Impaired muscle blood flow at the onset of heavy-intensity exercise may transiently reduce microvascular O(2) pressure and decrease the rate of O(2) transfer from capillary to mitochondria in chronic heart failure (CHF). However, advances in the pharmacological treatment of CHF (e.g., angiotensin-converting enzyme inhibitors and third-generation beta-blockers) may have improved microvascular O(2) delivery to an extent that intramyocyte metabolic inertia might become the main locus of limitation of O(2) uptake (Vo(2)) kinetics. We assessed the rate of change of pulmonary Vo(2) (Vo(2)(p)), (estimated) fractional O(2) extraction in the vastus lateralis (approximately Delta[deoxy-Hb+Mb] by near-infrared spectroscopy), and cardiac output (Qt) during high-intensity exercise performed to the limit of tolerance (Tlim) in 10 optimally treated sedentary patients (ejection fraction = 29 + or - 8%) and 11 controls. Sluggish Vo(2)(p) and Qt kinetics in patients were significantly related to lower Tlim values (P < 0.05). The dynamics of Delta[deoxy-Hb+Mb], however, were faster in patients than controls [mean response time (MRT) = 15.9 + or - 2.0 s vs. 19.0 + or - 2.9 s; P < 0.05] with a subsequent response "overshoot" being found only in patients (7/10). Moreover, tauVo(2)/MRT-[deoxy-Hb+Mb] ratio was greater in patients (4.69 + or - 1.42 s vs. 2.25 + or - 0.77 s; P < 0.05) and related to Qt kinetics and Tlim (R = 0.89 and -0.78, respectively; P < 0.01). We conclude that despite the advances in the pharmacological treatment of CHF, disturbances in "central" and "peripheral" circulatory adjustments still play a prominent role in limiting Vo(2)(p) kinetics and tolerance to heavy-intensity exercise in nontrained patients.
Exercise ventilation (') relative to carbon dioxide output (' ) is particularly relevant to patients limited by the respiratory system, those with chronic obstructive pulmonary disease (COPD). High'-' (poor ventilatory efficiency) has been found to be a key physiological abnormality in symptomatic patients with largely preserved forced expiratory volume in 1 s (FEV). Establishing an association between high '-' and exertional dyspnoea in mild COPD provides evidence that exercise intolerance is not a mere consequence of detraining. As the disease evolves, poor ventilatory efficiency might help explaining "out-of-proportion" breathlessness (to FEV impairment). Regardless, disease severity, cardiocirculatory co-morbidities such as heart failure and pulmonary hypertension have been found to increase '-' In fact, a high '-' has been found to be a powerful predictor of poor outcome in lung resection surgery. Moreover, a high '-' has added value to resting lung hyperinflation in predicting all-cause and respiratory mortality across the spectrum of COPD severity. Documenting improved ventilatory efficiency after lung transplantation and lung volume reduction surgery provides objective evidence of treatment efficacy. Considering the usefulness of exercise ventilatory efficiency in different clinical scenarios, the '-' relationship should be valued in the interpretation of cardiopulmonary exercise tests in patients with mild-to-end-stage COPD.
Sperandio PA, Oliveira MF, Rodrigues MK, Berton DC, Treptow E, Nery LE, Almeida DR, Neder JA. Sildenafil improves microvascular O 2 delivery-to-utilization matching and accelerates exercise O 2 uptake kinetics in chronic heart failure. Am J Physiol Heart Circ Physiol 303: H1474 -H1480, 2012. First published September 28, 2012; doi:10.1152/ajpheart.00435.2012 can temporally and spatially match microvascular oxygen (O 2) delivery (Q O2mv) to O2 uptake (V O2) in the skeletal muscle, a crucial adjustment-to-exercise tolerance that is impaired in chronic heart failure (CHF). To investigate the effects of NO bioavailability induced by sildenafil intake on muscle Q O2mv-to-O2 utilization matching and V O2 kinetics, 10 males with CHF (ejection fraction ϭ 27 Ϯ 6%) undertook constant work-rate exercise (70 -80% peak). Breath-bybreath V O2, fractional O2 extraction in the vastus lateralis {ϳdeoxy-genated hemoglobin ϩ myoglobin ([deoxy-Hb ϩ Mb]) by nearinfrared spectroscopy}, and cardiac output (CO) were evaluated after sildenafil (50 mg) or placebo. Sildenafil increased exercise tolerance compared with placebo by ϳ20%, an effect that was related to faster onand off-exercise V O2 kinetics (P Ͻ 0.05). Active treatment, however, failed to accelerate CO dynamics (P Ͼ 0.05). On-exercise [deoxy-Hb ϩ Mb] kinetics were slowed by sildenafil (ϳ25%), and a subsequent response "overshoot" (n ϭ 8) was significantly lessened or even abolished. In contrast, [deoxy-Hb ϩ Mb] recovery was faster with sildenafil (ϳ15%). Improvements in muscle oxygenation with sildenafil were related to faster on-exercise V O2 kinetics, blunted oscillations in ventilation (n ϭ 9), and greater exercise capacity (P Ͻ 0.05). Sildenafil intake enhanced intramuscular Q O2mv-to-V O2 matching with beneficial effects on V O2 kinetics and exercise tolerance in CHF. The lack of effect on CO suggests that improvement in blood flow to and within skeletal muscles underlies these effects.sildenafil; blood flow; heart failure; hemodynamics; near-infrared spectroscopy; oxygen consumption; kinetics THE INABILITY TO MAINTAIN an adequate driving pressure for blood-myocite oxygen (O 2 ) diffusion [i.e., microvascular partial pressure of O 2 (PO 2mv )] is paramount to explain the slowness of exercise O 2 uptake (V O 2 ) kinetics in patients with chronic heart failure [CHF; as recently reviewed by Poole and colleagues (34)]. To keep a sufficiently high PO 2mv , however, O 2 delivery should be spatially and temporally matched to V O 2 of individual fibers. In this context, seminal studies found that intramuscular PO 2mv in rodents with CHF was critically low either at rest-to-contractions transition (7,14) or during early recovery (12), i.e., when V O 2 should be increasing or decreasing most rapidly, respectively. Importantly, it was demonstrated that reduced nitric oxide (NO) bioavailability exerted a key mechanistic role on on-and off-exercise O 2 delivery-toutilization uncoupling in these animal preparations (24,25).In intact humans with CHF, previous studies have concomitant...
BackgroundExercise training (ET) improves functional capacity in chronic heart failure (HF). However, ET effects in acute HF are unknown.ObjectiveTo investigate the effects of ET alone or combined with noninvasive ventilation (NIV) compared with standard medical treatment during hospitalization in acute HF patients.MethodsTwenty-nine patients (systolic HF) were randomized into three groups: control (Control - only standard medical treatment); ET with placebo NIV (ET+Sham) and ET+NIV (NIV with 14 and 8 cmH2O of inspiratory and expiratory pressure, respectively). The 6MWT was performed on day 1 and day 10 of hospitalization and the ET was performed on an unloaded cycle ergometer until patients' tolerance limit (20 min or less) for eight consecutive days. For all analyses, statistical significance was set at 5% (p < 0.05).ResultsNone of the patients in either exercise groups had adverse events or required exercise interruption. The 6MWT distance was greater in ET+NIV (Δ120 ± 72 m) than in ET+Sham (Δ73 ± 26 m) and Control (Δ45 ± 32 m; p < 0.05). Total exercise time was greater (128 ± 10 vs. 92 ± 8 min; p < 0.05) and dyspnea was lower (3 ± 1 vs. 4 ± 1; p < 0.05) in ET+NIV than ET+Sham. The ET+NIV group had a shorter hospital stay (17 ± 10 days) than ET+Sham (23 ± 8 days) and Control (39 ± 15 days) groups (p < 0.05). Total exercise time in ET+Sham and ET+NIV had significant correlation with length of hospital stay (r = -0.75; p = 0.01).ConclusionExercise training in acute HF was safe, had no adverse events and, when combined with NIV, improved 6MWT and reduce dyspnea and length of stay.
Systolic heart failure is a common and disabling co-morbidity of chronic obstructive pulmonary disease (COPD) which may increase exercise ventilation due to heightened neural drive and/or impaired pulmonary gas exchange efficiency. The influence of heart failure on exercise ventilation, however, remains poorly characterized in COPD. In a prospective study, 98 patients with moderate to very severe COPD [41 with coexisting heart failure; 'overlap' (left ventricular ejection fraction < 50%)] underwent an incremental cardiopulmonary exercise test (CPET). Compared to COPD, overlap had lower peak exercise capacity despite higher FEV. Overlap showed lower operating lung volumes, greater ventilatory inefficiency and larger decrements in end-tidal CO (PETCO) (P < 0.05). These results were consistent with those found in FEV-matched patients. Larger areas under receiver operating characteristic curves to discriminate overlap from COPD were found for ventilation ([Formula: see text]E)-CO output [Formula: see text]CO) intercept, [Formula: see text]E-[Formula: see text]CO slope, peak [Formula: see text]E/[Formula: see text]CO ratio and peak PETCO. Multiple logistic regression analysis revealed that [Formula: see text]CO intercept ≤ 3.5 L/minute [odds ratios (95% CI) = 7.69 (2.61-22.65), P < 0.001] plus [Formula: see text]E-[Formula: see text]CO slope ≥ 34 [2.18 (0.73-6.50), P = 0.14] or peak [Formula: see text]E/[Formula: see text]CO ratio ≥ 37 [5.35 (1.96-14.59), P = 0.001] plus peak PETCO ≤ 31 mmHg [5.73 (1.42-23.15), P = 0.01] were indicative of overlapping. Heart failure increases the ventilatory response to metabolic demand in COPD. Variables reflecting excessive ventilation might prove useful to assist clinical interpretation of CPET responses in COPD patients presenting heart failure as co-morbidity.
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