The controversy about a valid demarcation of different exercise intensity domains is an ongoing discussion in sports and exercise physiology. To-date, thresholds are mostly determined by concentration changes of molecules and biomarkers determining energy-yielding pathways in the blood (i.e., lactate) or by exchange of pulmonary gases (Poole, Rossiter, Brooks, & Gladden, 2020). Besides that, critical power has recently been demonstrated to more accurately reflect a maximal metabolic steady-state than other measures using blood lactate concentration or respiratory gases (Jones, Burnley, Black, Poole, & Vanhatalo, 2019). However, none of these afore mentioned estimates of thresholds intensity takes into account what perturbations occur inside a muscle cell or a mitochondrion where ATP (i.e., the energy currency of the human body) are rephosphorylated using oxidative pathways. Lately, Nilsson, Bjornson, Flockhart, Larsen, and Nielsen (2019) demonstrated in a model that respiratory Complex I is bypassed during high intensity exercise using oxygen uptake (VO2) data derived from an incremental exercise test. Complex I is one of four enzyme complexes that is involved in the electron transport chain that transport protons across the inner mitochondrial membrane in order to create a proton motive force that is used to generate ATP from ADP and inorganic phosphate in Complex V (also known as the enzyme ATPase). The bypass of Complex I is suggested to be based on a trade-off between maximizing power output (i.e., higher flow rate) and maximizing substrate efficiency (i.e., lower flow rate). Complex I max (CImax) refers to this threshold where Complex I is bypassed. The aim of this study is therefore to provide a potential study design for a physiological validation of CImax, i.e., the relation of CImax to the intensity associated with lactate threshold (LT) and the onset of blood lactate accumulation (OBLA).
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