Aerobic Capacity In Patients Research Articles

Habitual Activities and Peak Aerobic Capacity in Patients With Asymptomatic and Symptomatic Left Ventricular Dysfunction

A reduced level of daily activities is thought to be an important determinant of aerobic exercise intolerance in patients with chronic heart failure chronic heart failure; however, few data exist about the relationship between habitual physical activity level and peak aerobic capacity in patients at different clinical stages of left ventricular dysfunction. The purposes of this study were as follow: (1) to validate a simple interviewer-administered scoring system for evaluation of habitual physical activity level of patients with chronic heart failure and asymptomatic left ventricular dysfunction (ALVD); (2) to determine the relationship between habitual physical activity level and peak aerobic capacity in chronic heart failure and ALVD patients; and (3) to compare habitual activity levels among different New York Heart Association (NYHA) classes in these populations. Cardiology division at a tertiary-care hospital. We studied 167 consecutive patients with chronic heart failure (NYHA class I to III), 40 patients with ALVD, and 52 healthy subjects (HS). Habitual physical activity level was evaluated by means of an interview-based activity scoring system considering leisure time and occupational activities and also recent deconditioning events (eg, hospital admissions); a final activity score (AS) ranging from 0.8 to 5 was obtained. All patients and HS performed a symptom-limited cardiopulmonary exercise test up to a respiratory exchange ratio of > or = 1.1. AS was an independent predictor of peak oxygen consumption (VO(2)) in all groups, with a significantly higher VO(2) vs AS relationship slope in the ALVD and HS groups than in the chronic heart failure group. Moreover, AS was found to be significantly lower in chronic heart failure than in ALVD patients and HS (1.6 +/- 0.6 vs 2.2 +/- 0.7 vs 3.5 +/- 1.1, respectively; p < 0.0001), as was peak VO(2) (14.7 +/- 3.7 mL/kg/min vs 20 +/- 4 mL/kg/min vs 33.1 +/- 10 mL/kg/min, respectively; p < 0.0001), but the latter differences were canceled after adjusting for AS values. Significant AS and peak VO(2) reductions were observed in chronic heart failure patients with NYHA class progression from I to III. Habitual physical activity level is progressively decreased with worsening of heart failure symptoms and is related to peak aerobic capacity in both chronic heart failure and ALVD patients. However, this relationship appears to be weak in patients with chronic heart failure, whereas daily activity is a strong independent predictor of peak aerobic capacity both in ALVD patients and HS. This may be related to the intervention of factors other than skeletal muscle deconditioning in the exercise pathophysiology of chronic heart failure patients.

Impact of early ventricular unloading on exercise performance in preadolescents with single ventricle fontan physiology

OBJECTIVESWe sought to determine if early ventricular volume unloading improves aerobic capacity in patients with single ventricle Fontan physiology.BACKGROUNDSurgical strategies for patients with single ventricle include intermediate staging or early Fontan completion to reduce the adverse affects of prolonged ventricular volume load. The impact of this strategy on exercise performance has not been evaluated.METHODSRetrospectively, we reviewed the exercise stress test results of all preadolescents with single ventricle Fontan physiology. “Volume unloading” was considered to have occurred at the time of bidirectional cavopulmonary anastomosis or at the time of Fontan surgery in those patients who did not undergo intermediate staging. Potential predictors of aerobic capacity were analyzed using multivariate regression.RESULTSThe patients (n = 46) achieved a mean percentage predicted of maximal oxygen consumption (V̇O2max) of 76.1% ± 21.1%. The mean age at the time of volume unloading was 2.7 ± 2.4 years, and the mean age at testing was 8.7 ± 2 years. Intermediate staging was performed in 16 of 46 patients (35%). In multivariate analysis, younger age at volume unloading was associated with increased aerobic capacity (p = 0.003). Other variables were not predictive. The subgroup of patients who underwent volume unloading before two years of age achieved a mean percentage predicted V̇O2max of 88.6% ± 24.1%.CONCLUSIONSPreadolescents with single ventricle who undergo volume unloading surgery at an early age demonstrate superior aerobic capacity compared with those whose surgery is delayed until a later age.

An investigation of factors limiting aerobic capacity in patients with ankylosing spondylitis

Ankylosing spondylitis (AS) has been shown to produce exercise limitation and breathlessness. The purpose of this study was to investigate factors which may be responsible for limiting aerobic capacity in patients with AS. Twenty patients with no other cardio-respiratory disease performed integrative cardiopulmonary exercise testing (CPET). The results were compared to 20 age and gender matched healthy controls. Variables that might influence exercise tolerance, including pulmonary function tests (body plethysmography), respiratory muscle strength (MIP, MEP) and endurance (Tlim), AS severity assessment including chest expansion (CE), thoracolumber movement (TL), wall tragus distance and peripheral muscle strength assessed by maximum voluntary contraction of the knee extensors (Qds), hand grip strength and lean body mass (LBM), were measured in the patients with AS and used as explanatory variables against the peak V̇O 2 achieved during CPET. AS subjects achieved a lower peak V̇O 2 than controls (25·2 ± 1·4 vs. 33·1 ± 1·6 ml kg −1min −1, mean ± sem, P=0·001). When compared with controls, ventilatory response (V̇ E/V̇CO 2) in AS was elevated ( P=0·01); however gas exchange indices, transcutaneous blood gases and breathing reserve were similar to controls. AS subjects developed a higher HR/V̇O 2 response ( P<0·01) on exertion but without associated abnormalities in ECG, blood pressure response or anaerobic threshold. The AS group experienced a greater degree of leg fatigue ( P<0·01) than controls at peak exercise. Although the breathlessness scores (BS) were comparable to controls at peak exercise, the slopes of the relationship between BS and work rate (WR) [AS 0·054 (0·1), Controls 0·043 (0·06); P<0·05] and BS and % predicted oxygen uptake [AS 0·084 (0·18), Controls 0·045 (0·06); P<0·01] were steeper in the AS subjects. There was weak association between peak V̇O 2 and vital capacity ( r 2% 12·0), MIP (11·8) but no association between Tlim, CE, Wall tragus distance or TL movement. The strongest association with aerobic capacity was between measurements of peripheral muscle strength (Qds; r=0·75; hand grip; r=0·47) accounting for 53% ( P<0·001) and 23·5% ( P<0·01) of the total variance in peak V̇O 2, respectively. The addition of LBM to Qds in the regression model significantly improved the explained variance to 78·3% ( P<0·001). This study shows that peripheral muscle function is the most important determinant of exercise intolerance in AS patients suggesting that deconditioning is the main factor in the production of the reduced aerobic capacity.

Effect of Reduced Body Weight on Muscle Aerobic Capacity in Patients With COPD

Effect of Reduced Body Weight on Muscle Aerobic Capacity in Patients With COPD

Influence of Respiratory Function on Aerobic Capacity in Patients with Chronic Pulmonary Disease

Influence of Respiratory Function on Aerobic Capacity in Patients with Chronic Pulmonary Disease

Effect of Reduced Body Weight on Muscle Aerobic Capacity in Patients With COPD

Reduced muscle aerobic capacity in COPD patients has been demonstrated in several laboratories by phosphorus magnetic resonance spectroscopy and by analysis of oxygen uptake (VO2) kinetics. COPD patients are usually elderly, hypoxemic, poorly active with muscle atrophy, and often malnourished. Under these conditions there is usually reduction of O2 delivery to the tissues (bulk O2 flow), redistribution of fiber type within the muscle, capillary rarefaction, and decreased mitochondrial function, alterations all capable of reducing muscle aerobic capacity. In COPD, the effect of reduced body mass on muscle aerobic capacity has not been investigated (to our knowledge). We studied 24 patients with stable COPD with moderate-to-severe airway obstruction (68+/-5 [SD] years; FEV1, 39+/-12% predicted; PaO2, 66+/-8 mm Hg; PaCO2, 41+/-3 mm Hg) with poor to normal nutritional status, as indicated by a low-normal percent of ideal body weight (IBW). Each subject first underwent 1-min maximal incremental cycle ergometer exercise for determination of VO2 peak and lactate threshold (LT). Subsequently, they performed a 10-min moderate (80% of LT-VO2) constant load exercise for determination of oxygen deficit (O2DEF) and mean response time VO2 (MRT). VO2, CO2 output (VCO2), and minute ventilation were measured breath by breath. Patients displayed low VO2 peak (1,094+/-47 [SE] mL/min), LT-VO2 (35+/-3% predicted O2 max), and higher MRT-VO2 (67+/-4 s). Univariate regression analysis showed that percent of IBW correlated with indexes of maximal and submaximal aerobic capacity: vs VO2 peak, R=0.53 (p<0.01); vs MRT R=-0.77 (p<0.001). Using stepwise regression analysis, MRT correlated (R2=-0.70) with percent of IBW (p<0.01) and with PaO2 (p<0.05). Reduced body mass has an independent negative effect on muscle aerobic capacity in COPD patients: this effect may explain the variability in exercise tolerance among patients with comparable ventilatory limitation.

The Association Between Walking Distance and Predicted Aerobic Capacity in Patients with Chronic Low Back Pain

The Association Between Walking Distance and Predicted Aerobic Capacity in Patients with Chronic Low Back Pain

GREATER PERIPHERAL THAN CENTRAL ADAPTATION TO AEROBIC TRAINING IN MITOCHONDRIAL MYOPATHIES 186

In theory, limited aerobic capacity in patients with mitochondrial myopathies (MM) could be secondary to the primary disease process or effects of chronic deconditioning. The objectives of this study were to determine 1) whether patients with MM could respond to aerobic training and 2) their ability to adapt centrally versus peripherally relative to patients with other chronic non-metabolic myopathies (NM). 10 patients with MM, 6 patients with NM, and 5 sedentary healthy control subjects were evaluated before and after undergoing a similar aerobic training regimen for 8 weeks. Aerobic capacity(METs) was estimated from performance on a graded exercise test to 85% HRmax. Heart rate for an identical submaximal exercise workload was used as an index of central adaptation. Blood lactate at rest and after a constant submaximal workload, and muscle oxidative ATP resynthesis after ischemic exercise (as reflected by the ADP recovery half time [T1/2] estimated by phosphorus magnetic resonance spectroscopy) were used as indices of peripheral muscle oxidative capacity. The mean initial fitness level was similar in MM and NM, and significantly lower than that of healthy controls(p<.01). Training resulted in a significant improvement in aerobic capacity in all groups, but MM improved 20% more than NM and 27% more than controls. Decreases in HR were detected in both patient groups (p<.01) but only MM showed significant improvement (p<.01) in blood lactate concentrations(50%) and ADP T1/2 (over 2-fold) after training. Thus, both MM and NM benefit from aerobic training, but MM benefit even more than NM. The difference appears to be due to greater peripheral adaptation in MM and supports the hypothesis that partially reversible limitation at the muscle level dominates the training response in patients with mitochondrial myopathy.

Serial cardiorespiratory exercise testing in patients with congenital heart disease.

Aerobic capacity of patients with different forms of congenital heart disease was serially evaluated in 79 patients and the evolution was correlated with the lesion and the level of daily activity. The patients were divided into six groups: patients with a small ventricular septal defect (VSD) with mini shunt (n = 14), mild pulmonary valve stenosis with gradient < 40 mm Hg (PS) (n = 12), mild to moderate aortic valve stenosis (gradient 36 +/- 17 mmHg) (AS) (n = 12), patients 4.7 +/- 2.1 years after repair of tetralogy of Fallot (PO-TF) (n = 16), patients 2.2 +/- 2.9 years after closure of a high flow/high gradient VSD (PO-VSD) (n = 13), and patients 2.6 +/- 1.7 years after Fontan repair (Fontan-PO) (n = 12). Aerobic capacity was assessed by determination of the ventilatory anaerobic threshold (VAT). VAT reflects the highest aerobic exercise level prior to a disproportionate increase of CO2 and ventilation relative to O2 uptake; it is independent of patient motivation. Data are expressed as percentage of normal O2 uptake at VAT, determined in 234 age/gender matched controls. The habitual level of physical activity was assessed by a standardised questionnaire. Aerobic capacity in all subgroups of patients, even with very mild defects, was at or below the lower limit of normal. Children left unrestricted from physical exercise (VSD, PS, PO-VSD) had no change over the study period. However, aerobic capacity of patients with medically imposed physical restrictions (AS) and significant residual haemodynamic lesions (PO-TF, Fontan) decreased with age.(ABSTRACT TRUNCATED AT 250 WORDS)

788-4 Does Low Level Training Increase Peak Aerobic Capacity in Patients with Congestive Heart Failure?

Conventional high level exercise training at a workload consistent with 75% of peak oxygen consumption (pVO 2 , ml/min/kg) in patients with congestive heart failure (CHF) improves peak aerobic capacity and limb vasodilatory capacity. However, training at this workload may promote left ventricular dilatation in patients with CHF by prolonged exposure to substantially elevated filling pressure (PCWP). Whether training at low level, I.e., at a workload consistent with &lt;50% pVO 2 , would result in limited increases in PCWP while still improving peak aerobic capacity and peripheral vasodilatory function is unknown. Accordingly, 15 patients with stable advanced CHF underwent measurement of 1) the PCWP response to low vs high level exercise, and 2) the change in peak aerobic capacity and limb vasodilatory capacity resulting from participation in a low level training program. PCWP was measured by right heart catheterization at rest, and during low and high level exercise. Patients then performed 12 weeks of low level training, utilizing a semi-recumbent bicycle. Pre- and post-training evaluations included pVO 2 , calf and forearm peak hyperemic blood flow (PHBF, ml/min/100 ml), and resting heart rate (HR, b/min). 1)PCWP rose to 20 mmHg during low level exercise (Δ54% vs rest), and 34 mmHg during high level exercise (Δ162% vs rest). 2)Pre- and post-training data are as follows: pVO 2 calf PHBF forearm PHBF HR pre-train 99 18 23 99 post-train 14.1 36 20 80 p value 0.02 &lt;0.01 NS 0.02 1) The rise in PCWP is significantly less during low level exercise than during high level exercise. 2) Training at a workload consistent with ≤50% of pVO 2 significantly improves peak aerobic capacity. 3) PHBF in the trained calf increases 100% from baseline, while it does not change in the untrained forearm. Enhanced vasodilatory responses in exercising muscle may be an important contributor to improved peak aerobic capacity. Thus, low level training produces benefits similar to high level training with only a moderate rise in PCWP, and may therefore provide less of a stimulus for ventricular dilatation.

Effect of the renin-angiotensin system on limb circulation and metabolism during exercise in patients with heart failure

The maximal aerobic exercise capacity of patients with chronic heart failure is frequently decreased because of inadequate blood flow to working skeletal muscle. To investigate whether this reduced flow is in part due to interference by angiotensin II with arteriolar dilation in working muscle, the effect of the angiotensin-converting enzyme inhibitor captopril on leg blood flow, leg vascular resistance, leg oxygen consumption (VO2) and leg lactate release during maximal upright bicycle exercise was examined in 12 patients with heart failure (maximal VO2 10.7 +/- 3.1 ml/min per kg). Captopril decreased leg resistance at rest (258 +/- 115 to 173 +/- 67 U, p less than 0.01) and maximal exercise (68 +/- 69 to 45 +/- 29 U, p less than 0.01) associated with proportionately similar decreases in systemic vascular resistance. However, maximal exercise duration and maximal VO2 were unchanged and, at identical peak exercise work times, there was no improvement in leg blood flow (2.0 +/- 0.9 to 2.0 +/- 1.1 liters/min, p = NS), leg VO2 (261 +/- 104 to 281 +/- 157 ml/min, p = NS) or leg lactate release (269 +/- 149 to 227 +/- 151 mg/min, p = NS). These data suggest that, during exercise in patients with heart failure, angiotensin II does not interfere with blood flow to working skeletal muscle.

Effect of hydralazine on perfusion and metabolism in the leg during upright bicycle exercise in patients with heart failure.

The aerobic exercise capacity of patients with chronic heart failure is frequently impaired because of inadequate O2 transport to working skeletal muscle. To determine whether hydralazine improves O2 transport to working muscle, we examined the effect of intravenous hydralazine on blood flow (measured by thermodilution) and metabolism in the leg during maximal upright bicycle exercise in 10 patients with chronic heart failure. Hydralazine increased maximal exercise cardiac output (5.6 +/- 0.7 to 6.7 +/- 0.6 l/min; p less than .01) and decreased systemic O2 extraction (79 +/- 3% to 65 +/- 2%; p less than .01) but did not alter maximal O2 uptake (787 +/- 105 vs 779 +/- 82 ml/min). Leg blood flow at maximal exercise increased from 1.6 +/- 0.2 to 2.1 +/- 0.4 l/min (p less than .03); the proportion of cardiac output delivered to the leg remained unchanged (59 +/- 3% vs 57 +/- 9%). This increase in flow was associated with a decrease in O2 extraction in the leg (84 +/- 2% to 79 +/- 2%; p less than .01) and no change in peak femoral venous lactate (59.1 +/- 7.4 vs 54.1 +/- 5.3 mg/dl), suggesting that there is functional or anatomic shunting of the augmented limb flow rather than delivery to metabolizing muscle. These data suggest that hydralazine augments flow to the exercising limb in patients with heart failure but that this augmented flow does not increase oxygen availability within working muscle.

Interaction of physiological mechanisms during exercise.

obtained from such studies is often difficult to interpret because the precise work intensity is not known and/or the duration of the exercise is too short for cardiorespiratory function to stabilize and a “Steady state” of exercise to be achieved. WASSERMAN, KARLMAN, ANTONIUS L. VAN KESSEL, AND GEORGE G. BURTON. Interaction of physiological mechanisms during exercise. J. Appl. Physiol. 22(1): 71-85. rg67.-The effects of work intensity and duration on the metabolic circulatory and ventilatory response to exercise are quantitated in healthy male subjects during cycle ergometer exercise. There is a wellordered relationship between work rate and oxidatve energy sources. Steady-state time for 02 consumption (Vo,) is dependent on work intensity (the time arterial blood lactate concentration stops increasing). At moderate work, anaerobic metabolism is a very small part of credit oxidation, while at very heavy work, the pyruvate-lactate mechanism is the major creditor. The increase in gas exchange ratio (R) reflecting the production of CO2 from bicarbonate (buffering of lactic aid) is transient. After the steady state is reached, R decreases. The heart rate increase during constant-load exercise parallels the increase in vo,. Physiological dead space/tidal volume ratio decreases from .33 to .17 during exercise. The reduction is independent of work duration and only slightly reduced as work intensity increases. Arterial 02 tension does not decrease during exercise at sea level even at maximal rates of 02 transport. Arterial-end tidal CO2 tension differences suggest a fluctuation in pulmonary capillary CO2 tension of approximately 8 mm Hg during the respiratory cycle of the exercising subject. Changes in minute ventilation are best predicted from the rate of CO2 production and the extent of respiratory compensation for metabolic acidosis.