Blood volume expansion does not explain the increase in peak oxygen uptake induced by 10 weeks of endurance training
Øyvind Skattebo, A W Bjerring, Marius Auensen, Sebastian Imre Sarvari, Kristoffer Toldnes Cumming, Carlo Capelli, Jostein Hallén
Abstract
Abstract Purpose The endurance training (ET)-induced increases in peak oxygen uptake ( $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak ) and cardiac output ( $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> 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 $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak and $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> peak are preserved following phlebotomy of the BV gained with ET during supine but not during upright cycling. Arteriovenous O 2 difference (a- $$\bar{\text{v}}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mrow><mml:mtext>v</mml:mtext></mml:mrow><mml:mrow><mml:mo>¯</mml:mo></mml:mrow></mml:mover></mml:math> O 2 diff; $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2 / $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> ), cardiac dimensions and muscle morphology were studied to assess their role for the $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak improvement. Methods Twelve untrained subjects ( $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak : 44 ± 6 ml kg −1 min −1 ) completed 10 weeks of supervised ET (3 sessions/week). Echocardiography, muscle biopsies, haemoglobin mass (Hb mass ) and BV were assessed pre- and post-ET. $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak and $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> peak during upright and supine cycling were measured pre-ET, post-ET and immediately after Hb mass was reversed to the individual pre-ET level by phlebotomy. Results ET increased the Hb mass (3.3 ± 2.9%; P = 0.005), BV (3.7 ± 5.6%; P = 0.044) and $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak during upright and supine cycling (11 ± 6% and 10 ± 8%, respectively; P ≤ 0.003). After phlebotomy, improvements in $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak compared with pre-ET were preserved in both postures (11 ± 4% and 11 ± 9%; P ≤ 0.005), as was $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> peak (9 ± 14% and 9 ± 10%; P ≤ 0.081). The increased $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> peak and a- $$\bar{\text{v}}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mrow><mml:mtext>v</mml:mtext></mml:mrow><mml:mrow><mml:mo>¯</mml:mo></mml:mrow></mml:mover></mml:math> O 2 diff accounted for 70% and 30% of the $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak 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 $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak was preserved despite removing the increases in Hb mass and BV by phlebotomy, independent of posture. $$\dot{V}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>V</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> O 2peak increased primarily through elevated $$\dot{Q}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mi>Q</mml:mi><mml:mo>˙</mml:mo></mml:mover></mml:math> peak but also through a widened a- $$\bar{\text{v}}$$ <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mover><mml:mrow><mml:mtext>v</mml:mtext></mml:mrow><mml:mrow><mml:mo>¯</mml:mo></mml:mrow></mml:mover></mml:math> O 2 diff, potentially mediated by cardiac remodelling and mitochondrial biogenesis.