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Updated: Dec 26, 2025

Assessment of Pulmonary Capillary Blood Volume, Membrane Diffusing Capacity, and Intrapulmonary Arteriovenous Anastomoses During Exercise
Published on: February 20, 2017
Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10 weeks of endurance training
Øyvind Skattebo1, Anders Wold Bjerring2,3, Marius Auensen4
1Department of Physical Performance, Norwegian School of Sport Sciences, Post box 4014 Ullevål Stadion, 0806, Oslo, Norway. oyvind.skattebo@nih.no.
Purpose:
The endurance training (ET)-induced increases in peak oxygen uptake ([Formula: see text]O2peak) and cardiac output ([Formula: see text]peak) during upright cycling are reversed to pre-ET levels after removing the training-induced increase in blood volume (BV). We hypothesised that ET-induced improvements in [Formula: see text]O2peak and [Formula: see text]peak are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O2 difference (a-[Formula: see text]O2diff; [Formula: see text]O2/[Formula: see text]), cardiac dimensions and muscle morphology were studied to assess their role for the [Formula: see text]O2peak improvement.
Methods:
Twelve untrained subjects ([Formula: see text]O2peak: 44 ± 6 ml kg-1 min-1) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hbmass) and BV were assessed pre- and post-ET. [Formula: see text]O2peak and [Formula: see text]peak during upright and supine cycling were measured pre-ET, post-ET and immediately after Hbmass was reversed to the individual pre-ET level by phlebotomy.
Results:
ET increased the Hbmass (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and [Formula: see text]O2peak during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in [Formula: see text]O2peak compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was [Formula: see text]peak (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased [Formula: see text]peak and a-[Formula: see text]O2diff accounted for 70% and 30% of the [Formula: see text]O2peak improvements, respectively. Markers of mitochondrial density (CS and COX-IV; P ≤ 0.007) and left ventricular mass (P = 0.027) increased.
Conclusion:
The ET-induced increase in [Formula: see text]O2peak was preserved despite removing the increases in Hbmass and BV by phlebotomy, independent of posture. [Formula: see text]O2peak increased primarily through elevated [Formula: see text]peak but also through a widened a-[Formula: see text]O2diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.
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