The Training‐Induced Increase in Critical Power Is Strongly Related to Changes in Vascular Function in Young Adults

Abstract

Homeostatic or steady‐state conditions are necessary to sustain exercise. When steady state cannot be achieved, muscle fatigue quickly grows, and task failure promptly occurs. Critical Power (PCRIT) is the highest power output at which steady‐state conditions can be achieved during a given exercise and is strongly related to aerobic capacity. Endurance training increases PCRIT, but the extent to which changes in vascular function, exercise blood flow and mitochondrial function are related to training‐induced changes in PCRIT is unknown.PurposeDetermine the relationship between training‐induced changes in blood flow, mitochondrial function and PCRIT.Methods20 untrained adults participated in either 6 weeks of high‐intensity knee extension exercise (3x per week, n=10) or 6 weeks of sham therapy (3x per week of sham heat therapy, n=10). PCRIT and work‐prime (W′) were determined during single‐leg knee extension (KE) before and after training. Maximum exercise blood flow (Doppler Ultrasound during maximum KE), resistance artery function (passive‐leg‐movement (PLM) technique) and maximum mitochondrial respiration (i.e., State 3 respiration of permeabilized muscle fibers biopsied from the vastus lateralis) were also assessed before and after training.ResultsPCRIT increased by 28% in the exercise group (Figure A, P=0.01), but did not change in the sham group (Figure A). W′ did not significantly change with the intervention (P=0.23). Maximum exercise blood flow (P=0.03), peak flow during PLM (P=0.02), and maximum coupled mitochondrial respiration (i.e., State 3 Respiration, P=0.03) all tended to increase in the exercise group, but not the sham group (P=0.82, 0.18, 0.76, respectively). As illustrated in Figures B, C and D, Pearson correlation indicated that the change in PCRIT was related to the changes in maximum exercise blood flow (R2=0.29, P=0.01), PLM Peak Flow (R2=0.54, P<0.01), and State 3 respiration (R2=0.29, P=0.03).ConclusionsWhile changes maximum exercise blood flow and maximum coupled mitochondrial respiration were related to training‐induced changes in PCRIT, the change in resistance artery function best predicted the training‐induced increase in PCRIT. While not tested in this study, resistance artery function may potentially relate to PCRIT by improving the precision of oxygen delivery and reducing oxygen deficit at the start of exercise. Interventions seeking to improve PCRIT and exercise tolerance, should consider focusing on strategies to enhance resistance artery function in the exercising muscles.