The effect of increasing work rate amplitudes from a common metabolic baseline on the kinetic response of V̇o2p, blood flow, and muscle deoxygenation.

A step-transition in external work rate (WR) increases pulmonary O2 uptake (V̇o2p) in a monoexponential fashion. Although the rate of this increase, quantified by the time constant (τ), has frequently been shown to be similar between multiple different WR amplitudes (ΔWR), the adjustment of O2 delivery to the muscle (via blood flow; BF), a potential regulator of V̇o2p kinetics, has not been extensively studied. To investigate the role of BF on V̇o2p kinetics, 10 participants performed step-transitions on a knee-extension ergometer from a common baseline WR (3 W) to: 24, 33, 45, 54, and 66 W. Each transition lasted 8 min and was repeated four to six times. Volume turbinometry and mass spectrometry, Doppler ultrasound, and near-infrared spectroscopy were used to measure V̇o2p, BF, and muscle deoxygenation (deoxy[Hb + Mb]), respectively. Similar transitions were ensemble-averaged, and phase II V̇o2p, BF, and deoxy[Hb + Mb] were fit with a monoexponential nonlinear least squares regression equation. With increasing ΔWR, τV̇o2p became larger at the higher ΔWRs (P < 0.05), while τBF did not change significantly, and the mean response time (MRT) of deoxy[Hb + Mb] became smaller. These findings that V̇o2p kinetics become slower with increasing ΔWR, while BF kinetics are not influenced by ΔWR, suggest that O2 delivery could not limit V̇o2p in this situation. However, the speeding of deoxy[Hb + Mb] kinetics with increasing ΔWR does imply that the O2 delivery-to-O2 utilization of the microvasculature decreases at higher ΔWRs. This suggests that the contribution of O2 delivery and O2 extraction to V̇O2 in the muscle changes with increasing ΔWR.NEW & NOTEWORTHY A step increase in work rate produces a monoexponential increase in V̇o2p and blood flow to a new steady-state. We found that step transitions from a common metabolic baseline to increasing work rate amplitudes produced a slowing of V̇o2p kinetics, no change in blood flow kinetics, and a speeding of muscle deoxygenation kinetics. As work rate amplitude increased, the ratio of blood flow to V̇o2p became smaller, while the amplitude of muscle deoxygenation became greater. The gain in vascular conductance became smaller, while kinetics tended to become slower at higher work rate amplitudes.

Data analysis technique influences blood flow kinetics parameter estimates for moderate- and heavy-intensity exercise transitions.

NEW FINDINGS: What is the central question of this study? During exercise, there are fluctuations in conduit artery blood flow (BF) caused by both cardiac and muscle contraction-relaxation cycles. What is the optimal method to process Doppler ultrasound-measured BF for the purpose of characterizing the dynamic response of BF during step-transitions in exercise? What is the main finding and its importance? Continuous BF data were processed in relation to either cardiac or muscle contraction-relaxation cycles and computed based on 'binned' or 'rolling' averages over one, two or five consecutive cycles. Kinetics characterization revealed no data processing technique-specific differences in steady-state BF, but variability in the rapidity at which BF attained steady-state (i.e., mean response time) was observed. ABSTRACT: The overall rate of blood flow (BF) adjustment (i.e., kinetics) from the onset of an exercise transition can be quantified by the mean response time (MRT). However, the BF response profile can be distorted during rhythmic, dynamic exercise consequent to variations caused by the cardiac cycle (HR) and the muscle contraction-relaxation (CR) cycle. We examined the extent to which distortions imposed by HR and CR cycles affected BF kinetics. Eight healthy, young men (27 (4) years; mean (SD)) performed transitions of alternate-leg knee-extension exercise from 3 W to either a moderate- (MOD) or heavy-intensity (HVY) power output. Femoral artery BF was continuously measured by Doppler ultrasound and averaged over one, two or five 'binned' (e.g., HR2b, etc.) or 'rolling' (e.g., CR5r, etc.) HR and CR cycles. Among analysis techniques, there were no differences for steady-state BF values at the 3 W baseline. In MOD, MRT using contraction-relaxation cycle (CR1) was smaller than most other analysis techniques. For both MOD and HVY, the 95% confidence interval for MRT was generally larger when using HR- compared to CR-related methods, and monoexponential fits based on 'rolling' averages (HR2r, HR5r, CR2r, CR5r) had a poorer ability to estimate the true end-exercise BF in HVY than in MOD. When modelling BF kinetics, we conclude that the CR1 method is a good option because of its ability to accurately estimate the 'data-determined' end-exercise BF value from the 'model-derived' response, maintain a relatively high density of data points during the transition and yield a relatively small 95% CI.

Power reserve following ramp-incremental cycling to exhaustion: implications for muscle fatigue and function.

In ramp-incremental cycling exercise, some individuals are capable of producing power output (PO) in excess of that produced at their limit of tolerance (LoT) whereas others cannot. This study sought to describe the 1) prevalence of a "power reserve" within a group of young men ( n = 21; mean ± SD: age 25 ± 4 yr; V̇o2max 45 ± 8 ml·kg-1·min-1); and 2) muscle fatigue characteristics of those with and without a power reserve. "Power reserve" (ΔPReserve) was determined as the difference between peak PO achieved during a ramp-incremental test to exhaustion and maximal, single-leg isokinetic dynamometer power determined within 45 s of completing the ramp-incremental test. Between-group differences in pre- vs. postexercise changes in voluntary and electrically stimulated single-leg muscle force production measures (maximal voluntary contraction torque, voluntary activation, maximal isotonic velocity and isokinetic power; 1-, 10-, 50-Hz torque; and 10/50-Hz ratio), V̇o2max, and constant-PO cycling time-to-exhaustion also were assessed. Frequency distribution analysis revealed a dichotomy in the prevalence of a power reserve within the sample resulting in two groups: 1) "No Reserve" (NRES: power reserve <5%; n = 10) and 2) "Reserve" (RES: power reserve >15%; n = 11). At the LoT, all participants had achieved V̇o2max. Muscle fatigue was evident in both groups, although the NRES group had greater reductions ( P < 0.05) in 10-Hz peak torque (PT), 10/50 Hz ratio, and maximal velocity. Time to the LoT during the constant PO test was 22 ± 16% greater ( P < 0.05) in RES (116 ± 19 s; PO = 317 ± 52 W) than in NRES (90 ± 23 s; PO = 337 ± 71 W), despite similar ramp-incremental exercise durations and V̇o2max between groups. Compared with the RES group, the NRES group accrued greater peripheral muscle fatigue at the LoT, suggesting that the mechanisms contributing to exhaustion in a ramp-incremental protocol are not uniform. NEW & NOTEWORTHY This study demonstrates that the mechanisms associated with the limit of tolerance during ramp-incremental cycling exercise differ between those who are capable of generating power output in excess of that at exercise termination vs. those who are not. Those without a "power reserve" exhibit greater peripheral muscle fatigue and reduced muscle endurance, supporting the hypothesis that exhaustion occurs at a specific level of neuromuscular fatigue. In contrast, those with a power reserve likely are limited by other mechanisms.

The slow component of pulmonary O2 uptake accompanies peripheral muscle fatigue during high-intensity exercise.

During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O2 uptake (V̇o2 p) features a developing slow component (V̇o2 pSC). This progressive increase in O2 cost of exercise is suggested to be related to the effects of muscle fatigue development. We hypothesized that peripheral muscle fatigue as assessed by contractile impairment would be associated with the V̇o2 pSC Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ∼Δ60 (very heavy, VH) where Δ is 60% of the difference between LT and peak V̇o2 p The VH exercise was completed for each of 3, 8, 13, and 18 min (i.e., VH3, VH8, VH13, VH18) with each preceded by 3 min of cycling at 20 W. Peripheral muscle fatigue was assessed via pre- vs. postexercise measurements of quadriceps torque in response to brief trains of electrical stimulation delivered at low (10 Hz) and high (50 Hz) frequencies. During exercise, breath-by-breath V̇o2 p was measured by mass spectrometry and volume turbine. The magnitude of V̇o2 pSC increased (P < 0.05) from 224 ± 81 ml/min at VH3 to 520 ± 119, 625 ± 134, and 678 ± 156 ml/min at VH8, VH13, and VH18, respectively. The ratio of the low-to-high frequency (10/50 Hz) response was reduced (P < 0.05) at VH3 (-12 ± 9%) and further reduced (P < 0.05) at VH8 (-25 ± 11%), VH13 (-42 ± 19%), and VH18 (-46 ± 16%), mirroring the temporal pattern of V̇o2 pSC development. The reduction in 10/50 Hz ratio was correlated (P < 0.001, r(2) = 0.69) with V̇o2 pSC amplitude. The temporal and quantitative association of decrements in muscle torque production and V̇o2 pSC suggest a common physiological mechanism between skeletal muscle fatigue and loss of muscle efficiency.