Hemodynamic effects of high intensity interval training in COPD patients exhibiting exercise-induced dynamic hyperinflation.

Dynamic hyperinflation (DH) has a significant adverse effect on cardiovascular function during exercise in COPD patients. COPD patients with (n = 25) and without (n = 11) exercise-induced DH undertook an incremental (IET) and a constant-load exercise test (CLET) sustained at 75% peak work (WRpeak) prior to and following an interval cycling exercise training regime (set at 100% WRpeak with 30-s work/30-s rest intervals) lasting for 12 weeks. Cardiac output (Q) was assessed by cardio-bio-impedance (PhysioFlow, enduro, PF-O7) to determine Q mean response time (QMRT) at onset (QMRT(ON)) and offset (QMRT(OFF)) of CLET. Post-rehabilitation only those patients exhibiting exercise-induced DH demonstrated significant reductions in QMRT(ON) (from 82.2 ± 4.3 to 61.7 ± 4.2 s) and QMRT(OFF) (from 80.5 ± 3.8 to 57.2 ± 4.9 s ). These post-rehabilitation adaptations were associated with improvements in inspiratory capacity, thereby suggesting that mitigation of the degree of exercise-induced DH improves central hemodynamic responses in COPD patients.

Activity monitoring reflects cardiovascular and metabolic variations in COPD patients across GOLD stages II to IV.

We investigated whether activity monitoring reliably reflects variations in oxygen transport and utilization during walking in COPD patients. Forty-two patients (14 in each GOLD stage II, III and IV) performed an incremental treadmill protocol to the limit of tolerance. Breath-by-breath gas exchange, central hemodynamic variables and activity monitoring were simultaneously recorded. Physiological variables and accelerometer outputs rose linearly with walking speeds. Strong correlations (r[interquartile range, IQR]) were found between treadmill walking intensity (WI: range 0.8-2.0 ms(-2)) and oxygen consumption (0.95 [IQR 0.87-0.97]), (range 7.6-15.5 ml kg(-1)min(-1)); minute ventilation (0.95 [IQR 0.86-0.98]), (range 20-37 l min(-1)); cardiac output (0.89 [IQR 0.73-0.94]), (range 6.8-11.5 l min(-1)) and arteriovenous oxygen concentration difference (0.84 [IQR 0.76-0.90]), (range 7.7-12.1 ml O2100 ml(-1)). Correlations between WI and gas exchange or central hemodynamic parameters were not different across GOLD stages. In conclusion, central hemodynamic, respiratory and muscle metabolic variations during incremental treadmill exercise are tightly associated to changes in walking intensity as recorded by accelerometry across GOLD stages II to IV. Interestingly, the magnitude of these associations is not different across GOLD stages.

On- and off-exercise kinetics of cardiac output in response to cycling and walking in COPD patients with GOLD Stages I-IV.

Exercise-induced dynamic hyperinflation and large intrathoracic pressure swings may compromise the normal increase in cardiac output (Q) in Chronic Obstructive Pulmonary Disease (COPD). Therefore, it is anticipated that the greater the disease severity, the greater would be the impairment in cardiac output during exercise. Eighty COPD patients (20 at each GOLD Stage) and 10 healthy age-matched individuals undertook a constant-load test on a cycle-ergometer (75% WR(peak)) and a 6min walking test (6MWT). Cardiac output was measured by bioimpedance (PhysioFlow, Enduro) to determine the mean response time at the onset of exercise (MRTon) and during recovery (MRToff). Whilst cardiac output mean response time was not different between the two exercise protocols, MRT responses during cycling were slower in GOLD Stages III and IV compared to Stages I and II (MRTon: Stage I: 45±2, Stage II: 65±3, Stage III: 90±3, Stage IV: 106±3s; MRToff: Stage I: 42±2, Stage II: 68±3, Stage III: 87±3, Stage IV: 104±3s, respectively). In conclusion, the more advanced the disease severity the more impaired is the hemodynamic response to constant-load exercise and the 6MWT, possibly reflecting greater cardiovascular impairment and/or greater physical deconditioning.