Maximal Exercise In Patients Research Articles

Blood pressure response during exercise testing in individuals with and without hypertension: The value of the recovery phase.

Hypertension and exercise testing are essential for cardiovascular risk assessment. However, an exact description of blood pressure (BP) in patients with a hypertensive response during exercise (HRE), especially in the recovery phase is lacking. Herein, we aimed to analyse BP and heart rate during exercise testing and recovery in patients with an HRE. 800 patients aged 17-90 with an HRE during a standardized bicycle ergometry test were recruited. The BP behaviour during exercise testing was correlated with clinical data. Furthermore, data were analysed according to the presence of pre-existent hypertension. Of the 800 patients included in this study 497 (62%) were previously diagnosed with hypertension. Analysis of covariance showed a significantly faster systolic (β [95% CI] 8.0 [4.9-11.1]) and diastolic (2.4 [0.4-4.4]) BP recovery 3 min after maximal exercise in patients without hypertension in univariable models. These results remained robust in fully adjusted models taking into account age, sex, body mass index, cardiovascular disease, and antihypertensive treatment for systolic (5.3 [1.2-9.4]) and diastolic BP (4.5 [1.9-7.0]). Furthermore, patients with hypertension displayed higher systolic BP during maximal exercise in univariable (3.8 [0.1-7.5]) and fully adjusted (5.5 [1.1-10.0]) models. There was no difference in maximum diastolic BP between groups. In this large cohort study, patients without hypertension showed a faster systolic and diastolic BP recovery and lower maximal systolic BP compared to patients with hypertension. Overall, this study provides new insights into cardiovascular health during recovery phase.

Muscle oxygen supply impairment during maximal exercise in patients undergoing dialysis therapy

This study aimed to investigate whether Chronic Kidney Disease (CKD) influences O2 supply including O2 delivery and release to the active muscles during maximal physical exercise. Twelve CKD patients undergoing dialysis therapy (HD group) and twelve healthy adults (CTR group) performed an incremental exercise test to determine maximal oxygen uptake (VO2peak). Throughout the exercise, near-infrared spectroscopy allowed the investigation of changes in oxyhemoglobin (∆O2Hb), deoxyhemoglobin (∆HHb), and total hemoglobin (∆THb) in the vastus lateralis muscle. VO2peak was significantly lower in HD group. In addition, HD patients had impaired changes in muscular oxygenation (∆HHb and ∆O2Hb) and blood volume (∆THb) during the exercise (p < 0.05). Moreover, a positive correlation was observed between VO2peak and muscle blood volume (∆THb) in both groups (p < 0.05). This study provides the first evidence that HD patients displayed lower VO2peak and blunted muscular deoxyhemoglobin increase during exercise. This result supports the hypothesis of an increase in oxygen affinity and/or mitochondrial dysfunction in this population.

Limits to submaximal and maximal exercise in patients with hypertrophic cardiomyopathy.

Patients with hypertrophic cardiomyopathy (HCM) often have reduced exercise capacity, and it is unclear whether cardiovascular regulation during exercise is intact in these patients. We aimed to determine the relationship between cardiac output (Q̇c) and oxygen uptake (V̇o2), and stroke volume (SV) reserve in HCM compared with healthy participants and participants with left ventricular hypertrophy (LVH) but not HCM. Sixteen patients with HCM (48 ± 7 yr, 44% female), 16 participants with LVH (49 ± 5 yr, 44% female), and 61 healthy controls (CON: 52 ± 5 yr, 52% female) completed submaximal steady-state treadmill exercise followed by a maximal exercise test. V̇o2, Q̇c, SV, and arteriovenous oxygen difference were measured during rest and exercise, and Q̇c/V̇o2 slopes were constructed, The Q̇c/V̇o2 slope was blunted in HCM compared with CON and LVH [HCM 4.9 ± 0.7 vs. CON 5.5 ± 1.0 (P = 0.027) vs. LVH 6.0 ± 1.0 AU (P = 0.002)] and participants with HCM had a lower SV reserve (HCM 53 ± 33%, controls 83 ± 33%, LVH 82 ± 22%; HCM vs. controls P = 0.002; HCM vs. LVH P = 0.015). Despite a blunted Q̇c/V̇o2 slope, 75% of patients with HCM achieved ≥80% predicted V̇o2max by augmenting a-vo2 difference at maximal exercise (16.0 ± 0.8 mL/100 mL vs. 13.8 ± 2.7 mL/100 mL, P = 0.021). Patients with HCM do not appropriately match Q̇c to metabolic demand, primarily due to inadequate stroke volume augmentation. Despite this central limitation, many patients achieve normal exercise capacities by significantly increasing peripheral oxygen extraction.NEW & NOTEWORTHY Through state-of-the-art hemodynamic and oxygen uptake methodologies, this study found the cardiac output response to increasing metabolic demand is blunted among patients with hypertrophic cardiomyopathy (HCM), primarily due to a reduced stroke volume reserve. Many patients with HCM augment their peripheral oxygen extraction during maximal exercise to achieve normal exercise capacity and overcome ineffective matching of cardiac output. Peripheral adaptations that compensate for cardiac limitations may contribute to the heterogeneity of functional limitations observed within this patient population.

Toward a Better Understanding of Muscle Microvascular Perfusion During Exercise in Patients With Peripheral Artery Disease: The Effect of Lower-Limb Revascularization

Purpose: Leg muscle microvascular blood flow (perfusion) is impaired in response to maximal exercise in patients with peripheral artery disease (PAD); however, during submaximal exercise, microvascular perfusion is maintained due to a greater increase in microvascular blood volume compared with that seen in healthy adults. It is unclear whether this submaximal exercise response reflects a microvascular impairment, or whether it is a compensatory response for the limited conduit artery flow in PAD. Therefore, to clarify the role of conduit artery blood flow, we compared whole-limb blood flow and skeletal muscle microvascular perfusion responses with exercise in patients with PAD (n=9; 60±7 years) prior to, and following, lower-limb endovascular revascularization. Materials and Methods: Microvascular perfusion (microvascular volume × flow velocity) of the medial gastrocnemius muscle was measured before and immediately after a 5 minute bout of submaximal intermittent isometric plantar-flexion exercise using contrast-enhanced ultrasound imaging. Exercise contraction-by-contraction whole-leg blood flow and vascular conductance were measured using strain-gauge plethysmography. Results: With revascularization there was a significant increase in whole-leg blood flow and conductance during exercise (p<0.05). Exercise-induced muscle microvascular perfusion response did not change with revascularization (pre-revascularization: 3.19±2.32; post-revascularization: 3.89±1.67 aU.s−1; p=0.38). However, the parameters that determine microvascular perfusion changed, with a reduction in the microvascular volume response to exercise (pre-revascularization: 6.76±3.56; post-revascularization: 2.42±0.69 aU; p<0.01) and an increase in microvascular flow velocity (pre-revascularization: 0.25±0.13; post-revascularization: 0.59±0.25 s−1; p=0.02). Conclusion: These findings suggest that patients with PAD compensate for the conduit artery blood flow impairment with an increase in microvascular blood volume to maintain muscle perfusion during submaximal exercise. Clinical Impact The findings from this study support the notion that the impairment in conduit artery blood flow in patients with PAD leads to compensatory changes in microvascular blood volume and flow velocity to maintain muscle microvascular perfusion during submaximal leg exercise. Moreover, this study demonstrates that these microvascular changes are reversed and become normalized with successful lower-limb endovascular revascularization.

A Cardiac Rehabilitation Program Increases the Acute Response of Endothelial Progenitor Cells to Maximal Exercise in Heart Failure Patients.

The purpose of this study was to investigate the effect of a cardiac rehabilitation program on the acute response on endothelial progenitor cells and circulating endothelial cells after maximal exercise in patients with chronic heart failure of different severity. Forty-four chronic heart failure patients were enrolled in a 36-session cardiac rehabilitation program. All patients underwent an initial maximal cardiopulmonary exercise test before and a final maximal cardiopulmonary exercise test after the cardiac rehabilitation program. The patients were divided in two groups of severity according to the median value of peak VO2. Blood was collected at 4 time points; 2 time points at rest, and 2 time points after each cardiopulmonary exercise test. Five endothelial cellular populations were quantified by flow cytometry. Although there was a higher increase in the mobilization of subgroups of endothelial progenitor cells and circulating endothelial cells after the final cardiopulmonary exercise test compared to the initial test within each severity group (p < 0.05), no significant differences between severity groups were observed (p > 0.05). A 36-session cardiac rehabilitation program had similar beneficial effects on the acute response of endothelial progenitor cells and circulating endothelial cells after maximal exercise in patients with chronic heart failure of different severity.

The acute and long-term effects of a cardiac rehabilitation program on endothelial progenitor cells in chronic heart failure patients: Comparing two different exercise training protocols.

BackgroundVascular endothelial dysfunction is an underlying pathophysiological feature of chronic heart failure (CHF). Endothelial progenitor cells (EPCs) are also impaired. The purpose of the study was to assess the effect of a cardiac rehabilitation (CR) program on the increase of EPCs at rest and on the acute response after maximal exercise in patients with CHF and investigate whether there were differences between two exercise training protocols and patients of NYHA II and III classes.MethodsForty-four patients with stable CHF enrolled in a 36-session CR program and were randomized in one training protocol; either high-intensity interval training (HIIT) or HIIT combined with muscle strength (COM). All patients underwent maximum cardiopulmonary exercise testing (CPET) before and after the CR program and venous blood was drawn before and after each CPET. Five endothelial cellular populations, expressed as cells/106 enucleated cells, were quantified by flow cytometry.ResultsAn increase in all endothelial cellular populations at rest was observed after the CR program (p < 0.01). The acute response after maximum exercise increased in 4 out of 5 endothelial cellular populations after rehabilitation. Although there was increase in EPCs at rest and the acute response after rehabilitation in each exercise training group and each NYHA class, there were no differences between HIIT and COM groups or NYHA II and NYHA III classes (p > 0.05).ConclusionsA 36-session CR program increases the acute response after maximum CPET and stimulates the long-term mobilization of EPCs at rest in patients with CHF. These benefits seem to be similar between HIIT and COM exercise training protocols and between patients of different functional classes.

Peak Oxygen Uptake Recovery Delay After Maximal Exercise in Patients With Heart Failure.

Peak oxygen uptake recovery delay (V˙o2peakRD), measured as the time until post-exercise oxygen uptake (V˙o2) decreases below V˙o2peak following maximal cardiopulmonary exercise testing (CPX), has been recognized as an abnormal response, associated with reduced cardiac output reserve during exercise in patients with heart failure (HF). In the current study we examined the association of V˙o2peakRD during routine CPX testing of patients with symptomatic HF across a wide range of left ventricular ejection fraction (LVEF) values with clinical biomarkers. In this retrospective study, 80 clinically stable symptomatic HF patients across a wide range of LVEF at our institution were evaluated that put forth a minimally acceptable effort during CPX testing (respiratory exchange ratio ≥ 1.00). The V˙o2peakRD was measured in 10-sec intervals following maximal CPX testing. Markers of elevated cardiac filling pressures (N-terminal pro-brain natriuretic peptide [NTproBNP] and echocardio-Doppler E/e') and other key CPX parameters were explored for their association with V˙o2peakRD. The mean V˙o2peakRD and V˙o2peak were 10 (interquartile range 10, 40) sec and 13.9 (11.6, 16.4) mL· kg · min, respectively. V˙o2peakRD demonstrated a positive linear trend with serum NTproBNP levels and E/e' (TJT = 1239.500, z = 2.634, P < .01; TJT = 1081.000, z = 2.046, P = .04, respectively). Prolonged V˙o2peakRD following exercise is associated with markers of greater disease severity in patients with HF.

Combining Dynamic Hyperinflation with Dead Space Volume during Maximal Exercise in Patients with Chronic Obstructive Pulmonary Disease.

Physiological dead space volume (VD) and dynamic hyperinflation (DH) are two different types of abnormal pulmonary physiology. Although they both involve lung volume, their combination has never been advocated, and thus their effect and implication are unclear. This study aimed (1) to combine VD and DH, and (2) investigate their relationship and clinical significance during exercise, as well as (3) identify a noninvasive variable to represent the VD fraction of tidal volume (VD/VT). Forty-six male subjects with chronic obstructive pulmonary disease (COPD) and 34 healthy male subjects matched for age and height were enrolled. Demographic data, lung function, and maximal exercise were investigated. End-expiratory lung volume (EELV) was measured for the control group and estimated for the study group using the formulae reported in our previous study. The VD/VT ratio was measured for the study group, and reference values of VD/VT were used for the control group. In the COPD group, the DHpeak/total lung capacity (TLC, DHpeak%) was 7% and the EELVpeak% was 70%. After adding the VDpeak% (8%), the VDDHpeak% was 15% and the VDEELVpeak% was 78%. Both were higher than those of the healthy controls. In the COPD group, the VDDHpeak% and VDEELVpeak% were more correlated with dyspnea score and exercise capacity than that of the DHpeak% and EELV%, and had a similar strength of correlation with minute ventilation. The VTpeak/TLC (VTpeak%), an inverse marker of DH, was inversely correlated with VD/VT (R2 ≈ 0.50). Therefore, we recommend that VD should be added to DH and EELV, as they are physiologically meaningful and VTpeak% represents not only DH but also dead space ventilation. To obtain VD, the VD/VT must be measured. Because obtaining VD/VT requires invasive arterial blood gases, further studies on noninvasive predicting VD/VT is warranted.

Exercise responses in children and adults with a Fontan circulation at simulated altitude.

BackgroundTraveling to high altitude has become more popular. High‐altitude exposure causes hypobaric hypoxia. Exposure to acute high altitude, during air travel or mountain stays, seems to be safe for most patients with congenital heart disorders (CHD). Still, current guidelines for CHD patients express concerns regarding safety of altitude exposure for patients with a Fontan circulation. Therefore, investigating hemodynamic and pulmonary responses of acute high‐altitude exposure (±2500 m) at rest and during maximal exercise in patients with Fontan circulation can provide clarity in this dispute and may contribute to improvement of clinical counseling.MethodsTwenty‐one Fontan patients with 21 age‐matched healthy controls, aged 8‐40 years, were enrolled in an observational study. Participants performed two cardiopulmonary exercise tests on a cycle ergometer with breath‐by‐breath respiratory gas analyses combined with noninvasive impedance cardiac output measurements: one at sea level (±6 m) and one at simulated high altitude (±2500 m), respectively.ResultsThe effect of altitude exposure was different in rest for saturation (−2.3% vs −4.1%) between Fontan patients and healthy controls (P < .05). At peak exercise the effects of high altitude exposure was different on VO2 (−5.1% vs 9.6%) and AvO2‐diff (−0.3% vs −12.8%) between Fontan patients and healthy controls.ConclusionAlthough, acute high‐altitude exposure has a detrimental effect on exercise capacity, the impact on pulmonary and hemodynamic responses of high‐altitude exposure is comparable between Fontan patients and healthy controls.

Thick Hearts Can't Keep Up: Exercise Limitations in Patients With Hypertrophic Cardiomyopathy

Patients with hypertrophic cardiomyopathy (HCM) may experience intolerance to submaximal and maximal exercise. While ejection fraction is generally preserved, reduced left ventricular end diastolic volume may limit stroke volume reserve and potentially attenuate maximal oxygen uptake (V̇O2max). Whether the relationship between supply (cardiac output, Q̇c) and demand (oxygen uptake, V̇O2) remains intact in these patients is unclear.PURPOSETo quantify the cardiac output response to a given metabolic demand during submaximal and maximal exercise in patients with HCM.METHODSEight patients with HCM (45.8±8.8 years, 75% female, left ventricular outflow tract pressure gradient 13±12mmHg) completed two bouts of submaximal steady‐state treadmill exercise (SS1 ~45% and SS2 ~60% V̇O2max), followed by an incremental treadmill test to exhaustion. V̇O2 (Douglas bag technique), Q̇c, (acetylene rebreathing), stroke volume (Q̇c/heart rate) and arterio‐venous difference (av‐O2 diff, Fick principle) were measured during rest, SS1, SS2 and maximal exercise. Stroke volume reserve was calculated as the percent increase in stroke volume from rest to maximal exercise. The relationship between Q̇c and V̇O2 (Q̇c/V̇O2 slope) was quantified using data collected at rest, submaximal and maximal exercise. Healthy sedentary adults (n=8) and subjects with left ventricular hypertrophy from hypertension (LVH, n=8) were included for age and sex‐matched comparison.RESULTSPatients with HCM had lower relative V̇O2max than healthy subjects and patients with LVH (HCM: 21.1±4.8mL/kg/min, healthy: 27.5±3.4 mL/kg/min, LVH 24.4±7.5 mL/kg/ min). The Q̇c response to a given metabolic demand was impaired in patients with HCM when compared to healthy controls and patients with LVH (HCM: 4.6, control: 5.4, LVH: 5.5; Figure 1). The blunted Q̇c/V̇O2 slope was primarily due to a smaller stroke volume reserve (HCM 28.8±27.0%, healthy 52.2±19.6%, LVH 48.6±25.0%), but also a significantly lower maximal heart rate compared to healthy controls (154±24 vs. 178±10 beats per minute, respectively; P&lt;0.05), though 75% of HCM patients were on beta‐blockade and/or calcium channel‐blockade therapy. Remarkably, five HCM patients were able to compensate for a blunted Q̇c/V̇O2 slope (4.2±0.4) and still achieve &gt;80% of predicted V̇O2max by significantly augmenting av‐O2 diff from rest to maximal exercise (Δav‐O2 diff 10.6±1.6 vs. 6.2±1.5 in HCM patients who did not achieve 80% of predicted V̇O2 max, P&lt;0.05).CONCLUSIONAlthough ejection fraction is preserved, patients with HCM may be unable to sufficiently match Q̇c to metabolic demands. However, some patients appear to compensate by significantly augmenting peripheral oxygen extraction and achieve at least 80% of predicted V̇O2max.Support or Funding InformationSupported by The Center for Regenerative Science and Medicine, UTSW Medical Center, Biotronik Inc., and the Research Endowment from The American College of Sports Medicine Foundation.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Coagulation factor VIII is vital for increasing global coagulation after physical exercise.

In a previous smaller study, we found evidence of a diminished global coagulation capacity after maximal exercise in patients with severe haemophilia A (HA). To validate these results, we repeated the study in a larger cohort. We also examined if the exercise-induced increased levels of von Willebrand factor (VWF) might prolong the effect of factor concentrate administered just before exercise. We studied individual and global coagulation parameters after maximal physical exercise in 10 persons with severe HA and 10 healthy matched control subjects. Blood samples were taken before, 10minutes, 60minutes and 4hours after exercise. Rotational thromboelastometry (ROTEM) and thrombin generation assay-calibrated automated thrombogram (TGA-CAT) showed significantly increased coagulation capacity after maximal exercise in healthy controls but not in patients with severe HA. VWF antigen and activity levels increased significantly in both groups, whereas FVIII:C only showed a significant increase in the control group. No statistically significant differences were seen between FVIII pharmacokinetic results obtained with and without exercise. Our findings do not support the presence of a FVIII-independent mechanism that increases global coagulation, but rather underscores the importance of FVIII in mediating the increased coagulation capacity seen after exercise. Our results could not support the hypothesis that exercise-induced increased levels of VWF for patients with severe HA lead to a prolonged effect of factor concentrate administered just before exercise.

Antioxidant Supplementation Improves Skeletal Muscle Metabolism During Maximal Exercise In Patients With Cystis Fibrosis

INTRODUCTION: Patients with cystic fibrosis (CF) exhibit high levels of oxidative stress that contribute to multiple systemic dysfunctions, including exercise intolerance. Antioxidant supplementation has been shown to mitigate oxidative stress and improve exercise intolerance in other populations. Recently, our group has described that patients with CF exhibit impairments in skeletal muscle metabolism that may contribute to exercise intolerance. Whether or not antioxidants can impact muscle metabolism during exercise in patients with CF, however, has yet to be elucidated. PURPOSE: This study sought to test the hypothesis that 4 weeks of oral antioxidant supplementation will improve skeletal muscle metabolism during maximal exercise in patients with CF. METHODS: Eight patients with CF (25 ± 11 yrs.) completed an incremental exercise test on a cycle ergometer before (Pre) and after 4 weeks of oral supplementation with an antioxidant cocktail (AOC: vitamin C, vitamin E and α- lipoic). Skeletal muscle metabolism was evaluated at rest and during maximal exercise (max) through: (I) O2 extraction (O2Ex) calculated using a derivation of the Fick equation, (II) muscle O2 utilization (HHb), using near-infrared spectroscopy and (III) exercise factor (EF), as the relative contribution of O2 supply to O2 consumption. RESULTS: A significant (p=0.039) increase in O2EXmax was observed after 4 weeks of AOC when compared to baseline (Pre: 57 ± 8%, AOC: 64 ± 7%). In addition, HHbmax was significantly (p=0.046) greater (Pre: 0.97 ± 3.4 μM, AOC: 5.9 ± 2.9 μM) and EFmax was significantly (p=0.048) reduced (Pre: 7.1 ± 1.4 AU; AOC: 6.3 ± 1.3 AU) after completing the AOC treatment. No changes in resting skeletal muscle metabolism (p≥0.446) were observed following 4 weeks of supplementation. CONCLUSIONS: For the first time, we have documented that four weeks of AOC supplementation improves skeletal muscle metabolism during maximal exercise in patients with CF. These findings suggest that oxidative stress may be partially involved in the reduced O2 extraction and muscle O2 utilization during exercise observed in patients with CF. Future studies are warranted to investigate the long term effects of antioxidants on muscle metabolism and exercise tolerance in CF. Supported in part by CFFT HARRIS14A0 (RAH).

Mixed Venous Oxygen Saturation is Impaired During Maximal Exercise in Patients with Cystic Fibrosis

Mixed Venous Oxygen Saturation is Impaired During Maximal Exercise in Patients with Cystic Fibrosis

Endothelial Dysfunction Predicts Systolic Blood Pressure Slope During Whole Body Maximal Exercise In Patients With Chronic Kidney Disease

Chronic kidney disease (CKD) patients have exercise intolerance and poor physical capacity that increases the risk of adverse cardiovascular events during and after physical activity. Previous studies in our lab demonstrate that CKD patients have exaggerated increases in blood pressure (BP) and sympathetic nervous system activation during handgrip exercises. However, whether CKD patients also have exaggerated increases in BP during whole‐body exercise or high intensity exercise is unknown. Furthermore, CKD patients often have endothelial dysfunction which could potentially lead to an impaired ability to vasodilate during exercise. Whether this might contribute to the augmented pressor response in CKD is also unknown. We hypothesized that CKD patients have exaggerated increases in BP during maximal whole body exercise and that endothelial dysfunction predicts a greater pressor response during exercise in these patients. 56 participants (35 CKD, 21 age‐matched controls) underwent maximal treadmill exercise using the modified Balke protocol. BP, heart rate (HR), and rate of perceived exertion were continuously monitored. Levels of mixed expired oxygen, carbon dioxide, and ventilation were recorded at rest and every 30 seconds during exercise. The peak oxygen uptake (VO2 max) was defined as the highest VO2 rate observed during maximal exercise. Endothelial function was assessed via brachial artery flow‐mediated dilation (FMD) just before and repeated 1 hour after exercise. CKD patients had significantly lower VO2 max compared to controls (21.8±1.1 ml/min/kg vs. 30.3±1.7, p&lt;0.001). There was no significant difference in maximal systolic BP (SBP), diastolic BP, or mean arterial pressure achieved during exercise between groups. However, CKD patients had a greater slope of rise in SBP (10.3 mmHg/stage vs. 7.7, p&lt;0.001). Maximum achieved HR was significantly lower in CKD versus controls (134.9±4.4 bpm vs. 150.0±3.6, p=0.011). Similar to BP response, the slope of rise in HR was significantly steeper in CKD patients (11.9 bpm/stage vs. 10.7, p=0.032). Before exercise, FMD (2.76±0.42% vs. 5.84±0.97, p=0.007), and FMD controlled for peak shear rate (FMDshear) (4.01±0.62% vs. 6.85±1.11, p=0.033) were significantly lower in CKD patients. A lower pre‐exercise FMD (p=0.039) and FMDshear (p&lt;0.001) were significantly associated with a greater slope of rise in SBP during exercise in CKD, but not in controls. There was no significant change in FMD before and after exercise in either group. CKD patients exhibit an accelerated rise in SBP and HR during whole body maximal exercise compared to controls. Further, impaired FMD predicts an accelerated SBP and HR response during exercise in CKD patients, but not in controls. These data suggest that endothelial dysfunction is associated with the exaggerated pressor response during exercise in CKD patients.Support or Funding InformationSupported by NIH HL‐098744.

Attenuated Microcirculatory Response to Maximal Exercise in Patients With Chronic Heart Failure.

Exercise training programs improve microcirculatory alternations in patients with chronic heart failure (CHF). However less is known about the acute effect of maximum exercise on the skeletal muscle microcirculation. We aimed to assess the effect of acute exercise on peripheral microcirculation of patients with CHF, as assessed by near-infrared spectroscopy with vascular occlusion technique. Tissue oxygenation was evaluated in 8 stable patients with CHF (7 males; mean age, 60 ± 9 years; body mass index, 26.3 ± 3.8 kg/m) and 8 healthy subjects (matched for age, sex, and body mass index) before and after cardiopulmonary exercise testing. Tissue oxygen saturation (StO2), StO2peak, oxygen consumption rate, and endothelial function (reperfusion rate), before and after maximum exercise, were assessed. Patients with CHF had lower StO2 and reperfusion rate compared with healthy subjects (71.4% ± 9.8% vs 81.0% ± 5.4% and 9 ± 1 %/min vs 13.9 ± 5.8%/min, respectively; P < .05) at rest. Oxygen consumption rate increased after exercise in patients with CHF and healthy subjects (from -31.7 ± 8.2 to -43.7 ± 12.7 and from -35.7 ± 6.7 to -42.4 ± 6.4, respectively; P < .05). StO2 decreased significantly after maximal exercise in patients with CHF (from 71.4 ± 9.8 to 65.2 ± 12.7; P < .05), whereas it returned to the preexercise values in healthy subjects (from 81.0 ± 5.4 to 80.3 ± 7.0). There was a significant between-group difference (P < .05). Patients with CHF present microcirculatory alternations. Acute exercise exerts an effect on microcirculation in peripheral, nonexercising muscles, with altered response in patients with CHF compared with healthy subjects.

Usefulness of High-Sensitive Troponin Elevation After Effort Stress to Unveil Vulnerable Myocardium in Patients With Heart Failure

Elevation of resting high-sensitivity troponin (hs-Tn) holds prognostic value in heart failure (HF), but its pathophysiological meaning is unclear. We aimed to investigate hs-Tn elevation after maximal exercise in patients with systolic HF and its neurohormonal and hemodynamic correlates: 30 patients diagnosed with systolic HF (left ventricular ejection fraction 32 ± 8%, mean ± SD), on guideline-directed medical therapy and not recognized inducible ischemia, underwent maximal cardiopulmonary stress test, with assay of plasma N-terminal proB-type natriuretic peptide (NT-proBNP), norepinephrine (NE), and hs-TnT (hs-TnT) at baseline, peak, and 1 and 4hours after exercise. Cardiac output (CO) was measured during effort, with a rebreathing technique. The natural logarithm of the ratio between percentage (%) increase in CO and NT-proBNP (ln[CO%/NT-proBNP% increase]) was evaluated, as a noninvasive estimate of Frank-Starling adaptation to effort, with NT-proBNP variation considered as a surrogate of end-diastolic left ventricular pressure variation. Hs-TnT increased during exercise with a 4-hour peak (p= 0.001); 10 patients had hs-TnT increase >20%. Patients with Hs-TnT increase >20% were more symptomatic at rest (p= 0.039) and showed greater NE at peak exercise (p= 0.003) and less ln[CO%/NT-proBNP% increase] (p= 0.034). A lower ln[CO%/NT-proBNP% increase] correlated with greater NE at peak exercise (r=-0.430, p= 0.018). In conclusion, acute troponin elevation after maximal exercise was detected in 1/3 of this series. The association of troponin release with NE, CO, and NT-proBNP changes after effort suggests a pathophysiological link among transient hemodynamic overload, adrenergic activation, and myocardial cell damage, likely identifying a clinical subset at greater risk for HF progression.

The Hemodynamic Response during Submaximal and Maximal Exercise in Patients with Cystic Fibrosis

The Hemodynamic Response during Submaximal and Maximal Exercise in Patients with Cystic Fibrosis

Attenuated Heart Rate Recovery is Associated with Sympathetic Hyperactivity in Patients with Metabolic Syndrome and Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) and metabolic syndrome (MetS) are independently associated with impaired heart rate recovery (HRR) after maximal exercise. We tested the hypotheses that: 1) MetS+OSA would have an additive effect on attenuation of HRR; 2) The sympathetic hyperactivation would be involved on slower HRR. Newly diagnosed MetS (ATP III) patients, sedentary were divided into: MetS+OSA (n=18, 49±2y) and MetS‐OSA (n=21, 44±2y). Normal individuals were also studied (C, n=13, 47±2y). OSA was characterized by apnea‐hypopnea index (AHI) &gt;;15events/h (polysomnography). Muscle sympathetic nerve activity (MSNA, microneurography), heart rate (EKG), low (LF) and high (HF) frequency power bands and sympatho‐vagal balance (LF/HF‐Spectral analysis) were measured. The HRR was calculated (HRpeak minus HHR at 1st, 2nd, 4th min). MetS+OSA had higher MSNA, LF and LF/HF compared with MetS‐OSA and C. MSNA was higher in MetS‐OSA than in C. HF power was lower in MetS+OSA compared with MetS‐OSA and C. HRR at 1st, 2nd min was lower in MetS+OSA compared with C (P&lt;0.01) and lower at 4th min compared with Met‐OSA and C (P&lt;0.01). Further analyses showed an association between MSNA levels and HRR (P&lt;0.01). In conclusion, OSA exacerbates the attenuation of HRR after maximal exercise in patients with MetS. In addition, the attenuation of HRR is associated with sympathetic hyperactivation.(FAPESP#2011/17533–6)

260: Cognitive performance, cerebral oxygenation, exercise capacity and cardiac output in patients with coronary heart disease

Recent data suggested that coronary heart disease (CHD) is associated with non-amnesic mild cognitive impairment. Our purpose was to assess cognitive performances at rest, VO2max, cardiac output (CO), and cerebral hemodynamic changes during maximal exercise in patients with stable CHD. 22 stable fit CHD patients (70,9±9,3 years), 10 healthy age-matched (68,6±8,6 years), 10 middle aged controls and 10 young controls (< 40y) were included. We assessed cognitive performance with a standard battery of paper and pencil tests, maximal exercise test on ergocycle with gas exchange analysis with non-invasive CO measurement and Near-Infrared Spectroscopy (NIRS) oxygenation indices at the brain level. There was no intergroup difference in VO2max or maximal CO between cardiac and healthy age-matched individuals. Some cognitive tests, especially for executive functioning, were significantly better for the healthy matched group (Trail Making Test-B; Inhibition/Flexibility Stroop Task and Backward Digit Span, p<0.05). For NIRS signals, we observed an increase in deoxyhemoglobin (HHb) for maximal intensities and the classical inverted U-shape curve for oxyhemoglobin (O2Hb) and hemoglobin difference (Hbdiff=O2Hb-HHb) in each group. Considering fitness, intra-CHD group differences were observed with lower amplitudes in HHb signalss for less fit subjects. In control groups, middle aged and young subjects had significant higher performances in VO2max, most of cognitive tests and higher amplitudes changes for NIRS indices while exercising. Despite comparable maximal exercise tolerances and CO, CHD individuals presented reduced cognitive performances compared to healthy age-matched subjects. We evidenced an inter-individual variability among CHD patients for cerebral NIRS signals changes, especially with age and fitness. These results suggest that variations in HHb are much more related to exercise capacity than O2Hb in CHD patients.

749 Cognitive Performance, Cerebral Oxygenation, Exercise Capacity and Cardiac Output in Patients with Coronary Heart Disease

Recent data suggested that coronary heart disease (CHD) was associated with non-amnesic mild cognitive impairment. The purpose of our study was to assess cognitive performances at rest, VO2max, cardiac output, and cerebral hemodynamic changes during maximal exercise in patients with stable CHD. 22 stable fit CHD patients (70,9 ± 9,3 years), 10 healthy age-matched (68,6 ± 8,6 years), 10 middle aged controls and 10 young controls (< 40ans) were included. We assessed cognitive performance with a standard battery of pen and paper tests, maximal exercise test on ergocycle with gas exchange analysis with non-invasive cardiac output measurement and Near-Infrared Spectroscopy (NIRS) oxygenation indices at the brain level. There was no intergroup difference in VO2max or maximal cardiac output between cardiac and healthy age-matched individuals. Some cognitive tests, especially for executive functioning, were significantly better for the healthy matched group (Trail Making Test-B ; Inhibition/Flexibility Stroop Task and Backward Digit Span p < 0.05). For NIRS signals, we observed an increase in deoxyhemoglobin (hHb) for maximal intensities and the classical inverted U-shaped curves for oxyhemoglobin (O2Hb) and hemoglobin difference (Diff Hb=O2Hb-HHb) in each group. About fitness, intra-CHD group differences were observed with higher amplitudes in hHb changes for fit CHD subjects. In control groups, middle aged and young subjects had significant higher performances in VO2max, most of cognitive tests and higher amplitudes changes for NIRS indices while exercising. In spite of comparable maximal exercise tolerances and cardiac outputs, CHD individuals presented some reduced cognitive performances compared to healthy age-matched subjects. We also found an inter-individual variability among CHD patients for cerebral NIRS signals changes especially with age and fitness. These results suggest that variations in deoxyhemoglobin are much more related to exercise capacity than oxyhemoglobin, especially in CHD patients.