Difference between revisions of "Schiffer 2014 FASEB J"
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{{Publication | {{Publication | ||
|title=Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ (2014) Dynamic regulation of metabolic efficiency explains tolerance to acute hypoxia in humans. FASEB J 28:4303-11. Β | |title=Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ (2014) Dynamic regulation of metabolic efficiency explains tolerance to acute hypoxia in humans. FASEB J 28:4303-11. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/24970395 PMID: 24970395] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/24970395 PMID: 24970395] | ||
|authors=Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ | |authors=Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ | ||
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drop in Wmax in hypoxia An acute shift in efficiency was | drop in Wmax in hypoxia An acute shift in efficiency was | ||
also demonstrated in isolated mitochondria exposed to | also demonstrated in isolated mitochondria exposed to | ||
physiological levels of hypoxia as | physiological levels of hypoxia as P/O ratio increased | ||
from 0.9 to 1.3 with hypoxic exposure. These findings | from 0.9 to 1.3 with hypoxic exposure. These findings | ||
suggest the existence of a physiological adaptive response | suggest the existence of a physiological adaptive response | ||
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optimized to maximize power production. | optimized to maximize power production. | ||
|keywords=Altitude, Maximum power principle, Mitochondria, Mitochondrial oxygen affinity | |keywords=Altitude, Maximum power principle, Mitochondria, Mitochondrial oxygen affinity | ||
|mipnetlab=SE Stockholm Weitzberg E, SE Stockholm Sahlin K, | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Exercise physiology;nutrition;life style | ||
|instruments=Oxygraph-2k | |organism=Human | ||
|tissues=Skeletal muscle | |||
|preparations=Isolated mitochondria | |||
|injuries=Hypoxia | |||
|couplingstates=OXPHOS, ETS | |||
|substratestates=CI, CII | |||
|instruments=Oxygraph-2k, TIP2k | |||
|additional=Labels | |additional=Labels | ||
}} | }} |
Revision as of 15:37, 24 February 2015
Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ (2014) Dynamic regulation of metabolic efficiency explains tolerance to acute hypoxia in humans. FASEB J 28:4303-11. |
Schiffer TA, Ekblom B, Lundberg JO, Weitzberg E, Larsen FJ (2014) FASEB J
Abstract: The maximum power principle dictates that open biological systems tend to self-organize to a level of efficiency that allows maximal power production. Applying this principle to cellular energetics and whole-body physiology would suggest that for every metabolic challenge, an optimal efficiency exists that maximizes power production. On exposure to hypoxia, it would be favorable if metabolic efficiency would rapidly adjust so as to better preserve work performance. We tested this idea in humans by measuring metabolic efficiency and exercise tolerance under normoxic (FiO2=20.9%) and hypoxic (FiO2=16%) conditions, where FiO2 is fraction of inhaled oxygen. The results were compared with respirometric analyses of skeletal muscle mitochondria from the same individuals. We found that among healthy trained subjects (n=14) with a wide range of metabolic efficiency (ME), those with a high ME during normoxic exercise were able to better maintain exercise capacity (WFmax) in hypoxia. On hypoxic exposure, these subjects acutely decreased their efficiency from 19.2 to 17.4%, thereby likely shifting it closer to a degree of efficiency where maximal power production is achieved. In addition, mitochondria from these subjects had a lower intrinsic respiration compared to subjects that showed a large drop in Wmax in hypoxia An acute shift in efficiency was also demonstrated in isolated mitochondria exposed to physiological levels of hypoxia as P/O ratio increased from 0.9 to 1.3 with hypoxic exposure. These findings suggest the existence of a physiological adaptive response by which metabolic efficiency is dynamically optimized to maximize power production. β’ Keywords: Altitude, Maximum power principle, Mitochondria, Mitochondrial oxygen affinity
β’ O2k-Network Lab: SE Stockholm Weitzberg E, SE Stockholm Sahlin K
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Stress:Hypoxia Organism: Human Tissue;cell: Skeletal muscle Preparation: Isolated mitochondria
Coupling state: OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k, TIP2k
Labels