in satisfied and dissatisfied shift workers across a shift cycle
  • 2003
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 95:5, s. 2099-2105
  • Tidskriftsartikel (refereegranskat)abstract
    • Although the literature claims that shift work is harmful, it overlooks the fact that that many shift workers are satisfied and stay healthy. There is little knowledge of the biological mechanisms mediating the differences in susceptibility. The present study compared satisfied and dissatisfied shift workers with respect to major anabolic and catabolic hormones. Forty-two male shift workers, with an extremely rapidly rotating shift schedule, were divided into two groups according to their ratings of satisfaction with their work hours. Morning blood samples were taken during the first and last morning shift in the shift cycle. Serum was analyzed with respect to testosterone, cortisol, and prolactin. Dissatisfied shift workers had lower morning testosterone than satisfied ones, but they did not significantly differ with respect to cortisol or prolactin. Low testosterone levels were, in addition, associated with a greater sleep need, disturbed sleep/wakefulness, and an increased need for recovery after the work period, the latter being the best predictor of testosterone levels. The only change across the shift cycle concerned a significant decrease of morning cortisol at the end of the shift cycle. High morning cortisol was related to having a morning personality and fewer sleep problems before the morning shift. Dissatisfaction with the shift system seems related to lower testosterone levels, which in turn are related to disturbed sleep/wakefulness and increased need for sleep and recovery. Furthermore, morning cortisol was reduced across a shift cycle. It is suggested that reduced testosterone levels may be part of a mechanism of shift work maladjustment.
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27.
  • Axelsson, Michael, 1958, et al. (författare)
  • A Novel Fully Implantable Multi-Channel Biotelemetry System for Measurement of Blood Flow, Pressure, ECG and Temperature
  • 2007
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 102:3, s. 1220-1228
  • Tidskriftsartikel (refereegranskat)abstract
    • Biotelemetry provides high-quality data in awake, free-ranging animals without the effects of anesthesia and surgery. Although many biological parameters can be measured using biotelemetry, simultaneous telemetric measurements of pressure and flow have not been available. The objective of this study was to evaluate simultaneous measurements of blood flow, pressure, ECG, and temperature in a fully implantable system. This novel system allows the measurement of up to four channels of blood flow, up to three channels of pressure, and a single channel each of ECG and temperature. The system includes a bidirectional radio-frequency link that allows the implant to send data and accept commands to perform various tasks. The system is controlled by a base station decoder/controller that decodes the data stream sent by the implant into analog signals. The system also converts the data into a digital data stream that can be sent via ethernet to a remote computer for storage and/or analysis. The system was chronically implanted in swine and alligators for up to 5 wk. Both bench and in vivo animal tests were performed to evaluate system performance. Results show that this biotelemetry system is capable of long-term accurate monitoring of simultaneous blood flow and pressure. The system allows, within the room, recordings, since the implant transmission range is between 6 and 10 m, and, with a relay, backpack transmission distance of up to 500 m can be achieved. This system will have significant utility in chronic models of cardiovascular physiology and pathology.
  •  
28.
  • Backstrom, T, et al. (författare)
  • Cardiac outflow of amino acids and purines during myocardial ischemia and reperfusion
  • 2003
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 94:3, s. 1122-1128
  • Tidskriftsartikel (refereegranskat)abstract
    • A novel application of microdialysis was studied, in which myocardial outflow of amino acids and purines was monitored by intravasal microdialysis in the myocardial venous outflow during ischemia and reperfusion. Microdialysis catheters were introduced into the great cardiac vein, pulmonary artery, and external jugular vein in 20 anesthetized pigs. The left anterior descending artery was occluded in four groups of pigs for 0, 10, 15, and 60 min. Ischemia was followed by 120 min of reperfusion. Microdialysis samples were analyzed for taurine, aspartate, glutamate, hypoxanthine, inosine, and guanosine. Myocardial infarction developed when ischemia exceeded 10 min. Taurine, aspartate, inosine, and guanosine increased early in the great cardiac vein during ischemia. We found the outflow patterns of amino acids and purines to be graded in response to different lengths of ischemia. In this study we have demonstrated a graded outflow of amino acids and purines in response to ischemia and a positive correlation between infarct size and myocardial outflow of amino acids and purines. This could be of value in a clinical setting to quantify the extent of myocardial damage.
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29.
  •  
30.
  •  
31.
  • Berg, HE, et al. (författare)
  • Lower limb skeletal muscle function after 6 wk of bed rest
  • 1997
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 82:1, s. 182-188
  • Tidskriftsartikel (refereegranskat)abstract
    • Berg, H. E., L. Larsson, and P. A. Tesch. Lower limb skeletal muscle function after 6 wk of bed rest. J. Appl. Physiol. 82(1): 182–188, 1997.—Force, electromyographic (EMG) activity, muscle mass, and fiber characteristics were studied in seven healthy men before and after 6 wk of bed rest. Maximum voluntary isometric and concentric knee extensor torque decreased ( P < 0.05) uniformly across angular velocities by 25–30% after bed rest. Maximum quadricep rectified EMG decreased by 19 ± 23%, whereas submaximum (100-Nm isometric action) EMG increased by 44 ± 28%. Knee extensor muscle cross-sectional area (CSA), assessed by using magnetic resonance imaging, decreased by 14 ± 4%. Maximum torque per knee extensor CSA decreased by 13 ± 9%. Vastus lateralis fiber CSA decreased 18 ± 14%. Neither type I, IIA, and IIB fiber percentages nor their relative proportions of myosin heavy chain (MHC) isoforms were altered after bed rest. Because the decline in strength could not be entirely accounted for by decreased muscle CSA, it is suggested that the strength loss is also due to factors resulting in decreased neural input to muscle and/or reduced specific tension of muscle, as evidenced by a decreased torque/EMG ratio. Additionally, it is concluded that muscle unloading in humans does not induce important changes in fiber type or MHC composition or in vivo muscle contractile properties.
  •  
32.
  • Berg, J., et al. (författare)
  • Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume
  • 2020
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 128:2, s. 252-263
  • Tidskriftsartikel (refereegranskat)abstract
    • Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1-2 h after AMI in a microembolization model (n = 12) and an ischemia-reperfusion model (n = 14). A subset of pigs (n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased (P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease (P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (-29 ± 14% vs. -15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas (P < 0.001), and A-wave AVPD remained unchanged (P = 0.93) whereas E-wave AVPD decreased (P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction.NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.
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33.
  • Bergfeldt, L, et al. (författare)
  • Power spectral and Poincaré plot characteristics in sinus node dysfunction
  • 2003
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 94:6, s. 2217-2224
  • Tidskriftsartikel (refereegranskat)abstract
    • A salient feature of the normal sinus node activity is its prominent beat-to-beat variability, which shows self-similarity on different time scales (fractal dynamics). However, in patients with sinus node dysfunction, short-term time sinus cycles show exaggerated variability, the characteristics of which have not been analyzed. Therefore, Poincaré plots and power spectral analysis were applied to short-term variations of sinus cycles in 30 patients with and 30 patients without sinus node disease. Three patterns of behavior were observed in sick sinus patients: type 1, completely normal ( n = 3); type 2, randomlike pattern in the Poincaré plots with “white noise” power spectra ( n = 9); and type 3, a transitional pattern, characterized by remnants of normal behavior mixed with scattered points ( n = 18). In control subjects, only type 1 ( n = 27) and type 3 ( n = 3) patterns were observed, P < 0.0001. The power spectral changes in sinus node dysfunction are thus characterized by a loss of the inverse power law relationship, which both has implications for heart rate variability analysis and might offer a new diagnostic approach.
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34.
  • Berlin, Gösta, 1944-, et al. (författare)
  • Low-O2 affinity erythrocytes improve performance of ischemic myocardium
  • 2002
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 92:3, s. 1267-1276
  • Tidskriftsartikel (refereegranskat)abstract
    • O2 transport and O2 diffusion interact in providing O2 to tissue, but the extent to which diffusion may be critical in the heart is unclear. If O2 diffusion limits mitochondrial oxygenation, a change in blood O2 affinity at constant total O2 transport should alter cardiac O2 consumption (VO2) and function. To test this hypothesis, we perfused isolated isovolumically working rabbit hearts with erythrocytes at physiological blood-gas values and P50 (PO2 required to half-saturate hemoglobin) values at Ph of 7.4 of 17 ▒ 1 Torr (2,3-bisphosphoglycerate depletion) and 33 ▒ 5 Torr (inositol hexaphosphate incorporation). When perfused at 40 and 20% of normal coronary flow, mean VO2 decreased from the control value by 37 and 46% (P < 0.001), and function, expressed as cardiac work, decreased by 38 and 52%, respectively (P < 0.001). Perfusion at higher P50 during low-flow ischemia improved VO2 by 20% (P < 0.001) and function by 36% (P < 0.02). There was also modest improvement at basal flow (P < 0.02 and P < 0.002, respectively). The improvement in VO2 and function due to the P50 increase demonstrates the importance of O2 diffusion in this cardiac ischemia model.
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35.
  • Berner, J, et al. (författare)
  • Altered respiratory pattern and hypoxic response in transgenic newborn mice lacking the tachykinin-1 gene
  • 2007
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 103:2, s. 552-559
  • Tidskriftsartikel (refereegranskat)abstract
    • Substance P is known to be involved in respiratory rhythm and central pattern-generating mechanisms, especially during early development. We therefore studied respiratory responses in transgenic newborn mice (Tac1−/−) lacking substance P and neurokinin A (NKA). In vivo, the effects of intermittent isocapnic hypoxia (IH) and hypercapnia were studied using whole body flow plethysmography at P2-3 and P8-10. In vitro, anoxic responses and the effects of hypocapnic and hypercapnic conditions were studied in brain stem-spinal cord preparations (C4 activity) at P2. Hypoxic challenge considerably modified the respiratory activity in transgenic mice displayed in vivo as an attenuated increase in tidal volume during IH. Transgenic mice also showed a more prominent posthypoxic frequency decline in vivo, and posthypoxic neuronal arrests appeared more often in vitro. We recognized two types of sigh activity: with or without a following pause. During IH, the amount of sighs with a pause decreased and those without increased, a redistribution that became stronger with age only in controls. Intermittent anoxia induced long-term facilitation effects in controls, but not in Tac1−/− animals, manifested as an increase in burst frequency in vitro and by an augmentation of ventilation during posthypoxic periods in vivo. Thus our data demonstrate that a functional substance P/NKA system is of great importance for the generation of an adequate respiratory response to hypoxic provocation in newborn mice and during early maturation. It also indicates that substance P (and/or NKA) is involved in the development of the plasticity of the respiratory system.
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36.
  • Berner, J, et al. (författare)
  • Hypoxic ventilatory response in Tac1-/- neonatal mice following exposure to opioids
  • 2012
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 113:11, s. 1718-1726
  • Tidskriftsartikel (refereegranskat)abstract
    • Morphine is the dominating analgetic drug used in neonates, but opioid-induced respiratory depression limits its therapeutic use. In this study, we examined acute morphine effects on respiration during intermittent hypoxia in newborn Tac1 gene knockout mice (Tac1−/−) lacking substance P and neurokinin A. In vivo, plethysmography revealed a blunted hypoxic ventilatory response (HVR) in Tac1−/− mice. Morphine (10 mg/kg) depressed the HVR in wild-type animals through an effect on respiratory frequency, whereas it increased tidal volumes in Tac1−/− during hypoxia, resulting in increased minute ventilation. Apneas were reduced during the first hypoxic episode in both morphine-exposed groups, but were restored subsequently in Tac1−/− mice. Morphine did not affect ventilation or apnea prevalence during baseline conditions. In vitro, morphine (50 nM) had no impact on anoxic response of brain stem preparations of either strain. In contrast, it suppressed the inspiratory rhythm during normoxia and potentiated development of posthypoxic neuronal arrest, especially in Tac1−/−. Thus this phenotype has a higher sensitivity to the depressive effects of morphine on inspiratory rhythm generation, but morphine does not modify the reactivity to oxygen deprivation. In conclusion, although Tac1−/− mice are similar to wild-type animals during normoxia, they differed by displaying a reversed pattern with an improved HVR during intermittent hypoxia both in vivo and in vitro. These data suggest that opioids and the substance P-ergic system interact in the HVR, and that reducing the activity in the tachykinin system may alter the respiratory effects of opioid treatment in newborns.
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37.
  • Bersch, Ines, et al. (författare)
  • Upper and lower motor neuron lesions in tetraplegia: implications for surgical nerve transfer to restore hand function.
  • 2020
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 129:5, s. 1214-1219
  • Tidskriftsartikel (refereegranskat)abstract
    • Nerve transfers (neurotizations) performed under optimal conditions can restore some voluntary control in muscles of the upper extremities in patients with tetraplegia. However, the type of motoneuron lesions in target muscles for nerve transfers influences the functional outcome. Using standardized maps of motor point topography, surface electrical stimulation reliably defines the kind and extent of motoneuron lesion in the sel,ected muscles. In a muscle with an intact lower motor motoneuron, nerve transfers can often successfully reinnervate the chosen key muscle. Conversely, in a lower motoneuron lesion, the nerve transfer outcome is less predictable. However, direct muscle stimulation appears to ameliorate the morphological precondition, a finding that necessitates new preoperative approaches to optimize reinnervation in denervated/partially denervated muscles. Therefore, understanding the impact of electrical stimulation in diagnostics, prognostics, and treatments of upper limbs in tetraplegia is critical for neurotization procedures.
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38.
  • Biselli, P. J. C., et al. (författare)
  • Nasal high-flow therapy reduces work of breathing compared with oxygen during sleep in COPD and smoking controls: a prospective observational study
  • 2017
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 122:1, s. 82-88
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with chronic obstructive pulmonary disease (COPD) endure excessive resistive and elastic loads leading to chronic respiratory failure. Oxygen supplementation corrects hypoxemia but is not expected to reduce mechanical loads. Nasal high-flow (NHF) therapy supports breathing by reducing dead space, but it is unclear how it affects mechanical loads of patients with COPD. The objective of this study was to compare the effects of low-flow oxygen and NHF therapy on ventilation and work of breathing (WOB) in patients with COPD and controls during sleep. Patients with COPD (n = 12) and controls (n = 6) were recruited and submitted to polysomnography to measure sleep parameters and ventilation in response to administration of oxygen and NHF. A subset of six patients also had an esophageal catheter inserted for the purpose of measuring WOB. Patients with COPD had similar minute ventilation (V-E) but lower tidal volumes than matched controls. With oxygen, SaO(2) was increased and V-E was reduced in both controls and patients with COPD, but there was an increase in transcutaneous CO2 levels. NHF produced a greater reduction in V-E and was associated with a reduction in CO2 levels. Although NHF halved WOB, oxygen produced only a minor reduction in this parameter. We conclude that oxygen produced little change in WOB, which was associated with CO2 elevations. On the other hand, NHF produced a large reduction in V-E and WOB with a concomitant decrease in CO2 levels. Our data indicate that NHF improves alveolar ventilation during sleep compared with oxygen and room air in patients with COPD and therefore can decrease their cost of breathing. NEW & NOTEWORTHY Nasal high-flow (NHF) therapy can support ventilation in patients with chronic obstructive pulmonary disease during sleep by decreasing the work of breathing and improving CO2 levels. On the other hand, oxygen supplementation corrects hypoxemia, but it produces only a minimal reduction in work of breathing and is associated with increased CO2 levels. Therefore, NHF can be a useful method to assist ventilation in patients with increased respiratory mechanical loads.
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39.
  • Bjarnegård, Niclas, et al. (författare)
  • Arterial properties along the upper arm in humans: age-related effects and the consequence of anatomical location
  • 2010
  • Ingår i: JOURNAL OF APPLIED PHYSIOLOGY. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 108:1, s. 34-38
  • Tidskriftsartikel (refereegranskat)abstract
    • The normal aging process of the brachial artery (BA) wall is of specific interest since it is often selected as a model artery in studies of vascular function. With echo-tracking ultrasound, diameter, absolute diameter change, and intima-media thickness (IMT) were registered in 60 healthy subjects, 21-86 yr (30 men), at a proximal, upper third, and distal arterial site along the upper arm. Blood pressure was recorded noninvasively, and the distensibility coefficient (DC) was calculated. The diameter at the proximal site increased with age from 5.5 +/- 0.2 mm in the young subjects to 6.9 +/- 0.3 mm (P andlt; 0.01) in the elderly subjects, concomitantly as IMT increased from 0.40 +/- 0.01 to 0.65 +/- 0.03 mm (P andlt; 0.001). The diameter at the other sites was similar in the young and elderly subjects, whereas IMT increased slightly with age. At the proximal site, DC decreased dramatically from 40.7 +/- 2.2 to 10.1 +/- 0.8 10(-3)/kPa (P andlt; 0.001) with age, whereas hardly no change was seen in the distal upper arm. The principal transit zone between elastic to predominantly muscular artery behavior seems to be located within the proximal part of the brachial artery, emphasizing the importance of carefully defining the arterial examination site.
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40.
  • Bjornsen, T., et al. (författare)
  • High-frequency blood flow-restricted resistance exercise results in acute and prolonged cellular stress more pronounced in type I than in type II fibers
  • 2021
  • Ingår i: Journal of Applied Physiology. - Rockville : American Physiological Society. - 8750-7587 .- 1522-1601. ; 131:2, s. 643-660
  • Tidskriftsartikel (refereegranskat)abstract
    • Myocellular stress with high-frequency blood flow-restricted resistance exercise (BFRRE) was investigated by measures of heat shock protein (HSP) responses, glycogen content, and inflammatory markers. Thirteen participants [age: 24 +/- 2 yr (means +/- SD), 9 males] completed two 5-day blocks of seven BFRRE sessions, separated by 10 days. Four sets of unilateral knee extensions to failure at 20% of one-repetition maximum (1RM) were performed. Muscle samples obtained before, 1 h after the first session in the first and second block (acute 1 and acute 2), after three sessions (day 4), during the "rest week," and at 3 (post 3) and 10 days postintervention (post 10) were analyzed for HSP70, alpha beta-crystallin, glycogen [periodic acid-Schiff (PAS) staining], mRNAs, miRNAs, and CD68(+) (macrophages) and CD661D(+) (neutrophils) cell numbers. alpha beta-crystallin translocated from the cytosolic to the cytoskeletal fraction after acute 1 and acute 2 (P < 0.05) and immunostaining revealed larger responses in type I than in type II fibers (acute 1, 225 +/- 184% vs. 92 +/- 81%, respectively, P = 0.001). HSP70 was increased in the cytoskeletal fraction at day 4 and post 3, and immunostaining intensities were more elevated in type I than in type II fibers at day 4 (206 +/- 84% vs. 72 +/- 112%, respectively, P <0.001), during the rest week (98 +/- 66% vs. 42 +/- 79%, P < 0.001), and at post 3 (115 +/- 82% vs. 28 +/- 78%, P = 0.003). Glycogen content was reduced in both fiber types, but most pronounced in type I, which did not recover until the rest week (-15% to 29%, P <= 0.001). Intramuscular macrophage numbers were increased by similar to 65% postintervention, but no changes were observed in muscle neutrophils. We conclude that high-frequency BFRRE with sets performed till failure stresses both fiber types, with type I fibers being most affected. NEW & NOTEWORTHY BFRRE has been reported to preferentially stress type I muscle fibers, as evidenced by HSP responses. We extend these findings by showing that the HSP responses occur in both fiber types but more so in type I fibers and that they can still be induced after a short-term training period. Furthermore, the reductions in glycogen content of type I fibers after strenuous frequent BFRRE in unaccustomed subjects can be prolonged (>= 5 days), probably due to microdamage.
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41.
  • Bjørnsen, Thomas, et al. (författare)
  • Delayed myonuclear addition, myofiber hypertrophy and increases in strength with high-frequency low-load blood flow restricted training to volitional failure.
  • 2019
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 126:3, s. 578-592
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate muscle hypertrophy, strength, myonuclear and satellite cell (SC) responses to high-frequency blood flow restricted resistance exercise (BFRRE).Thirteen individuals (24±2 years [mean ± SD], 9 males) completed two 5-day-blocks of 7 BFRRE sessions, separated by a 10-day rest period. Four sets of unilateral knee extensions to voluntary failure at 20% of 1RM were conducted with partial blood flow restriction (90-100 mmHg). Muscle samples obtained before-, during, 3- and 10 days after training were analyzed for muscle fiber area (MFA), myonuclei, SC, and mRNA and miRNA expression. Muscle size was measured by ultrasonography and magnetic resonance imaging, and strength with 1RM knee-extension.With the first block of BFRRE, SC number increased in both fiber types (70-80%, p<0.05), while type I and II MFA decreased by 6±7% and 15±11% (p<0.05), respectively. With the second block of training, muscle size increased by 6-8%, while the number of SC (type I: 80±63%, type II 147±95%), myonuclei (type I: 30±24%, type II: 31±28%) and MFA (type I: 19±19%, type II: 11±19%) peaked 10 days after the second block of BFRRE, whereas strength peaked after 20 days of detraining (6±6%, p<0.05). Pax7- and p21 mRNA expression were elevated during the intervention, while myostatin, IGF1R, MyoD, myogenin, cyclinD1 and -D2 mRNA did not change until 3-10 days post intervention.High frequency low-load BFRRE induced robust increases in SC, myonuclei and muscle size, but modest strength gains. Intriguingly, the responses were delayed and peaked 10-20 days after the training intervention, indicating overreaching.
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42.
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43.
  • Bojsen-Møller, Jens, et al. (författare)
  • Differential displacement of the human soleus and medial gastrocnemius aponeuroses during isometric plantar flexor contractions in vivo.
  • 2004
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 97:5, s. 1908-14
  • Tidskriftsartikel (refereegranskat)abstract
    • The human triceps surae muscle-tendon complex is a unique structure with three separate muscle compartments that merge via their aponeuroses into the Achilles tendon. The mechanical function and properties of these structures during muscular contraction are not well understood. The purpose of the study was to investigate the extent to which differential displacement occurs between the aponeuroses of the medial gastrocnemius (MG) and soleus (Sol) muscles during plantar flexion. Eight subjects (mean +/- SD; age 30 +/- 7 yr, body mass 76.8 +/- 5.5 kg, height 1.83 +/- 0.06 m) performed maximal isometric ramp contractions with the plantar flexor muscles. The experiment was performed in two positions: position 1, in which the knee joint was maximally extended, and position 2, in which the knee joint was maximally flexed (125 degrees ). Plantarflexion moment was assessed with a strain gauge load cell, and the corresponding displacement of the MG and Sol aponeuroses was measured by ultrasonography. Differential shear displacement of the aponeurosis was quantified by subtracting displacement of Sol from that of MG. Maximal plantar flexion moment was 36% greater in position 1 than in position 2 (132 +/- 20 vs. 97 +/- 11 N.m). In position 1, the displacement of the MG aponeurosis at maximal force exceeded that of the Sol (12.6 +/- 1.7 vs. 8.9 +/- 1.5 mm), whereas in position 2 displacement of the Sol was greater than displacement of the MG (9.6 +/- 1.0 vs. 7.9 +/- 1.2 mm). The amount and "direction" of shear between the aponeuroses differed significantly between the two positions across the entire range of contraction, indicating that the Achilles tendon may be exposed to intratendinous shear and stress gradients during human locomotion.
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44.
  • Bolger, C., et al. (författare)
  • Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes
  • 2011
  • Ingår i: Journal of Applied Physiology. - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 111:4, s. 1059-1065
  • Tidskriftsartikel (refereegranskat)abstract
    • Bolger C, Tufvesson E, Anderson SD, Devereux G, Ayres JG, Bjermer L, Sue-Chu M, Kippelen P. Effect of inspired air conditions on exercise-induced bronchoconstriction and urinary CC16 levels in athletes. J Appl Physiol 111: 1059-1065, 2011. First published July 28, 2011; doi:10.1152/japplphysiol.00113.2011.-Injury to the airway epithelium has been proposed as a key susceptibility factor for exercise-induced bronchoconstriction (EIB). Our goals were to establish whether airway epithelial cell injury occurs during EIB in athletes and whether inhalation of warm humid air inhibits this injury. Twenty-one young male athletes (10 with a history of EIB) performed two 8-min exercise tests near maximal aerobic capacity in cold dry (4 degrees C, 37% relative humidity) and warm humid (25 degrees C, 94% relative humidity) air on separate days. Postexercise changes in urinary CC16 were used as a biomarker of airway epithelial cell perturbation and injury. Bronchoconstriction occurred in eight athletes in the cold dry environment and was completely blocked by inhalation of warm humid air [maximal fall in forced expiratory volume in 1 s = 18.1 +/- 2.1% (SD) in cold dry air and 1.7 +/- 0.8% in warm humid air, P < 0.01]. Exercise caused an increase in urinary excretion of CC16 in all subjects (P < 0.001), but this rise in CC16 was blunted following inhalation of warm humid air [median CC16 increase pre- to postchallenge = 1.91 and 0.35 ng/mu mol in cold dry and warm humid air, respectively, in athletes with EIB (P = 0.017) and 1.68 and 0.48 ng/mu mol in cold dry and warm humid air, respectively, in athletes without EIB (P = 0.002)]. The results indicate that exercise hyperpnea transiently disrupts the airway epithelium of all athletes (not only in those with EIB) and that inhalation of warm moist air limits airway epithelial cell perturbation and injury.
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45.
  • Bood, JR, et al. (författare)
  • Urinary excretion of lipid mediators in response to repeated eucapnic voluntary hyperpnea in asthmatic subjects
  • 2015
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 119:3, s. 272-279
  • Tidskriftsartikel (refereegranskat)abstract
    • Exercise-induced bronchoconstriction displays refractoriness manifested as a decreased response to repeated exercise challenge within hours. The refractoriness may be attenuated by inhibition of the biosynthesis of prostaglandins (PG). The aim of the study was to determine which PGs and other lipid mediators are excreted during the refractory period. First, 16 subjects with mild stable asthma performed two repeated 4-min challenges with eucapnic voluntary hyperpnea (EVH) 1 and 3 h apart. There was a similar degree of refractoriness in both protocols (∼15% protection). The 1-h interval was too short to study mediator excretion because the urinary levels did not return to baseline before the second challenge. With the 3-h protocol, there was increased urinary excretion of cysteinyl-leukotrienes and metabolites of the mast cell product PGD2after both challenges. Next, another eight subjects performed two 6-min challenges with EVH 3 h apart, which produced a greater bronchoconstrictor response than the 4-min protocol (30.0 ± 5.4 vs. 17.7 ± 1.5%; P = 0.0029) and a greater degree of refractoriness (∼30%). Analysis by ultra-performance liquid chromatography triple quadrupole mass spectrometry confirmed excretion of the bronchoconstrictor cysteinyl-leukotrienes and PGD2during both challenges. In addition, there was increased excretion of the bronchoprotective PGE2, and also of the main metabolite of PGI2. This is the first report of excretion of PGE2and PGI2during the refractory period to EVH challenge, suggesting that they may mediate the refractoriness. Maintained excretion of PGD2and leukotriene E4following the repeat challenge argues against mast cell mediator depletion as the mechanism of refractoriness.
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46.
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47.
  • Borges, João Batista, et al. (författare)
  • Regional Lung Perfusion estimated by Electrical Impedance Tomography in a piglet model of lung collapse
  • 2011
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 112:1, s. 225-236
  • Tidskriftsartikel (refereegranskat)abstract
    • The assessment of the regional match between alveolar ventilation and perfusion in critically ill patients requires simultaneous measurements of both parameters. Ideally, assessment of lung perfusion should be performed in real-time with an imaging technology which provides, through fast acquisition of sequential images, information about the regional dynamics or regional kinetics of an appropriate tracer. We present a novel electrical impedance tomography (EIT) based method that quantitatively estimates regional lung perfusion based on first-pass kinetics of a bolus of hypertonic saline contrast. Pulmonary blood flow was measured in six piglets during control and unilateral or bilateral lung collapse conditions. The first-pass kinetics method showed good agreement with the estimates obtained by single-photon-emission computerized tomography (SPECT). The mean difference (SPECT minus EIT) between fractional blood flow to lung areas suffering atelectasis was -0.6 %, with a standard deviation of 2.9 %. This method outperformed the estimates of lung perfusion based on impedance-pulsatility. In conclusion, we describe a novel method based on Electrical Impedance Tomography for estimating regional lung perfusion at the bedside. In both, healthy and injured lung conditions, the distribution of pulmonary blood flow as assessed by EIT agreed well with the one obtained by SPECT. The method proposed in this paper has the potential to contribute to a better understanding of the behavior of regional perfusion under different lung and therapeutic conditions.
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48.
  • Brage, Søren, et al. (författare)
  • Hierarchy of individual calibration levels for heart rate and accelerometry to measure physical activity.
  • 2007
  • Ingår i: J Appl Physiol. - : American Physiological Society. - 8750-7587. ; 103:2, s. 682-92
  • Tidskriftsartikel (refereegranskat)abstract
    • Combining accelerometry with heart rate (HR) monitoring may improve precision of physical activity measurement. Considerable variation exists in the relationships between physical activity intensity (PAI) and HR and accelerometry, which may be reduced by individual calibration. However, individual calibration limits feasibility of these techniques in population studies, and less burdensome, yet valid, methods of calibration are required. We aimed to evaluate the precision of different individual calibration procedures against a reference calibration procedure: a ramped treadmill walking-running test with continuous measurement of PAI by indirect calorimetry in 26 women and 25 men [mean (SD): 35 ( 9 ) yr, 1.69 (0.10) m, 70 ( 14 ) kg]. Acceleration (along the longitudinal axis of the trunk) and HR were measured simultaneously. Alternative calibration procedures included treadmill testing without calorimetry, submaximal step and walk tests with and without calorimetry, and nonexercise calibration using sleeping HR and gender. Reference accelerometry and HR models explained >95% of the between-individual variance in PAI ( P < 0.001). This fraction dropped to 73 and 81%, respectively, for accelerometry and HR models calibrated with treadmill tests without calorimetry. Step-test calibration captured 62–64% (accelerometry) and 68% (HR) of the variance between individuals. Corresponding values were 63–76% and 59–61% for walk-test calibration. There was only little benefit of including calorimetry during step and walk calibration for HR models. Nonexercise calibration procedures explained 54% (accelerometry) and 30% (HR) of the between-individual variance. In conclusion, a substantial proportion of the between-individual variance in relationships between PAI, accelerometry, and HR is captured with simple calibration procedures, feasible for use in epidemiological studies.
  •  
49.
  • Brink-Elfegoun, Tibault, et al. (författare)
  • Maximal oxygen uptake is not limited by a central nervous system governor.
  • 2007
  • Ingår i: Journal of applied physiology. - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 102:2, s. 781-6
  • Tidskriftsartikel (refereegranskat)abstract
    • We tested the hypothesis that the work of the heart was not a limiting factor in the attainment of maximal oxygen uptake (VO2 max). We measured cardiac output (Q) and blood pressures (BP) during exercise at two different rates of maximal work to estimate the work of the heart through calculation of the rate-pressure product, as a part of the ongoing discussion regarding factors limiting VO2 max. Eight well-trained men (age 24.4 +/- 2.8 yr, weight 81.3 +/- 7.8 kg, and VO2 max 59.1 +/- 2.0 ml x min(-1) x kg(-1)) performed two maximal combined arm and leg exercises, differing 10% in watts, with average duration of time to exhaustion of 4 min 50 s and 3 min 40 s, respectively. There were no differences between work rates in measured VO2 max, maximal Q, and peak heart rate between work rates (0.02 l/min, 0.3 l/min, and 0.8 beats/min, respectively), but the systolic, diastolic, and calculated mean BP were significantly higher (19, 5, and 10 mmHg, respectively) in the higher than in the lower maximal work rate. The products of heart rate times systolic or mean BP and Q times systolic or mean BP were significantly higher (3,715, 1,780, 569, and 1,780, respectively) during the higher than the lower work rate. Differences in these four products indicate a higher mechanical work of the heart on higher than lower maximal work rate. Therefore, this study does not support the theory, which states that the work of the heart, and consequently VO2 max, during maximal exercise is hindered by a command from the central nervous system aiming at protecting the heart from being ischemic.
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50.
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