Symmorphosis and skeletal muscle : in vivo and in vitro measures reveal differing constraints in the exercise‐trained and untrained human

Key points The concept of symmorphosis predicts that the capacity of each step of the oxygen cascade is attuned to the task demanded of it during aerobic exercise at maximal rates of oxygen consumption ( ) such that no single process is limiting or in excess at . The present study challenges the applicability of this concept to humans by revealing clear, albeit very different, limitations and excesses in oxygen supply and consumption among untrained and endurance‐trained humans. Among untrained individuals, is limited by the capacity of the mitochondria to consume oxygen, despite an excess of oxygen supply, whereas, among trained individuals, is limited by the supply of oxygen to the mitochondria, despite an excess of mitochondrial respiratory capacity. 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 2 ) supply and demand during maximal skeletal muscle O 2 consumption ( ) in humans is unclear. Therefore, in vitro skeletal muscle mitochondrial ( Mito , mitochondrial respiration of fibres biopsied from vastus lateralis) was compared with in vivo skeletal muscle during single leg knee extensor exercise ( KE , direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole‐body during cycling ( Body , indirect calorimetry) in 10 endurance exercise‐trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O 2 supply ( KE O 2max ) exceeded (462 ± 37 ml kg −1 min −1 , P 0.05) Mito (364 ± 16 ml kg −1 min −1 ). Conversely, in trained subjects, both KE O 2max (557 ± 35 ml kg −1 min −1 ) and KE (458 ± 24 ml kg −1 min −1 ) fell far short of Mito (743 ± 35 ml kg −1 min −1 , P < 0.05). Although Mito was related to KE ( r = 0.69, P < 0.05) and Body ( r = 0.91, P < 0.05) in untrained subjects, these variables were entirely unrelated in trained subjects. Therefore, in untrained subjects, is limited by mitochondrial O 2 demand, with evidence of adequate O 2 supply, whereas, in trained subjects, an exercise training‐induced mitochondrial reserve results in skeletal muscle being markedly limited by O 2 supply. Taken together, these in vivo and in vitro measures reveal clearly differing limitations and excesses at in untrained and trained humans and challenge the concept of symmorphosis as it applies to O 2 supply and demand in humans.