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

Highlights

• Interval exercise training improves cardiac output at peak levels of exercise in COPD.

• Interval exercise training reduces the magnitude of dynamic hyperinflation in COPD.

• Mitigation of dynamic hyperinflation improves central hemodynamic responses to a given power output in hyperinflated COPD.

• Rehabilitative exercise training induces a more efficient hemodynamic response to a given power output in patients with COPD.

• Non-invasive measurement of cardiac output in patients with COPD may improve the evaluation of the efficacy of pharmacological and non-pharmacological interventions.

Abstract

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.

Introduction

In patients with Chronic Obstructive Pulmonary Disease (COPD) exercise intolerance is often the result of malfunction and lack of co-ordination between the various physiological systems, namely the ventilatory, the cardiovascular, and the locomotor muscle metabolism. Such malfunction may primarily occur consequently to: (i) the inability of the ventilatory capacity to suffice the ventilatory requirement (O’Donnell and Webb, 2008); (ii) the reduced capacity for O₂ utilization at the level of the peripheral muscles (ATS, 1995, Debigaré and Maltais, 2008) and (iii) the adverse hemodynamic consequences of exercise-induced lung dynamic hyperinflation (DH) commonly in conjunction with profound expiratory abdominal muscle recruitment (Aliverti and Macklem, 2001, Vogiatzis and Zakynthinos, 2012).

In the absence of overt primary cardiovascular disease (such as valvular or ischemic heart disease) the normal increase in cardiac output during exercise in COPD is impeded by two major physiological mechanisms, namely: (i) heart compression due to exercise-induced lung DH (Jörgensen et al., 2003, Jörgensen et al., 2007) and (ii) intra-thoracic hypovolemia secondary to decreased venous return resulting from persistent expiratory abdominal muscle recruitment (Aliverti and Macklem, 2008). Previous studies have shown that approximately 70–80% of patients with moderate to severe COPD experience a decrease from rest in inspiratory capacity (IC) during exercise and are thus characterised as hyperinflators (O’Donnell et al., 2006, O’Donnell et al., 2001, Vogiatzis et al., 2011b). In contrast, there is a subgroup of COPD patients with absence of DH (non-hyperinflators) during exercise (Aliverti et al., 2004).

Previous studies (Berton et al., 2010, Chiappa et al., 2009, Laveneziana et al., 2009, Laveneziana et al., 2011, Vogiatzis et al., 2011a) have shown that in COPD patients exhibiting profound lung DH during exercise, the administration of Heliox or bronchodilators reduces the work of breathing and results in the acceleration of the cardiovascular response to exercise, thereby enhancing systemic and leg muscle O₂ availability along with exercise tolerance.

In this context, implementation of pulmonary rehabilitation has also shown to substantially decrease the magnitude of exercise-induced DH and the degree of expiratory abdominal muscle recruitment at a given level of submaximal exercise, thereby improving indirect measures of cardio-circulatory function, exercise tolerance and peak oxygen uptake (Georgiadou et al., 2007, Porszasz et al., 2005, Ramponi et al., 2012). The effect of lessening the degree of exercise-induced DH on central hemodynamic responses during exercise following pulmonary rehabilitation remains however, currently unknown.

Accordingly, the purpose of the present study was to investigate whether exercise training-induced reductions in the amount of exercise-induced DH are associated with improved hemodynamic responses during exercise. Based on the findings of earlier studies (Berton et al., 2010, Laveneziana et al., 2009) demonstarting positive effects of pharmachological alleviation of DH on cardiovascular response to submaximal exercise, it was reasoned that rehabilitative-induced reductions in the magnitude of DH during exercise would be associated with improvement in central hemodynamic responses to a given external work load only in those patients exhibiting significant dynamic hyperinflation during exercise.