Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10 weeks of endurance training
Peer reviewed, Journal article
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Original versionEuropean Journal of Applied Physiology. 2020, 120(5), 985-999. 10.1007/s00421-020-04336-2
Purpose: The endurance training (ET)-induced increases in peak oxygen uptake (V˙O2peak) and cardiac output (Q˙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 V˙O2peak and Q˙peak are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O2 difference (a-v¯O2diff; V˙O2/Q˙), cardiac dimensions and muscle morphology were studied to assess their role for the V˙O2peak improvement. Methods: Twelve untrained subjects (V˙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. V˙O2peak and Q˙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 V˙O2peak during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in V˙O2peak compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was Q˙peak (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased Q˙peak and a-v¯O2diff accounted for 70% and 30% of the V˙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 V˙O2peak was preserved despite removing the increases in Hbmass and BV by phlebotomy, independent of posture. V˙O2peak increased primarily through elevated Q˙peak but also through a widened a-v¯O2diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.
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