Greater exercise sweating in obese women with polycystic ovary syndrome compared with obese controls.

PURPOSE

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.

METHODS

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.

RESULTS

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).

CONCLUSIONS

Thermoregulation was adequate in women with PCOS; however, the women with PCOS achieved thermoregulation at the expense of producing higher sweat volumes.