ABSTRACT
BACKGROUND: Increases in maximal oxygen uptake (VO2max) are widely reported in response to completion of high intensity interval training (HIIT), yet the mechanism explaining this result is poorly understood. This study examined changes in VO2max and cardiac output (CO) in response to 10 sessions of low-volume HIIT. METHODS: Participants included 30 active men and women (mean age and VO2max=22.9±5.4 years and 39.6±5.6 mL/kg/min) who performed HIIT and 30 men and women (age and VO2max=25.7±4.5 years and 40.7±5.2 mL/kg/min) who served as non-exercising controls (CON). High intensity interval training consisted of 6-10 s bouts of cycling per session at 90-110 percent peak power output (PPO) interspersed with 75 s recovery. Before and after training, progressive cycling to exhaustion was completed during which CO, stroke volume (SV), and heart rate (HR) were estimated using thoracic impedance. To confirm VO2max attainment, a verification test was completed after progressive cycling at a work rate equal to 110%PPO. RESULTS: Data demonstrated significant improvements in VO2max (2.71±0.63 L/min to 2.86±0.63 L/min, P<0.001) and COmax (20.0±3.1 L/min to 21.7±3.2 L/min, P=0.04) via HIIT that were not exhibited in CON. Maximal SV was increased in HIIT (P=0.04) although there was no change in maximal HR (P=0.57). CONCLUSIONS: The increase in VO2max seen in response to ten sessions of HIIT is due to improvements in oxygen delivery.
Subject(s)
Cardiac Output , High-Intensity Interval Training , Oxygen/metabolism , Adolescent , Adult , Female , Heart/physiology , Heart Rate , Humans , Male , Oxygen Consumption , Young AdultABSTRACT
PURPOSE: Increased capacity for fat oxidation (FatOx) is demonstrated in response to chronic endurance training as well as high-intensity interval training (HIIT). This study examined changes in maximal fat oxidation (MFO) in response to 20 sessions of periodized HIIT in an attempt to identify if various regimes of HIIT similarly augment capacity for FatOx. METHODS: Thirty-nine habitually active men and women (mean age and VO2max = 22.5 ± 4.4 year and 40.0 ± 5.6 mL/kg/min) completed training and 32 men and women with similar physical activity and fitness level served as non-exercising controls (CON). Training consisted of ten sessions of progressive low-volume HIIT on the cycle ergometer after which participants completed an additional ten sessions of sprint interval training (SIT), high-volume HIIT, or periodized HIIT, whose assignment was randomized. Before and throughout training, MFO, FatOx, and carbohydrate oxidation (CHOOx) were assessed during progressive cycling to exhaustion. RESULTS: Compared to CON, there was no effect of HIIT on MFO (p = 0.11). Small increases (p = 0.03) in FatOx were evident in response to HIIT leading to an additional 4.3 g of fat oxidized, although this value may not be clinically meaningful. CONCLUSIONS: Our results refute the widely reported increases in capacity for FatOx demonstrated with HIIT, which is likely due to marked day-to-day variability in determinations of MFO and exercise fat oxidation as well as the heterogeneity of our sample.
Subject(s)
High-Intensity Interval Training , Lipid Metabolism , Adult , Carbohydrate Metabolism , Energy Metabolism , Female , Humans , Male , Oxidation-ReductionABSTRACT
Increases in maximal oxygen uptake (VËO2max) frequently occur with high-intensity interval training (HIIT), yet the specific adaptation explaining this result remains elusive. PURPOSE: This study examined changes in VËO2max and cardiac output (CO) in response to periodized HIIT. METHODS: Thirty-nine active men and women (mean age and VËO2max = 22.9 ± 5.4 yr and 39.6 ± 5.6 mL·kg·min) performed HIIT and 32 men and women (age and VËO2max = 25.7 ± 4.5 yr and 40.7 ± 5.2 mL·kg·min) were nonexercising controls (CON). The first 10 sessions of HIIT required eight to ten 60 s bouts of cycling at 90%-110% percent peak power output interspersed with 75 s recovery, followed by randomization to one of three regimes (sprint interval training (SIT), high-volume interval training (HIITHI), or periodized interval training (PER) for the subsequent 10 sessions. Before, midway, and at the end of training, progressive cycling to exhaustion was completed during which VËO2max and maximal CO were estimated. RESULTS: Compared with CON, significant (P < 0.001) increases in VËO2max in HIIT + SIT (39.8 ± 7.3 mL·kg·min to 43.6 ± 6.1 mL·kg·min), HIIT + HIITHI (41.1 ± 4.9 mL·kg·min to 44.6 ± 7.0 mL·kg·min), and HIIT + PER (39.5 ± 5.6 mL·kg·min to 44.1 ± 5.4 mL·kg·min) occurred which were mediated by significant increases in maximal CO (20.0 ± 3.1 L·min to 21.7 ± 3.2 L·min, P = 0.04). Maximal stroke volume was increased with HIIT (P = 0.04), although there was no change in maximal HR (P = 0.88) or arteriovenous O2 difference (P = 0.36). These CO data are accurate and represent the mean changes from pre- to post-HIIT across all three training groups. CONCLUSIONS: Increases in VËO2max exhibited in response to different HIIT regimes are due to improvements in oxygen delivery.
