Gifford 2016 J Physiol: Difference between revisions

Revision as of 10:27, 7 December 2015

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 (2015) Symmorphosis and skeletal muscle V_O2max: in vivo and in vitro measures reveal differing constraints in the exercise-trained and untrained human. J Physiol [Epub ahead of print].

» PMID: 26614395

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 (2015) 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 (V_O2max) in humans is unclear. Therefore, in vitro skeletal muscle mitochondrial V_O2max (Mito V_O2max, mitochondrial respiration of fibers biopsied from vastus lateralis) was compared to in vivo skeletal muscle V_O2max during single leg knee extensor exercise (_KEV_O2max, direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole-body V_O2max during cycling (_BodyV_O2max, indirect calorimetry) in 10 endurance-exercise trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O₂ supply (_KEQ_O2max) exceeded (462 ± 37 ml∙kg-1 ∙min-1, P<0.05) and _KEV_O2max matched (340 ± 22 ml∙kg-1 ∙min-1, P>0.05) Mito V_O2max (364 ± 16 ml∙kg-1 ∙min-1). Conversely, in trained subjects both _KEQ_O2max (557 ± 35 ml∙kg-1 ∙min-1) and _KEV_O2max (458 ± 24 ml∙kg-1 ∙min-1) fell far short of _MitoV_O2max (743 ± 35 ml∙kg-1 ∙min-1, P<0.05). While _MitoV_O2max was related to _KEV_O2max (r = 0.69, P<0.05) and _BodyV_O2max (r = 0.91, P<0.05) in the untrained subjects, these variables were entirely unrelated in the trained subjects. Therefore, in the untrained, V_O2max 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 V_O2max being markedly limited by O₂ supply. Together these in vivo and in vitro measures reveal clearly differing limitations and excesses at V_O2max 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

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

Organism: Human Tissue;cell: Skeletal muscle

Regulation: Oxygen kinetics

@@ Line 5: / Line 5: @@
 |year=2015
 |journal=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 (O<sub>2</sub>) supply and demand during maximal skeletal muscle O<sub>2</sub> consumption (''V''<sub>O2max</sub>) in humans is unclear. Therefore, ''in vitro'' skeletal muscle mitochondrial ''V''<sub>O2max</sub> (Mito ''V''<sub>O2max</sub>, mitochondrial respiration of fibers biopsied from ''vastus lateralis'') was compared to ''in vivo'' skeletal muscle ''V''<sub>O2max</sub> during single leg knee extensor exercise (<sub>KE</sub>''V''<sub>O2max</sub>, direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole-body ''V''<sub>O2max</sub> during cycling (<sub>Body</sub>''V''<sub>O2max</sub>, indirect calorimetry) in 10 endurance-exercise trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O<sub>2</sub> supply (<sub>KE</sub>''Q''<sub>O2max</sub>) exceeded (462 ± 37 ml∙kg-1 ∙min-1, ''P''<0.05) and <sub>KE</sub>''V''<sub>O2max</sub> matched (340 ± 22 ml∙kg-1 ∙min-1, ''P''>0.05) Mito ''V''<sub>O2max</sub (364 ± 16 ml∙kg-1 ∙min-1). Conversely, in trained subjects both <sub>KE</sub>''Q''<sub>O2max</sub> (557 ± 35 ml∙kg-1 ∙min-1) and <sub>KE</sub>''V''<sub>O2max</sub (458 ± 24 ml∙kg-1 ∙min-1) fell far short of <sub>Mito</sub>''V''<sub>O2max</sub (743 ± 35 ml∙kg-1 ∙min-1, ''P''<0.05). While <sub>Mito</sub>''V''<sub>O2max</sub was related to <sub>KE</sub>''V''<sub>O2max</sub (''r'' = 0.69, ''P''<0.05) and Body ''V''<sub>O2max</sub (''r'' = 0.91, ''P''<0.05) in the untrained subjects, these variables were entirely unrelated in the trained subjects. Therefore, in the untrained, ''V''<sub>O2max</sub is limited by mitochondrial O<sub>2</sub> demand, with evidence of adequate O<sub>2</sub> supply, while in trained subjects an exercise training-induced mitochondrial reserve results in skeletal muscle ''V''<sub>O2max</sub> being markedly limited by O<sub>2</sub> supply. Together these ''in vivo'' and ''in vitro'' measures reveal clearly differing limitations and excesses at ''V''<sub>O2max</sub in untrained and trained humans and challenge the concept of symmorphosis as it applies to O<sub>2</sub> supply and demand in humans. This article is protected by copyright. All rights reserved.
+|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 (O<sub>2</sub>) supply and demand during maximal skeletal muscle O<sub>2</sub> consumption (''V''<sub>O2max</sub>) in humans is unclear. Therefore, ''in vitro'' skeletal muscle mitochondrial ''V''<sub>O2max</sub> (Mito ''V''<sub>O2max</sub>, mitochondrial respiration of fibers biopsied from ''vastus lateralis'') was compared to ''in vivo'' skeletal muscle ''V''<sub>O2max</sub> during single leg knee extensor exercise (<sub>KE</sub>''V''<sub>O2max</sub>, direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole-body ''V''<sub>O2max</sub> during cycling (<sub>Body</sub>''V''<sub>O2max</sub>, indirect calorimetry) in 10 endurance-exercise trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O<sub>2</sub> supply (<sub>KE</sub>''Q''<sub>O2max</sub>) exceeded (462 ± 37 ml∙kg-1 ∙min-1, ''P''<0.05) and <sub>KE</sub>''V''<sub>O2max</sub> matched (340 ± 22 ml∙kg-1 ∙min-1, ''P''>0.05) Mito ''V''<sub>O2max</sub> (364 ± 16 ml∙kg-1 ∙min-1). Conversely, in trained subjects both <sub>KE</sub>''Q''<sub>O2max</sub> (557 ± 35 ml∙kg-1 ∙min-1) and <sub>KE</sub>''V''<sub>O2max</sub> (458 ± 24 ml∙kg-1 ∙min-1) fell far short of <sub>Mito</sub>''V''<sub>O2max</sub> (743 ± 35 ml∙kg-1 ∙min-1, ''P''<0.05). While <sub>Mito</sub>''V''<sub>O2max</sub> was related to <sub>KE</sub>''V''<sub>O2max</sub> (''r'' = 0.69, ''P''<0.05) and <sub>Body</sub>''V''<sub>O2max</sub> (''r'' = 0.91, ''P''<0.05) in the untrained subjects, these variables were entirely unrelated in the trained subjects. Therefore, in the untrained, ''V''<sub>O2max</sub> is limited by mitochondrial O<sub>2</sub> demand, with evidence of adequate O<sub>2</sub> supply, while in trained subjects an exercise training-induced mitochondrial reserve results in skeletal muscle ''V''<sub>O2max</sub> being markedly limited by O<sub>2</sub> supply. Together these ''in vivo'' and ''in vitro'' measures reveal clearly differing limitations and excesses at ''V''<sub>O2max</sub> in untrained and trained humans and challenge the concept of symmorphosis as it applies to O<sub>2</sub> supply and demand in humans. This article is protected by copyright. All rights reserved.
 |keywords=BMI, VO2max
 }}