Lactate metabolism during exercise in patients with mitochondrial myopathy
Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10...
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| Published in | Neuromuscular disorders : NMD Vol. 23; no. 8; pp. 629 - 636 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier B.V
01.08.2013
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0960-8966 1873-2364 1873-2364 |
| DOI | 10.1016/j.nmd.2013.05.007 |
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| Abstract | Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10 matched healthy control subjects at rest and during cycle exercise with a combination of femoral arterio-venous differences of lactate, and lactate tracer dilution methodology. During exercise, lactate concentration and production rates were several-fold higher in patients, but despite mitochondrial dysfunction, lactate was oxidized in muscle to the same extent as in healthy control subjects. This surprisingly high ability to burn lactate in working muscle with defective mitochondria, probably relates to the variability of oxidative capacity among muscle fibers. The data suggests that lactate is not solely an indicator of impaired oxidative capacity, but an important fuel for oxidative metabolism, even in muscle with severely impaired mitochondrial function. |
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| AbstractList | Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10 matched healthy control subjects at rest and during cycle exercise with a combination of femoral arterio-venous differences of lactate, and lactate tracer dilution methodology. During exercise, lactate concentration and production rates were several-fold higher in patients, but despite mitochondrial dysfunction, lactate was oxidized in muscle to the same extent as in healthy control subjects. This surprisingly high ability to burn lactate in working muscle with defective mitochondria, probably relates to the variability of oxidative capacity among muscle fibers. The data suggests that lactate is not solely an indicator of impaired oxidative capacity, but an important fuel for oxidative metabolism, even in muscle with severely impaired mitochondrial function. Abstract Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10 matched healthy control subjects at rest and during cycle exercise with a combination of femoral arterio-venous differences of lactate, and lactate tracer dilution methodology. During exercise, lactate concentration and production rates were several-fold higher in patients, but despite mitochondrial dysfunction, lactate was oxidized in muscle to the same extent as in healthy control subjects. This surprisingly high ability to burn lactate in working muscle with defective mitochondria, probably relates to the variability of oxidative capacity among muscle fibers. The data suggests that lactate is not solely an indicator of impaired oxidative capacity, but an important fuel for oxidative metabolism, even in muscle with severely impaired mitochondrial function. Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10 matched healthy control subjects at rest and during cycle exercise with a combination of femoral arterio-venous differences of lactate, and lactate tracer dilution methodology. During exercise, lactate concentration and production rates were several-fold higher in patients, but despite mitochondrial dysfunction, lactate was oxidized in muscle to the same extent as in healthy control subjects. This surprisingly high ability to burn lactate in working muscle with defective mitochondria, probably relates to the variability of oxidative capacity among muscle fibers. The data suggests that lactate is not solely an indicator of impaired oxidative capacity, but an important fuel for oxidative metabolism, even in muscle with severely impaired mitochondrial function.Patients with mitochondrial DNA mutations often have elevated plasma lactate at rest and during exercise, but it is unknown whether the high lactate levels are caused by a high production, an impaired oxidation or a combination. We studied lactate kinetics in 10 patients with mtDNA mutations and 10 matched healthy control subjects at rest and during cycle exercise with a combination of femoral arterio-venous differences of lactate, and lactate tracer dilution methodology. During exercise, lactate concentration and production rates were several-fold higher in patients, but despite mitochondrial dysfunction, lactate was oxidized in muscle to the same extent as in healthy control subjects. This surprisingly high ability to burn lactate in working muscle with defective mitochondria, probably relates to the variability of oxidative capacity among muscle fibers. The data suggests that lactate is not solely an indicator of impaired oxidative capacity, but an important fuel for oxidative metabolism, even in muscle with severely impaired mitochondrial function. |
| Author | Van Hall, Gerrit Orngreen, Mette C. Vissing, John Jeppesen, Tina D. |
| Author_xml | – sequence: 1 givenname: Tina D. surname: Jeppesen fullname: Jeppesen, Tina D. email: Tina@Dysgaard.dk organization: Neuromuscular Research Unit, Section 3342, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark – sequence: 2 givenname: Mette C. surname: Orngreen fullname: Orngreen, Mette C. organization: Neuromuscular Research Unit, Section 3342, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark – sequence: 3 givenname: Gerrit surname: Van Hall fullname: Van Hall, Gerrit organization: Department of Biomedical Sciences, Rigshospitalet, University of Copenhagen, Denmark – sequence: 4 givenname: John surname: Vissing fullname: Vissing, John organization: Neuromuscular Research Unit, Section 3342, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark |
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| Keywords | Premature fatigue Mitochondrial myopathy Lactate acidosis Lactate kinetics |
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| SubjectTerms | Adult Analysis of Variance Blood Pressure - physiology Burns DNA, Mitochondrial - genetics Epinephrine - metabolism Exercise - physiology Female Gas Chromatography-Mass Spectrometry Humans Insulin - metabolism Lactate acidosis Lactate kinetics Lactic Acid - metabolism Male Middle Aged Mitochondrial Myopathies - genetics Mitochondrial Myopathies - metabolism Mitochondrial Myopathies - physiopathology Mitochondrial myopathy Mutation - genetics Neurology Norepinephrine - metabolism Oxygen Consumption Premature fatigue Time Factors |
| Title | Lactate metabolism during exercise in patients with mitochondrial myopathy |
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