Quantifying the effects of four weeks of low-volume high-intensity sprint interval training on V̇O2max through assessment of hemodynamics.

Abstract

Sprint interval training is a popular workout modality. Studies have eluded to a positive effect on maximal oxygen uptake, however little is known about the mechanistic basis of this adaptation. Therefore, the purpose of this study was to determine the effects of a short-term high-intensity sprint interval training (SIT) intervention on V̇O2max through quantification of both the respiratory and hemodynamic responses. Thirty-six physically active participants undertook 4 weeks of either cycling-based SIT (8×20 s at 170% P-V̇O2max with 10 s recovery) or continuous exercise training (CET) (30 min at 70% P-V̇O2max) 3 times per week. V̇O2max, blood-based markers and hemodynamic responses were assessed pre and post the intervention period. V̇O2max was assessed using breath-by-breath open circuit spirometry, while hemodynamic responses were monitored using thoracic impedance cardiography. V̇O2max exhibited a non-significant 4.1% increase (ES=0.24) for SIT with 7.0% P=0.007 (ES=0.40) increase for CET. Hemodynamic responses (maximal cardiac output, maximal stroke volume) displayed non-significant responses for CET and SIT while a-vO2dif-max increased from 15.8±4.8 to 18.3±2.9 mL/100 mL) (P=0.02) (ES=0.63) in SIT. V̇O2max is a function of maximal cardiac output and a-vO2dif-max, so for a meaningful change to occur in cardiorespiratory fitness, there must be a concomitant increase in O2 delivery. This study demonstrates that a low volume SIT intervention evokes peripherally mediated responses (a-vO2dif) and anaerobic substrate utilization rather than O2 delivery components. Future works should address the time course of the responses and when assessing V̇O2max-based responses that due attention be given to the hemodynamic responses as means of quantification of the response.