The oxygen uptake (VCombining Dot AboveO2) at the respiratory compensation point (RCP) closely identifies with the maximal metabolic steady state. However, the power output (PO) at RCP cannot be ...determined from contemporary ramp-incremental exercise protocols.
This study aimed to test the efficacy of a "step-ramp-step" (SRS) cycling protocol for estimating the PO at RCP and the validity of RCP as a maximal metabolic steady-state surrogate.
Ten heathy volunteers (5 women; age: 30 ± 7 yr; VCombining Dot AboveO2max: 54 ± 6 mL·kg·min) performed in the following series: a moderate step transition to 100 W (MOD), ramp (30 W·min), and after 30 min of recovery, step transition to ~50% POpeak (HVY). Ventilatory and gas exchange data from the ramp were used to identify the VCombining Dot AboveO2 at lactate threshold (LT) and RCP. The PO at LT was determined by the linear regression of the VCombining Dot AboveO2 versus PO relationship after adjusting ramp data by the difference between the ramp PO at the steady-state VCombining Dot AboveO2 from MOD and 100 W. Linear regression between the VCombining Dot AboveO2-PO values associated with LT and HVY provided, by extrapolation, the PO at RCP. Participants then performed 30-min constant-power tests at the SRS-estimated RCP and 5% above this PO.
All participants completed 30 min of constant-power exercise at the SRS-estimated RCP achieving steady-state VCombining Dot AboveO2 of 3176 ± 595 mL·min that was not different (P = 0.80) from the ramp-identified RCP (3095 ± 570 mL·min) and highly consistent within participants (bias = -26 mL·min, r = 0.97, coefficient of variation = 2.3% ± 2.8%). At 5% above the SRS-estimated RCP, four participants could not complete 30 min and all, but two exhibited non-steady-state responses in blood lactate and VCombining Dot AboveO2.
In healthy individuals cycling at their preferred cadence, the SRS protocol and the RCP are capable of accurately predicting the PO associated with maximal metabolic steady state.
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.
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 (P ETC O2) at two isoxic end‐tidal PO2 (P ET O2) 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 P ET O2 of 150 and 50 mmHg. During rebreathing, the P ETC O2 values at which ventilation (L min−1) and total MSNA (units) began to rise were identified (P ETC O2 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 P ETC O2 recruitment thresholds but individual ventilatory responsiveness does not predict sympathetic sensitivities of either chemoreflex.
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.
A variety of health benefits associated with physical activity depends upon the frequency, intensity, duration, and type of exercise. Intensity of exercise is the most elusive of these elements and ...yet has important implications for the health benefits and particularly cardiovascular outcomes elicited by regular physical activity. Authorities recommend that we obtain 150min of moderate to vigorous intensity physical activity (MVPA) each week. The current descriptions of moderate to vigorous intensity are not sufficient, and we wish to enhance understanding of MVPA by recognition of important boundaries that define these intensities. There are two key thresholds identified in incremental tests: ventilatory and lactate thresholds 1 and 2, which reflect boundaries related to individualized disturbance to homeostasis that are appropriate for prescribing exercise. VT2 and LT2 correspond with critical power/speed and respiratory compensation point. Moderate intensity physical activity approaches VT1 and LT1 and vigorous intensity physical activity is between the two thresholds (1 and 2). The common practice of prescribing exercise at a fixed metabolic rate (# of METs) or percentage of maximal heart rate or of maximal oxygen uptake (V̇O
2
max) does not acknowledge the individual variability of these metabolic boundaries. As training adaptations occur, these boundaries will change in absolute and relative terms. Reassessment is necessary to maintain regular exercise in the moderate to vigorous intensity domains. Future research should consider using these metabolic boundaries for exercise prescription, so we will gain a better understanding of the specific physical activity induced health benefits.
Common methods to prescribe exercise intensity are based on fixed percentages of maximum rate of oxygen uptake (V˙O2max), peak work rate (WRpeak), maximal HR (HRmax). However, it is unknown how these ...methods compare to the current models to partition the exercise intensity spectrum.
Thus, the aim of this study was to compare contemporary gold-standard approaches for exercise prescription based on fixed percentages of maximum values to the well-established, but underutilized, "domain" schema of exercise intensity.
One hundred individuals participated in the study (women, 46; men, 54). A cardiopulmonary ramp-incremental test was performed to assess V˙O2max, WRpeak, HRmax, and the lactate threshold (LT), and submaximal constant-work rate trials of 30-min duration to determine the maximal lactate steady-state (MLSS). The LT and MLSS were used to partition the intensity spectrum for each individual in three domains of intensity: moderate, heavy, and severe.
V˙O2max in women and men was 3.06 ± 0.41 L·min and 4.10 ± 0.56 L·min, respectively. Lactate threshold and MLSS occurred at a greater %V˙O2max and %HRmax in women compared with men (P < 0.05). The large ranges in both sexes at which LT and MLSS occurred on the basis of %V˙O2max (LT, 45%-74%; MLSS, 69%-96%), %WRpeak (LT, 23%-57%; MLSS, 44%-71%), and %HRmax (LT, 60%-90%; MLSS, 75%-97%) elicited large variability in the number of individuals distributed in each domain at the fixed-percentages examined.
Contemporary gold-standard methods for exercise prescription based on fixed-percentages of maximum values conform poorly to exercise intensity domains and thus do not adequately control the metabolic stimulus.
The inspection of aquatic environments is a challenging activity, which is made more difficult if the environment is complex or confined, such as those that are found in nuclear storage facilities ...and accident sites, marinas and boatyards, liquid storage tanks, or flooded tunnels and sewers. Human inspections of these environments are often dangerous or infeasible, so remote inspection using unmanned underwater vehicles (UUVs) is used. Due to access restrictions and environmental limitations, such as low illumination levels, turbidity, and a lack of salient features, traditional localisation systems that have been developed for use in large bodies of water cannot be used. This means that UUV capabilities are severely restricted to manually controlled low-quality visual inspections, generating non-geospatially located data. The localisation of UUVs in these environments would enable the autonomous behaviour and the development of accurate maps. This article presents a review of the state-of-the-art in localisation technologies for these environments and identifies areas of future research to overcome the challenges posed.
This study aimed to compare the concordance between CP and MLSS estimated by various models and criteria and their agreement with MMSS.
After a ramp test, 10 recreationally active males performed ...four to five severe-intensity constant-power output (PO) trials to estimate CP and three to four constant-PO trials to determine MLSS and identify MMSS. CP was computed using the three-parameter hyperbolic (CP3-hyp), two-parameter hyperbolic (CP2-hyp), linear (CPlin), and inverse of time (CP1/Tlim) models. In addition, the model with the lowest combined parameter error identified the "best-fit" CP (CPbest-fit). MLSS was determined as an increase in blood lactate concentration ≤1 mM during constant-PO cycling from the 5th (MLSS5-30), 10th (MLSS10-30), 15th (MLSS15-30), 20th (MLSS20-30), or 25th (MLSS25-30) to 30th minute. MMSS was identified as the greatest PO associated with the highest submaximal steady-state V˙O2 (MV˙O2ss).
Concordance between the various CP and MLSS estimates was greatest when MLSS was identified as MLSS15-30, MLSS20-30, and MLSS25-30. The PO at MV˙O2ss was 243 ± 43 W. Of the various CP models and MLSS criteria, CP2-hyp (244 ± 46 W) and CPlin (248 ± 46 W) and MLSS15-30 and MLSS20-30 (both 245 ± 46 W), respectively, displayed, on average, the greatest agreement with MV˙O2ss. Nevertheless, all CP models and MLSS criteria demonstrated some degree of inaccuracies with respect to MV˙O2ss.
Differences between CP and MLSS can be reconciled with optimal methods of determination. When estimating MMSS, from CP the error margin of the model estimate should be considered. For MLSS, MLSS15-30 and MLSS20-30 demonstrated the highest degree of accuracy.
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.
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).
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).
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.
We aimed to test the extended capabilities of the SRS protocol by validating its capacity to predict the power outputs for targeted metabolic rates (V̇O 2 ) and time-to-task failure ( Tlim ) within ...the heavy- and severe-intensity domain, respectively.
Fourteen young individuals completed (i) an SRS protocol from which the power outputs at GET and RCP (RCP CORR ), and the work accruable above RCP CORR , defined as W ' RAMP , were derived; (ii) one heavy-intensity bout at a power output predicted to elicit a targeted V̇O 2 equidistant from GET and RCP; and (iii) four severe-intensity trials at power outputs predicted to elicit targeted Tlim at minutes 2.5, 5, 10, and 13. These severe-intensity trials were also used to compute the constant-load-derived critical power and W ´ ( W ' CONSTANT ).
Targeted (2.41 ± 0.52 L·min -1 ) and measured (2.43 ± 0.52 L·min -1 ) V̇O 2 at the identified heavy-intensity power output (162 ± 43 W) were not different ( P = 0.71) and substantially concordant (CCC = 0.95). Likewise, targeted and measured Tlim for the four identified severe-intensity power outputs were not different ( P > 0.05), and the aggregated coefficient of variation was 10.7% ± 8.9%. The derived power outputs at RCP CORR (192 ± 53 W) and critical power (193 ± 53 W) were not different ( P = 0.65) and highly concordant (CCC = 0.99). There were also no differences between W ' RAMP and W ' CONSTANT ( P = 0.51).
The SRS protocol can accurately predict power outputs to elicit discrete metabolic rates and exercise durations, thus providing, with time efficiency, a high precision for the control of the metabolic stimulus during exercise.
Neutrophils are recruited from the blood to sites of sterile inflammation, where they contribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital ...microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating neutrophils to adhere within liver sinusoids. Subsequently, generation of an intravascular chemokine gradient directed neutrophil migration through healthy tissue toward foci of damage. Lastly, formyl-peptide signals released from necrotic cells guided neutrophils through nonperfused sinusoids into the injury. Thus, dynamic in vivo imaging revealed a multistep hierarchy of directional cues that guide neutrophil localization to sites of sterile inflammation.
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