McCue Alexus, Munten Stephanie, Herzig Karl-Heinz, Gagnon Dominique D
Laboratory of Environmental Exercise Physiology, School of Kinesiology and Health Sciences, Laurentian University, Sudbury, Ontario, Canada; Center of Research in Occupational Health and Safety, Laurentian University, Sudbury, Ontario, Canada.
Institute of Biomedicine, Medical Research Center, Faculty of Medicine, University of Oulu, Oulu University Hospital, Oulu, Finland; Department of Gastroenterology and Metabolism, Poznan University of Medical Sciences, Poznan, Poland.
J Therm Biol. 2021 May;98:102912. doi: 10.1016/j.jtherbio.2021.102912. Epub 2021 Mar 17.
Metabolic flexibility is compromised in individuals suffering from metabolic diseases, lipo- and glucotoxicity, and mitochondrial dysfunctions. Exercise studies performed in cold environments have demonstrated an increase in lipid utilization, which could lead to a compromised substrate competition, glycotoxic-lipotoxic state, or metabolic inflexibility. Whether metabolic flexibility is altered during incremental maximal exercise to volitional fatigue in a cold environment remains unclear.
Ten young healthy participants performed four maximal incremental treadmill tests to volitional fatigue, in a fasted state, in a cold (0 °C) or a thermoneutral (22.0 °C) environment, with and without a pre-exercise ingestion of a 75-g glucose solution. Metabolic flexibility was assessed via indirect calorimetry using the change in respiratory exchange ratio (ΔRER), maximal fat oxidation (ΔMFO), and where MFO occurred along the exercise intensity spectrum (ΔFat), while circulating lactate and glucose levels were measured pre and post exercise.
Multiple linear mixed-effects regressions revealed an increase in glucose oxidation from glucose ingestion and an increase in lipid oxidation from the cold during exercise (p < 0.001). No differences were observed in metabolic flexibility as assessed via ΔRER (0.05 ± 0.03 vs. 0.05 ± 0.03; p = 0.734), ΔMFO (0.21 ± 0.18 vs. 0.16 ± 0.13 g min; p = 0.133) and ΔFat (13.3 ± 19.0 vs. 0.6 ± 21.3 %V̇O; p = 0.266) in cold and thermoneutral, respectively.
Following glucose loading, metabolic flexibility was unaffected during exercise to volitional fatigue in a cold environment, inducing an increase in lipid oxidation. These results suggest that competing pathways responsible for the regulation of fuel selection during exercise and cold exposure may potentially be mechanistically independent. Whether long-term metabolic influences of high-fat diets and acute lipid overload in cold and warm environments would impact metabolic flexibility remain unclear.
代谢灵活性在患有代谢疾病、脂肪毒性和糖毒性以及线粒体功能障碍的个体中受损。在寒冷环境中进行的运动研究表明脂质利用率增加，这可能导致底物竞争受损、糖毒性-脂肪毒性状态或代谢不灵活性。在寒冷环境中进行递增式最大运动直至自愿性疲劳期间，代谢灵活性是否会发生改变仍不清楚。
10名年轻健康参与者在禁食状态下，于寒冷（0°C）或热中性（22.0°C）环境中，进行了4次最大递增式跑步机测试直至自愿性疲劳，测试分为运动前摄入75克葡萄糖溶液和未摄入两种情况。通过间接量热法，利用呼吸交换率变化（ΔRER）、最大脂肪氧化量（ΔMFO）以及最大脂肪氧化量在运动强度谱上的出现位置（ΔFat）来评估代谢灵活性，同时在运动前后测量循环中的乳酸和葡萄糖水平。
多元线性混合效应回归显示，运动期间葡萄糖摄入使葡萄糖氧化增加，寒冷使脂质氧化增加（p < 0.001）。通过ΔRER（0.05±0.03对0.05±0.03；p = 0.734）、ΔMFO（0.21±0.18对0.16±0.13克/分钟；p = 0.133）和ΔFat（13.3±19.0对0.6±21.3%V̇O；p = 0.266）评估的代谢灵活性在寒冷和热中性环境中未观察到差异。
葡萄糖负荷后，在寒冷环境中进行运动直至自愿性疲劳期间，代谢灵活性未受影响，脂质氧化增加。这些结果表明，运动和寒冷暴露期间负责调节燃料选择的竞争途径可能在机制上是独立的。高脂肪饮食以及寒冷和温暖环境中的急性脂质过载对代谢灵活性的长期代谢影响仍不清楚。
