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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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
19.	Apple, F.S, et al. (författare) CK and LD isozymes in human single muscle fibers in trained athletes 1989 Ingår i: Journal of applied physiology. - 8750-7587 .- 1522-1601. ; 66:6, s. 2717-2720 Tidskriftsartikel (refereegranskat)
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 0.5mv 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.
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.
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.
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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