Muscle Capillary

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David C Poole - One of the best experts on this subject based on the ideXlab platform.

  • August Krogh: Muscle Capillary function and oxygen delivery.
    Comparative biochemistry and physiology. Part A Molecular & integrative physiology, 2020
    Co-Authors: David C Poole, Yutaka Kano, Shunsaku Koga, Timothy I. Musch
    Abstract:

    Abstract The Capillary bed constitutes the obligatory pathway for almost all oxygen (O2) and substrate molecules as they pass from blood to individual cells. As the largest organ, by mass, skeletal Muscle contains a prodigious surface area of capillaries that have a critical role in metabolic homeostasis and must support energetic requirements that increase as much as 100-fold from rest to maximal exercise. In 1919 Krogh's 3 papers, published in the Journal of Physiology, brilliantly conflated measurements of Muscle Capillary function at rest and during contractions with Agner K. Erlang's mathematical model of O2 diffusion. These papers single-handedly changed the perception of capillaries from passive vessels serving at the mercy of their upstream arterioles into actively contracting vessels that were recruited during exercise to elevate blood-myocyte O2 flux. Although seminal features of Krogh's model have not withstood the test of time and subsequent technological developments, Krogh is credited with helping found the field of Muscle microcirculation and appreciating the role of the Capillary bed and Muscle O2 diffusing capacity in facilitating blood-myocyte O2 flux. Today, thanks in large part to Krogh, it is recognized that comprehending the role of the microcirculation, as it supports perfusive and diffusive O2 conductances, is fundamental to understanding skeletal Muscle plasticity with exercise training and resolving the mechanistic bases by which major pathologies including heart failure and diabetes cripple exercise tolerance and cerebrovascular dysfunction predicates impaired executive function.

  • skeletal Muscle Capillary function contemporary observations and novel hypotheses
    Experimental Physiology, 2013
    Co-Authors: David C Poole, Steven W. Copp, Scott K. Ferguson, Timothy I. Musch
    Abstract:

    New findings • What is the topic of this review?This review presents the paradigm shift in our understanding of Capillary structure and function that has occurred since 1920 (August Krogh's Nobel Prize-winning work). • What advances does it highlight?The compelling weight of evidence supports the concept that most capillaries support red blood cell (RBC) flux in resting Muscle. Increased blood–myocyte flux during contractions thus occurs via elevated RBC flux, velocity and haematocrit in already flowing capillaries, with Capillary surface area being recruited along the length of already flowing capillaries. Heart failure, diabetes and sepsis impair blood–myocyte O2 (and glucose) flux by increasing the proportion of non-RBC/plasma flowing capillaries and compromising the matching of O2 delivery to O2 requirements. The Capillary bed constitutes a vast surface that facilitates exchange of O2, substrates and metabolites between blood and organs. In contracting skeletal Muscle, Capillary blood flow and O2 diffusing capacity, as well as O2 flux, may increase two orders of magnitude above resting values. Chronic diseases, such as heart failure and diabetes, and also sepsis impair these processes, leading to compromised energetic, metabolic and, ultimately, contractile function. Among researchers seeking to understand blood–myocyte exchange in health and the basis for dysfunction in disease, there is a fundamental disconnect between microcirculation specialists and many physiologists and physiologist clinicians. While the former observe capillaries and Capillary function directly (Muscle intravital microscopy), the latter generally use indirect methodologies (e.g. post-mortem tissue analysis, 1-methyl xanthine, contrast-enhanced ultrasound, permeability–surface area product) and interpret their findings based upon August Krogh's observations made nearly a century ago. ‘Kroghian’ theory holds that only a small fraction of capillaries support red blood cell (RBC) flux in resting Muscle, leaving the vast majority to be ‘recruited’ (i.e. to initiate RBC flux) during contractions, which would constitute the basis for increasing surface area for Capillary exchange and reducing Capillary–mitochondrial diffusion distances. Experimental techniques each have their strengths and weaknesses, and often the correct or complete answer to a problem emerges from integration across multiple technologies. Today, Krogh's entrenched ‘Capillary recruitment’ hypothesis is challenged by direct observations of capillaries in contracting Muscle, which is something that he and his colleagues could not do. Moreover, in the peer-reviewed scientific literature, application of a range of contemporary physiological technologies, including intravital microscopy of contracting Muscle, magnetic resonance, near-infrared spectroscopy and phosphorescence quenching, combined with elegant in situ and in vivo models, suggest that the role of the Capillary bed, at least in contracting Muscle, is subserved without the necessity for de novo Capillary recruitment of previously non-flowing capillaries. When viewed within the context of the Capillary recruitment hypothesis, this evidence casts serious doubt on the interpretation of those data that are based upon Kroghian theory and indirect methodologies. Thus, today a wealth of evidence calls for a radical revision of blood–Muscle exchange theory to one in which most capillaries support RBC flux at rest and, during contractions, Capillary surface area is ‘recruited’ along the length of previously flowing capillaries. This occurs, in part, by elevating Capillary haematocrit and extending the length of the Capillary available for blood–myocyte exchange (i.e. longitudinal recruitment). Our understanding of blood–myocyte O2 and substrate/metabolite exchange in health and the mechanistic basis for dysfunction in disease demands no less.

  • Skeletal Muscle Capillary function: contemporary observations and novel hypotheses
    Experimental physiology, 2013
    Co-Authors: David C Poole, Steven W. Copp, Scott K. Ferguson, Timothy I. Musch
    Abstract:

    The Capillary bed constitutes a vast surface that facilitates exchange of O2, substrates and metabolites between blood and organs. In contracting skeletal Muscle, Capillary blood flow and O2 diffusing capacity, as well as O2 flux, may increase two orders of magnitude above resting values. Chronic diseases, such as heart failure and diabetes, and also sepsis impair these processes, leading to compromised energetic, metabolic and, ultimately, contractile function. Among researchers seeking to understand blood-myocyte exchange in health and the basis for dysfunction in disease, there is a fundamental disconnect between microcirculation specialists and many physiologists and physiologist clinicians. While the former observe capillaries and Capillary function directly (Muscle intravital microscopy), the latter generally use indirect methodologies (e.g. post-mortem tissue analysis, 1-methyl xanthine, contrast-enhanced ultrasound, permeability-surface area product) and interpret their findings based upon August Krogh's observations made nearly a century ago. 'Kroghian' theory holds that only a small fraction of capillaries support red blood cell (RBC) flux in resting Muscle, leaving the vast majority to be 'recruited' (i.e. to initiate RBC flux) during contractions, which would constitute the basis for increasing surface area for Capillary exchange and reducing Capillary-mitochondrial diffusion distances. Experimental techniques each have their strengths and weaknesses, and often the correct or complete answer to a problem emerges from integration across multiple technologies. Today, Krogh's entrenched 'Capillary recruitment' hypothesis is challenged by direct observations of capillaries in contracting Muscle, which is something that he and his colleagues could not do. Moreover, in the peer-reviewed scientific literature, application of a range of contemporary physiological technologies, including intravital microscopy of contracting Muscle, magnetic resonance, near-infrared spectroscopy and phosphorescence quenching, combined with elegant in situ and in vivo models, suggest that the role of the Capillary bed, at least in contracting Muscle, is subserved without the necessity for de novo Capillary recruitment of previously non-flowing capillaries. When viewed within the context of the Capillary recruitment hypothesis, this evidence casts serious doubt on the interpretation of those data that are based upon Kroghian theory and indirect methodologies. Thus, today a wealth of evidence calls for a radical revision of blood-Muscle exchange theory to one in which most capillaries support RBC flux at rest and, during contractions, Capillary surface area is 'recruited' along the length of previously flowing capillaries. This occurs, in part, by elevating Capillary haematocrit and extending the length of the Capillary available for blood-myocyte exchange (i.e. longitudinal recruitment). Our understanding of blood-myocyte O2 and substrate/metabolite exchange in health and the mechanistic basis for dysfunction in disease demands no less.

  • Temporal profile of rat skeletal Muscle Capillary haemodynamics during recovery from contractions
    The Journal of Physiology, 2006
    Co-Authors: Leonardo F Ferreira, Timothy I. Musch, Danielle J. Padilla, David C Poole
    Abstract:

    In skeletal Muscle capillaries, red blood cell (RBC) flux (F RBC), velocity (V RBC) and haematocrit (HctCAP) are key determinants of microvascular O2 exchange. However, the mechanisms leading to the changes in F RBC, V RBC and HctCAP during Muscle contractions and recovery thereafter are not fully understood. To address this issue we used intravital microscopy to investigate the temporal profile of the rat spinotrapezius Muscle (n = 5) Capillary haemodynamics during recovery from 3 min of twitch Muscle contractions (1 Hz, 4‐6 V). Specifically, we hypothesized that (1) during early recovery F RBC and V RBC would decrease rapidly and F RBC would display a biphasic response (consistent with a Muscle pump effect on Capillary haemodynamics), and (2) there would be a dynamic relationship between changes (Δ )i nV RBC and HctCAP. The values at rest (R) and end-recovery (ER) were significantly lower (P 0.05). Based on the early decrease in F RBC (within 5 s), overall dynamic profile of F RBC and the ∼20 s ‘delay’ to the decrease in V RBC we conclude that the Muscle pump does not appear to contribute substantially to the steady-state Capillary haemodynamics in the contracting rat spinotrapezius Muscle. Moreover, our findings suggest that alterations in V RBC do not obligate proportional changes in HctCAP within individual capillaries following Muscle contractions.

  • Temporal profile of rat skeletal Muscle Capillary haemodynamics during recovery from contractions.
    The Journal of physiology, 2006
    Co-Authors: Leonardo F Ferreira, Timothy I. Musch, Danielle J. Padilla, David C Poole
    Abstract:

    In skeletal Muscle capillaries, red blood cell (RBC) flux (F(RBC)), velocity (V(RBC)) and haematocrit (Hct(CAP)) are key determinants of microvascular O2 exchange. However, the mechanisms leading to the changes in F(RBC), V(RBC) and Hct(CAP) during Muscle contractions and recovery thereafter are not fully understood. To address this issue we used intravital microscopy to investigate the temporal profile of the rat spinotrapezius Muscle (n = 5) Capillary haemodynamics during recovery from 3 min of twitch Muscle contractions (1 Hz, 4-6 V). Specifically, we hypothesized that (1) during early recovery F(RBC) and V(RBC) would decrease rapidly and F(RBC) would display a biphasic response (consistent with a Muscle pump effect on Capillary haemodynamics), and (2) there would be a dynamic relationship between changes (Delta) in V(RBC) and Hct(CAP). The values at rest (R) and end-recovery (ER) were significantly lower (P < 0.05) than at end-contraction (EC) for F(RBC) (in cells s(-1), R = 30.1 +/- 7.8, EC = 46.2 +/- 7.3 and ER = 26.0 +/- 6.1), V(RBC) (in microm s(-1), R = 368 +/- 83, EC = 497 +/- 62 and ER = 334 +/- 59) and Hct(CAP) (R = 0.193 +/- 0.016, EC = 0.214 +/- 0.023 and ER = 0.185 +/- 0.019). The first data point where a significant decrease in F(RBC), Hct(CAP) and V(RBC) occurred was at 5, 5 and 20 s post-contraction, respectively. The decrease in F(RBC) approximated a monoexponential response (half-time of approximately 26 s). The relationship between DeltaV(RBC) and DeltaHct(CAP) was not significant (P > 0.05). Based on the early decrease in F(RBC) (within 5 s), overall dynamic profile of F(RBC) and the approximately 20 s 'delay' to the decrease in V(RBC) we conclude that the Muscle pump does not appear to contribute substantially to the steady-state Capillary haemodynamics in the contracting rat spinotrapezius Muscle. Moreover, our findings suggest that alterations in V(RBC) do not obligate proportional changes in Hct(CAP) within individual capillaries following Muscle contractions.

Pål Aukrust - One of the best experts on this subject based on the ideXlab platform.

  • cardiac resynchronization therapy improves minute ventilation carbon dioxide production slope and skeletal Muscle Capillary density without reversal of skeletal Muscle pathology or inflammation
    Europace, 2013
    Co-Authors: Alf Inge Larsen, Sigurd Lindal, Kate Myreng, Christer Ogne, Jan Terje Kvaløy, Peter Scott Munk, Pål Aukrust
    Abstract:

    Aims We evaluated the effects of cardiac resynchronization therapy (CRT) on skeletal Muscle pathology and inflammation in patients with heart failure. Methods and results Stable patients ( n = 21, 14 males, mean age 70 ± 7 years) with symptomatic heart failure (mean left ventricular ejection fraction 24 ± 6%) and an indication for CRT were included. Ergospirometry, skeletal Muscle open biopsy, and blood sampling were performed prior to implantation and after 6 months of CRT. After CRT there was a reduction in both left ventricular end-diastolic diameter (LVEDD; 6.8 ± 0.8 vs. 6.3 ± 0.7 cm, P < 0.001) and native QRS duration (D) minus biventricular paced QRSD (172.9 ± 23 vs. 136.3 ± 23 ms, P ≤ 0.001). These changes were associated with an increase in peak slope oxygen uptake (consumption) (VO2) (13.3 ± 2.2 vs. 14.5 ± 2.6 mL/kg/min, P = 0.07) and an improvement in the minute ventilation/carbon dioxide production slope (VE/VCO2) slope (41.6 ± 7.4 vs. 39.1 ± 5.6, P = 0.012). There were no statistically significant changes in levels of pro-inflammatory cytokines, in mediators of mitochondrial biosynthesis or skeletal Muscle pathology, except for an increase in skeletal Muscle Capillary density (4.5 ± 2.4 vs. 7.7 ± 3.3%, P = 0.002). Both the reduction of QRS duration and the increase in peak VO2 correlated significantly with the change in mitochondrial density ( r = 0.57, P = 0.008 and r = 0.54, P = 0.027, respectively). Conclusion Cardiac resynchronization therapy, with improved functional status and reduced LVEDD resulted in increased peak VO2, improvement in VE/VCO2 slope and Capillary density in skeletal Muscle, with no reduction in systemic pro-inflammatory cytokines, increase in intramuscular levels of mediators of mitochondrial biosynthesis or improvement in skeletal Muscle ultrastructure per se . ClinicalTrials.gov Identifier: [NCT01019915][1]. [1]: /lookup/external-ref?link_type=CLINTRIALGOV&access_num=NCT01019915&atom=%2Feuropace%2Fearly%2F2013%2F01%2F14%2Feuropace.eus428.atom

  • Cardiac resynchronization therapy improves minute ventilation/carbon dioxide production slope and skeletal Muscle Capillary density without reversal of skeletal Muscle pathology or inflammation
    Europace : European pacing arrhythmias and cardiac electrophysiology : journal of the working groups on cardiac pacing arrhythmias and cardiac cellula, 2013
    Co-Authors: Alf Inge Larsen, Sigurd Lindal, Kate Myreng, Christer Ogne, Jan Terje Kvaløy, Peter Scott Munk, Pål Aukrust, Arne Yndestad, Kenneth Dickstein, Dennis W.t. Nilsen
    Abstract:

    We evaluated the effects of cardiac resynchronization therapy (CRT) on skeletal Muscle pathology and inflammation in patients with heart failure. Stable patients (n = 21, 14 males, mean age 70 ± 7 years) with symptomatic heart failure (mean left ventricular ejection fraction 24 ± 6%) and an indication for CRT were included. Ergospirometry, skeletal Muscle open biopsy, and blood sampling were performed prior to implantation and after 6 months of CRT. After CRT there was a reduction in both left ventricular end-diastolic diameter (LVEDD; 6.8 ± 0.8 vs. 6.3 ± 0.7 cm, P < 0.001) and native QRS duration (D) minus biventricular paced QRSD (172.9 ± 23 vs. 136.3 ± 23 ms, P ≤ 0.001). These changes were associated with an increase in peak slope oxygen uptake (consumption) (VO₂) (13.3 ± 2.2 vs. 14.5 ± 2.6 mL/kg/min, P = 0.07) and an improvement in the minute ventilation/carbon dioxide production slope (VE/VCO₂) slope (41.6 ± 7.4 vs. 39.1 ± 5.6, P = 0.012). There were no statistically significant changes in levels of pro-inflammatory cytokines, in mediators of mitochondrial biosynthesis or skeletal Muscle pathology, except for an increase in skeletal Muscle Capillary density (4.5 ± 2.4 vs. 7.7 ± 3.3%, P = 0.002). Both the reduction of QRS duration and the increase in peak VO₂ correlated significantly with the change in mitochondrial density (r = 0.57, P = 0.008 and r = 0.54, P = 0.027, respectively). Cardiac resynchronization therapy, with improved functional status and reduced LVEDD resulted in increased peak VO₂, improvement in VE/VCO₂ slope and Capillary density in skeletal Muscle, with no reduction in systemic pro-inflammatory cytokines, increase in intramuscular levels of mediators of mitochondrial biosynthesis or improvement in skeletal Muscle ultrastructure per se. ClinicalTrials.gov Identifier: NCT01019915.

Ylva Hellsten - One of the best experts on this subject based on the ideXlab platform.

  • the effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian Journal of Medicine & Science in Sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P < 0.05) and was unchanged in the HIIT group with no difference between groups. Endothelium thickness increased (P < 0.05), basement membrane thickness decreased (P < 0.05), and the Capillary lumen tended (P = 0.07) to increase in the END group, whereas these structural indicators were unchanged after HIIT. In contrast, skeletal Muscle endothelial nitric oxide synthase (eNOS) increased after HIIT (P < 0.05), but not END, whereas there was no change in vascular endothelial growth factor (VEGF), superoxide dismutase (SOD)-2, or NADPH oxidase after both training protocols. In contrast to END training, HIIT did not alter capillarization or Capillary structure in individuals with type 2 diabetes. In conclusion, HIIT appears to be a less effective strategy to treat Capillary rarefaction and reduce basement thickening in type 2 diabetes.

  • The effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian journal of medicine & science in sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P 

  • exercise induced Capillary growth in human skeletal Muscle and the dynamics of vegf
    Microcirculation, 2014
    Co-Authors: Birgitte Hoier, Ylva Hellsten
    Abstract:

    In skeletal Muscle, growth of capillaries is an important adaptation to exercise training that secures adequate diffusion capacity for oxygen and nutrients even at high-intensity exercise when increases in Muscle blood flow are profound. Mechanical forces present during Muscle activity, such as shear stress and passive stretch, lead to cellular signaling, enhanced expression of angiogenic factors, and initiation of Capillary growth. The most central angiogenic factor in skeletal Muscle Capillary growth is VEGF. During Muscle contraction, VEGF increases in the Muscle interstitium, acts on VEGF receptors on the Capillary endothelium, and thereby stimulates angiogenic processes. A primary source of Muscle interstitial VEGF during exercise is the skeletal Muscle fibers which contain large stores of VEGF within vesicles. We propose that, during Muscle activity, these VEGF-containing vesicles are redistributed toward the sarcolemma where the contents are secreted into the extracellular fluid. VEGF mRNA expression is increased primarily after exercise, which allows for a more rapid replenishment of VEGF stores lost through secretion during exercise. Future studies should focus on elucidating mechanisms and regulation of VEGF secretion.

Stefan P. Mortensen - One of the best experts on this subject based on the ideXlab platform.

  • the effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian Journal of Medicine & Science in Sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P < 0.05) and was unchanged in the HIIT group with no difference between groups. Endothelium thickness increased (P < 0.05), basement membrane thickness decreased (P < 0.05), and the Capillary lumen tended (P = 0.07) to increase in the END group, whereas these structural indicators were unchanged after HIIT. In contrast, skeletal Muscle endothelial nitric oxide synthase (eNOS) increased after HIIT (P < 0.05), but not END, whereas there was no change in vascular endothelial growth factor (VEGF), superoxide dismutase (SOD)-2, or NADPH oxidase after both training protocols. In contrast to END training, HIIT did not alter capillarization or Capillary structure in individuals with type 2 diabetes. In conclusion, HIIT appears to be a less effective strategy to treat Capillary rarefaction and reduce basement thickening in type 2 diabetes.

  • The effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian journal of medicine & science in sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P 

Oliver Baum - One of the best experts on this subject based on the ideXlab platform.

  • the effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian Journal of Medicine & Science in Sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P < 0.05) and was unchanged in the HIIT group with no difference between groups. Endothelium thickness increased (P < 0.05), basement membrane thickness decreased (P < 0.05), and the Capillary lumen tended (P = 0.07) to increase in the END group, whereas these structural indicators were unchanged after HIIT. In contrast, skeletal Muscle endothelial nitric oxide synthase (eNOS) increased after HIIT (P < 0.05), but not END, whereas there was no change in vascular endothelial growth factor (VEGF), superoxide dismutase (SOD)-2, or NADPH oxidase after both training protocols. In contrast to END training, HIIT did not alter capillarization or Capillary structure in individuals with type 2 diabetes. In conclusion, HIIT appears to be a less effective strategy to treat Capillary rarefaction and reduce basement thickening in type 2 diabetes.

  • The effect of two exercise modalities on skeletal Muscle Capillary ultrastructure in individuals with type 2 diabetes
    Scandinavian journal of medicine & science in sports, 2019
    Co-Authors: Stefan P. Mortensen, Kamilla Winding, Ulrik Winning Iepsen, Gregers Winding Munch, Niels Marcussen, Ylva Hellsten, Bente Klarlund Pedersen, Oliver Baum
    Abstract:

    Type 2 diabetes is associated with microvascular dysfunction, but little is known about how Capillary ultrastructure is affected by exercise training. To investigate the effect of two types of exercise training on skeletal Muscle Capillary ultrastructure and capillarization in individuals with type 2 diabetes, 21 individuals with type 2 diabetes were allocated (randomized controlled trial) to 11 weeks of aerobic exercise training consisting of either moderate-intensity endurance training (END; n = 10) or low-volume high-intensity interval training (HIIT; n = 11). Skeletal Muscle biopsies (m vastus lateralis) were obtained before and after the training intervention. At baseline, there was no difference in capillarization, Capillary structure, and exercise hyperemia between the two groups. After the training intervention, Capillary-to-fiber ratio increased by 8% ± 3% in the END group (P