Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10 weeks of endurance training.

Purpose: The endurance training (ET)-induced increases in peak oxygen uptake ([Formula: see text]O) and cardiac output ([Formula: see text]) 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]O and [Formula: see text] are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O difference (a-[Formula: see text]Odiff; [Formula: see text]O/[Formula: see text]), cardiac dimensions and muscle morphology were studied to assess their role for the [Formula: see text]O improvement.

Methods: Twelve untrained subjects ([Formula: see text]O: 44 ± 6 ml kg min) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hb) and BV were assessed pre- and post-ET. [Formula: see text]O and [Formula: see text] during upright and supine cycling were measured pre-ET, post-ET and immediately after Hb was reversed to the individual pre-ET level by phlebotomy.

Results: ET increased the Hb (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and [Formula: see text]O during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in [Formula: see text]O compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was [Formula: see text] (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased [Formula: see text] and a-[Formula: see text]Odiff accounted for 70% and 30% of the [Formula: see text]O 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]O was preserved despite removing the increases in Hb and BV by phlebotomy, independent of posture. [Formula: see text]O increased primarily through elevated [Formula: see text] but also through a widened a-[Formula: see text]Odiff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.