Abstract
BackgroundLittle is known about the mechanistic basis for the exercise intolerance characteristic of patients with respiratory disease; a lack of clearly defined, distinct patient groups limits interpretation of many studies. The purpose of this pilot study was to investigate the pulmonary oxygen uptake ( overset{.}{V} O2) response, and its potential determinants, in patients with emphysema and idiopathic pulmonary fibrosis (IPF).MethodsFollowing a ramp incremental test for the determination of peak overset{.}{V} O2 and the gas exchange threshold, six emphysema (66 ± 7 years; FEV1, 36 ± 16%), five IPF (65 ± 12 years; FEV1, 82 ± 11%) and ten healthy control participants (63 ± 6 years) completed three repeat, heavy-intensity exercise transitions on a cycle ergometer. Throughout each transition, pulmonary gas exchange, heart rate and muscle deoxygenation ([HHb], patients only) were assessed continuously and subsequently modelled using a mono-exponential with ( overset{.}{V} O2, [HHb]) or without (HR) a time delay.ResultsThe overset{.}{V} O2 phase II time-constant (τ) did not differ between IPF and emphysema, with both groups significantly slower than healthy controls (Emphysema, 65 ± 11; IPF, 69 ± 7; Control, 31 ± 7 s; P < 0.05). The HR τ was slower in emphysema relative to IPF, with both groups significantly slower than controls (Emphysema, 87 ± 19; IPF, 119 ± 20; Control, 58 ± 11 s; P < 0.05). In contrast, neither the [HHb] τ nor [HHb]:O2 ratio differed between patient groups.ConclusionsThe slower overset{.}{V} O2 kinetics in emphysema and IPF may reflect poorer matching of O2 delivery-to-utilisation. Our findings extend our understanding of the exercise dysfunction in patients with respiratory disease and may help to inform the development of appropriately targeted rehabilitation strategies.
Highlights
Little is known about the mechanistic basis for the exercise intolerance characteristic of patients with respiratory disease; a lack of clearly defined, distinct patient groups limits interpretation of many studies
Skeletal muscle dysfunction characterized by a decreased capillary network [11], McNarry et al BMC Pulmonary Medicine (2017) 17:26 reduced myoglobin level [12], abnormal oxidative capacity [13, 14] and altered muscle fibre type distribution have been suggested to be associated with the slower V_ : O2 kinetics [2, 15] and positive responses to training reported in some previous studies [5, 8]
Others have suggested that the cardiovascular derangements often present in those with chronic obstructive pulmonary disease (COPD) may engender an oxygen delivery limitation leading to the slower dynamic V_ : O2 response observed [3, 16], a contention supported by the limited evidence available regarding the V_ : O2 response during heavy intensity exercise [4]
Summary
Little is known about the mechanistic basis for the exercise intolerance characteristic of patients with respiratory disease; a lack of clearly defined, distinct patient groups limits interpretation of many studies. Others have suggested that the cardiovascular derangements often present in those with COPD may engender an oxygen delivery limitation leading to the slower dynamic V_ : O2 response observed [3, 16], a contention supported by the limited evidence available regarding the V_ : O2 response during heavy intensity exercise [4] Further interpretation of these findings is limited, by methodological limitations such as the reliance on a single exercise bout for the derivation of V_ : O2 kinetics, which may not reflect the true response [17], and significant potential variability in patient populations. Some or all of these entities may be present within an individual in varying proportion
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