Gifford 2016 J Physiol

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Gifford JR, Garten RS, Nelson AD, Trinity JD, Layec G, Witman MA, Weavil JC, Mangum T, Hart C, Etheredge C, Jessop J, Bledsoe A, Morgan DE, Wray DW, Richardson RS (2016) Symmorphosis and skeletal muscle VO2max: in vivo and in vitro measures reveal differing constraints in the exercise-trained and untrained human. https://doi.org/10.1113/JP271229

» J Physiol 594:1741-51. PMID: 26614395 Open Access

Gifford JR, Garten RS, Nelson AD, Trinity JD, Layec G, Witman MA, Weavil JC, Mangum T, Hart C, Etheredge C, Jessop J, Bledsoe A, Morgan DE, Wray DW, Richardson Russell S (2016) J Physiol

Abstract: The concept of symmorphosis postulates a matching of structural capacity to functional demand within a defined physiological system, regardless of endurance exercise training status. Whether this concept applies to oxygen (O2) supply and demand during maximal skeletal muscle O2 consumption (VO2max) in humans is unclear. Therefore, in vitro skeletal muscle mitochondrial VO2max (Mito VO2max, mitochondrial respiration of fibers biopsied from vastus lateralis) was compared to in vivo skeletal muscle VO2max during single leg knee extensor exercise (KEVO2max, direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole-body VO2max during cycling (BodyVO2max, indirect calorimetry) in 10 endurance-exercise trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O2 supply (KEQO2max) exceeded (462 ± 37 mL∙kg-1∙min-1, P<0.05) and KEVO2max matched (340 ± 22 mL∙kg-1∙min-1, P>0.05) Mito VO2max (364 ± 16 mL∙kg-1∙min-1). Conversely, in trained subjects both KEQO2max (557 ± 35 mL∙kg-1∙min-1) and KEVO2max (458 ± 24 mL∙kg-1∙min-1) fell far short of MitoVO2max (743 ± 35 mL∙kg-1∙min-1, P<0.05). While MitoVO2max was related to KEVO2max (r = 0.69, P<0.05) and BodyVO2max (r = 0.91, P<0.05) in the untrained subjects, these variables were entirely unrelated in the trained subjects. Therefore, in the untrained, VO2max is limited by mitochondrial O2 demand, with evidence of adequate O2 supply, while in trained subjects an exercise training-induced mitochondrial reserve results in skeletal muscle VO2max being markedly limited by O2 supply. Together these in vivo and in vitro measures reveal clearly differing limitations and excesses at VO2max in untrained and trained humans and challenge the concept of symmorphosis as it applies to O2 supply and demand in humans. This article is protected by copyright. All rights reserved.
Keywords: BMI, VO2max

O2k-Network Lab: US UT Salt Lake City Richardson RS, US MA Amherst Busa MA

Selected quotations

  • The unique combination of in vivo and in vitro measures utilized in the present study clarifies the determinants of ̇VO2max and identifies two very different sources of limitation to ̇VO2max in untrained and endurance exercise-trained individuals. Among untrained individuals, ̇VO2max appears to be limited and therefore determined by mitochondrial O2 demand, despite evidence of adequate O2 supply. By contrast, among trained individuals, O2 supply appears to limit ̇VO2max, despite the presence of a large mitochondrial respiratory reserve capacity.


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 


Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized cells 

Regulation: Oxygen kinetics  Coupling state: OXPHOS  Pathway: N, NS 


BMI, VO2max, MitoFit2022Hypoxia