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 modified step-ramp-step protocol to prescribe constant-speed exercise in treadmill running.

PURPOSE: This study investigated whether a running-adapted version of the cycling-based "step-ramp-step" (SRS) protocol would improve prediction of V ˙ O2 in treadmill exercise compared to the traditional prescriptive approach. METHODS: Fourteen healthy individuals (6 females; 25 ± 6 years; 66.1 ± 12.7 kg) performed a treadmill-based SRS protocol including a ramp-incremental test to task failure followed by two constant-speed bouts within the moderate-(MODstep-below estimated lactate threshold; θLT), and heavy-intensity domains (HVYstep-between θLT and respiratory compensation point; RCP). Using the uncorrected V ˙ O2-to-speed relationship from the ramp exercise, three constant-speed bouts were performed at 40-50% between: baseline and θLT (CSEMOD); θLT and RCP (CSEHVY); and RCP and peak (CSESEV). For CSEMOD, CSEHVY, and CSESEV measured end-exercise V ˙ O2 was compared to predicted V ˙ O2 based on the: (i) "SRS-corrected" V ˙ O2-to-speed relationship (where MODstep and HVYstep were used to adjust the V ˙ O2 relative to speed); and (ii) linear "uncorrected" data. RESULTS: Average treadmill speeds for CSEMOD and CSEHVY were 7.8 ± 0.8 and 11.0 ± 1.4 km·h-1, respectively, eliciting end-exercise V ˙ O2 of 1979 ± 390 and 2574 ± 540 mL·min-1. End-exercise V ˙ O2 values were not different compared to SRS-predicted V ˙ O2 at CSEMOD (mean difference: 5 ± 166 mL·min-1; p = 0.912) and CSEHVY (20 ± 128 mL·min-1; p = 0.568). The linear "uncorrected" estimates were not different for CSEMOD (- 91 ± 172 mL·min-1; p = 0.068) but lower for CSEHVY (- 195 ± 146 mL·min-1; p < 0.001). For CSESEV (running speed: 13.8 ± 1.7 km·h-1), the end-exercise V ˙ O2 was not different from peak V ˙ O2 achieved during the ramp (3027 ± 682 vs. 2979 ± 655 mL·min-1; p = 0.231). CONCLUSION: In healthy individuals, the SRS protocol more accurately predicts speeds for a target V ˙ O2 compared to traditional approaches.

The Effects of a 90-km Outdoor Cycling Ride on Performance Outcomes Derived From Ramp-Incremental and 3-Minute All-Out Tests.

ABSTRACT: Bitel, M, Keir, DA, Grossman, K, Barnes, M, Murias, JM, and Belfry, GR. The effects of a 90-km outdoor cycling ride on performance outcomes derived from ramp-incremental and 3-minute all-out tests. J Strength Cond Res 38(3): 540-548, 2024-The purpose of this study was to determine whether laboratory-derived exercise intensity and performance demarcations are altered after prolonged outdoor cycling. Male recreational cyclists ( n = 10; RIDE) performed an exhaustive ramp-incremental test (RAMP) and a 3-minute all-out test (3MT) on a cycle ergometer before and after a 90-km cycling ride. RAMP-derived maximal oxygen uptake (V̇O 2max ), gas exchange threshold (GET), respiratory compensation point (RCP), and associated power output (PO), as well as 3MT-derived critical power (CP) and work performed above CP, were compared before and after ∼3 hours of outdoor cycling. Six active men served as "no-exercise" healthy controls (CON), who, instead, rested for 3 hours between repeated RAMP and 3MT tests. During the 90-km ride, the duration within the moderate-intensity, heavy-intensity, and severe-intensity domains was 59 ± 24%, 40 ± 24%, and 1 ± 1%, respectively. Compared with pre-90 km, post-RAMP exhibited reductions in (a) V̇O 2max (4.04 ± 0.48 vs. 3.80 ± 0.38 L·min -1 ; p = 0.026) and associated PO (392 ± 30 W vs. 357 ± 26 W; p = 0.002); (b) the V̇O 2 and PO at RCP (3.49 ± 0.46 vs. 3.34 ± 0.43 L·min -1 ; p = 0.040 and 312 ± 40 W vs. 292 ± 24 W; p = 0.023); and (c) the PO (214 ± 32 W vs. 198 ± 25 W; p = 0.027), but not the V̇O 2 at GET (2.52 ± 0.44 vs. 2.44 ± 0.38 L·min -1 ; p = 0.388). Pre-90 km vs. post-90 km 3MT variables showed reduced W' (9.8 ± 3.4 vs. 6.8 ± 2.6 kJ; p = 0.002) and unchanged CP (304 ± 26 W and 297 ± 34 W; p = 0.275). In the CON group, there were no differences in V̇O 2max , GET, RCP, W', CP, or associated power outputs ( p > 0.05) pre-to-post 3 hours of rest. The preservation of critical power demonstrates that longer-duration maximal efforts may be sustained after long-duration cycle. However, shorter sprints and higher-intensity efforts eliciting V̇O 2max will exhibit decreased PO after 3 hours of a predominantly moderate-intensity cycle.

A test of the interaction between central and peripheral respiratory chemoreflexes in humans.

How central and peripheral chemoreceptor drives to breathe interact in humans remains contentious. We measured the peripheral chemoreflex sensitivity to hypoxia (PChS) at various isocapnic CO2 tensions ( P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) to determine the form of the relationship between PChS and central P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ . Twenty participants (10F) completed three repetitions of modified rebreathing tests with end-tidal P O 2 ${P_{{{\mathrm{O}}_{\mathrm{2}}}}}$ ( P ET O 2 ${P_{{\mathrm{ET}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) clamped at 150, 70, 60 and 45 mmHg. End-tidal P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ( P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ), P ET O 2 ${P_{{\mathrm{ET}}{{\mathrm{O}}_{\mathrm{2}}}}}$ , ventilation ( V ̇ $\dot{V}$ E ) and calculated oxygen saturation (SC O2 ) were measured breath-by-breath by gas-analyser and pneumotach. The V ̇ $\dot{V}$ E - P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ relationship of repeat-trials were linear-interpolated, combined, averaged into 1 mmHg bins, and fitted with a double-linear function ( V ̇ $\dot{V}$ E S, L min-1 mmHg-1 ). PChS was computed at intervals of 1 mmHg of P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ as follows: the difference in V ̇ $\dot{V}$ E between the three hypoxic profiles and the hyperoxic profile (∆ V ̇ $\dot{V}$ E ) was calculated; three ∆ V ̇ $\dot{V}$ E values were plotted against corresponding SC O2 ; and linear regression determined PChS (Lmin-1 mmHg-1 %SC O2 -1 ). These processing steps were repeated at each P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ to produce the PChS vs. isocapnic P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ relationship. These were fitted with linear and polynomial functions, and Akaike information criterion identified the best-fit model. One-way repeated measures analysis of variance assessed between-condition differences. V ̇ $\dot{V}$ E S increased (P < 0.0001) with isoxic P ET O 2 ${P_{{\mathrm{ET}}{{\mathrm{O}}_{\mathrm{2}}}}}$ from 3.7 ± 1.5 L min-1 mmHg-1 at 150 mmHg to 4.4 ± 1.8, 5.0 ± 1.6 and 6.0 ± 2.2 Lmin-1 mmHg-1 at 70, 60 and 45 mmHg, respectively. Mean SC O2 fell progressively (99.3 ± 0%, 93.7 ± 0.1%, 90.4 ± 0.1% and 80.5 ± 0.1%; P < 0.0001). In all individuals, PChS increased with P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ , and this relationship was best described by a linear model in 75%. Despite increasing central chemoreflex activation, PChS increased linearly with P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ indicative of an additive central-peripheral chemoreflex response. KEY POINTS: How central and peripheral chemoreceptor drives to breathe interact in humans remains contentious. We measured peripheral chemoreflex sensitivity to hypoxia (PChS) at various isocapnic carbon dioxide tensions ( P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) to determine the form of the relationship between PChS and central P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ . Participants performed three repetitions of modified rebreathing with end-tidal P O 2 ${P_{{{\mathrm{O}}_{\mathrm{2}}}}}$ fixed at 150, 70, 60 and 45 mmHg. PChS was computed at intervals of 1 mmHg of end-tidal P C O 2 ${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ( P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ ) as follows: the difference in V ̇ $\dot{V}$ E between the three hypoxic profiles and the hyperoxic profile (∆ V ̇ $\dot{V}$ E ) was calculated; three ∆ V ̇ $\dot{V}$ E values were plotted against corresponding calculated oxygen saturation (SC O2 ); and linear regression determined PChS (Lmin-1 mmHg-1 %SC O2 -1 ). In all individuals, PChS increased with P ETC O 2 ${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$ , and this relationship was best described by a linear (rather than polynomial) model in 15 of 20. Most participants did not exhibit a hypo- or hyper-additive effect of central chemoreceptors on the peripheral chemoreflex indicating that the interaction was additive.

Coupling of [Formula: see text] and [Formula: see text] kinetics: insights from multiple exercise transitions below the estimated lactate threshold.

During a step-change in exercise power output (PO), ventilation ([Formula: see text]) increases with a similar time course to the rate of carbon dioxide delivery to the lungs ([Formula: see text]). To test the strength of this coupling, we compared [Formula: see text] and [Formula: see text] kinetics from ten independent exercise transitions performed within the moderate-intensity domain. Thirteen males completed 3-5 repetitions of ∆40 W step transitions initiated from 20, 40, 60, 80, 100, and 120 W on a cycle ergometer. Preceding the ∆40 W step transitions from 60, 80, 100, and 120 W was a 6 min bout of 20 W cycling from which the transitions of variable ∆PO were examined. Gas exchange ([Formula: see text] and oxygen uptake, [Formula: see text]) and [Formula: see text] were measured by mass spectrometry and volume turbine. The kinetics of the responses were characterized by the time constant (τ) and amplitude (Δ[Formula: see text]/Δ[Formula: see text]). Overall, [Formula: see text] kinetics were consistently slower than [Formula: see text] kinetics (by ~ 45%) and τ[Formula: see text] rose progressively with increasing baseline PO and with heightened ∆PO from a common baseline. Compared to τ[Formula: see text], τ[Formula: see text] was on average slightly greater (by ~ 4 s). Repeated-measures analysis of variance revealed that there was no interaction between τ[Formula: see text] and τ[Formula: see text] in either the variable baseline (p = 0.49) and constant baseline (p = 0.56) conditions indicating that each changed in unison. Additionally, for Δ[Formula: see text]/Δ[Formula: see text], there was no effect of either variable baseline PO (p = 0.05) or increasing ΔPO (p = 0.16). These data provide further evidence that, within the moderate-intensity domain, both the temporal- and amplitude-based characteristics of V̇E kinetics are inextricably linked to those of [Formula: see text].

An undergraduate laboratory to study exercise thresholds.

In exercise physiology, laboratory components help students connect theoretical concepts to their own exercise experiences and introduce them to data collection, analysis, and interpretation using classic techniques. Most courses include a lab protocol that involves exhaustive incremental exercise during which expired gas volumes and concentrations of oxygen and carbon dioxide are measured. During these protocols, there are characteristic alterations in gas exchange and ventilatory profiles that give rise to two exercise thresholds: the gas exchange threshold (GET) and the respiratory compensation point (RCP). The ability to explain why these thresholds occur and how they are identified is fundamental to learning in exercise physiology and requisite to the understanding of core concepts including exercise intensity, prescription, and performance. Proper identification of GET and RCP requires the assembly of eight data plots. In the past, the burden of time and expertise required to process and prepare data for interpretation has been a source of frustration. In addition, students often express a desire for more opportunities to practice/refine their skills. The objective of this article is to share a blended laboratory model that features the "Exercise Thresholds App," a free online resource that eliminates postprocessing of data and provides a bank of profiles on which end-users can practice threshold identification skills with immediate feedback. In addition to including prelaboratory and postlaboratory recommendations, we present student accounts of understanding, engagement, and satisfaction following completion of the laboratory experience and introduce a new quiz feature of the app to assist instructors with evaluating student learning.NEW & NOTEWORTHY We present a laboratory to study exercise thresholds from gas exchange and ventilatory measures that features the "Exercise Thresholds App," a free online resource that eliminates postprocessing of data and provides a bank of profiles on which end-users can practice threshold identification skills. In addition to including prelaboratory and postlaboratory recommendations, we present student accounts of understanding, engagement, and satisfaction and introduce a new quiz feature of the app to assist instructors with evaluating learning.

Influence of sex and age on the relationship between aerobic fitness and muscle sympathetic nerve activity in healthy adults.

We examined the influence of sex and age on the relationship between aerobic fitness and muscle sympathetic nerve activity (MSNA) in healthy adults. Data were assessed from 224 volunteers (88 females), aged 18-76 yr, in whom resting MSNA (microneurography) and peak oxygen uptake (V̇o2peak; incremental exercise test) were evaluated. When separated into younger (<50 yr) and older (≥50 yr) subgroups, there were inverse relationships between relative V̇o2peak (mL·kg-1·min-1) and MSNA burst frequency in younger males (R2 = 0.21, P < 0.0001) and older females (R2 = 0.36, P < 0.01), but not older males (R2 = 0.05, P = 0.08) or younger females (R2 = 0.03, P = 0.14). Similar patterns were observed with absolute V̇o2peak (L·min-1) and percent-predicted (based on age, sex, weight, height, and modality), and with burst incidence. Sex and age influence the relationship between aerobic fitness and resting MSNA, and, thus, must be considered as key variables when studying these potential associations; inverse relationships are strongest in younger males and older females.NEW & NOTEWORTHY Our data reveal for the first time that associations between aerobic fitness and resting muscle sympathetic nerve activity are sex and age specific; inverse relationships are evident in younger males (<50 yr) and older females (≥50 yr), but absent in younger females (<50 yr) and older males (≥50 yr).

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.

Strategies to improve respiratory chemoreflex characterization by Duffin's rebreathing.

NEW FINDINGS: What is the central question of this study? We assessed the test-retest variability of respiratory chemoreflex characterization by Duffin's modified rebreathing method and explored whether signal averaging of repeated trials improves confidence in parameter estimation. What is the main finding and its importance? Modified rebreathing is a reproducible method to characterize responses of central and peripheral respiratory chemoreflexes. Signal averaging of multiple repeated tests minimizes within- and between-test variability, improves the confidence of chemoreflex characterization and reduces the minimal change in parameters required to establish an effect. Future experiments that apply this method might benefit from signal averaging to improve its discriminatory effect. ABSTRACT: We assessed the test-retest variability of central and peripheral respiratory chemoreflex characterization by Duffin's modified rebreathing method and explored whether signal averaging of repeated trials improves confidence in parameter estimation. Over four laboratory visits, 13 participants (mean ± SD age, 25 ± 5 years) performed six repetitions of modified rebreathing in isoxic-hypoxic conditions [end-tidal P O 2 ${P_{{{\rm{O}}_{\rm{2}}}}}$ ( P ET , O 2 ${P_{{\rm{ET,}}{{\rm{O}}_{\rm{2}}}}}$ )  = 50 mmHg] and isoxic-hyperoxic conditions ( P ET , O 2 ${P_{{\rm{ET,}}{{\rm{O}}_{\rm{2}}}}}$   = 150 mmHg). End-tidal P C O 2 ${P_{{\rm{C}}{{\rm{O}}_{\rm{2}}}}}$ ( P ET , C O 2 ${P_{{\rm{ET,C}}{{\rm{O}}_{\rm{2}}}}}$ ), P ET , O 2 ${P_{{\rm{ET,}}{{\rm{O}}_{\rm{2}}}}}$ and minute ventilation ( V ̇ $\dot {\rm V}$ E ) were measured breath-by-breath, by gas analyser and pneumotachograph. The V ̇ $\dot {\rm V}$ E versus P ET , C O 2 ${P_{{\rm{ET,C}}{{\rm{O}}_{\rm{2}}}}}$ relationships were fitted with a piecewise model to estimate the ventilatory recruitment threshold (VRT) and the slope above the VRT ( V ̇ $\dot {\rm V}$ E S). Breath-by-breath data from the three within- and between-day trials were averaged using two approaches [simple average (fit then average) and ensemble average (average then fit)] and compared with a single-trial fit. Variability was assessed by intraclass correlation (ICC) and coefficient of variance (CV), and the minimal detectable change was computed for each approach using two independent sets of three trials. Within days, the VRT and V ̇ $\dot {\rm V}$ E S exhibited excellent test-retest variability in both hyperoxic conditions (VRT: ICC = 0.965, CV = 2.3%; V ̇ $\dot {\rm V}$ E S: ICC = 0.932, CV = 15.5%) and hypoxic conditions (VRT: ICC = 0.970, CV = 2.9%; V ̇ $\dot {\rm V}$ E S: ICC = 0.891, CV = 17.2%). Between-day reproducibility was also excellent (hyperoxia, VRT: ICC = 0.930, CV = 2.2%; V ̇ $\dot {\rm V}$ E S: ICC = 0.918, CV = 14.2%; and hypoxia, VRT: ICC = 0.940, CV = 3.0%; V ̇ $\dot {\rm V}$ E S: ICC = 0.880, CV = 18.1%). Compared with a single-trial fit, there were no differences in VRT or V ̇ $\dot {\rm V}$ E S using the simple average or ensemble average approaches; however, ensemble averaging reduced the minimal detectable change for V ̇ $\dot {\rm V}$ E S from 2.95 to 1.39 L min-1  mmHg-1 (hyperoxia) and from 3.64 to 1.82 L min-1  mmHg-1 (hypoxia). Single trials of modified rebreathing are reproducible; however, signal averaging of repeated trials improves confidence in parameter estimation.

Evaluating the suitability of supra-POpeak verification trials after ramp-incremental exercise to confirm the attainment of maximum O2 uptake.

During exhaustive ramp-incremental cycling tests, the incidence of O2 uptake (V̇o2) plateaus is low. To verify the attainment of maximum V̇o2 (V̇o2max), it is recommended that a trial at a power output (PO) corresponding to 110% of the ramp-derived peak (POpeak) is performed. It remains unclear whether verification trials set at this PO can be tolerated for long enough to allow attainment of V̇o2max. Eleven recreationally trained individuals performed five ramp tests of varying slope (5, 10, 15, 25, and 30 W/min), each followed, in series, by two verification trials: the first at 110% POpeak of the 25 W/min ramp and the second at 110% POpeak attained in the preceding ramp test. Exercise duration of the first verification trial was on average 81 ± 15 s (CV = 9 ± 3%) versus 162 ± 32, 121 ± 24, 103 ± 15, and 73 ± 10 s for the second verification trials at 110% of POpeak of the 5, 10, 15, and 30 W/min ramp tests, respectively (P < 0.05). Compared with the highest V̇o2 recorded during ramp tests, V̇o2 from the subsequent verification trials was not different for the 5, 10, and 15 W/min ramp tests (P > 0.05) but was lower for the 25 and 30 W/min ramp tests (P < 0.05). Verification trials at 110% POpeak of rapidly incrementing ramp tests (i.e., 25 W/min) were not sustained for long enough to allow the attainment of V̇o2max. With commonly used rapidly incrementing ramp tests engendering exhaustion within 8-12 min, verification trials less than POpeak should be preferred as they can be sustained sufficiently long to allow the attainment of V̇o2max.

Simultaneous assessment of central and peripheral chemoreflex regulation of muscle sympathetic nerve activity and ventilation in healthy young men.

KEY POINTS: Central chemoreceptor stimulation, by hypercapnia (acidosis), and peripheral, by hypoxia plus hypercapnia, evoke reflex increases in ventilation and sympathetic outflow. The assumption that central or peripheral chemoreceptor-mediated sympathetic activation elicited when PCO2 increases parallels concurrent ventilatory responses is unproven. Applying a modified rebreathing protocol that equilibrates central and peripheral chemoreceptor PCO2 whilst clamping O2 tension at either hypoxic or hyperoxic concentrations, the independent ventilatory and muscle sympathetic stimulus-response properties of the central and peripheral chemoreflexes were quantified and compared in young men. The novel findings were that ventilatory and sympathetic responses to central and peripheral chemoreflex stimulation are initiated at similar PCO2 recruitment thresholds but individual specific sympathetic responsiveness cannot be predicted from the ventilatory sensitivities of either chemoreceptor reflex. Such findings in young men, if replicated in heart failure or hypertension, should temper present enthusiasm for trials targeting the peripheral chemoreflex based solely on ventilatory responsiveness to non-specific chemoreceptor stimulation. ABSTRACT: In humans, stimulation of peripheral or central chemoreceptor reflexes is assumed to evoke equivalent ventilatory and sympathetic responses. We evaluated whether central or peripheral chemoreceptor-mediated sympathetic activation elicited by increases in CO2 tension ( PCO2 ) parallels concurrent ventilatory responses. Twelve healthy young men performed a modified rebreathing protocol designed to equilibrate central and peripheral chemoreceptor PCO2 tensions with end-tidal PCO2 ( PETCO2 ) at two isoxic end-tidal PO2 ( PETO2 ) such that central responses can be segregated, by hyperoxia, from the net response (hypoxia minus hyperoxia). Ventilation and muscle sympathetic nerve activity (MSNA) were recorded continuously during rebreathing at isoxic PETO2 of 150 and 50 mmHg. During rebreathing, the PETCO2 values at which ventilation (L min-1 ) and total MSNA (units) began to rise were identified ( PETCO2 recruitment thresholds) and their slopes above the recruitment threshold were determined (sensitivity). The central chemoreflex recruitment threshold for ventilation (46 ± 3 mmHg) and MSNA (45 ± 4 mmHg) did not differ (P = 0.55) and slopes were 2.3 ± 0.9 L min-1  mmHg-1 and 2.1 ± 1.5 units mmHg-1 , respectively. The peripheral chemoreflex recruitment thresholds, at 41 ± 3 mmHg for both ventilation and MSNA were lower (P < 0.05) compared to the central chemoreflex recruitment thresholds. Peripheral chemoreflex sensitivity was 1.7 ± 0.1 L min-1  mmHg-1 for ventilation and 2.9 ± 2.6 units mmHg-1 for MSNA. There was no relationship between the ventilatory and MSNA sensitivity for either the central (r2  = 0.01, P = 0.76) or peripheral (r2  = 0.01, P = 0.73) chemoreflex. In healthy young men, ventilatory and sympathetic responses to central and peripheral chemoreceptor reflex stimulation are initiated at similar PETCO2 recruitment thresholds but individual ventilatory responsiveness does not predict sympathetic sensitivities of either chemoreflex.

Training heart failure patients with reduced ejection fraction attenuates muscle sympathetic nerve activation during mild dynamic exercise.

Muscle sympathetic nerve activity (MSNA) decreases during low-intensity dynamic one-leg exercise in healthy subjects but increases in patients with heart failure with reduced ejection fraction (HFrEF). We hypothesized that increased peak oxygen uptake (V̇o2peak) after aerobic training would be accompanied by less sympathoexcitation during both mild and moderate one-leg dynamic cycling, an attenuated muscle metaboreflex, and greater skin vasodilation. We studied 27 stable, treated HFrEF patients (6 women; mean age: 65 ± 2 SE yr; mean left ventricular ejection fraction: 30 ± 1%) and 18 healthy age-matched volunteers (6 women; mean age: 57 ± 2 yr). We assessed V̇o2peak (open-circuit spirometry) and the skin microcirculatory response to reactive hyperemia (laser flowmetry). Fibular MSNA (microneurography) was recorded before and during one-leg cycling (2 min unloaded and 2 min at 50% of V̇o2peak) and, to assess the muscle metaboreflex, during posthandgrip ischemia (PHGI). HFrEF patients were evaluated before and after 6 mo of exercise-based cardiac rehabilitation. Pretraining V̇o2peak and skin vasodilatation were lower (P < 0.001) and resting MSNA higher (P = 0.01) in HFrEF than control subjects. Training improved V̇o2peak (+3.0 ± 1.0 mL·kg-1·min-1; P < 0.001) and cutaneous vasodilation and diminished resting MSNA (-6.0 ± 2.0, P = 0.01) plus exercise MSNA during unloaded (-4.0 ± 2.5, P = 0.04) but not loaded cycling (-1.0 ± 4.0 bursts/min, P = 0.34) and MSNA during PHGI (P < 0.05). In HFrEF patients, exercise training lowers MSNA at rest, desensitizes the sympathoexcitatory metaboreflex, and diminishes MSNA elicited by mild but not moderate cycling. Training-induced downregulation of resting MSNA and attenuated reflex sympathetic excitation may improve exercise capacity and survival.

Identification of critical intensity from a single lactate measure during a 3-min, submaximal cycle-ergometer test.

We tested the hypothesis that critical intensity in cycling can be determined from a single delta blood lactate in the third minute of a submaximal cycle ergometer trial. Fourteen healthy young men performed four to six constant-power-output trials on a cycle ergometer to the limit of tolerance. Critical intensity was calculated via a linear model and subsequently validated. Lactate was measured at baseline and at 3 min from exercise onset. Delta lactate was the difference between these measures. Based on individual trials, we obtained the delta lactate-% validated critical intensity relationship and thereafter an estimate of critical intensity was computed. Validated and estimated critical intensity were compared by effects sizes, paired-sample t-test and Bland-Altman analysis. Delta lactate was a linear function of the intensity of exercise, expressed as % validated critical intensity (R2 = 0.89). Estimated critical intensity was not different from (d = 0.03, P = 0.98) and highly correlated with (R2 = 0.88) validated critical intensity. The bias between measures was 0.03 W (≠0) with a precision of 7 W. The results suggest that critical intensity in cycling can be accurately and precisely determined from delta lactate during a sub-maximal trial and so provides a practical and valid alternative to direct determination.

The influence of metabolic and circulatory heterogeneity on the expression of pulmonary oxygen uptake kinetics in humans.

We examined the relationship amongst baseline work rate (WR), phase II pulmonary oxygen uptake (V̇(O2p)) time constant (τV̇(O2p)) and functional gain (G(P)=ΔV̇(O2p)/ΔWR) during moderate-intensity exercise. Transitions were initiated from a constant or variable baseline WR. A validated circulatory model was used to examine the role of heterogeneity in muscle metabolism (V̇(O2m)) and blood flow (Q̇(m)) in determining V̇(O2p) kinetics. We hypothesized that τV̇(O2p) and G(P) would be invariant in the constant baseline condition but would increase linearly with increased baseline WR. Fourteen men completed three to five repetitions of ∆40 W step transitions initiated from 20, 40, 60, 80, 100 and 120 W on a cycle ergometer. The ∆40 W step transitions from 60, 80, 100 and 120 W were preceded by 6 min of 20 W cycling, from which the progressive ΔWR transitions (constant baseline condition) were examined. The V̇(O2p) was measured breath by breath using mass spectrometry and a volume turbine. For a given ΔWR, both τV̇(O2p) (22-35 s) and G(P) (8.7-10.5 ml min(-1) W(-1)) increased (P < 0.05) linearly as a function of baseline WR (20-120 W). The τV̇(O2p) was invariant (P < 0.05) in transitions initiated from 20 W, but G(P) increased with ΔWR (P < 0.05). Modelling the summed influence of multiple muscle compartments revealed that τV̇(O2p) could appear fast (24 s), and similar to in vivo measurements (22 ± 6 s), despite being derived from τV̇(O2p) values with a range of 15-40 s and τQ̇(m) with a range of 20-45 s, suggesting that within the moderate-intensity domain phase II V̇(O2p) kinetics are slowed dependent on the pretransition WR and are strongly influenced by muscle metabolic and circulatory heterogeneity.

Breath-by-breath pulmonary O2 uptake kinetics: effect of data processing on confidence in estimating model parameters.

To improve the signal-to-noise ratio of breath-by-breath pulmonary O2 uptake (V̇O2p) data, it is common practice to perform multiple step transitions, which are subsequently processed to yield an ensemble-averaged profile. The effect of different data-processing techniques on phase II V̇O2p kinetic parameter estimates (V̇O2p amplitude, time delay and phase II time constant (τV̇O2p)] and model confidence [95% confidence interval (CI95)] was examined. Young (n = 9) and older men (n = 9) performed four step transitions from a 20 W baseline to a work rate corresponding to 90% of their estimated lactate threshold on a cycle ergometer. Breath-by-breath V̇O2p was measured using mass spectrometry and volume turbine. Mono-exponential kinetic modelling of phase II V̇O2p data was performed on data processed using the following techniques: (A) raw data (trials time aligned, breaths of all trials combined and sorted in time); (B) raw data plus interpolation (trials time aligned, combined, sorted and linearly interpolated to second by second); (C) raw data plus interpolation plus 5 s bin averaged; (D) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 1; points joined by straight-line segments), ensemble averaged]; (E) 'D' plus 5 s bin averaged; (F) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 2; points copied until subsequent point appears), ensemble averaged]; and (G) 'F' plus 5 s bin averaged. All of the model parameters were unaffected by data-processing technique; however, the CI95 for τV̇O2p in condition 'D' (4 s) was lower (P < 0.05) than the CI95 reported for all other conditions (5-10 s). Data-processing technique had no effect on parameter estimates of the phase II V̇O2p response. However, the narrowest interval for CI95 occurred when individual trials were linearly interpolated and ensemble averaged.

Pulmonary O2 uptake kinetics during moderate-intensity exercise transitions initiated from low versus elevated metabolic rates: insights from manipulations in cadence.

INTRODUCTION: The rate of adjustment (τ) of phase II pulmonary O2 uptake (VO2p) is slower when exercise transitions are initiated from an elevated baseline work rate (WR) and metabolic rate (MR). In this study, combinations of cycling cadence (40 vs. 90 rpm) and external WR were used to examine the effect of prior MR on τVO2p. METHODS: Eleven young men completed transitions from 20 W (BSL) to 90% lactate threshold, with transitions performed as two steps of equal ∆WR (LS, lower step; US, upper step), while maintaining a cadence of (1) 40 rpm, (2) 90 rpm, and (3) 40 rpm but with the WRs elevated to match the higher VO2p associated with 90 rpm cycling (40MATCH); transitions lasted 6 min. VO2p was measured breath-by-breath using mass spectrometry and turbinometry; vastus lateralis muscle deoxygenation [HHb] was measured using near-infrared spectroscopy. VO2p and HHb responses were modeled using nonlinear least squares regression analysis. RESULTS: VO2p at BSL, LS and US was similar for 90 rpm and 40MATCH, but greater than in 40 rpm. Compared to 90 rpm, τVO2p at 40 rpm was shorter (p < 0.05) in LS (18 ± 5 vs. 28 ± 8 s) but not in US (26 ± 8 vs. 33 ± 9 s), and at 40MATCH, τVO2p was lower (p < 0.05) (19 ± 6 s) in LS but not in US (34 ± 13 s) despite differing external WR and ∆WR. CONCLUSIONS: A similar overall adjustment of [HHb] and VO2p in LS and US across conditions suggested dynamic matching between microvascular blood flow and O2 utilization. Prior MR (rather than external WR per se) plays a role in the dynamic adjustment of pulmonary (and muscle) VO2p.

Evaluation of the "Step-Ramp-Step" Protocol: Accurate Aerobic Exercise Prescription with Different Steps and Ramp Slopes.

PURPOSE: To assess whether: i) a lower amplitude constant-load MOD is appropriate to determine the mean response time (MRT); ii) the method accurately corrects the dissociation in the V̇O 2 -PO relationship during ramp compared with constant-load exercise when using different ramp slopes. METHODS: Eighteen participants (7 females) performed three SRS tests including: i) step-transitions into MOD from 20 to 50 W (MOD 50 ) and 80 W (MOD 80 ); and ii) slopes of 15, 30, and 45 W·min -1 . The V̇O 2 and PO at the gas exchange threshold (GET) and the corrected respiratory compensation point (RCP CORR ) were determined. Two to three 30-min constant-load trials evaluated the V̇O 2 and PO at the maximal metabolic steady state (MMSS). RESULTS: There were no differences in V̇O 2 at GET (1.97 ± 0.36, 1.99 ± 0.36, 1.95 ± 0.30 L·min -1 ), and RCP (2.81 ± 0.57, 2.86 ± 0.59, 2.84 ± 0.59) between 15, 30, and 45 W·min -1 ramps, respectively ( P > 0.05). The MRT in seconds was not affected by the amplitude of the MOD or the slope of the ramp (range 19 ± 10 s to 23 ± 20 s; P > 0.05). The mean PO at GET was not significantly affected by the amplitude of the MOD or the slope of the ramp (range 130 ± 30 W to 137 ± 30 W; P > 0.05). The PO at RCP CORR was similar for all conditions ((range 186 ± 43 W to 193 ± 47 W; P > 0.05). CONCLUSIONS: The SRS protocol accounts for the V̇O 2 MRT when using smaller amplitude steps, and for the V̇O 2 slow component when using different ramp slopes, allowing for accurate partitioning of the exercise intensity domains in a single test.

Variability of cardiopulmonary exercise testing in patients with atrial fibrillation and determination of exercise responders to high-intensity interval training and moderate-to-vigorous intensity continuous training.

Disabling atrial fibrillation (AF)-related symptoms and different testing settings may influence day-to-day cardiopulmonary exercise testing (CPET) measurements, which can affect exercise prescription for high-intensity interval training (HIIT) and moderate-to-vigorous intensity continuous training (M-VICT) and their outcomes. This study examined the reliability of CPET in patients with AF and assessed the proportion of participants achieving minimal detectable changes (MDC) in peak oxygen consumption (V̇O2peak) following HIIT and M-VICT. Participants were randomized into HIIT or M-VICT after completing two baseline CPETs: one with cardiac stress technologists (CPETdiag) and the other with a research team of exercise specialists (CPETresearch). Additional CPET was completed following 12 weeks of twice-weekly training. Reliability of CPETdiag and CPETresearch was assessed by intraclass correlation coefficient (ICC) and dependent t-tests. The MDC score was calculated for V̇O2peak using a reliable change index. The proportion of participants achieving MDC was compared between HIIT and M-VICT using chi-square analysis. Eighteen participants (69±7 years, 33% females) completed two baseline CPETs. ICC was significant for all measured variables. However, peak power output (POpeak: 124±40 vs. 148±40 watts, p<0.001) and HR (HRpeak: 136±22 vs. 148±30 bpm, p=0.023) were significantly greater in CPETresearch than CPETdiag. Few participants achieved MDC in V̇O2peak (5.6 mL/kg/min) with no difference between HIIT (0%) and M-VICT (10.0%, p=0.244). POpeak and HRpeak differed significantly in patients with AF when CPETs were repeated under different settings. Caution must be practiced when prescribing exercise intensity based on these measures as under-prescription may increase the number of exercise non-responders.

The Respiratory Compensation Point: Mechanisms and Relation to the Maximal Metabolic Steady State.

At a point during the latter third of an incremental exercise protocol, ventilation begins to exceed the rate of clearance of carbon dioxide (CO2) at the lungs ( V ˙ CO2). The onset of this hyperventilation, which is confirmed by a fall from a period of stability in end-tidal and arterial CO2 tensions (PCO2), is referred to as the respiratory compensation point (RCP). The mechanisms that contribute to the RCP remain debated as does its surrogacy for the maximal metabolic steady state of constant-power exercise (i.e., the highest work rate associated with maintenance of physiological steady state). The objective of this current opinion is to summarize the original research contributions that support and refute the hypotheses that: (i) the RCP represents a rapid, peripheral chemoreceptor-mediated reflex response engaged when the metabolic rate at which the buffering systems can no longer constrain the rise in hydrogen ions ([H+]) associated with rising lactate concentration and metabolic CO2 production is surpassed; and (ii) the metabolic rate at which this occurs is equivalent to the maximal metabolic steady state of constant power exercise. In doing so, we will shed light on potential mechanisms contributing to the RCP, attempt to reconcile disparate findings, make a case for its adoption for exercise intensity stratification and propose strategies for the use of RCP in aerobic exercise prescription.