Looking Beyond A-vo2 Difference: Peripheral Adaptations And Vo2Max In Trained And Untrained Adults

Abstract

PURPOSE: Observing little-to-no increase in arterial-venous oxygen difference (a-vO2diff) following endurance training, some previous investigations have attributed little importance to factors peripheral to the heart, such as maximal mitochondrial oxygen consumption (MitoVO2max) and convective (QmO2) and diffusive (DmO2) muscle oxygen delivery in the training-induced increase in VO2max. As lack of change in a-vO2diff does not necessarily indicate a lack of change in peripheral function, the purpose of this study was to determine the combined influences of adaptations peripheral to the heart in the endurance-training-associated increase in VO2max. METHODS: Arterial-venous blood draws and Doppler ultrasound during maximal single leg knee extension (KE) exercise were used to quantify QmO2, DmO2, a-vO2diff and KEVO2max when free of upstream limitations from the heart in 10 untrained and 10 trained young males. Mitochondrial respiration of muscle biopsied from the vastus lateralis was used to quantify MitoVO2max when free from upstream oxygen supply limitations. RESULTS: In agreement with previous investigations, QmO2 and KEVO2max were 20-35% greater in the trained (P<0.05), while a-vO2diff was not markedly different (P>0.05, See Figures A-C). Nevertheless, training was associated with a 50-100% increases in DmO2 and MitoVO2max, (P<0.05). When plotted as a Wagner diagram (Figure D), it becomes clear that the greater KEVO2max in the trained is the result of 3 synergistic adaptations (1. increased MitoVO2max, 2. increased QmO2 and 3. enhanced DmO2), which, together, raise VO2max more than each adaptation would alone. CONCLUSIONS: Despite minimal changes in a-vO2diff, the training-associated increase in KEVO2max is dependent upon specific peripheral factors within the muscle exhibiting a greater capacity, including mitochondrial respiratory capacity, as well as convective and diffusive muscle oxygen delivery.