Arteriovenous O2 Difference Research Articles

6-Year Follow-Up of a World Record Breaking Master Marathon Runner.

Endurance performance declines with advancing age. Of the three main physiological factors that determine endurance running performance (maximal oxygen consumption [V̇O2max], lactate threshold, and running economy [RE]), V̇O2max appears to be most affected by age. While endurance performance declines with age, recently, endurance performance has rapidly improved in master athletes as the number of master athletes competing in endurance events has increased. Master athletes represent an intriguing model to study healthy aging. In this case study, we reassessed the physiological profile of a 76-year-old distance runner who broke the marathon world record for men over 70 years of age in 2018. This runner was tested a few months before breaking the world record and retested in 2024. Between 2018 and 2024, his marathon running velocity decreased significantly. Therefore, the purpose of this case study was to determine the physiological changes that explain his performance decline. RE remained similar to 2018, and while there was not a clear breakpoint in blood lactate, he still likely runs marathons at a high percentage (~90%) of his V̇O2max. However, V̇O2max declined by 15.1%. HRmax declined by 3.2% and maximal O2 pulse declined by 12.4%, suggesting that maximal stroke volume and/or arteriovenous O2 difference decreased. Altogether, although this marathoner continues to compete at an elite level, his performance has declined since his record-breaking marathon due to a reduction in V̇O2max. This is likely caused by reductions in maximal stroke volume and/or arteriovenous O2 difference. We speculate that these changes reflect primarily age-related processes.

Lean body mass and the cardiorespiratory phenotype: An ethnic-specific relationship in Hans Chinese women and men.

Lean body mass (LBM) and the functional capacity of cardiovascular (CV) and respiratory systems constitute a female-specific relationship in European-American individuals. Whether this recent finding be extrapolated to the world's largest ethnic group, that is, Hans Chinese (HC, a population characterized by low LBM), is unknown. Healthy HC adults (n=144, 50% ♀) closely matched by sex, age and physical activity were included. Total and regional (leg, arm and trunk) LBM and body composition were measured via dual-energy X-ray absorptiometry. Cardiac structure, stiffness, central/peripheral haemodynamics and peak O2 consumption (VO2peak) were assessed via transthoracic echocardiography and pulmonary gas analyses at rest and during exercise up to peak effort. Regression analyses determined the sex-specific relationship of LBM with cardiac and aerobic phenotypes. Total and regional LBM were lower and body fat percentage higher in women compared with men (P<0.001). In both sexes, total LBM positively associated with left ventricular (LV) mass and peak volumes (r≥0.33, P≤0.005) and negatively with LV end-systolic and central arterial stiffness (r≥-0.34, P≤0.004). Total LBM strongly associated with VO2peak (r≥0.60, P<0.001) and peak cardiac output (r≥0.40, P<0.001) in women and men. Among regional LBM, leg LBM prominently associated with the arterio-venous O2 difference at peak exercise in both sexes (r≥0.43, P<0.001). Adjustment by adiposity or CV risk factors did not modify the results. LBM independently determines internal cardiac dimensions, ventricular mass, distensibility and the capacity to deliver and consume O2 in HC adults irrespective of sex.

The Chinese cardiorespiratory and circulatory system at work in women and men: a case–control study

The physiology of prominent prognostic factors in the cardiorespiratory system remains unchartered in the world's largest ethnic group: Hans Chinese (HC). This study assessed and contrasted the fundamental variables in HC and European-American (EA) individuals. Healthy HC and EA adults (n=140, 43% ♀) closely matched by age, sex and physical activity were included. Body composition (DXA) and haematological variables (haemoglobin mass, blood volume (BV)) were measured at rest. Pulmonary O2 uptake (VO2) measurements along with cycle ergometry designed for accurate transthoracic echocardiography were implemented to assess cardiorespiratory structure/function up to peak effort. HC presented with higher body fat and lower lean body mass (LBM) percentage than EA irrespective of sex (P≤0.014). BV did not differ whereas blood haemoglobin concentration was lower in HC compared with EA, particularly in females (P=0.009). Myocardial diastolic and overall function at rest was enhanced in HC versus EA (P<0.001). During exercise, heart volumes and output per unit of body size did not differ between ethnicities, whereas larger heart volumes per unit of LBM were found in HC versus EA in females (P≤0.003). At high exercise intensities, VO2 (-16%) and the arteriovenous O2 difference (-28%) were markedly reduced in HC compared with EA in females (P≤0.024). In males, no physiological difference between HC and EA was observed during exercise. Notwithstanding lower LBM, HC are characterised by similar BV and cardiac capacity but reduced peak VO2 than EA in females, partly explained by low ethnic-specific blood O2 carrying capacity. Early Career Scheme (106210224, to D.M.) and Seed Fund (104006024, to D.M.).

Insulin resistance without coexisting hyperglycaemia is not independently associated with cardiorespiratory fitness or its components in women

Abstract Background Insulin resistance (IR) is a globally prevalent condition in which tissues’ response to insulin is diminished. Cardiorespiratory fitness (peak O2 uptake (VO2peak)) is determined by Fick’s equation (VO2 = cardiac output (CO) × arteriovenous O2 difference (Ca-vO2) = heart rate × stroke volume (SV) × Ca-vO2) and diffusion law (VO2 = diffusive O2 conductance (DO2) × constant k × venous O2 pressure (PvO2)). Several studies suggest an association between IR and decreased VO2peak, but the association has been questioned by analyses taking account of body size and composition, and potential mechanisms behind the association are unknown. Purpose To test a hypothesis that IR is not independently associated with VO2peak or its components. Methods Fifty of 144 women, who had participated in baseline experiments of three intervention studies, were included in this retrospective cross-sectional study; see Table 1 for subject characteristics. The inclusion criteria were age 18-40 years, body mass index 18.5-40 kg/m2, Caucasian origin, and available data on key measures. The exclusion criteria were diseases, medications, and other factors possibly affecting VO2peak. We measured haemoglobin, fasting glucose, and fasting insulin concentrations (blood), assessed IR (homeostasis model assessment (HOMA-IR)), and measured body size and composition (bioimpedance). The subjects performed an incremental cycling test to volitional fatigue; we measured ventilatory gas exchange (spiroergometry), arterial O2 saturation (oximetry), and SV and CO (impedance cardiography), and calculated Ca-vO2, DO2, and PvO2. We analysed VO2peak and its components as absolute (e.g. L/min) and ratiometrically scaled values (e.g. mL/min/kg), and when appropriate, also as allometrically scaled values (e.g. mL/min/kg^x, where 0 &amp;lt; x &amp;lt; 1) after identifying optimal variable-specific exponents. Results VO2peak scaled to body mass (BM) as well as SVpeak and COpeak scaled to body surface area (BSA) were inversely associated with the body size variables they were scaled to (all P &amp;lt; 0.013). Contrariwise, this was not the case when we optimally scaled VO2peak to fat-free mass (FFM), SVpeak to FFM^0.55, COpeak to FFM^0.50, and DO2peak to FFM (all 0.066 &amp;lt; P &amp;lt; 0.977). HOMA-IR was inversely associated with VO2peak scaled to BM but not in a multivariate analysis, whereas HOMA-IR was not associated with VO2peak scaled to FFM (Table 2); we made alike observations with SVpeak and COpeak (data not shown). Further, VO2peak scaled to BM as well as SVpeak and COpeak scaled to BSA were or tended to be up to 15 % higher in a group with HOMA-IR&amp;lt;3.0 than in a group with HOMA-IR≥3.0, while other peak exercise data did not differ between the groups (Table 1). Conclusion Body size and composition significantly affect conclusions drawn regarding VO2peak and its components. Taking this into account, IR without coexisting hyperglycaemia is not independently associated with VO2peak or its components in women.Table 1Table 2

Cardiovascular responses of exercises performed within the extreme exercise domain.

Stroke volume (SV), heart rate (HR) and arterio-venous O2 difference (a-vO2diff) responses to heavy and severe-intensity exercise have been well documented; however, there is a lack of information on the SV, HR and a v-O2diff responses of work rates within extreme exercise domain. The aim of this study was, therefore, to focus on central and peripheral components of VO2 responses to exercises performed within the heavy, severe and extreme exercise domain. Eight well-trained male cyclists participated in this study. Maximal O2 consumption (VO2max) and corresponding work rate (P@VO2max) were determined by multisession constant work rate exercises. Cardiovascular responses to exercises were evaluated by nitrous-oxide rebreathing method with work rates from 40 % to 160 % of P@VO2max, VO2max corresponded to 324+/-39.4 W; however, maximal SV responses occurred at 205+/-54.3 W (p<0.01). Maximal cardiac output (Q), HR, and a vO2diff responses were revealed by the P@VO2max. VO2 response to exercise significantly decreased from severe-intense exercises to the first work rate of extreme exercise domain due to significant decreases in Q, SV, and HR responses (p<0.05), except a v-O2diff (p>0.05). Moreover, non-significant decreases in Q, SV, and a v-O2diff were evaluated as response to increase in work rate belonging to extreme work rates (p>0.05), except the HR (p<0.05). Work rates within the lower district of the extreme exercise domain have an important potential to improve peripheral component of VO2, while the P@VO2max seems the most appropriate intensity for aerobic endurance development as it maximizes the central component of VO2max.

Development potentials of commonly used high-intensity training strategies on central and peripheral components of maximal oxygen consumption

The aim of this study was to reveal the development potentials of five high-intensity training models on central and peripheral components of maximal oxygen consumption (VO2max). Following VO2max determination, maximal cardiac output (Qmax), maximal stroke volume (SVmax), and maximal arteriovenous O2 difference (a−vO2diff_max) were analysed. Short-interval- (short-HIIT), long-interval (long-HIIT), alternating work-rate continuous (alter-HIT), constant work-rate continuous (const-HIT), and sprint interval (SIT) sessions were performed on separate days with iso-effort and iso-time methods. Time spent (tspent) at > 95% of VO2max was the highest in long-HIIT (p < 0.05). The tspent at > 90% of Qmax was higher in alter-HIT than long-HIIT and SIT (p < 0.05), while there was no significant difference for tspent at > 90% of SVmax amongst high-intensity trainings. The tspent at > 90% of a−vO2diff_max was higher in short-HIIT and long-HIIT than other modalities (p < 0.05). It can be said that continuous modalities seem to have a higher potential to improve central part of VO2max, while interval modalities may be better to develop peripheral component.

Energy Cost of Running in Well-Trained Athletes: Toward Slope-Dependent Factors

This study aimed to determine the contribution of metabolic, cardiopulmonary, neuromuscular, and biomechanical factors to the energy cost (ECR) of graded running in well-trained runners. Eight men who were well-trained trail runners (age: 29 [10]y, mean [SD]; maximum oxygen consumption: 68.0 [6.4]mL·min-1·kg-1) completed maximal isometric evaluations of lower limb extensor muscles and 3 randomized trials on a treadmill to determine their metabolic and cardiovascular responses and running gait kinematics during downhill (DR: -15% slope), level (0%), and uphill running (UR: 15%) performed at similar O2 uptake (approximately 60% maximum oxygen consumption). Despite similar O2 demand, ECR was lower in DR versus level running versus UR (2.5 [0.2] vs 3.6 [0.2] vs 7.9 [0.5]J·kg-1·m-1, respectively; all P < .001). Energy cost of running was correlated between DR and level running conditions only (r2 = .63; P = .018). Importantly, while ECR was correlated with heart rate, cardiac output, and arteriovenous O2 difference in UR (all r2 > .50; P < .05), ECR was correlated with lower limb vertical stiffness, ground contact time, stride length, and step frequency in DR (all r2 > .58; P < .05). Lower limb isometric extension torques were not related to ECR whatever the slope. The determining physiological factors of ECR might be slope specific, mainly metabolic and cardiovascular in UR versus mainly neuromuscular and mechanical in DR. This possible slope specificity of ECR during incline running opens the way for the implementation of differentiated physiological evaluations and training strategies to optimize performance in well-trained trail runners.

The effect of age on mechanisms of exercise tolerance: Reduced arteriovenous oxygen difference causes lower oxygen consumption in older people.

To assess the effect of age on mechanisms of exercise tolerance. Prospective observational study recruited 71 healthy individuals divided into two groups according to their age i.e. younger (≤40years of age, N=43); and older (≥55years of age, N=28). All participants underwent maximal graded cardiopulmonary exercise stress testing using cycle ergometer with simultaneous non-invasive gas-exchange and central haemodynamic measurements. Using the Fick equation, arteriovenous O2 difference was calculated as the ratio between measured O2 consumption and cardiac output. The mean age of younger and older participants was 26.0±5.7years, and 65.1±6.6years respectively. Peak O2 consumption was significantly lower in older compared to the younger age group (18.8±5.2 vs 34.4±9.8mL/kg/min, p<0.01). Peak exercise cardiac output and cardiac index were not significantly different between the younger and older age groups (22.7±5.0 vs 22.1±3.9L/min, p=0.59; and 12.4±2.9 vs 11.8±1.9L/min/m2, p=0.29). Despite demonstrating significantly lower peak heart rate by 33 beats/min (129±18.3 vs 162±19.9, p<0.01), older participants demonstrated significantly higher stroke volume and stroke volume index compared to the younger age group (173±41.5 vs 142±34.9mL/min, p<0.01; and 92.1±18.1 vs 78.3±19.5mL/m2, p<0.01). Arteriovenous O2 difference was significantly lower in older compared to younger age group participants (9.01±3.0 vs 15.8±4.3 mlO2/100mL blood, p<0.01). Ability of skeletal muscles to extract delivered oxygen represented by reduced arteriovenous O2 difference at peak exercise appears to be the key determinant of exercise tolerance in healthy older individuals.

Veno-arterial CO2 difference and cardiac index in children after cardiac surgery.

Veno-arterial CO2 difference has been considered as a marker of low cardiac output. This study aimed to evaluate the correlation between veno-arterial CO2 difference and cardiac index estimated by MostCareTM in children after cardiac surgery and its association with other indirect perfusion parameters and the complex clinical course (vasoactive inotropic score above 15 or length of stay above 5 days).Data from 40 patients and 127 arterial and venous CO2 measurements for gap calculation taken 0-5 days postoperatively were available. The median (range) veno-arterial CO2 difference value was 9 (1-25 mmHg). The correlation between veno-arterial CO2 difference and cardiac index was not significant (r: -0.16, p = 0.08). However, there was a significant correlation between veno-arterial CO2 difference and vasoactive inotropic score (r: 0.21, p = 0.02), systolic arterial pressure (r: -0.43, p = 0.0001), dP/dtMAX (r: 0.26, p = 0.004), and arterio-venous O2 difference (r: 0.63, p = 0.0001). Systolic arterial pressure (OR 0.95, 95% CI 0.90-0.99), dP/dtMAX (OR 0.00, 95% CI 0.00-0.06), lactates (OR 1.87, 95% CI 1.21-3.31), and veno-arterial CO2 difference (OR 1.13, 95% CI 1.01-1.35) showed a significant univariate association with the complex clinical course. In conclusion, veno-arterial CO2 difference did not correlate with cardiac index estimated by MostCareTM in our cohort of post-cardiosurgical children, but it identified patients with the complex clinical course, especially when combined with other direct and indirect variables of perfusion.

Large Vs Small Skeletal Muscle Mass Training: A Study On Solid Organ Transplanted Recipients

Heart, kidney and liver transplanted patiences (HTR, KTR and LTR) suffer from a reduced exercise capacity. Several studies pointed out the impairments of both central and peripheral factors as responsible for the decreased peak oxygen consumption (V’O2peak) and diminished peak work rate (WRpeak); however, if the main limitation comes from central or peripheral origin is still unclear (Williams and McKenna, 2012). In healthy humans, V’O2peak is mainly constrained by central factors with peripheral factors playing a minor role, indeed endurance training (ET) involving small muscle mass fails to increase whole-body V’O2peak (Rud et al, 2012). Given the skeletal muscle abnormalities reported in HTR, KTR and LTR the limitation conferred by peripheral factors might be important as the central one. PURPOSE: The study investigated if ET of small muscle mass, e.g. single leg cycling (SL), induces higher increase in V’O2peak and WRpeak than ET with large muscle masses, e.g. double leg cycling (DL), in HTR, KTR and LTR. METHODS: 33 sedentary patience were enrolled and divided into SL group (SLG) (n= 17; HTR=6, KTR=6 and LTR=5) and DL (DLG) (n= 16; HTR=7, KTR=5 and LTR=4). Subjects completed DL incremental tests to determine V’O2peak and WRpeak; peak cardiac output (Q’peak) was assessed by cardio-impedance and peak systemic arterio-venous O2 difference (Ca-vO2peak) was calculated as: V’O2peak/Q’peak. All subjects were asked to attend 24 ET sessions: the DLG performed traditional cycling and the SLG the first half of the session with the one leg and the second half with the other limb. RESULTS: SLG and DLG increased V’O2peak by 19.7 ± 2.7% (mean ± SE) and 23.2 ± 3.1% (Time effect: P<0.001), respectively; WRpeak became 15.3 ± 2.2% and 18.2 ±3.2% larger in SLG and DLG (Time effect: P<0.001), respectively. Q’peak changed by -1.5 ± 5.5% in SLG (n=11) and by 6.7 ± 5.3% in DLG (n=10), however no effect of ET was found Q’peak. Ca-vO2peak improved by 17.6 ± 6.5% and 12.7 ± 6.2% in SLG (n=11) and DLG (n=10) (Time effect: P: 0.003), respectively. CONCLUSIONS: Given the absence of improvement in Q’peak after ET, the accretion of V’O2peak and WRpeak seems to be induced by a greater Ca-vO2peak, suggesting a key role of peripheral factors in impairing exercise capacity in HTR, KTR and LTR.

Contribution of oxygen extraction fraction to maximal oxygen uptake in healthy young men.

We analysed the importance of systemic and peripheral arteriovenous O2 difference ( a-v¯O2 difference and a‐vfO2 difference, respectively) and O2 extraction fraction for maximal oxygen uptake ( V˙O2max). Fick law of diffusion and the Piiper and Scheid model were applied to investigate whether diffusion versus perfusion limitations vary with V˙O2max. Articles (n = 17) publishing individual data (n = 154) on V˙O2max, maximal cardiac output ( Q˙max; indicator‐dilution or the Fick method), a-v¯O2 difference (catheters or the Fick equation) and systemic O2 extraction fraction were identified. For the peripheral responses, group‐mean data (articles: n = 27; subjects: n = 234) on leg blood flow (LBF; thermodilution), a‐vfO2 difference and O2 extraction fraction (arterial and femoral venous catheters) were obtained. Q˙max and two‐LBF increased linearly by 4.9‐6.0 L · min–1 per 1 L · min–1 increase in V˙O2max (R 2 = .73 and R 2 = .67, respectively; both P < .001). The a-v¯O2 difference increased from 118‐168 mL · L–1 from a V˙O2max of 2‐4.5 L · min–1 followed by a reduction (second‐order polynomial: R 2 = .27). After accounting for a hypoxemia‐induced decrease in arterial O2 content with increasing V˙O2max (R 2 = .17; P < .001), systemic O2 extraction fraction increased up to ~90% ( V˙O2max: 4.5 L · min–1) with no further change (exponential decay model: R 2 = .42). Likewise, leg O2 extraction fraction increased with V˙O2max to approach a maximal value of ~90‐95% (R 2 = .83). Muscle O2 diffusing capacity and the equilibration index Y increased linearly with V˙O2max (R 2 = .77 and R 2 = .31, respectively; both P < .01), reflecting decreasing O2 diffusional limitations and accentuating O2 delivery limitations. In conclusion, although O2 delivery is the main limiting factor to V˙O2max, enhanced O2 extraction fraction (≥90%) contributes to the remarkably high V˙O2max in endurance‐trained individuals.

Increased oxygen extraction and mitochondrial protein expression after small muscle mass endurance training.

When exercising with a small muscle mass, the mass-specific O2 delivery exceeds the muscle oxidative capacity resulting in a lower O2 extraction compared with whole-body exercise. We elevated the muscle oxidative capacity and tested its impact on O2 extraction during small muscle mass exercise. Nine individuals conducted six weeks of one-legged knee extension (1L-KE) endurance training. After training, the trained leg (TL) displayed 45% higher citrate synthase and COX-IV protein content in vastus lateralis and 15%-22% higher pulmonary oxygen uptake ( ) and peak power output ( ) during 1L-KE than the control leg (CON; all P<.05). Leg O2 extraction (catheters) and blood flow (ultrasound Doppler) were measured while both legs exercised simultaneously during 2L-KE at the same submaximal power outputs (real-time feedback-controlled). TL displayed higher O2 extraction than CON (main effect: 1.7±1.6% points; P=.010; 40%-83% of ) with the largest between-leg difference at 83% of (O2 extraction: 3.2±2.2% points; arteriovenous O2 difference: 7.1±4.8mL· L-1 ; P<.001). At 83% of , muscle O2 conductance (DM O2 ; Fick law of diffusion) and the equilibration index Y were higher in TL (P<.01), indicating reduced diffusion limitations. The between-leg difference in O2 extraction correlated with the between-leg ratio of citrate synthase and COX-IV (r=.72-.73; P=.03), but not with the difference in the capillary-to-fiber ratio (P=.965). In conclusion, endurance training improves O2 extraction during small muscle mass exercise by elevating the muscle oxidative capacity and the recruitment of DM O2, especially evident during high-intensity exercise exploiting a larger fraction of the muscle oxidative capacity.

Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10\xa0weeks of endurance training

PurposeThe endurance training (ET)-induced increases in peak oxygen uptake (dot{V}O2peak) and cardiac output (dot{Q}peak) during upright cycling are reversed to pre-ET levels after removing the training-induced increase in blood volume (BV). We hypothesised that ET-induced improvements in dot{V}O2peak and dot{Q}peak are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O2 difference (a-bar{text{v}}O2diff; dot{V}O2/dot{Q}), cardiac dimensions and muscle morphology were studied to assess their role for the dot{V}O2peak improvement.MethodsTwelve untrained subjects (dot{V}O2peak: 44 ± 6 ml kg−1 min−1) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hbmass) and BV were assessed pre- and post-ET. dot{V}O2peak and dot{Q}peak during upright and supine cycling were measured pre-ET, post-ET and immediately after Hbmass was reversed to the individual pre-ET level by phlebotomy.ResultsET increased the Hbmass (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and dot{V}O2peak during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in dot{V}O2peak compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was dot{Q}peak (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased dot{Q}peak and a-bar{text{v}}O2diff accounted for 70% and 30% of the dot{V}O2peak improvements, respectively. Markers of mitochondrial density (CS and COX-IV; P ≤ 0.007) and left ventricular mass (P = 0.027) increased.ConclusionThe ET-induced increase in dot{V}O2peak was preserved despite removing the increases in Hbmass and BV by phlebotomy, independent of posture. dot{V}O2peak increased primarily through elevated dot{Q}peak but also through a widened a-bar{text{v}}O2diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.

Assessment of Exercise Stroke Volume and Its Prediction From Oxygen Pulse in Paralympic Athletes With Locomotor Impairments: Cardiac Long-Term Adaptations Are Possible.

The determinants of cardiac output (CO) during exercise, i.e., stroke volume (SV) and heart rate (HR), could differ in Paralympic athletes (PAthl) with spinal cord injury (SCI) with respect to PAthl with locomotor impairments caused by different health conditions (HCs). The purposes of the present study were the comparisons of two groups of PAthl, one with SCI and the other with either amputation (AMP) or post poliomyelitis syndrome (PM), assessing the (1) peak cardiorespiratory responses and determinants (SV and HR) of CO during maximal and submaximal arm cranking exercise (ACE), respectively; (2) correlations between peak oxygen uptake (VO2peak) and the highest SV obtained during submaximal exercise; and (3) correlations between oxygen pulse (O2 pulse, ratio between VO2 and HR) and both SV and O2 arterio-venous difference [(a-v)O2diff]. Each athlete (19 PAthl with SCI, 9 with AMP, and 5 with PM) completed a continuous incremental cardiopulmonary ACE test to volitional fatigue to assess peak responses. In a different session, CO was indirectly measured through carbon dioxide (CO2) rebreathing method at sub-maximal exercise intensities approximating 30, 50, and 70% of the VO2peak. There were no significant differences between the PAthl groups in age, anthropometry, and VO2peak. However, peak HR was significantly lower, and peak O2 pulse was significantly higher in PAthl with AMP/PM compared to those with SCI. During sub-maximal exercise, PAthl with AMP/PM displayed significantly higher SV values (154.8 ± 17.60 ml) than PAthl with SCI (117.1 ± 24.66 ml). SV correlated significantly with VO2peak in both PAthl with SCI (R2 = 0.796) and AMP/PM (R2 = 0.824). O2 pulse correlated significantly with SV in both PAthl with SCI (R2 = 0.888) and AMP/PM (R2 = 0.932) and in the overall sample (R2 = 0.896). No significant correlations were observed between O2 pulse and (a-v)O2diff. It was concluded that in PAthl with different HCs: (1) significant differences, as a consequence of the different HC, exist in the determinants of CO at maximal and submaximal ACE; (2) SV is a significant determinant of VO2peak, suggesting cardiac adaptations possible also in PAthl with SCI; and (3) SV can be predicted from O2 pulse measurements during submaximal exercise in both groups of PAthl.

Children with Burn Injury Have Impaired Cardiac Output during Submaximal Exercise.

Burn trauma damages resting cardiac function; however, it is currently unknown if the cardiovascular response to exercise is likewise impaired. We tested the hypothesis that, in children, burn injury lowers cardiac output (Q˙) and stroke volume (SV) during submaximal exercise. Five children with 49% ± 4% total body surface area (BSA) burned (two female, 11.7 ± 1 yr, 40.4 ± 18 kg, 141.1 ± 9 cm) and eight similar nonburned controls (five female, 12.5 ± 2 yr, 58.0 ± 17 kg, 147.3 ± 12 cm) with comparable exercise capacity (peak oxygen consumption [peak V˙O2]: 31.9 ± 11 vs 36.8 ± 8 mL O2·kg·min, P = 0.39) participated. The exercise protocol entailed a preexercise (pre-EX) rest period followed by 3-min exercise stages at 20 W and 50 W. V˙O2, HR, Q˙ (via nonrebreathing), SV (Q˙/HR), and arteriovenous O2 difference ([a-v]O2diff, Q˙/ V˙O2) were the primary outcome variables. Using a 2-way factorial ANOVA (group [G] × exercise [EX]), we found that Q˙ was approximately 27% lower in the burned than the nonburned group at 20 W of exercise (burned 5.7 ± 1.0 vs nonburned: 7.9 ± 1.8 L·min) and 50 W of exercise (burned 6.9 ± 1.6 vs nonburned 9.2 ± 3.2 L·min) (G-EX interaction, P = 0.012). SV did not change from rest to exercise in burned children but increased by approximately 24% in the nonburned group (main effect for EX, P = 0.046). Neither [a-v] O2diff nor V˙O2 differed between groups at rest or exercise, but HR response to exercise was reduced in the burn group (G-EX interaction, P = 0.004). When normalized to BSA, SV (index) was similar between groups; however, Q˙ (index) remained attenuated in the burned group (G-EX interaction, P < 0.008). Burned children have an attenuated cardiovascular response to submaximal exercise. Further investigation of hemodynamic function during exercise will provide insights important for cardiovascular rehabilitation in burned children.

Different Determinants of Ventilatory Inefficiency at Different Stages of Reduced Ejection Fraction Chronic Heart Failure Natural History.

BackgroundIt is not known whether determinants of ventilation (VE)/volume of exhaled carbon dioxide (VCO 2) slope during incremental exercise may differ at different stages of reduced ejection fraction chronic heart failure natural history.Methods and Results VE/VCO 2 slope was fitted up to lowest VE/VCO 2 ratio, that is, a proxy of the VE/perfusion ratio devoid of nonmetabolic stimuli to ventilatory drive. VE/VCO 2 slope tertiles were generated from our database (<27.5 [tertile 1], ≥27.5 to <32.0 [tertile 2], and ≥32.0 [tertile 3]), and 147 chronic heart failure patients with repeated tests yielding VE/VCO 2 slopes in 2 different tertiles were selected. Determinants of VE/VCO 2 slope changes across tertile pairs 1 versus 2, 2 versus 3, and 1 versus 3 were assessed by exploring changes in VE and VCO 2 at lowest VE/VCO 2 and those in VE/work rate (W) and VCO 2/W slope. Resting and peak cardiac output (CO) were calculated as VO 2/estimated arteriovenous O2 difference and the CO/W slope analyzed. Notwithstanding a progressively lower W with increasing tertile, VE at lowest VE/VCO 2 and VE/W slope were significantly higher in tertiles 2 and 3 versus tertile 1. Conversely, VCO 2 at lowest VE/VCO 2 and CO/W slope significantly decreased across tertiles, whereas VCO 2/W slope did not. Difference (Δ) in VE/W slope between tertiles accounted for 71% of ΔVE/VCO 2 slope variance, with ΔVCO 2/W slope explaining an additional 26% (model r=0.99; r 2=0.97; P<0.0001). Similar results were obtained substituting ΔVCO 2/W slope with ΔCO/W slope.ConclusionsVentilatory overactivation is the predominant cause of VE/VCO 2 slope increase at initial stages of chronic heart failure, whereas hemodynamic impairment plays an additional role at more‐advanced pathophysiological stages.

High-Intensity Interval Training Increases Cardiac Output and V˙O2max.

This study examined changes in V˙O2max and cardiac output (CO) in response to periodized HIIT. Thirty-nine active men and women (mean age and V˙O2max = 22.9 ± 5.4 yr and 39.6 ± 5.6 mL·kg·min) performed HIIT and 32 men and women (age and V˙O2max = 25.7 ± 4.5 yr and 40.7 ± 5.2 mL·kg·min) were nonexercising controls (CON). The first 10 sessions of HIIT required eight to ten 60 s bouts of cycling at 90%-110% percent peak power output interspersed with 75 s recovery, followed by randomization to one of three regimes (sprint interval training (SIT), high-volume interval training (HIITHI), or periodized interval training (PER) for the subsequent 10 sessions. Before, midway, and at the end of training, progressive cycling to exhaustion was completed during which V˙O2max and maximal CO were estimated. Compared with CON, significant (P < 0.001) increases in V˙O2max in HIIT + SIT (39.8 ± 7.3 mL·kg·min to 43.6 ± 6.1 mL·kg·min), HIIT + HIITHI (41.1 ± 4.9 mL·kg·min to 44.6 ± 7.0 mL·kg·min), and HIIT + PER (39.5 ± 5.6 mL·kg·min to 44.1 ± 5.4 mL·kg·min) occurred which were mediated by significant increases in maximal CO (20.0 ± 3.1 L·min to 21.7 ± 3.2 L·min, P = 0.04). Maximal stroke volume was increased with HIIT (P = 0.04), although there was no change in maximal HR (P = 0.88) or arteriovenous O2 difference (P = 0.36). These CO data are accurate and represent the mean changes from pre- to post-HIIT across all three training groups. Increases in V˙O2max exhibited in response to different HIIT regimes are due to improvements in oxygen delivery.

Lvad pump speed increase is associated with increased peak exercise cardiac output and vo2, postponed anaerobic threshold and improved ventilatory efficiency

BackgroundsPeak exercise cardiac output (CO) increase is associated with an increase of peak oxygen uptake (VO2), provided that arteriovenous O2 difference [Δ(Ca−Cv)O2] does not decrease. At anaerobic threshold, VO2, is related to CO.We tested the hypothesis that, in heart failure (HF) patients with left ventricular assistance device (LVAD), an acute increase of CO obtained through changes in LVAD pump speed is associated with peak exercise and anaerobic threshold VO2 increase. MethodsFifteen of 20 patients bearing LVAD (Jarvik 2000) enrolled in the study successfully performed peak exercise evaluation. All patients had severe HF as shown by clinical evaluation, laboratory tests, echocardiography, spirometry with alveolar-capillary diffusion, and maximal cardiopulmonary exercise testing (CPET). CPETs with non-invasive CO measurements at rest and peak exercise were done on 2days at LVAD pump speed set randomly at 2 and 4. ResultsIncreasing LVAD pump speed from 2 to 4 increased CO from 3.4±0.9 to 3.8±1.0L/min (ΔCO 0.4±0.6L/min, p=0.04) and from 5.3±1.3 to 5.9±1.4L/min (ΔCO 0.6±0.7L/min, p<0.01) at rest and peak exercise, respectively. Similarly, VO2 increased from 788±169 to 841±152mL/min (ΔVO2 52±76mL/min, p=0.01) and from 568±116 to 619±124mL/min (ΔVO2 69±96mL/min, p=0.02) at peak exercise and at anaerobic threshold, respectively. Δ(Ca−Cv)O2 did not change significantly, while ventilatory efficiency improved (VE/VCO2 slope from 39.9±5.4 to 34.9±8.3, ΔVE/VCO2 −5.0±6.4, p<0.01). ConclusionsIn HF, an increase in CO with a higher LVAD pump speed is associated with increased peak VO2, postponed anaerobic threshold, and improved ventilatory efficiency.

Effects of erythropoietin on systemic hematocrit and oxygen transport in the splenectomized horse

To test the hypotheses that erythropoietin (rhuEPO) treatment increases systemic hematocrit, maximal O2 uptake (V˙O2max, by elevated perfusive and diffusive O2 conductances) and performance five female horses (4–13 years) received 15IU/kg rhuEPO (erythropoietin) three times per week for three weeks. These horses had been splenectomized over 1 year previously to avoid confounding effects from the mobilization of splenic red blood cell reserves. Each horse performed three maximal exercise tests (one per month) on an inclined (4°) treadmill to the limit of tolerance; two control trials and one following EPO treatment. Measurements of hemoglobin concentration ([Hb] and hematocrit), plasma and blood volume, V˙O2, cardiac output as well as arterial and mixed venous blood gases were made at rest and during maximal exercise. EPO increased resting [Hb] by 18% from 13.3±0.6 to 15.7±0.8g/dL (mean±SD) corresponding to an increased hematocrit from 36±2 to 46±2% concurrent with 23 and 10% reductions in plasma and blood volume, respectively (all P<0.05). EPO elevated V˙O2max by 20% from 25.7±1.7 to 30.9±3.4L/min (P<0.05) via a 17% increase in arterial O2 content and 18% greater arteriovenous O2 difference in the face of an unchanged cardiac output. To achieve the greater V˙O2max after EPO, diffusive O2 conductance increased ∼30% (from 580±76 to 752±166mL O2/mmHg/min, P<0.05) which was substantially greater than the elevation of perfusive O2 conductance. These effects of EPO were associated with an increased exercise performance (total running time: control, 216±72; EPO, 264±48s, P<0.05). We conclude that EPO substantially increases V˙O2max and performance in the splenectomized horse via improved perfusive and diffusive O2 transport.

Altered cardiorespiratory response to exercise in overweight and obese women with polycystic ovary syndrome.

In polycystic ovary syndrome (PCOS), cardiovascular risk is increased. Peak O2 uptake (V˙O2peak) predicts the cardiovascular risk. We were the first to examine the contribution of systemic O2 delivery and arteriovenous O2 difference to V˙O2peak in overweight and obese women with PCOS. Fifteen overweight or obese PCOS women and 15 age‐, anthropometry‐, and physical activity‐matched control women performed a maximal incremental cycling exercise test. Alveolar gas exchange (volume turbine and mass spectrometry), arterial O2 saturation (pulse oximetry), and cardiac output (CO) (impedance cardiography) were monitored. Hb concentration was determined. Arterial O2 content and arteriovenous O2 difference (C(a‐v)O2) (Fick equation) were calculated. Insulin resistance was evaluated by homeostasis model assessment (HOMA‐IR). PCOS women had lower V˙O2peak than controls (40 ± 6 vs. 46 ± 5 mL/min/kg fat‐free mass [FFM], P = 0.011). Arterial O2 content was similarly maintained in the groups throughout the exercise test (P > 0.05). Linear regression analysis revealed a pronounced response of CO to increasing V˙O2 in PCOS women during the exercise test: A ∆CO/∆V˙O2 slope was steeper in PCOS women than in controls (β = 5.84 vs. β = 5.21, P = 0.004). Eventually, the groups attained similar peak CO and peak CO scaled to FFM (P > 0.05). Instead, C(a‐v)O2 at peak exercise was lower in PCOS women than in controls (13.2 ± 1.6 vs. 14.8 ± 2.4 mL O2/100 mL blood, P = 0.044). HOMA‐IR was similar in the groups (P > 0.05). The altered cardiorespiratory responses to exercise in overweight and obese PCOS women indicate that PCOS per se is associated with alterations in peripheral adjustments to exercise rather than with limitations of systemic O2 delivery.