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.

A stochastic simulation of skeletal muscle calcium transients in a structurally realistic sarcomere model using MCell.

Skeletal muscle contraction is initiated when an action potential triggers the release of Ca2+ into the sarcomere in a process referred to as excitation-contraction coupling. The speed and scale of this process makes direct observation very challenging and invasive. To determine how the concentration of Ca2+ changes within the myofibril during a single activation, several simulation models have been developed. These models follow a common pattern; divide the half sarcomere into a series of compartments, then use ordinary differential equations to solve reactions occurring within and between the compartments. To further develop this type of simulation, we have created a realistic structural model of a skeletal muscle myofibrillar half-sarcomere using MCell software that incorporates the myofilament lattice structure. Using this simulation model, we were successful in reproducing the averaged calcium transient during a single activation consistent with both the experimental and previous simulation results. In addition, our simulation demonstrated that the inclusion of the myofilament lattice within our model produced an asymmetric distribution of Ca2+, with more Ca2+ accumulating near the Z-disk and less Ca2+ reaching the m-line. This asymmetric distribution of Ca2+ is also apparent when we examine how the Ca2+ are bound to the troponin-C proteins along the actin filaments. Our simulation model also allowed us to produce advanced visualizations of this process, including two simulation animations, allowing us to view Ca2+ release, diffusion, binding and uptake within the myofibrillar half-sarcomere.

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.