Lundby, Carsten
Overview
Works: | 22 works in 24 publications in 1 language and 29 library holdings |
---|---|
Roles: | Contributor, dgs, Author, Other, Thesis advisor |
Publication Timeline
.
Most widely held works by
Carsten Lundby
Assessment of total haemoglobin mass: can it detect erythropoietin-induced blood manipulations? by
Carsten Lundby(
)
1 edition published in 2009 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2009 in English and held by 2 WorldCat member libraries worldwide
Effects of Exercise Training in Hypoxia Versus Normoxia on Vascular Health by
David Montero(
)
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
Screening for recombinant human erythropoietin using [Hb], reticulocytes, the OFFhr score, OFFz score and Hbz score: status
of the Blood Passport by Andreas Bornø(
)
1 edition published in 2010 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2010 in English and held by 2 WorldCat member libraries worldwide
Altered skeletal muscle (mitochondrial) properties in patients with mitochondrial DNA single deletion myopathy by
Saskia Maria Gehrig(
)
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2016 in English and held by 2 WorldCat member libraries worldwide
"Live High-Train High" increases hemoglobin mass in Olympic swimmers by
Thomas Christian Bonne(
)
1 edition published in 2014 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2014 in English and held by 2 WorldCat member libraries worldwide
Effects of endurance training on skeletal muscle mitochondrial function in Huntington disease patients by Sandro Manuel Mueller(
)
1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2017 in English and held by 2 WorldCat member libraries worldwide
Red Blood Cell Volume and the Capacity for Exercise at Moderate to High Altitude by
Robert A Jacobs(
)
1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2012 in English and held by 2 WorldCat member libraries worldwide
Cerebral net exchange of large neutral amino acids after lipopolysaccharide infusion in healthy humans by Ronan MG Berg(
)
1 edition published in 2010 in English and held by 2 WorldCat member libraries worldwide
1 edition published in 2010 in English and held by 2 WorldCat member libraries worldwide
Determination of plasma volume by means of carbon monoxide re-breathing and indocyanine green dilution : a comparison of the
two methods by Fabio Wyrsch(
Book
)
1 edition published in 2017 in English and held by 1 WorldCat member library worldwide
1 edition published in 2017 in English and held by 1 WorldCat member library worldwide
Hyperthermia-induced limitations and adaptations to exercise in the heat by
Stefanie Keiser(
Book
)
2 editions published in 2016 in English and held by 1 WorldCat member library worldwide
2 editions published in 2016 in English and held by 1 WorldCat member library worldwide
<<The>> impact of hypoxia on aerobic exercise capacity by
Christoph Andreas Siebenmann(
Book
)
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
Does 'altitude training' increase exercise performance in elite athletes?(
)
1 edition published in 2016 in English and held by 1 WorldCat member library worldwide
New Findings: What is the topic of this review? The aim is to evaluate the effectiveness of various altitude training strategies as investigated within the last few years. What advances does it highlight? Based on the available literature, the foundation to recommend altitude training to athletes is weak. Athletes may use one of the various altitude training strategies to improve exercise performance. The scientific support for such strategies is, however, not as sound as one would perhaps imagine. The question addressed in this review is whether altitude training should be recommended to elite athletes or not. Abstract
1 edition published in 2016 in English and held by 1 WorldCat member library worldwide
New Findings: What is the topic of this review? The aim is to evaluate the effectiveness of various altitude training strategies as investigated within the last few years. What advances does it highlight? Based on the available literature, the foundation to recommend altitude training to athletes is weak. Athletes may use one of the various altitude training strategies to improve exercise performance. The scientific support for such strategies is, however, not as sound as one would perhaps imagine. The question addressed in this review is whether altitude training should be recommended to elite athletes or not. Abstract
Carotid chemoreceptor control of muscle sympathetic nerve activity in hypobaric hypoxia(
)
1 edition published in 2017 in English and held by 1 WorldCat member library worldwide
1 edition published in 2017 in English and held by 1 WorldCat member library worldwide
Sirtuin 5 and activated protein-1 transcription factor JunD as therapeutic targets in acute ischemic stroke by
Candela Diaz-Cañestro(
Book
)
1 edition published in 2018 in English and held by 1 WorldCat member library worldwide
1 edition published in 2018 in English and held by 1 WorldCat member library worldwide
Hypovolemia explains the reduced stroke volume at altitude(
)
1 edition published in 2013 in English and held by 1 WorldCat member library worldwide
Abstract: During acute altitude exposure tachycardia increases cardiac output (Q) thus preserving systemic O2 delivery. Within days of acclimatization, however, Q normalizes following an unexplained reduction in stroke volume (SV). To investigate whether the altitude-mediated reduction in plasma volume (PV) and hence central blood volume (CBV) is the underlying mechanism we increased/decreased CBV by means of passive whole body head-down (HDT) and head-up (HUT) tilting in seven lowlanders at sea level (SL) and after 25/26days of residence at 3454m. Prior to the experiment on day 26, PV was normalized by infusions of a PV expander. Cardiovascular responses to whole body tilting were monitored by pulse contour analysis. After 25/26days at 3454m PV and blood volume decreased by 9±4% and 6±2%, respectively (P <0.001 for both). SV was reduced compared to SL for each HUT angle (P <0.0005). However, the expected increase in SV from HUT to HDT persisted and ended in the same plateau as at SL, albeit this was shifted 18±20° toward HDT (P =0.019). PV expansion restored SV to SL during HUT and to an ~8% higher level during HDT (P =0.003). The parallel increase in SV from HUT to HDT at altitude and SL to a similar plateau demonstrates an unchanged dependence of SV on CBV, indicating that the reduced SV during HUT was related to an attenuated CBV for a given tilt angle. Restoration of SV by PV expansion rules out a significant contribution of other mechanisms, supporting that resting SV at altitude becomes reduced due to a hypovolemia. Abstract : e00094 Abstract : We tested the hypothesis that stroke volume at altitude is reduced due to hypovolemia. In seven lowlanders exposed to 3454m for 4 weeks we manipulated central blood volume by whole body tilting and by plasma volume expansion. Stroke volume at altitude was reduced during head-up tilt but normalized by head-down tilt or plasma volume expansion, indicating that hypovolemia explains the reduced stroke volume at altitude
1 edition published in 2013 in English and held by 1 WorldCat member library worldwide
Abstract: During acute altitude exposure tachycardia increases cardiac output (Q) thus preserving systemic O2 delivery. Within days of acclimatization, however, Q normalizes following an unexplained reduction in stroke volume (SV). To investigate whether the altitude-mediated reduction in plasma volume (PV) and hence central blood volume (CBV) is the underlying mechanism we increased/decreased CBV by means of passive whole body head-down (HDT) and head-up (HUT) tilting in seven lowlanders at sea level (SL) and after 25/26days of residence at 3454m. Prior to the experiment on day 26, PV was normalized by infusions of a PV expander. Cardiovascular responses to whole body tilting were monitored by pulse contour analysis. After 25/26days at 3454m PV and blood volume decreased by 9±4% and 6±2%, respectively (P <0.001 for both). SV was reduced compared to SL for each HUT angle (P <0.0005). However, the expected increase in SV from HUT to HDT persisted and ended in the same plateau as at SL, albeit this was shifted 18±20° toward HDT (P =0.019). PV expansion restored SV to SL during HUT and to an ~8% higher level during HDT (P =0.003). The parallel increase in SV from HUT to HDT at altitude and SL to a similar plateau demonstrates an unchanged dependence of SV on CBV, indicating that the reduced SV during HUT was related to an attenuated CBV for a given tilt angle. Restoration of SV by PV expansion rules out a significant contribution of other mechanisms, supporting that resting SV at altitude becomes reduced due to a hypovolemia. Abstract : e00094 Abstract : We tested the hypothesis that stroke volume at altitude is reduced due to hypovolemia. In seven lowlanders exposed to 3454m for 4 weeks we manipulated central blood volume by whole body tilting and by plasma volume expansion. Stroke volume at altitude was reduced during head-up tilt but normalized by head-down tilt or plasma volume expansion, indicating that hypovolemia explains the reduced stroke volume at altitude
Mitochondrial function in human skeletal muscle following high-altitude exposure(
)
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
Abstract : Studies regarding mitochondrial modifications in human skeletal muscle following acclimatization to high altitude are conflicting, and these inconsistencies may be due to the prevalence of representing mitochondrial function through static and isolated measurements of specific mitochondrial characteristics. The aim of this study, therefore, was to investigate mitochondrial function in response to high-altitude acclimatization through measurements of respiratory control in the vastus lateralis muscle. Skeletal muscle biopsies were obtained from 10 lowland natives prior to and again after a total of 9-11 days of exposure to 4559 m. High-resolution respirometry was performed on the muscle samples to compare respiratory chain function and respiratory capacities. Respirometric analysis revealed that mitochondrial function was largely unaffected, because high-altitude exposure did not affect the capacity for fat oxidation or individualized respiration capacity through either complex I or complex II. Respiratory chain function remained unaltered, because neither coupling nor respiratory control changed in response to hypoxic exposure. High-altitude acclimatization did, however, show a tendency (P = 0.059) to limit mass-specific maximal oxidative phosphorylation capacity. These data suggest that 9-11 days of exposure to high altitude do not markedly modify integrated measures of mitochondrial functional capacity in skeletal muscle despite significant decrements in the concentrations of enzymes involved in the tricarboxylic acid cycle and oxidative phosphorylation
1 edition published in 2012 in English and held by 1 WorldCat member library worldwide
Abstract : Studies regarding mitochondrial modifications in human skeletal muscle following acclimatization to high altitude are conflicting, and these inconsistencies may be due to the prevalence of representing mitochondrial function through static and isolated measurements of specific mitochondrial characteristics. The aim of this study, therefore, was to investigate mitochondrial function in response to high-altitude acclimatization through measurements of respiratory control in the vastus lateralis muscle. Skeletal muscle biopsies were obtained from 10 lowland natives prior to and again after a total of 9-11 days of exposure to 4559 m. High-resolution respirometry was performed on the muscle samples to compare respiratory chain function and respiratory capacities. Respirometric analysis revealed that mitochondrial function was largely unaffected, because high-altitude exposure did not affect the capacity for fat oxidation or individualized respiration capacity through either complex I or complex II. Respiratory chain function remained unaltered, because neither coupling nor respiratory control changed in response to hypoxic exposure. High-altitude acclimatization did, however, show a tendency (P = 0.059) to limit mass-specific maximal oxidative phosphorylation capacity. These data suggest that 9-11 days of exposure to high altitude do not markedly modify integrated measures of mitochondrial functional capacity in skeletal muscle despite significant decrements in the concentrations of enzymes involved in the tricarboxylic acid cycle and oxidative phosphorylation
Adaptations of skeletal muscle mitochondria to exercise training(
)
1 edition published in 2015 in English and held by 1 WorldCat member library worldwide
Abstract : New Findings: What is the topic of this review? We review recent work relating to exercise-induced alterations in mitochondrial structure and function. What advances does it highlight? Training mitochondrial volume density increases due to 1) an increase cross sectional area and 2) longitudinal growth. Specific respiratory alterations appear dependent on exercise training intensity. Low-moderate endurance training primarily improves the capacity for fat oxidation whereas high-intensity interval training (HIT) improves global respiratory capacity. The latter includes maximal state 3 mass-specific respiration, which is the strongest individual measure predictive of endurance performance. This highlights the importance of training specificity in endurance athletes. Mitochondrial volume density (MitoVD) is composed of two distinct mitochondrial subpopulations-- intermyofibrillar mitochondria (MitoIMF) and subsarcolemmal mitochondria (MitoSS). With exercise training, MitoVD may increase by up to 40% and is, for the most part, related to an increase in MitoIMF . Exercise-induced adaptations in mitochondrial function depend on the intensity of training and appear to be explained predominately by an increased expression of mitochondrial enzymes that facilitate aerobic metabolism. Although mitochondrial content often increases with training, it seems that mitochondrial adaptations are not needed to facilitate maximal oxygen uptake, whereas such adaptations are of greater importance for endurance capacity. New Findings: What is the topic of this review? We review recent work relating to exercise-induced alterations in mitochondrial structure and function. What advances does it highlight? Training mitochondrial volume density increases due to 1) an increase cross sectional area and 2) longitudinal growth. Specific respiratory alterations appear dependent on exercise training intensity. Low-moderate endurance training primarily improves the capacity for fat oxidation whereas high-intensity interval training (HIT) improves global respiratory capacity. The latter includes maximal state 3 mass-specific respiration, which is the strongest individual measure predictive of endurance performance. This highlights the importance of training specificity in endurance athletes
1 edition published in 2015 in English and held by 1 WorldCat member library worldwide
Abstract : New Findings: What is the topic of this review? We review recent work relating to exercise-induced alterations in mitochondrial structure and function. What advances does it highlight? Training mitochondrial volume density increases due to 1) an increase cross sectional area and 2) longitudinal growth. Specific respiratory alterations appear dependent on exercise training intensity. Low-moderate endurance training primarily improves the capacity for fat oxidation whereas high-intensity interval training (HIT) improves global respiratory capacity. The latter includes maximal state 3 mass-specific respiration, which is the strongest individual measure predictive of endurance performance. This highlights the importance of training specificity in endurance athletes. Mitochondrial volume density (MitoVD) is composed of two distinct mitochondrial subpopulations-- intermyofibrillar mitochondria (MitoIMF) and subsarcolemmal mitochondria (MitoSS). With exercise training, MitoVD may increase by up to 40% and is, for the most part, related to an increase in MitoIMF . Exercise-induced adaptations in mitochondrial function depend on the intensity of training and appear to be explained predominately by an increased expression of mitochondrial enzymes that facilitate aerobic metabolism. Although mitochondrial content often increases with training, it seems that mitochondrial adaptations are not needed to facilitate maximal oxygen uptake, whereas such adaptations are of greater importance for endurance capacity. New Findings: What is the topic of this review? We review recent work relating to exercise-induced alterations in mitochondrial structure and function. What advances does it highlight? Training mitochondrial volume density increases due to 1) an increase cross sectional area and 2) longitudinal growth. Specific respiratory alterations appear dependent on exercise training intensity. Low-moderate endurance training primarily improves the capacity for fat oxidation whereas high-intensity interval training (HIT) improves global respiratory capacity. The latter includes maximal state 3 mass-specific respiration, which is the strongest individual measure predictive of endurance performance. This highlights the importance of training specificity in endurance athletes
The C57Bl/6 mouse serves as a suitable model of human skeletal muscle mitochondrial function(
)
1 edition published in 2013 in English and held by 1 WorldCat member library worldwide
Abstract : It is debatable whether differences in mitochondrial function exist across skeletal muscle types and whether mouse skeletal muscle mitochondrial function can serve as a valid model for human skeletal muscle mitochondrial function. The aims of this study were to compare and contrast three different mouse skeletal muscles and to identify the mouse muscle that most closely resembles human skeletal muscle respiratory capacity and control. Mouse quadriceps (QUADM), soleus (SOLM) and gastrocnemius (GASTM) skeletal muscles were obtained from 8- to 10-week-old healthy mice (n = 8), representing mixed, oxidative and glycolytic muscle, respectively. Skeletal muscle samples were also collected from young, active, healthy human subjects (n = 8) from the vastis lateralis (QUADH). High-resolution respirometry was used to examine mitochondrial function in all skeletal muscle samples, and mitochondrial content was quantified with citrate synthase activity. Mass-specific respiration was higher across all respiratory states in SOLM versus both GASTM and QUADH (P <0.01). When controlling for mitochondrial content, however, SOLM respiration was lower than GASTM and QUADH (P <0.05 and P <0.01, respectively). When comparing respiratory capacity between mouse and human muscle, QUADM exhibited only one different respiratory state when compared with QUADH . These results demonstrate that qualitative differences in mitochondrial function exist between different mouse skeletal muscles types when respiratory capacity is normalized to mitochondrial content, and that skeletal muscle respiratory capacity in young, healthy QUADM does correspond well with that of young, healthy QUADH
1 edition published in 2013 in English and held by 1 WorldCat member library worldwide
Abstract : It is debatable whether differences in mitochondrial function exist across skeletal muscle types and whether mouse skeletal muscle mitochondrial function can serve as a valid model for human skeletal muscle mitochondrial function. The aims of this study were to compare and contrast three different mouse skeletal muscles and to identify the mouse muscle that most closely resembles human skeletal muscle respiratory capacity and control. Mouse quadriceps (QUADM), soleus (SOLM) and gastrocnemius (GASTM) skeletal muscles were obtained from 8- to 10-week-old healthy mice (n = 8), representing mixed, oxidative and glycolytic muscle, respectively. Skeletal muscle samples were also collected from young, active, healthy human subjects (n = 8) from the vastis lateralis (QUADH). High-resolution respirometry was used to examine mitochondrial function in all skeletal muscle samples, and mitochondrial content was quantified with citrate synthase activity. Mass-specific respiration was higher across all respiratory states in SOLM versus both GASTM and QUADH (P <0.01). When controlling for mitochondrial content, however, SOLM respiration was lower than GASTM and QUADH (P <0.05 and P <0.01, respectively). When comparing respiratory capacity between mouse and human muscle, QUADM exhibited only one different respiratory state when compared with QUADH . These results demonstrate that qualitative differences in mitochondrial function exist between different mouse skeletal muscles types when respiratory capacity is normalized to mitochondrial content, and that skeletal muscle respiratory capacity in young, healthy QUADM does correspond well with that of young, healthy QUADH
Regulation of cerebral blood flow with emphasis on age and environment by
Daniela Katharina Flück(
Book
)
2 editions published in 2015 in English and held by 1 WorldCat member library worldwide
2 editions published in 2015 in English and held by 1 WorldCat member library worldwide
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- SpringerLink (Online service) Other
- Robach, Paul
- Jacobs, Robert A. Author
- Mueller, Sandro Manuel Author Contributor
- Mihaylova, Violeta Other Contributor
- Frese, Sebastian Other Contributor
- Petersen, Jens A. Other Contributor
- Ligon-Auer, Maria Other Contributor
- Gassmann, Max
- Keiser, Stefanie 1989- Author
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