We conclude that 12 weeks of aerobic exercise training improves cardiac autonomic modulation and functional capacity 4 months after GBS.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O2 uptake (V̇o2p) kinetics during exercise, which may stem from inadequate muscle O2 delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O2 delivery to uptake during exercise. We tested the hypothesis that, along with slowed V̇o2p kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Q̇t) following the onset of heavy-intensity exercise. We measured V̇o2p, Q̇t (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly ( P < 0.05) lower in patients and related to the kinetics of V̇o2p ( r = −0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of V̇o2p (42 ± 13 vs. 73 ± 24 s) and Q̇t (67 ± 11 vs. 96 ± 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 ± 2.4 vs. 16.5 ± 3.4 s). Consequently, the time constant ratio of O2 uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O2 delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O2 delivery and utilization and may contribute to the slower V̇o2p kinetics compared with age-matched controls.

The proposed approach evaluates complexity of the cardiovascular control and causality among cardiovascular regulatory mechanisms from spontaneous variability of heart period (HP), systolic arterial pressure (SAP) and respiration (RESP). It relies on construction of a multivariate embedding space, optimization of the embedding dimension and a procedure allowing the selection of the components most suitable to form the multivariate embedding space. Moreover, it allows the comparison between linear model-based (MB) and nonlinear model-free (MF) techniques and between MF approaches exploiting local predictability (LP) and conditional entropy (CE). The framework was applied to study age-related modifications of complexity and causality in healthy humans in supine resting (REST) and during standing (STAND). We found that: 1) MF approaches are more efficient than the MB method when nonlinear components are present, while the reverse situation holds in presence of high dimensional embedding spaces; 2) the CE method is the least powerful in detecting age-related trends; 3) the association of HP complexity on age suggests an impairment of cardiac regulation and response to STAND; 4) the relation of SAP complexity on age indicates a gradual increase of sympathetic activity and a reduced responsiveness of vasomotor control to STAND; 5) the association from SAP to HP on age during STAND reveals a progressive inefficiency of baroreflex; 6) the reduced connection from HP to SAP with age might be linked to the progressive exploitation of Frank-Starling mechanism at REST and to the progressive increase of peripheral resistances during STAND; 7) at REST the diminished association from RESP to HP with age suggests a vagal withdrawal and a gradual uncoupling between respiratory activity and heart; 8) the weakened connection from RESP to SAP with age might be related to the progressive increase of left ventricular thickness and vascular stiffness and to the gradual decrease of respiratory sinus arrhythmia.

Background: Respiratory muscle unloading during exercise could improve locomotor muscle oxygenation by increasing oxygen delivery (higher cardiac output and/or arterial oxygen content) in patients with chronic obstructive pulmonary disease (COPD). Methods: Sixteen non-hypoxaemic men (forced expiratory volume in 1 s 42.2 (13.9)% predicted) undertook, on different days, two constant work rate (70-80% peak) exercise tests receiving proportional assisted ventilation (PAV) or sham ventilation. Relative changes (D%) in deoxyhaemoglobin (HHb), oxyhaemoglobin (O 2 Hb), tissue oxygenation index (TOI) and total haemoglobin (Hb tot ) in the vastus lateralis muscle were measured by nearinfrared spectroscopy. In order to estimate oxygen delivery (DO 2 est, l/min), cardiac output and oxygen saturation (SpO 2 ) were continuously monitored by impedance cardiography and pulse oximetry, respectively. Results: Exercise tolerance (Tlim) and oxygen uptake were increased with PAV compared with sham ventilation. In contrast, end-exercise blood lactate/Tlim and leg effort/Tlim ratios were lower with PAV (p,0.05). There were no between-treatment differences in cardiac output and SpO 2 either at submaximal exercise or at Tlim (ie, DO 2 est remained unchanged with PAV; p.0.05). Leg muscle oxygenation, however, was significantly enhanced with PAV as the exercise-related decrease in D(O 2 Hb)% was lessened and TOI was improved; moreover, D(Hb tot )%, an index of local blood volume, was increased compared with sham ventilation (p,0.01). Conclusions: Respiratory muscle unloading during highintensity exercise can improve peripheral muscle oxygenation despite unaltered systemic DO 2 in patients with advanced COPD. These findings might indicate that a fraction of the available cardiac output had been redirected from ventilatory to appendicular muscles as a consequence of respiratory muscle unloading.

Neural control of heart rate, in addition to other clinically valuable measures, is positively altered in moderate-severe COPD patients following 6 weeks of aerobic exercise training. The improvement in submaximal performance after exercise training was associated with parasympathetic activity.

No abstract

Blood flow requirements of the respiratory muscles (RM) increase markedly during exercise in chronic heart failure (CHF). We reasoned that if the RM could subtract a fraction of the limited cardiac output (QT) from the peripheral muscles, RM unloading would improve locomotor muscle perfusion. Nine patients with CHF (left ventricle ejection fraction = 26 +/- 7%) undertook constant-work rate tests (70-80% peak) receiving proportional assisted ventilation (PAV) or sham ventilation. Relative changes (Delta%) in deoxy-hemoglobyn, oxi-Hb ([O2Hb]), tissue oxygenation index, and total Hb ([HbTOT], an index of local blood volume) in the vastus lateralis were measured by near infrared spectroscopy. In addition, QT was monitored by impedance cardiography and arterial O2 saturation by pulse oximetry (SpO2). There were significant improvements in exercise tolerance (Tlim) with PAV. Blood lactate, leg effort/Tlim and dyspnea/Tlim were lower with PAV compared with sham ventilation (P < 0.05). There were no significant effects of RM unloading on systemic O2 delivery as QT and SpO2 at submaximal exercise and at Tlim did not differ between PAV and sham ventilation (P > 0.05). Unloaded breathing, however, was related to enhanced leg muscle oxygenation and local blood volume compared with sham, i.e., higher Delta[O2Hb]% and Delta[HbTOT]%, respectively (P < 0.05). We conclude that RM unloading had beneficial effects on the oxygenation status and blood volume of the exercising muscles at similar systemic O2 delivery in patients with advanced CHF. These data suggest that blood flow was redistributed from respiratory to locomotor muscles during unloaded breathing.

The objective of this study was to (a) evaluate the impact of the leg press, at variable percentages of 1 repetition maximum (1RM), on heart rate variability (HRV) and blood lactate and (b) determine the relationship between HRV with blood lactate in a healthy elderly cohort. Ten healthy men (64 +/- 4 years) participated in a progressive leg-press protocol to maximal exertion. Initially, 1RM for the leg press was determined for all subjects. The protocol then began at 10% of 1RM, with subsequent increases of 10% until 30% of 1RM, followed by incremental adjustments of 5% until exhaustion. The measurement of instantaneous R-R interval variability from Poincare plots (SD1 and SD2) and time domain indexes (RMSSD and RMSM), blood pressure, and blood lactate were obtained at rest and all leg-press loads. Significant alterations of HRV and blood lactate were observed from 30% of 1RM leg press (p < 0.05). Additionally, significant correlations were found between the lactate threshold (LT) and the RMSSD threshold (r = 0.78; p < 0.01), and between the LT and SD1 threshold (r = 0.81, p < 0.01). We conclude that metabolic and cardiovascular alterations are apparent during relatively low resistance exercise (RE) loads in apparently healthy subjects. In addition, HRV indexes were associated with blood-lactate levels during RE. The practical applications is the possibility of using HRV as a noninvasive measure obtained at a relatively low cost may be used to identify neural and metabolic alterations during RE in older subjects.