Heavy-intensity priming exercise extends the V̇o2max plateau and increases peak-power output during ramp-incremental exercise.

This study investigated whether a heavy-intensity priming exercise precisely prescribed within the heavy-intensity domain would lead to a greater peak-power output (POpeak) and a longer maximal oxygen uptake (V̇o2max) plateau. Twelve recreationally active adults participated in this study. Two visits were required: 1) a step-ramp-step test [ramp-incremental (RI) control], and 2) an RI test preceded by a priming exercise within the heavy-intensity domain (RI primed). A piecewise equation was used to quantify the V̇o2 plateau duration (V̇o2plateau-time). The mean response time (MRT) was computed during the RI control condition. The delta (Δ) V̇o2 slope (S; mL·min-1·W-1) and V̇o2-Y intercept (Y; mL·min-1) within the moderate-intensity domain between conditions (RI primed minus RI control) were also assessed using a novel graphical analysis. V̇o2plateau-time (P = 0.001; d = 1.27) and POpeak (P = 0.003; d = 1.08) were all greater in the RI primed. MRT (P < 0.001; d = 2.45) was shorter in the RI primed compared with the RI control. A larger ΔV̇o2plateau-time was correlated with a larger ΔMRT between conditions (r = -0.79; P = 0.002). This study demonstrated that heavy-intensity priming exercise lengthened the V̇o2plateau-time and increased POpeak. The overall faster RI-V̇o2 responses seem to be responsible for the longer V̇o2plateau-time. Specifically, a shorter MRT, but not changes in RI-V̇o2-slopes, was associated with a longer V̇o2plateau-time following priming exercise.NEW & NOTEWORTHY It remains unclear whether priming exercise extends the maximal oxygen uptake (V̇o2max) plateau and increases peak-power output (POpeak) during ramp-incremental (RI) tests. This study demonstrates that a priming exercise, precisely prescribed within the heavy-intensity domain, extends the plateau at V̇o2max and leads to a greater POpeak. Specifically, the extended V̇o2max plateau was associated with accelerated RI-V̇o2 responses.

Five Weeks of Sprint Interval Training Improve Muscle Glycolytic Content and Activity But Not Time to Task Failure in Severe-Intensity Exercise.

PURPOSE: This study examined the impact of a 5-wk sprint interval training (SIT) intervention on time to task failure (TTF) during severe-intensity constant work rate (CWR) exercise, as well as in glycolytic enzymatic content and activity, and glycogen content. METHODS: Fourteen active males were randomized into either a SIT group ( n = 8) composed of 15 SIT sessions over 5 wk, or a control group ( n = 6). At pretraining period, participants performed i) ramp incremental test to measure the cardiorespiratory function; ii) CWR cycling TTF at 150% of the power output (PO) at the respiratory compensation point (RCP-PO) with muscle biopsies at rest and immediately following task failure. After 5 wk, the same evaluations were repeated (i.e., exercise intensities matched to current training status), and an additional cycling CWR matched to pretraining 150% RCP-PO was performed only for TTF evaluation. The content and enzymatic activity of glycogen phosphorylase (GPhos), hexokinase (HK), phosphofructokinase (PFK), and lactate dehydrogenase (LDH), as well as the glycogen content, were analyzed. Content of monocarboxylate transporter isoform 4 (MCT4) and muscle buffering capacity were also measured. RESULTS: Despite improvements in total work performed at CWR posttraining, no differences were observed for TTF. The GPhos, HK, PFK, and LDH content and activity, and glycogen content also improved after training only in the SIT group. Furthermore, the MCT4 concentrations and muscle buffering capacity were also improved only for the SIT group. However, no difference in glycogen depletion was observed between groups and time. CONCLUSIONS: Five weeks of SIT improved the glycolytic pathway parameters and total work performed; however, glycogen depletion was not altered during CWR severe-intensity exercise, and TTF remained similar.

Heart Rate Variability Thresholds: Agreement with Established Approaches and Reproducibility in Trained Females and Males.

PURPOSE: To determine in trained females and males i) the agreement between the gas exchange threshold (GET), lactate threshold 1 (LT1), and heart rate variability threshold 1 (HRVT1), as well as between the respiratory compensation point (RCP), lactate threshold 2 (LT2), and heart rate variability threshold 2 (HRVT2), and ii) the reproducibility of HRVT1 and HRVT2 during 2-min incremental step protocols. METHODS: Fifty-seven trained participants (24 females) completed a 2-min step incremental test to task failure. Nineteen participants (eight females) completed a second test to evaluate reproducibility. Gas exchange and ventilatory responses, blood lactate concentration, and RR time series were recorded to assess the oxygen consumption (V̇O 2 ) and heart rate (HR) associated with the GET, RCP, LT1, LT2, HRVT1, and HRVT2. RESULTS: V̇O 2 -GET versus V̇O 2 -HRVT1 and HR-GET versus HR-HRVT1 were statistically different for females (29.5 ± 4.0 vs 34.6 ± 6.1 mL·kg -1 ·min -1 ; 154 ± 11 vs 166 ± 12 bpm) and for males (33.9 ± 4.2 vs 42.7 ± 4.6 mL·kg -1 ·min -1 ; 145 ± 11 vs 165 ± 9 bpm; P < 0.001). V̇O 2 and HR at HRVT1 were greater than at LT1 ( P < 0.05). V̇O 2 -RCP versus V̇O 2 -HRVT2 and HR-RCP versus HR-HRVT2 were not statistically different for females (40.1 ± 4.7 vs 39.5 ± 6.7 mL·kg -1 ·min -1 ; 177 ± 9 vs 176 ± 9 bpm) and males (48.4 ± 5.4 vs 47.8 ± 4.8 mL·kg -1 ·min -1 ; 176 ± 8 vs 175 ± 9 bpm; P > 0.05). V̇O 2 and HR responses at LT2 were similar to HRVT2 ( P > 0.05). Intraclass correlation coefficient for V̇O 2 -HRVT1, HR-HRVT1, V̇O 2 -HRVT2, and HR-HRVT2 indicated good reproducibility when comparing the two different time points to standard methods. CONCLUSIONS: Whereas HRVT2 is a valid and reproducible estimate of the RCP/LT2, current approaches for HRVT1 estimation did not show good agreement with outcomes at GET and LT1.

A Ramp versus Step Transition to Constant Work Rate Exercise Decreases Steady-State Oxygen Uptake.

PURPOSE: This study aimed to investigate whether a ramp-to-constant WR (rCWR) transition compared with a square-wave-to-constant WR (CWR) transition within the heavy-intensity domain can reduce metabolic instability and decrease the oxygen cost of exercise. METHODS: Fourteen individuals performed (i) a ramp-incremental test to task failure, (ii) a 21-min CWR within the heavy-intensity domain, and (iii) an rCWR to the same WR. Oxygen uptake (V̇O 2 ), lactate concentration ([La - ]), and muscle oxygen saturation (SmO 2 ) were measured. V̇O 2 and V̇O 2 gain (V̇O 2 -G) during the first 10-min steady-state V̇O 2 were analyzed. [La - ] before, at, and after steady-state V̇O 2 and SmO 2 during the entire 21-min steady-state exercise were also examined. RESULTS: V̇O 2 and V̇O 2 -G during rCWR (2.49 ± 0.58 L·min -1 and 10.7 ± 0.2 mL·min -1 ·W -1 , respectively) were lower ( P < 0.001) than CWR (2.57 ± 0.60 L·min -1 and 11.3 ± 0.2 mL·min -1 ·W -1 , respectively). [La - ] before and at steady-state V̇O 2 during the rCWR condition (1.94 ± 0.60 and 3.52 ± 1.19 mM, respectively) was lower than the CWR condition (3.05 ± 0.82 and 4.15 ± 1.25 mM, respectively) ( P < 0.001). [La - ] dynamics after steady-state V̇O 2 were unstable for the rCWR ( P = 0.011). SmO 2 was unstable within the CWR condition from minutes 4 to 13 ( P < 0.05). CONCLUSIONS: The metabolic disruption caused by the initial minutes of square-wave exercise transitions is a primary contributor to metabolic instability, leading to an increased V̇O 2 -G compared with the rCWR condition approach. The reduced early reliance on anaerobic energy sources during the rCWR condition may be responsible for the lower V̇O 2 -G.

Can the heart rate response at the respiratory compensation point be used to retrieve the maximal metabolic steady state?

The metabolic rate (VO2) at the maximal metabolic steady state (MMSS) is generally not different from the VO2 at the respiratory compensation point (RCP). Based on this, it is often assumed that the heart rate (HR) at RCP would also be similar to that at MMSS. The study aims to compare the HR at RCP with that at MMSS. Seventeen individuals completed a ramp-incremental test, a series of severe-intensity trials to estimate critical power and two-to-three 30-min trials to confirm MMSS. The HR at RCP was retrieved by linear interpolation of the ramp-VO2/HR relationship and compared to the HR at MMSS recorded at 10, 15, 20, 25 and 30 min. The HR at RCP was 166 ± 12 bpm. The HR during MMSS at the timepoints of interest was 168 ± 8, 171 ± 8, 175 ± 9, 177 ± 9 and 178 ± 10 bpm. The HR at RCP was not different from the HR at MMSS at 10 min (P > 0.05) but lower at subsequent timepoints (P < 0.05) with this difference becoming progressively larger. For all timepoints, limits of agreement were large (~30 bpm). Given these differences and the variability at the individual level, the HR at RCP cannot be used to control the metabolic stimulus of endurance exercise.