Department of Physical Performance, Norwegian School of Sport Sciences, Post box 4014 Ullevål Stadion, 0806, Oslo, Norway.
Center for Cardiological Innovation, Oslo University Hospital, Oslo, Norway.
Eur J Appl Physiol. 2020 May;120(5):985-999. doi: 10.1007/s00421-020-04336-2. Epub 2020 Mar 14.
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.
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.
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.
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.
在直立式自行车运动中，耐力训练（ET）引起的峰值摄氧量（[Formula: see text]O）和心输出量（[Formula: see text]）的增加会在去除 ET 引起的血容量（BV）增加后恢复到 ET 前的水平。我们假设，在仰卧位而不是在直立位自行车运动期间，从 ET 获得的 BV 进行放血后，ET 引起的[Formula: see text]O 和[Formula: see text]的改善仍然得到保留。动静脉氧差（a-[Formula: see text]Odiff；[Formula: see text]O/[Formula: see text]）、心脏尺寸和肌肉形态学被研究以评估它们对[Formula: see text]O 改善的作用。
12 名未经训练的受试者（[Formula: see text]O：44±6 ml·kg·min）完成了 10 周的监督 ET（每周 3 次）。在 ET 前后评估超声心动图、肌肉活检、血红蛋白质量（Hb）和 BV。在 ET 前后和 Hb 通过放血恢复到个体 ET 前水平后，立即测量直立和仰卧位自行车运动时的[Formula: see text]O 和[Formula: see text]。
ET 增加了 Hb（3.3±2.9%；P=0.005）、BV（3.7±5.6%；P=0.044）和直立及仰卧位自行车运动时的[Formula: see text]O（分别增加 11±6%和 10±8%；P≤0.003）。在两种姿势下，与 ET 前相比，放血后[Formula: see text]O 的改善仍然保持（11±4%和 11±9%；P≤0.005），[Formula: see text]也保持（9±14%和 9±10%；P≤0.081）。增加的[Formula: see text]和 a-[Formula: see text]Odiff 分别占[Formula: see text]O 改善的 70%和 30%。线粒体密度标志物（CS 和 COX-IV；P≤0.007）和左心室质量（P=0.027）增加。
尽管通过放血去除了 Hb 和 BV 的增加，但 ET 引起的[Formula: see text]O 的增加仍然保持不变，与姿势无关。[Formula: see text]O 的增加主要通过升高的[Formula: see text]实现，但也通过加宽的 a-[Formula: see text]Odiff 实现，这可能是通过心脏重塑和线粒体生物发生介导的。
