Oxygen availability and skeletal muscle oxidative capacity in patients with peripheral artery disease: implications from in vivo and in vitro assessments
Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O 2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despit...
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| Published in | American journal of physiology. Heart and circulatory physiology Vol. 315; no. 4; pp. H897 - H909 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Physiological Society
01.10.2018
|
| Series | Energetics and Metabolism |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0363-6135 1522-1539 1522-1539 |
| DOI | 10.1152/ajpheart.00641.2017 |
Cover
| Abstract | Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V
max
) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O
2
supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O
2
availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O
2
delivery, tissue oxygenation, V
max
, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O
2
and RH + 100% O
2
). Compared with HC subjects, patients with PAD exhibited attenuated O
2
delivery at the same absolute work rate and attenuated tissue reoxygenation and V
max
after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O
2
significantly increased convective O
2
delivery (~44%), tissue reoxygenation (~54%), and V
max
(~60%) in patients with PAD ( P < 0.05), such that V
max
was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O
2
. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O
2
supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD.
NEW & NOTEWORTHY Currently, there is little accord as to the role of O
2
availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O
2
supply and not the impact of an intrinsic mitochondrial defect in this pathology. |
|---|---|
| AbstractList | Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V
) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O
supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O
availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O
delivery, tissue oxygenation, V
, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O
and RH + 100% O
). Compared with HC subjects, patients with PAD exhibited attenuated O
delivery at the same absolute work rate and attenuated tissue reoxygenation and V
after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O
significantly increased convective O
delivery (~44%), tissue reoxygenation (~54%), and V
(~60%) in patients with PAD ( P < 0.05), such that V
was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O
. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O
supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O
availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O
supply and not the impact of an intrinsic mitochondrial defect in this pathology. Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O 2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O 2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O 2 delivery, tissue oxygenation, V max , and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O 2 and RH + 100% O 2 ). Compared with HC subjects, patients with PAD exhibited attenuated O 2 delivery at the same absolute work rate and attenuated tissue reoxygenation and V max after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O 2 significantly increased convective O 2 delivery (~44%), tissue reoxygenation (~54%), and V max (~60%) in patients with PAD ( P < 0.05), such that V max was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O 2 . Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O 2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O 2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O 2 supply and not the impact of an intrinsic mitochondrial defect in this pathology. Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O 2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O 2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O 2 delivery, tissue oxygenation, V max , and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O 2 and RH + 100% O 2 ). Compared with HC subjects, patients with PAD exhibited attenuated O 2 delivery at the same absolute work rate and attenuated tissue reoxygenation and V max after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O 2 significantly increased convective O 2 delivery (~44%), tissue reoxygenation (~54%), and V max (~60%) in patients with PAD ( P < 0.05), such that V max was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O 2 . Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O 2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O 2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O 2 supply and not the impact of an intrinsic mitochondrial defect in this pathology. Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate (Vmax) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O2 delivery, tissue oxygenation, Vmax, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O2 and RH + 100% O2). Compared with HC subjects, patients with PAD exhibited attenuated O2 delivery at the same absolute work rate and attenuated tissue reoxygenation and Vmax after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O2 significantly increased convective O2 delivery (~44%), tissue reoxygenation (~54%), and Vmax (~60%) in patients with PAD (P < 0.05), such that Vmax was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O2. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( Vmax) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O2 delivery, tissue oxygenation, Vmax, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O2 and RH + 100% O2). Compared with HC subjects, patients with PAD exhibited attenuated O2 delivery at the same absolute work rate and attenuated tissue reoxygenation and Vmax after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O2 significantly increased convective O2 delivery (~44%), tissue reoxygenation (~54%), and Vmax (~60%) in patients with PAD ( P < 0.05), such that Vmax was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O2. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O2 supply and not the impact of an intrinsic mitochondrial defect in this pathology.Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( Vmax) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O2 delivery, tissue oxygenation, Vmax, and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O2 and RH + 100% O2). Compared with HC subjects, patients with PAD exhibited attenuated O2 delivery at the same absolute work rate and attenuated tissue reoxygenation and Vmax after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O2 significantly increased convective O2 delivery (~44%), tissue reoxygenation (~54%), and Vmax (~60%) in patients with PAD ( P < 0.05), such that Vmax was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O2. Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O2 supply and not the impact of an intrinsic mitochondrial defect in this pathology. Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated due to disease-related impairments in O 2 supply. However, in vitro assessments suggest intrinsic deficits in mitochondrial respiration despite ample O 2 availability. To address this conundrum, Doppler ultrasound, near-infrared spectroscopy, phosphorus magnetic resonance spectroscopy, and high-resolution respirometry were combined to assess convective O 2 delivery, tissue oxygenation, V max , and skeletal muscle mitochondrial capacity (complex I + II, state 3 respiration), respectively, in the gastrocnemius muscle of 10 patients with early stage PAD and 11 physical activity-matched healthy control (HC) subjects. All participants were studied in free-flow control conditions (FF) and with reactive hyperemia (RH) induced by a period of brief ischemia during the last 30 s of submaximal plantar flexion exercise. Patients with PAD repeated the FF and RH trials under hyperoxic conditions (FF + 100% O 2 and RH + 100% O 2 ). Compared with HC subjects, patients with PAD exhibited attenuated O 2 delivery at the same absolute work rate and attenuated tissue reoxygenation and V max after relative intensity-matched exercise. Compared with the FF condition, only RH + 100% O 2 significantly increased convective O 2 delivery (~44%), tissue reoxygenation (~54%), and V max (~60%) in patients with PAD ( P < 0.05), such that V max was now not different from HC subjects. Furthermore, there was no evidence of an intrinsic mitochondrial deficit in PAD, as assessed in vitro with adequate O 2 . Thus, in combination, this comprehensive in vivo and in vitro investigation implicates O 2 supply as the predominant factor limiting mitochondrial oxidative capacity in early stage PAD. NEW & NOTEWORTHY Currently, there is little accord as to the role of O 2 availability and mitochondrial function in the skeletal muscle dysfunction associated with peripheral artery disease. This is the first study to comprehensively use both in vivo and in vitro approaches to document that the skeletal muscle dysfunction associated with early stage peripheral artery disease is predominantly a consequence of limited O 2 supply and not the impact of an intrinsic mitochondrial defect in this pathology. |
| Author | Hart, Corey R. Gifford, Jayson R. Richardson, Russell S. Trinity, Joel D. Layec, Gwenael Le Fur, Yann Clifton, Heather L. |
| Author_xml | – sequence: 1 givenname: Corey R. surname: Hart fullname: Hart, Corey R. organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah, Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah – sequence: 2 givenname: Gwenael surname: Layec fullname: Layec, Gwenael organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah, Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah, Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah – sequence: 3 givenname: Joel D. surname: Trinity fullname: Trinity, Joel D. organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah, Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah, Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah – sequence: 4 givenname: Yann surname: Le Fur fullname: Le Fur, Yann organization: Centre de Résonance Magnétique Biologique et Médicale Unité Mixte de Recherché 7339, Aix-Marseille Université, Centre National de la Recherche Scientifique, Marseille, France – sequence: 5 givenname: Jayson R. surname: Gifford fullname: Gifford, Jayson R. organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah – sequence: 6 givenname: Heather L. surname: Clifton fullname: Clifton, Heather L. organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah, Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah – sequence: 7 givenname: Russell S. surname: Richardson fullname: Richardson, Russell S. organization: Geriatric Research, Education, and Clinical Center, George E. Whalen Veterans Affairs Medical Center, Salt Lake City, Utah, Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, Utah, Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, Utah |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29932772$$D View this record in MEDLINE/PubMed https://hal.science/hal-03606816$$DView record in HAL |
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| Snippet | Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V
max
) in patients with peripheral artery disease (PAD) may be attenuated... Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V ) in patients with peripheral artery disease (PAD) may be attenuated due... Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate (Vmax) in patients with peripheral artery disease (PAD) may be attenuated due... Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( Vmax) in patients with peripheral artery disease (PAD) may be attenuated due... Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated... Evidence suggests that the peak skeletal muscle mitochondrial ATP synthesis rate ( V max ) in patients with peripheral artery disease (PAD) may be attenuated... |
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| SubjectTerms | Assessments Attenuation Biochemistry, Molecular Biology Clinical trials Doppler effect Electron transport chain Flow control Gastrocnemius muscle Hyperemia In vivo methods and tests Infrared spectra Infrared spectroscopy Ischemia Life Sciences Magnetic resonance spectroscopy Mitochondria Muscle function Muscles Near infrared radiation Oxygen Oxygenation Pathology Patients Phosphorus Physical activity Physical training Plantar flexion Respiration Respirometry Skeletal muscle Spectroscopy Ultrasound Vascular diseases Vein & artery diseases |
| Title | Oxygen availability and skeletal muscle oxidative capacity in patients with peripheral artery disease: implications from in vivo and in vitro assessments |
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