School of Health and Kinesiology, University of Nebraska at Omaha, Omaha, NE 68182, USA.
School of Integrative Physiology and Athletic Training, University of Montana, Missoula, MT 59812, USA.
Int J Environ Res Public Health. 2022 May 3;19(9):5554. doi: 10.3390/ijerph19095554.
Recent aerobic exercise training in the heat has reported blunted aerobic power improvements and reduced mitochondrial-related gene expression in men. It is unclear if this heat-induced blunting of the training response exists in females. The purpose of the present study was to determine the impact of 60 min of cycling in the heat over three weeks on thermoregulation, gene expression, and aerobic capacity in females. Untrained females (n = 22; 24 ± 4yoa) were assigned to three weeks of aerobic training in either 20 °C (n = 12) or 33 °C (n = 10; 40%RH). Maximal aerobic capacity (39.5 ± 6.5 to 41.5 ± 6.2 mL·kg−1·min−1, p = 0.021, ηp2 = 0.240, 95% CI [0.315, 3.388]) and peak aerobic power (191.0 ± 33.0 to 206.7 ± 27.2 W, p < 0.001, ηp2 = 0.531, 95% CI [8.734, 22.383]) increased, while the absolute-intensity trial (50%VO2peak) HR decreased (152 ± 15 to 140 ± 13 b·min−1, p < 0.001, ηp2 = 0.691, 95% CI [15.925, 8.353]), but they were not different between temperatures (p = 0.440, p = 0.955, p = 0.341, respectively). Independent of temperature, Day 22 tolerance trial skin temperatures decreased from Day 1 (p = 0.006, ηp2 = 0.319, 95% CI [1.408, 0.266), but training did not influence core temperature (p = 0.598). Average sweat rates were higher in the 33 °C group vs. the 20 °C group (p = 0.008, ηp2 = 0.303, 95% CI [67.9, 394.9]) but did not change due to training (p = 0.571). Pre-training PGC-1α mRNA increased 4h-post-exercise (5.29 ± 0.70 fold change, p < 0.001), was lower post-training (2.69 ± 0.22 fold change, p = 0.004), and was not different between temperatures (p = 0.455). While training induced some diminished transcriptional stimulus, generally the training temperature had little effect on genes related to mitochondrial biogenesis, mitophagy, and metabolic enzymes. These female participants increased aerobic fitness and maintained an exercise-induced PGC-1α mRNA response in the heat equal to that of room temperature conditions, contrasting with the blunted responses previously observed in men.
最近的研究表明，在热环境中进行有氧训练会导致男性的有氧能力提高减弱和与线粒体相关的基因表达减少。目前尚不清楚这种热诱导的训练反应减弱是否存在于女性中。本研究的目的是确定在三周内，在热环境中进行 60 分钟的骑行对女性的体温调节、基因表达和有氧能力的影响。未经过训练的女性（n = 22；24 ± 4 岁）被分配到在 20°C（n = 12）或 33°C（n = 10；40%RH）下进行三周的有氧训练。最大有氧能力（39.5 ± 6.5 至 41.5 ± 6.2 mL·kg-1·min-1，p = 0.021，ηp2 = 0.240，95%CI [0.315，3.388]）和峰值有氧功率（191.0 ± 33.0 至 206.7 ± 27.2 W，p < 0.001，ηp2 = 0.531，95%CI [8.734，22.383]）增加，而绝对强度试验（50%VO2peak）的 HR 降低（152 ± 15 至 140 ± 13 b·min-1，p < 0.001，ηp2 = 0.691，95%CI [15.925，8.353]），但在温度之间没有差异（p = 0.440，p = 0.955，p = 0.341，分别）。无论温度如何，第 22 天的耐受试验皮肤温度从第 1 天开始下降（p = 0.006，ηp2 = 0.319，95%CI [1.408，0.266），但训练并没有影响核心温度（p = 0.598）。33°C 组的平均出汗率高于 20°C 组（p = 0.008，ηp2 = 0.303，95%CI [67.9，394.9]），但由于训练而没有变化（p = 0.571）。PGC-1α mRNA 在运动后 4 小时（5.29 ± 0.70 倍变化，p < 0.001）增加，训练后（2.69 ± 0.22 倍变化，p = 0.004）降低，且温度之间无差异（p = 0.455）。虽然训练诱导了一些转录刺激的减弱，但通常训练温度对与线粒体生物发生、线粒体自噬和代谢酶相关的基因几乎没有影响。这些女性参与者在热环境中提高了有氧能力，并保持了与在室温条件下相同的运动诱导的 PGC-1α mRNA 反应，与之前在男性中观察到的减弱反应形成对比。
