Morales-Alamo David, Guerra Borja, Santana Alfredo, Martin-Rincon Marcos, Gelabert-Rebato Miriam, Dorado Cecilia, Calbet José A L
Department of Physical Education, University of Las Palmas de Gran Canaria, Las Palmas de Gran Canaria, Spain.
Research Institute of Biomedical and Health Sciences, Las Palmas de Gran Canaria, Spain.
Front Physiol. 2018 Mar 19;9:188. doi: 10.3389/fphys.2018.00188. eCollection 2018.
Compared to normoxia, during sprint exercise in severe acute hypoxia the glycolytic rate is increased leading to greater lactate accumulation, acidification, and oxidative stress. To determine the role played by pyruvate dehydrogenase (PDH) activation and reactive nitrogen and oxygen species (RNOS) in muscle lactate accumulation, nine volunteers performed a single 30-s sprint (Wingate test) on four occasions: two after the ingestion of placebo and another two following the intake of antioxidants, while breathing either hypoxic gas (PO = 75 mmHg) or room air (PO = 143 mmHg). muscle biopsies were obtained before, immediately after, 30 and 120 min post-sprint. Antioxidants reduced the glycolytic rate without altering performance or VO. Immediately after the sprints, Ser- and Ser-PDH-E1α phosphorylations were reduced to similar levels in all conditions (~66 and 91%, respectively). However, 30 min into recovery Ser-PDH-E1α phosphorylation reached pre-exercise values while Ser-PDH-E1α was still reduced by 44%. Thirty minutes after the sprint Ser-PDH-E1α phosphorylation was greater with antioxidants, resulting in 74% higher muscle lactate concentration. Changes in Ser and Ser-PDH-E1α phosphorylation from pre to immediately after the sprints were linearly related after placebo ( = 0.74, < 0.001; = 18), but not after antioxidants ingestion ( = 0.35, = 0.15). In summary, lactate accumulation during sprint exercise in severe acute hypoxia is not caused by a reduced activation of the PDH. The ingestion of antioxidants is associated with increased PDH re-phosphorylation and slower elimination of muscle lactate during the recovery period. Ser re-phosphorylates at a faster rate than Ser-PDH-E1α during the recovery period, suggesting slightly different regulatory mechanisms.
与常氧相比，在严重急性低氧状态下进行短跑运动时，糖酵解速率增加，导致乳酸积累、酸化和氧化应激加剧。为了确定丙酮酸脱氢酶（PDH）激活以及活性氮和氧物种（RNOS）在肌肉乳酸积累中所起的作用，九名志愿者分四次进行了单次30秒的短跑（温盖特测试）：两次在摄入安慰剂后，另外两次在摄入抗氧化剂后，同时分别呼吸低氧气体（PO = 75 mmHg）或室内空气（PO = 143 mmHg）。在短跑前、短跑后即刻、短跑后30分钟和120分钟采集肌肉活检样本。抗氧化剂降低了糖酵解速率，同时不影响运动表现或VO。短跑后即刻，在所有条件下Ser-和Ser-PDH-E1α磷酸化水平均降至相似水平（分别约为66%和91%）。然而，恢复30分钟时，Ser-PDH-E1α磷酸化达到运动前值，而Ser-PDH-E1α仍降低44%。短跑后30分钟，抗氧化剂组的Ser-PDH-E1α磷酸化水平更高，导致肌肉乳酸浓度高出74%。安慰剂组短跑前至短跑后即刻Ser和Ser-PDH-E1α磷酸化的变化呈线性相关（ = 0.74， < 0.001； = 18），但摄入抗氧化剂后则无相关性（ = 0.35， = 0.15）。总之，严重急性低氧状态下短跑运动期间的乳酸积累并非由PDH激活降低所致。摄入抗氧化剂与恢复期间PDH再磷酸化增加以及肌肉乳酸清除减慢有关。恢复期间Ser再磷酸化的速率比Ser-PDH-E1α更快，提示调控机制略有不同。
