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Difference between revisions of "Larsen 2011 FASEB J"

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{{Publication
{{Publication
|title=Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO (2011) Mitochondrial oxygen affinity predicts basal metabolic rate in humans. FASEB J 25: 2843-2852.
|title=Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO (2011) Mitochondrial oxygen affinity predicts basal metabolic rate in humans. FASEB J 25:2843-52. doi:10.1096/fj.11-182139
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21576503 PMID:21576503]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21576503 PMID:21576503 Open Access]
|authors=Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO
|authors=Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO
|year=2011
|year=2011
|journal=FASEB J
|journal=FASEB J
|abstract=The [[basal respiration|basal metabolic rate]] (BMR) is referred to as the minimal rate of metabolism required to support basic body functions. It is well known that individual BMR varies greatly, even when correcting for body weight, fat content, and thyroid hormone levels, but the mechanistic determinants of this phenomenon remain unknown. Here, we show in humans that mass-related BMR correlates strongly to the mitochondrial oxygen affinity (''p''<sub>50</sub>(mito); ''R''<sup>2</sup>=0.66, ''P''=0.0004) measured in isolated skeletal muscle mitochondria. A similar relationship was found for oxygen affinity and efficiency during constant-load submaximal exercise (''R''<sup>2</sup>=0.46, ''P''=0.007). In contrast, BMR did not correlate to overall mitochondrial density or to proton leak. Mechanistically, part of the ''p''<sub>50</sub>(mito) seems to be controlled by the excess of cytochrome ''c'' oxidase (COX) protein and activity relative to other mitochondrial proteins. This is illustrated by the 5-fold increase in ''p''<sub>50</sub>(mito) after partial cyanide inhibition of COX at doses that do not affect maximal mitochondrial electron flux through the ETS. These data suggest that the interindividual variation in BMR in humans is primarily explained by differences in mitochondrial oxygen affinity. The implications of these findings are discussed in terms of a trade-off between aerobic efficiency and power.
|abstract=The [[basal respiration|basal metabolic rate]] (BMR) is referred to as the minimal rate of metabolism required to support basic body functions. It is well known that individual BMR varies greatly, even when correcting for body weight, fat content, and thyroid hormone levels, but the mechanistic determinants of this phenomenon remain unknown. Here, we show in humans that mass-related BMR correlates strongly to the mitochondrial oxygen affinity (''p''<sub>50</sub>(mito); ''R''<sup>2</sup>=0.66, ''P''=0.0004) measured in isolated skeletal muscle mitochondria. A similar relationship was found for oxygen affinity and efficiency during constant-load submaximal exercise (''R''<sup>2</sup>=0.46, ''P''=0.007). In contrast, BMR did not correlate to overall mitochondrial density or to proton leak. Mechanistically, part of the ''p''<sub>50</sub>(mito) seems to be controlled by the excess of cytochrome ''c'' oxidase (COX) protein and activity relative to other mitochondrial proteins. This is illustrated by the 5-fold increase in ''p''<sub>50</sub>(mito) after partial cyanide inhibition of COX at doses that do not affect maximal mitochondrial electron flux through the ET capacity. These data suggest that the interindividual variation in BMR in humans is primarily explained by differences in mitochondrial oxygen affinity. The implications of these findings are discussed in terms of a trade-off between aerobic efficiency and power.
|mipnetlab=SE_Stockholm_Weitzberg E, SE Stockholm Sahlin K
|mipnetlab=SE_Stockholm_Weitzberg E, SE Stockholm Sahlin K, SE Stockholm Larsen FJ
}}
}}
{{Labeling
{{Labeling
|area=Respiration, mt-Biogenesis; mt-density, Exercise physiology; nutrition; life style
|area=Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine
|organism=Human
|organism=Human
|tissues=Skeletal muscle
|tissues=Skeletal muscle
|preparations=Intact Organism, Isolated Mitochondria
|preparations=Isolated mitochondria
|topics=Inhibitor, O2
|topics=Inhibitor, Oxygen kinetics
|couplingstates=OXPHOS
|couplingstates=OXPHOS
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=proton leak, cytochrome c oxidase, efficiency
|additional=proton leak, cytochrome c oxidase, efficiency
}}
}}

Latest revision as of 09:42, 31 March 2022

Publications in the MiPMap
Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO (2011) Mitochondrial oxygen affinity predicts basal metabolic rate in humans. FASEB J 25:2843-52. doi:10.1096/fj.11-182139

Β» PMID:21576503 Open Access

Larsen FJ, Schiffer TA, Sahlin K, Ekblom B, Weitzberg E, Lundberg JO (2011) FASEB J

Abstract: The basal metabolic rate (BMR) is referred to as the minimal rate of metabolism required to support basic body functions. It is well known that individual BMR varies greatly, even when correcting for body weight, fat content, and thyroid hormone levels, but the mechanistic determinants of this phenomenon remain unknown. Here, we show in humans that mass-related BMR correlates strongly to the mitochondrial oxygen affinity (p50(mito); R2=0.66, P=0.0004) measured in isolated skeletal muscle mitochondria. A similar relationship was found for oxygen affinity and efficiency during constant-load submaximal exercise (R2=0.46, P=0.007). In contrast, BMR did not correlate to overall mitochondrial density or to proton leak. Mechanistically, part of the p50(mito) seems to be controlled by the excess of cytochrome c oxidase (COX) protein and activity relative to other mitochondrial proteins. This is illustrated by the 5-fold increase in p50(mito) after partial cyanide inhibition of COX at doses that do not affect maximal mitochondrial electron flux through the ET capacity. These data suggest that the interindividual variation in BMR in humans is primarily explained by differences in mitochondrial oxygen affinity. The implications of these findings are discussed in terms of a trade-off between aerobic efficiency and power.


β€’ O2k-Network Lab: SE_Stockholm_Weitzberg E, SE Stockholm Sahlin K, SE Stockholm Larsen FJ


Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine 


Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria 

Regulation: Inhibitor, Oxygen kinetics  Coupling state: OXPHOS 

HRR: Oxygraph-2k 

proton leak, cytochrome c oxidase, efficiency