The John B. Pierce Laboratory, 290 Congress Ave., New Haven, CT 06519, USA.
Med Sci Sports Exerc. 2010 Sep;42(9):1660-8. doi: 10.1249/MSS.0b013e3181d8cf68.
We examined estradiol and testosterone effects on thermoregulation in women with and without Polycystic Ovary syndrome (PCOS). We hypothesized that core temperature (Tc) threshold for sweating during exercise is delayed in women with PCOS and that testosterone delays the Tc set point for sweating during exercise.
For 16 d, we suppressed estrogens, progesterone, and testosterone with a gonadotropin-releasing hormone antagonist (GnRHant) in seven women with and seven women without PCOS (control); we added 17[beta]-estradiol (0.2 mg.d-1, two patches) on days 4-16 (E2) and testosterone (2.5 mg.d-1, orally) on days 13-16 (E2 + T). Under each hormone condition, subjects cycled in a temperature of 35 degrees C at 60% of age-predicted HRmax for 40 min.
Tc sweating threshold was lower in women in the PCOS group compared with those in the control during GnRHant (37.21 degrees C +/- 0.51 degrees C vs 37.70 degrees C +/- 0.12 degrees C, P < 0.05); neither E2 nor E2 + T influenced the thermoregulatory responses in PCOS. E2 decreased Tc sweating threshold in control (37.06 degrees C +/- 0.69 degrees C, P < 0.05), but E2 + T attenuated this response (37.53 degrees C +/- 0.19 degrees C). Peak sweating rate was greater in women in the PCOS group compared with those in the control group during GnRHant (1.06 +/- 0.47 vs 0.47 +/- 0.11 mg.cm-2.min-1) and E2 + T (0.85 +/- 0.41 vs 0.44 +/- 0.10 mg.cm-2.min-1, P < 0.05). Compared with the control group, total sweat losses were greater in the PCOS group during GnRHant (0.614 +/- 0.189 vs 0.419 +/- 0.098 L) and during E2 + T (0.696 +/- 0.281 vs 0.434 +/- 0.164 L, P < 0.05) but not during E2 (0.639 +/- 0.231 and 0.505 +/- 0.214 L for PCOS and control groups, respectively, P = 0.09).
Thermoregulation was adequate in women with PCOS; however, the women with PCOS achieved thermoregulation at the expense of producing higher sweat volumes.
我们研究了雌二醇和睾酮对多囊卵巢综合征（PCOS）妇女和非多囊卵巢综合征妇女的体温调节的影响。我们假设，在患有 PCOS 的女性中，运动时出汗的核心温度（Tc）阈值会延迟，而睾酮会延迟运动时出汗的 Tc 设定点。
在 16 天内，我们用促性腺激素释放激素拮抗剂（GnRHant）抑制了七名患有 PCOS 和七名无 PCOS 的女性（对照组）的雌激素、孕激素和睾酮；我们在第 4-16 天添加了 17[β]-雌二醇（0.2 mg.d-1，两个贴片）（E2）和睾酮（2.5 mg.d-1，口服）（E2 + T）在第 13-16 天。在每种激素条件下，受试者在 35 度的温度下以 60%的年龄预测 HRmax 循环 40 分钟。
与对照组相比，在 GnRHant 期间，PCOS 组女性的 Tc 出汗阈值较低（37.21 摄氏度 +/- 0.51 摄氏度 vs 37.70 摄氏度 +/- 0.12 摄氏度，P < 0.05）；E2 或 E2 + T 均未影响 PCOS 的体温调节反应。E2 降低了对照组的 Tc 出汗阈值（37.06 摄氏度 +/- 0.69 摄氏度，P < 0.05），但 E2 + T 减弱了这种反应（37.53 摄氏度 +/- 0.19 摄氏度）。与对照组相比，在 GnRHant 期间（1.06 +/- 0.47 对 0.47 +/- 0.11 mg.cm-2.min-1）和 E2 + T 期间（0.85 +/- 0.41 对 0.44 +/- 0.10 mg.cm-2.min-1，P < 0.05），PCOS 组女性的峰值出汗率更高。与对照组相比，在 GnRHant 期间（0.614 +/- 0.189 对 0.419 +/- 0.098 L）和 E2 + T 期间（0.696 +/- 0.281 对 0.434 +/- 0.164 L，P < 0.05），PCOS 组的总汗量更多，但在 E2 期间则没有（分别为 PCOS 和对照组的 0.639 +/- 0.231 和 0.505 +/- 0.214 L，P = 0.09）。
患有 PCOS 的女性体温调节正常；然而，患有 PCOS 的女性通过产生更高的汗液量来实现体温调节。
