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Tidal breathing in awake humans is variable. This variability causes changes in lung gas stores that affect gas exchange measurements. To overcome this, several algorithms provide solutions for breath‐by‐breath alveolar gas exchange measurement; however, there is no consensus on a physiologically robust method suitable for widespread application. A recent approach, the ‘independent‐breath’ (IND) algorithm, avoids the complexity of measuring breath‐by‐breath changes in lung volume by redefining what is meant by a ‘breath’. Specifically, it defines a single breathing cycle as the time between equal values of the FO2 ${F_{{{\\mathrm{O}}_2}}}$ /FN2 ${F_{{{\\mathrm{N}}_2}}}$(or FCO2 ${F_{{\\mathrm{C}}{{\\mathrm{O}}_2}}}$ /FN2 ${F_{{{\\mathrm{N}}_2}}}$ ) ratio, that is, the ratio of fractional concentrations of lung‐expired O2 (or CO2) and nitrogen (N2). These developments imply that the end of one breath is not, by necessity, aligned with the start of the next. Here we demonstrate how the use of the IND algorithm fails to conserve breath‐by‐breath mass balance of O2 and CO2 exchanged between the atmosphere and tissues (and vice versa). We propose a new term, within the IND algorithm, designed to overcome this limitation. We also present the far‐reaching implications of using algorithms based on alternative definitions of the breathing cycle, including challenges in measuring and interpreting the respiratory exchange ratio, pulmonary gas exchange efficiency, dead space fraction of the breath, control of breathing, and a broad spectrum of clinically relevant cardiopulmonary exercise testing variables. Therefore, we do not support the widespread adoption of currently available alternative definitions of the breathing cycle as a legitimate solution for breath‐by‐breath alveolar gas exchange measurement in research or clinical settings. What is the central question of this study? The IND algorithm for breath‐by‐breath alveolar gas exchange computation redefines ‘a breath’: what are the implications of this approach for the measurement of gas exchange at rest and during exercise? What is the main finding and its importance? The IND algorithm does not maintain continuity between consecutive breaths, violating the conservation of mass for breath‐by‐breath alveolar gas exchange measurements. A volume correction to the algorithm is provided to address this discrepancy and preserve mass balance. However, by redefining the conventional breathing cycle, the IND algorithm has additional implications for cardiopulmonary exercise testing interpretation because variables with demonstrated diagnostic and prognostic value cannot be accurately determined.

This study compared cardiovascular and metabolic responses during concentric and eccentric stepping. Eight participants (5 m, 3f; 22 ± 2 years) performed maximal concentric and eccentric ramp incremental tests on a modified stepping ergometer. Subsequently, three randomized 15‐min constant‐power tests were performed (1) concentric stepping at 90% of the concentric lactate threshold (LT), (2) eccentric stepping at the same power, and (3) eccentric stepping at the same oxygen uptake (V̇O2). At equivalent power (36 ± 6 W, p = 0.62), eccentric stepping resulted in 46 ± 8% lower V̇O2, 16 ± 6% lower heart rate (HR), and 11 ± 5% lower mean arterial blood pressure compared to concentric (p < 0.01). Matching V̇O2 required 65 ± 19% more power during eccentric stepping (p < 0.01). During this test, eccentric V̇O2 and HR continued to increase, resulting in a 22 ± 29% higher V̇O2 and 19 ± 16% higher HR in the final minute (p < 0.001). Reduced cardiorespiratory demand during eccentric stepping at the same power as concentric demonstrates a higher eccentric power is required to produce the same V̇O2. However, despite being below the concentric LT, eccentric V̇O2 and HR continued to increase past the predicted steady state, indicating a higher exercise intensity.

Background Menopause represents a turning point where vascular damage begins to outweigh reparative processes, leading to increased cardiovascular disease (CVD) risk. Exercise training reduces CVD risk in postmenopausal females via improvements in traditional risk factors and direct changes to the vasculature. We assessed the effect of moderate (MODERATE‐IT) versus heavy (HEAVY‐IT) intensity interval exercise training upon markers of cardiovascular health and vascular repair in postmenopausal females. Methods Twenty‐seven healthy postmenopausal females (56 ± 4 yr) were assigned to 12 weeks of either MODERATE‐IT or HEAVY‐IT, twice per week. MODERATE‐IT consisted of 10s work, and 10s active recovery repeated for 30 min. HEAVY‐IT comprised 30s work, and 30s active recovery repeated for 21 ± 2 min. Endothelial function (flow‐mediated dilation), arterial stiffness (pulse wave velocity), and V̇O2peak were assessed pre‐training and post‐training. Blood samples were obtained pre‐training and post‐training for enumeration of circulating angiogenic cells (CACs), culture of CACs, and lipoprotein profile. Results V̇O2peak increased 2.4 ± 2.8 ml/kg/min following HEAVY‐IT only (p < 0.05). Brachial blood pressure and endothelial function were unchanged with exercise training (p > 0.05). Peripheral pulse wave velocity reduced 8% with exercise training, irrespective of intensity (p < 0.05). Exercise training had no effect on lipoprotein profile or endothelin‐1 (p > 0.05). CAC adhesion to vascular smooth muscle cells (VSMC) increased 30 min post plating following MODERATE‐IT only (p < 0.05). Conclusions HEAVY‐IT was more effective at increasing V̇O2peak in postmenopausal females. The ability of CACs to adhere to VSMC improved following MODERATE‐IT but not HEAVY‐IT. Interval training had the same effect on endothelial function (no change) and arterial stiffness (reduced), regardless of exercise intensity.

Athletic training leads to remodelling of both left and right ventricles with increased myocardial mass and cavity dilatation. Whether changes in cardiac strain parameters occur in response to training is less well established. In this study we investigated the relationship in trained athletes between cardiovascular magnetic resonance (CMR) derived strain parameters of cardiac function and fitness. Thirty five endurance athletes and 35 age and sex matched controls underwent CMR at 3.0 T including cine imaging in multiple planes and tissue tagging by spatial modulation of magnetization (SPAMM). CMR data were analysed quantitatively reporting circumferential strain and torsion from tagged images and left and right ventricular longitudinal strain from feature tracking of cine images. Athletes performed a maximal ramp-incremental exercise test to determine the lactate threshold (LT) and maximal oxygen uptake (V̇O2max). LV circumferential strain at all levels, LV twist and torsion, LV late diastolic longitudinal strain rate, RV peak longitudinal strain and RV early and late diastolic longitudinal strain rate were all lower in athletes than controls. On multivariable linear regression only LV torsion (beta = −0.37, P = 0.03) had a significant association with LT. Only RV longitudinal late diastolic strain rate (beta = −0.35, P = 0.03) had a significant association with V̇O2max. This cohort of endurance athletes had lower LV circumferential strain, LV torsion and biventricular diastolic strain rates than controls. Increased LT, which is a major determinant of performance in endurance athletes, was associated with decreased LV torsion. Further work is needed to understand the mechanisms by which this occurs.

The tolerable duration of continuous high-intensity exercise is determined by the hyperbolic Speed-tolerable duration (S-tLIM) relationship. However, application of the S-tLIM relationship to normalize the intensity of High-Intensity Interval Training (HIIT) has yet to be considered, with this the aim of present study. Subjects completed a ramp-incremental test, and series of 4 constant-speed tests to determine the S-tLIM relationship. A sub-group of subjects (n = 8) then repeated 4 min bouts of exercise at the speeds predicted to induce intolerance at 4 min (WR4), 6 min (WR6) and 8 min (WR8), interspersed with bouts of 4 min recovery, to the point of exercise intolerance (fixed WR HIIT) on different days, with the aim of establishing the work rate that could be sustained for 960 s (i.e. 4×4 min). A sub-group of subjects (n = 6) also completed 4 bouts of exercise interspersed with 4 min recovery, with each bout continued to the point of exercise intolerance (maximal HIIT) to determine the appropriate protocol for maximizing the amount of high-intensity work that can be completed during 4×4 min HIIT. For fixed WR HIIT tLIM of HIIT sessions was 399±81 s for WR4, 892±181 s for WR6 and 1517±346 s for WR8, with total exercise durations all significantly different from each other (P<0.050). For maximal HIIT, there was no difference in tLIM of each of the 4 bouts (Bout 1: 229±27 s; Bout 2: 262±37 s; Bout 3: 235±49 s; Bout 4: 235±53 s; P>0.050). However, there was significantly less high-intensity work completed during bouts 2 (153.5±40. 9 m), 3 (136.9±38.9 m), and 4 (136.7±39.3 m), compared with bout 1 (264.9±58.7 m; P>0.050). These data establish that WR6 provides the appropriate work rate to normalize the intensity of HIIT between subjects. Maximal HIIT provides a protocol which allows the relative contribution of the work rate profile to physiological adaptations to be considered during alternative intensity-matched HIIT protocols.

Aims Heart failure with reduced ejection fraction (HFrEF) induces skeletal muscle mitochondrial abnormalities that contribute to exercise limitation; however, specific mitochondrial therapeutic targets remain poorly established. This study quantified the relationship and contribution of distinct mitochondrial respiratory states to prognostic whole‐body measures of exercise limitation in HFrEF. Methods and results Male patients with HFrEF (n = 22) were prospectively enrolled and underwent ramp‐incremental cycle ergometry cardiopulmonary exercise testing to determine exercise variables including peak pulmonary oxygen uptake (V̇O2peak), lactate threshold (V̇O2LT), the ventilatory equivalent for carbon dioxide (V̇E/V̇CO2LT), peak circulatory power (CircPpeak), and peak oxygen pulse. Pectoralis major was biopsied for assessment of in situ mitochondrial respiration. All mitochondrial states including complexes I, II, and IV and electron transport system (ETS) capacity correlated with V̇O2peak (r = 0.40–0.64; P < 0.05), V̇O2LT (r = 0.52–0.72; P < 0.05), and CircPpeak (r = 0.42–0.60; P < 0.05). Multiple regression analysis revealed that combining age, haemoglobin, and left ventricular ejection fraction with ETS capacity could explain 52% of the variability in V̇O2peak and 80% of the variability in V̇O2LT, respectively, with ETS capacity (P = 0.04) and complex I (P = 0.01) the only significant contributors in the model. Conclusions Mitochondrial respiratory states from skeletal muscle biopsies of patients with HFrEF were independently correlated to established non‐invasive prognostic cycle ergometry cardiopulmonary exercise testing indices including V̇O2peak, V̇O2LT, and CircPpeak. When combined with baseline patient characteristics, over 50% of the variability in V̇O2peak could be explained by the mitochondrial ETS capacity. These data provide optimized mitochondrial targets that may attenuate exercise limitations in HFrEF.

PurposePathogen transmission during cardio-pulmonary exercise testing (CPET) is caused by carrier aerosols generated during respiration.MethodsTen healthy volunteers (age range: 34 ± 15; 4 females) were recruited to see if the physiological reactions to ramp-incremental CPET on a cycle ergometer were affected using an in-line filter placed between the mouthpiece and the flow sensor. The tests were in random order with or without an in-line bacterial/viral spirometer filter. The work rate aligned, time interpolated 10 s bin data were compared throughout the exercise period.ResultsFrom rest to peak exercise, filter use increased only minute ventilation (V˙E) (ΔV˙E = 1.56 ± 0.70 L/min, P < 0.001) and tidal volume (VT) (ΔVT = 0.10 ± 0.11 L, P = 0.014). Over the entire test, the slope of the residuals for V˙CO2 was positive (0.035 ± 0.041 (ΔL/L), P = 0.027). During a ramp-incremental CPET in healthy subjects, an in-line filter increased V˙E and VT but not metabolic rate.ConclusionIn conclusion, using an in-line filter is feasible, does not affect appreciably the physiological variables, and may mitigate risk of aerosol dispersion during CPET.

Objectives: Fatigue is a prominent feature of long COVID (LC) and may be related to several pathophysiologic mechanisms, including immune hyperstimulation. Aerobic endurance exercise training may be a useful therapy, with appropriate attention to preventing post-exertional malaise. Methods: Fourteen participants completed a pilot study of aerobic exercise training (twenty 1.5 h sessions of over 10 weeks). Cardiorespiratory fitness, 6 min walk distance, quality of life, symptoms, 7-day physical activity, immunophenotype, and inflammatory biomarkers were measured before and after exercise training. Results: The participant characteristics at baseline were as follows: 53.5 ± 11.6 yrs, 53% f, BMI 32.5 ± 8.4, 42% ex-smokers, 15.1 ± 8.8 months since initial COVID-19 infection, low normal pulmonary function testing, V.O2peak 19.3 ± 5.1 mL/kg/min, 87 ± 17% predicted. After exercise training, participants significantly increased their peak work rate (+16 ± 20 W, p = 0.010) and V.O2peak (+1.55 ± 2.4 mL/kg/min, p = 0.030). Patients reported improvements in fatigue severity (−11%), depression (−42%), anxiety (−29%), and dyspnea level (−46%). There were no changes in 6MW distance or physical activity. The circulating number of CD3+, CD4+, CD19+, CD14++CD16, and CD16++CD14+ monocytes and CD56+ cells (assessed with flow cytometry) increased with acute exercise (rest to peak) and was not diminished or augmented by exercise training. Plasma concentrations of TNF-α, IL-6, IL-8, IL-10, INF-γ, and INF-λ were normal at study entry and not affected by training. Conclusions: Aerobic endurance exercise training in individuals with LC delivered beneficial effects on cardiorespiratory fitness, quality of life, anxiety, depression, and fatigue without detrimental effects on immunologic function.

BackgroundCMR image acquisition techniques during exercise typically require transient cessation of exercise or complex post-processing analysis, potentially compromising its clinical utility. We evaluated the feasibility and reproducibility of a novel image acquisition Method for the assessment of biventricular physiological response during continuous physical exercise.Methods10 healthy volunteers (80% men, age 25±2 years) underwent supine cycle ergometer (Lode) induced exercise CMR (Philips 1.5T Ingenia) on two separate occasions using a free-breathing, multi-shot, navigated, balanced steady-state free precession cine pulse sequence. Individual target heart rates (HR) for both moderate and high-intensity exercise were prescribed based on a prior supine cardiopulmonary exercise test (CPET). The scan protocol included a short axis ventricular volume stack and a 40 phase 4-chamber cine. Images were acquired at baseline, and during steady-state moderate and high-intensity exercise (55% and 75% maximal heart rate, respectively). Data were analysed by two independent observers and left and right ventricular (LV, RV) indices calculated.ResultsEnd-diastolic volume (EDV) of both LV and RV decreased during moderate and high-intensity exercise, although the reduction in indexed RVEDV (RVEDVi) was only observed during maximal exercise (table 1). Similarly, a significant reduction in end-systolic volumes (ESV) was seen in both ventricles, whilst the reduction in indexed LVESV (LVESVi) was only evident during high-intensity exercise. Ejection fraction (EF) increased from rest to moderate and high intensity exercise in the LV (LVEF 58±5% vs 61±8% vs 68±3%, respectively; p<0.001), whereas RVEF was only significantly higher during high-intensity exercise (RVEF 58±7% vs 62±7% vs 66±4%; p<0.01). A biphasic change in global longitudinal strain (GLS) was observed; there was a significant increase in GLS during moderate-intensity exercise which appeared to plateau at maximal exercise. A similar biphasic change was observed for GLS rate (table 1).Intra-observer reproducibility of LV parameters was excellent at all three stages (Table 2), although measurements of RVESV were more variable. The reproducibility of both RVEF and RV cardiac indexes was however excellent. Similarly, inter-observer reproducibility of LV volumes, EF and cardiac indexes was excellent. Inter-scan LV and RV ejection fraction were highly reproducible at all 3 stages; RVESVi reproducibility was suboptimal.ConclusionThis exercise CMR protocol using a novel free-breathing, multi-shot, navigated imaging Method allows simultaneous assessment of the left and right ventricular response to continuous exercise. Intra and inter-observer reproducibility were excellent. Clinical feasibility and utility now needs to be established.Abstract 51 Table 1 Volumetric data for both left and right ventricle at baseline, and during steady state moderate and high-intensity exerciseAbstract 51 Table 2