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

Abstract

Abstract There is a lack of knowledge regarding the contribution of central and peripheral factors to the increases in VO 2max following sprint‐interval training (SIT). This study investigated the importance of maximal cardiac output (Q max ) in relation to VO 2max improvements following SIT and the relative importance of the hypervolemic response on Q max and VO 2max . We also investigated whether systemic O 2 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 Q max , arterial O 2 content (c a O 2 ), mixed venous O 2 content (c v O 2 ), blood volume (BV) and VO 2max before and after the intervention. In order to assess the relative contribution of the hypervolemic response to the increases in VO 2max , BV was re‐established to pre‐training levels by phlebotomy. Following the intervention, VO 2max , BV and Q max increased by 11% ( P < 0.001), 5.4% ( P = 0.013) and 8.8% ( P = 0.004), respectively. c v O 2 decreased by 12.4% ( P = 0.011) and systemic O 2 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, VO 2max and Q max 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 VO 2max after phlebotomy was linear to the amount of blood removed ( P = 0.007, R = −0.82). The causal relationship between BV, Q max and VO 2max shows that the hypervolemic response is a key mediator of the increases in VO 2max following SIT. image Key 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 (VO 2max ). In contrast to the commonly accepted view where central haemodynamic adaptations are considered to be the key mediators of increases in VO 2max there have been propositions highlighting peripheral adaptations as the main mediators in the context of SIT‐induced changes in VO 2max . 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 VO 2max 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 VO 2max and maximal cardiac output similar to those that have previously been reported for traditional endurance exercise.

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