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COPD patients exhibit lower peak oxygen consumption (V̇O 2  PEAK ), altered muscle metabolism and impaired exercise tolerance compared with age-matched controls. Whether these traits reflect muscle level deconditioning (impacted by ventilatory constraints) and/or dysfunction in mitochondrial ATP production capacity is debated. By studying aerobic exercise training (AET) at a matched relative intensity and subsequent exercise withdrawal period (EW) we aimed to elucidate the whole-body and muscle mitochondrial responsiveness of healthy-young (HY), healthy-older (HO) and COPD volunteers to whole-body exercise.  The HY (n=10), HO (n=10) and COPD (n=20) volunteers were studied before, after eight-weeks AET (65% V̇O 2  PEAK ) and after four-weeks EW. V̇O 2  PEAK , muscle maximal mitochondrial ATP production rates (MAPR), mitochondrial content, mitochondrial DNA copy number and abundance of 59 targeted fuel metabolism mRNAs were determined at all time-points.  Muscle MAPR (normalised for mitochondrial content) was not different for any substrate combination in HO, HY and COPD at baseline, but mitochondrial DNA copy number relative to a nuclear-encoded house-keeping gene was greater in HY (mean± sd ) (804±67) than in HO (631±69), p=0.041. AET increased V̇O 2  PEAK  in HO (17%, p=0.002) and HY (21%, p&lt;0.001) but not COPD (p=0.603). Muscle MAPR for palmitate increased with training in HO (57%, p=0.041) and HY (56%, p=0.003) and decreased with EW in HO (−45%, p=0.036) and HY (−30%, p=0.016), but was unchanged in COPD (p=0.594). Mitochondrial DNA copy number increased with AET in HY (66%, p=0.001) but not HO (p=0.081) or COPD (p=0.132). The observed changes in muscle mRNA abundance were similar in all groups after AET and EW.  Intrinsic mitochondrial function was not impaired by ageing or COPD in the untrained state. Whole-body and muscle mitochondrial responses to AET were robust in HY, evident in HO, but deficient in COPD. All showed robust muscle mRNA responses. Higher relative exercise intensities during whole-body training may be needed to maximise whole-body and muscle mitochondrial adaptation in COPD.

Whole-body and muscle responses to aerobic exercise training and withdrawal in ageing and COPD