Increased maximal oxygen uptake after sprint‐interval training is mediated by central haemodynamic factors as determined by right heart catheterization

Abstract

AbstractThere is a lack of knowledge regarding the contribution of central and peripheral factors to the increases in VO2max following sprint‐interval training (SIT). This study investigated the importance of maximal cardiac output (Qmax) in relation to VO2max improvements following SIT and the relative importance of the hypervolemic response on Qmax and VO2max. We also investigated whether systemic O2 extraction increased with SIT as has been previously suggested. Healthy men and women (n = 9) performed 6 weeks of SIT. State‐of‐the‐art measurements: right heart catheterization, carbon monoxide rebreathing and respiratory gas exchange analysis were used to assess Qmax, arterial O2 content (caO2), mixed venous O2 content (cvO2), blood volume (BV) and VO2max before and after the intervention. In order to assess the relative contribution of the hypervolemic response to the increases in VO2max, BV was re‐established to pre‐training levels by phlebotomy. Following the intervention, VO2max, BV and Qmax increased by 11% (P < 0.001), 5.4% (P = 0.013) and 8.8% (P = 0.004), respectively. cvO2 decreased by 12.4% (P = 0.011) and systemic O2 extraction increased by 4.0% (P = 0.009) during the same period, both variables were unaffected by phlebotomy (P = 0.589 and P = 0.548, respectively). After phlebotomy, VO2max and Qmax reverted back to pre‐intervention values (P = 0.064 and P = 0.838, respectively) and were significantly lower compared with post‐intervention (P = 0.016 and P = 0.018, respectively). The decline in VO2max after phlebotomy was linear to the amount of blood removed (P = 0.007, R = −0.82). The causal relationship between BV, Qmax and VO2max shows that the hypervolemic response is a key mediator of the increases in VO2max following SIT. imageKey points Sprint‐interval training (SIT) is an exercise model involving supramaximal bouts of exercise interspersed with periods of rest known for its efficiency in improving maximal oxygen uptake (VO2max). In contrast to the commonly accepted view where central haemodynamic adaptations are considered to be the key mediators of increases in VO2max there have been propositions highlighting peripheral adaptations as the main mediators in the context of SIT‐induced changes in VO2max. By combining right heart catheterization, carbon monoxide rebreathing and phlebotomy, this study shows that increases in maximal cardiac output due to the expansion of the total blood volume is a major explanatory factor for the improvement in VO2max following SIT, with a smaller contribution from improved systemic oxygen extraction. The present work not only clarifies a controversy in the field by using state‐of‐the‐art methods, but also encourages future research to investigate regulatory mechanisms that could explain how SIT can lead to improvements in VO2max and maximal cardiac output similar to those that have previously been reported for traditional endurance exercise.