Jacobs 2011 J Appl Physiol
|Jacobs R, Rasmussen P, Siebenmann C, Díaz V, Pesta D, Gnaiger E, Nordsborg NB, Robach P, Lundby C (2011) Determinants of time trial performance and maximal incremental exercise in highly trained endurance athletes. J Appl Physiol 111:1422–30.|
Jacobs R, Rasmussen P, Siebenmann C, Diaz V, Pesta D, Gnaiger Erich, Nordsborg NB, Robach P, Lundby C (2011) J Appl Physiol
Abstract: Human endurance performance can be predicted by the product of maximal oxygen consumption (VO2max), lactate threshold, and exercise economy. These physiologic parameters, however, are not wholly exclusive from one another and their interplay is complex. Accordingly, we sought to identify more specific measurements explaining the division of performance among athletes. Out of 150 separate variables we identified 10 principal factors responsible for hematological, cardiovascular, respiratory, musculoskeletal, and neurologic variation in 16 highly trained cyclists. These principal factors were then correlated with a 26 km time trial and test of maximal incremental power output. Average power output during a 26 km time trial was attributed to, in order of importance, oxidative phosphorylation capacity of the m. vastus lateralis (p=0.0005), steady state submaximal blood lactate concentrations (p=0.0017), and maximal leg oxygenation (O2LEG) (p=0.0295) accounting for 78% of the variation in time trial performance. Variability in maximal incremental power output, on the other hand, was attributed to total body hemoglobin mass (Hbmass; p=0.0038), VO2max (p=0.0213), and O2LEG (p=0.0463). In conclusion: 1) Skeletal muscle oxidative capacity is the primary predictor of time trial performance in highly trained cyclists; 2) The strongest predictor for maximal incremental power output is Hbmass; and 3) Overall exercise performance (time trial performance + maximal incremental power output) correlates most strongly to measures regarding the capability for oxygen transport, high VO2max and Hbmass, in addition to measures of oxygen utilization, maximal oxidative phosphorylation and electron transport system capacities in the skeletal muscle.
• O2k-Network Lab: CH Zurich Lundby C, AT Innsbruck Gnaiger E, US CO Colorado Springs Jacobs RA
Stress:Ischemia-reperfusion Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ET Pathway: F, N, S, NS HRR: Oxygraph-2k