【摘要】 目的：探讨低氧环境下单次高强度间歇运动（High Intensity Interval Exercise, HIIE）对健康成人骨骼肌线粒体生物发生标志物的急性调控效应，并通过常氧环境下的不同强度匹配，比较不同氧环境与负荷模式对线粒体生物合成通路的差异化影响。方法：采用交叉研究设计，10名健康男性受试者（年龄28岁±5岁，BMI 23.6 kg/m²±3.4 kg/m²）分别完成3次HIIE干预：1)常压低氧（HY，吸入氧分数FiO₂为14%，模拟海拔3 200 m）;2)常氧绝对强度（NA,FiO₂为21%，海拔25 m）匹配HY条件下绝对功率输出)；3)常氧相对强度（NR，匹配HY绝对功率输出）。HIIE方案为6×4 min自行车间歇运动（组间间歇2 min），其中，HY和NR干预分别以各自环境下85.8%±1.9%与87.4%±1.7%的峰值功率输出执行，NA干预维持HY的绝对功率（相当于78.2%±2.4%峰值）。采用活检技术于运动前（Baseline）、运动后即刻（P0H）、3 h（P3H）及24 h（P24H）采集股外侧肌肉样本，进行多维度分析：1)实时荧光定量PCR（qPCR）定量线粒体生物合成相关基因表达；2)蛋白免疫印迹（Western blot）分析PGC-1α蛋白水平；3)高分辨率呼吸测定仪（Oroboros）评估线粒体氧化功能。结果：1)基因层面：HY和NR干预在P3H时间点均呈现HIF-1α、VEGF及PGC-1α mRNA的显著上调（P<0.05），其下游线粒体生物合成关键基因（PGC-1α1/4、PPARα）、呼吸链调控（HSP70、p53）及代谢相关基因（PDK4、SLC27A4、UCP3、CD36）呈现出时序性激活。2)蛋白表达层面：仅NR干预检测到运动后即刻PGC-1α蛋白的显著升高。3)功能层面：3次干预后线粒体呼吸功能及柠檬酸合成酶活性等指标均未见统计学差异（P>0.05）。结论：在相对强度匹配条件下，低氧与常氧HIIE可产生相似的线粒体生物合成基因急性激活效应，但该分子级联反应尚未转化为功能性线粒体适应性改变。低氧环境通过激活HIF-1α及PGC-1α等基因，产生与常氧相对强度等效的分子效应，这一发现为低氧-常氧运动强度的生物学等效转换提供了重要的证据。更多还原

【Abstract】 Objective: This study aimed to investigate the acute regulatory effects of a single session of high-intensity interval exercise（HIIE） under hypoxic conditions on skeletal muscle mitochondrial biogenesis markers in healthy adults. By incorporating normoxic trials with matched intensities, the study further sought to systematically compare the differential impacts of oxgen availability and workload patterns on mitochondrial biogenesis pathways. Methods:Using a crossover design, ten healthy males（age 28±5 years; BMI 26. 0±3. 4 kg/m²） completed three HIIE sessions:（1） hypoxia（HY, FiO₂ = 14%, simulated altitude 3200 m）;（2） normoxia-absolute intensity（NA, FiO₂ = 21%, altitude 25m）, matched to the absolute peak power output（ PPO） of HY; and（3） normoxia-relative intensity（NR）, matched to the relative PPO of HY. The HIIE protocol consisted of six 4-minute cycling intervals with 2-minute rest. HY and NR were performed at 85. 8 ± 1. 9% and 87. 4 ± 1. 7% of their respective environment-specific PPO, whereas NA was performed at the absolute workload corresponding to HY, which equated to 78. 2 ± 2. 4% of PPO under normoxia. Muscle biopsies from the vastus lateralis were collected at baseline, immediately post-exercise（P0H）, 3 h post-exercise（P3H）, and 24 h post-exercise（P24H）. Analyses included:（ 1） quantitative real-time PCR for mitochondrial biogenesis-related gene expression;（2） Western blot for PGC-1α protein levels; and（3） high-resolution respirometry（Oroboros） for mitochondrial oxidative function.Results:（1） Gene expression: At P3H, HIF-1α, VEGF, and PGC-1α gene expression were significantly upregulated in HY and NR（P<0. 05）, along with time-dependent activation of downstream genes related to mitochondrial biogenesis（PGC-1α1/4, PPARα）, respiratory regulation（HSP70, p53）, and metabolism（PDK4, SLC27A4, UCP3, CD36）.（2） Protein expression: PGC-1α protein increased immediately post-exercise only in NR.（3） Mitochondrial function: Mitochondrial respiration and citrate synthase activity showed no differences across the three conditions（P>0. 05）.Conclusion:This study provides the first evidence that relative-intensity matched HIIE under hypoxia and normoxia conditions induces similar acute activation of mitochondrial biogenesis-related genes, although these molecular cascades do not translate into functional mitochondrial adaptations. Hypoxia-induced activation of HIF-1α and PGC-1α produces molecular effects equivalent to those observed under normoxia at matched relative intensity. These findings offer novel evidence supporting the biological equivalence of hypoxia-and normoxia-based exercise intensity.更多还原