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

ABSTRACT: During exhaustive ramp-incremental cycling tests, the incidence of O₂ uptake (V̇o₂) plateaus is low. To verify the attainment of maximum V̇o₂ (V̇o_2max), it is recommended that a trial at a power output (PO) corresponding to 110% of the ramp-derived peak (PO_peak) is performed. It remains unclear whether verification trials set at this PO can be tolerated for long enough to allow attainment of V̇o_2max. 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% PO_peak of the 25 W/min ramp and the second at 110% PO_peak 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 PO_peak 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% PO_peak of rapidly incrementing ramp tests (i.e., 25 W/min) were not sustained for long enough to allow the attainment of V̇o_2max. With commonly used rapidly incrementing ramp tests engendering exhaustion within 8-12 min, verification trials less than PO_peak should be preferred as they can be sustained sufficiently long to allow the attainment of V̇o_2max.

SUBMITTER: Iannetta D

PROVIDER: S-EPMC7509256 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The dissociation between constant work rate of O2 uptake (V?o2) and ramp V?o2 at a given work rate might be mitigated during slowly increasing ramp protocols. This study characterized the V?o2 dynamics in response to five different ramp protocols and constant-work-rate trials at the maximal metabolic steady state (MMSS) to characterize 1) the V?o2 gain (G) in the moderate, heavy, and severe domains, 2) the mean response time of V?o2 (MRT), and 3) the work rates at lactate threshold (LT) and respiratory compensation point (RCP). Eleven young individuals performed five ramp tests (5, 10, 15, 25, and 30 W/min), four to five time-to-exhaustions for critical power estimation, and two to three constant-work-rate trials for confirmation of the work rate at MMSS. G was greatest during the slowest ramp and progressively decreased with increasing ramp slopes (from ~12 to ~8 ml·min-1·W-1, P < 0.05). The MRT was smallest during the slowest ramp slopes and progressively increased with faster ramp slopes (1?±?1, 2?±?1, 5?±?3, and 10?±?4, 15?±?6 W, P < 0.05). After "left shifting" the ramp V?o2 by the MRT, the work rate at LT was constant regardless of the ramp slope (~150 W, P > 0.05). The work rate at MMSS was 215?±?55 W and was similar and highly correlated with the work rate at RCP during the 5 W/min ramp (P > 0.05, r?=?0.99; Lin's concordance coefficient?=?0.99; bias?=?-3 W; root mean square error?=?6 W). Findings showed that the dynamics of V?o2 (i.e., G) during ramp exercise explain the apparent dichotomy existing with constant-work-rate exercise. When these dynamics are appropriately "resolved", LT is constant regardless of the ramp slope of choice, and RCP and MMSS display minimal variations between each other.NEW & NOTEWORTHY This study demonstrates that the dynamics of V?o2 during ramp-incremental exercise are dependent on the characteristics of the increments in work rate, such that during slow-incrementing ramp protocols the magnitude of the dissociation between ramp V?o2 and constant V?o2 at a given work rate is reduced. Accurately accounting for these dynamics ensures correct characterizations of the V?o2 kinetics at ramp onset and allows appropriate comparisons between ramp and constant-work-rate exercise-derived indexes of exercise intensity.

Project description:BackgroundMechanical ventilation can lead to ventilator-induced lung injury (VILI). In addition to the well-known mechanical forces of volutrauma, barotrauma, and atelectrauma, non-mechanical mechanisms have recently been discussed as contributing to the pathogenesis of VILI. One such mechanism is oscillations in partial pressure of oxygen (PO2) which originate in lung tissue in the presence of within-breath recruitment and derecruitment of alveoli. The purpose of this study was to investigate this mechanism's possible independent effects on lung tissue and inflammation in a porcine model.MethodsTo separately study the impact of PO2 oscillations on the lungs, an in vivo model was set up that allowed for generating mixed-venous PO2 oscillations by the use of veno-venous extracorporeal membrane oxygenation (vvECMO) in a state of minimal mechanical stress. While applying the identical minimal-invasive ventilator settings, 16 healthy female piglets (weight 50 ± 4 kg) were either exposed for 6 h to a constant mixed-venous hemoglobin saturation (SmvO2) of 65% (which equals a PmvO2 of 41 Torr) (control group), or an oscillating SmvO2 (intervention group) of 40-90% (which equals PmvO2 oscillations of 30-68 Torr)-while systemic normoxia in both groups was maintained. The primary endpoint of histologic lung damage was assessed by ex vivo histologic lung injury scoring (LIS), the secondary endpoint of pulmonary inflammation by qRT-PCR of lung tissue. Cytokine concentration of plasma was carried out by ELISA. A bioinformatic microarray analysis of lung samples was performed to generate hypotheses about underlying pathomechanisms.ResultsThe LIS showed significantly more severe damage of lung tissue after exposure to PO2 oscillations compared to controls (0.53 [0.51; 0.58] vs. 0.27 [0.23; 0.28]; P = 0.0025). Likewise, a higher expression of TNF-α (P = 0.0127), IL-1β (P = 0.0013), IL-6 (P = 0.0007), and iNOS (P = 0.0013) in lung tissue was determined after exposure to PO2 oscillations. Cytokines in plasma showed a similar trend between the groups, however, without significant differences. Results of the microarray analysis suggest that inflammatory (IL-6) and oxidative stress (NO/ROS) signaling pathways are involved in the pathology linked to PO2 oscillations.ConclusionsArtificial mixed-venous PO2 oscillations induced lung damage and pulmonary inflammation in healthy animals during lung protective ventilation. These findings suggest that PO2 oscillations represent an independent mechanism of VILI.

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

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Dataset Information

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

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OmicsDI is part of the ELIXIR infrastructure

Tweets

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