We tested two hypotheses about the disruption of luteinizing hormone (LH) pulsatility in exercising women by assaying LH in blood samples drawn at 10-min intervals over 24 h from nine young, habitually sedentary, regularly menstruating women on days 8, 9, or 10 of two menstrual cycles after 4 days of intense exercise [E = 30 kcal.kg lean body mass (LBM)-1.day-1 at 70% of aerobic capacity]. To test the hypothesis that LH pulsatility is disrupted by low energy availability, we controlled the subjects' dietary energy intakes (I) to set their energy availabilities (A = I - E) at 45 and 10 kcal.kg LBM-1.day-1 during the two trials. To test the hypothesis that LH pulsatility is disrupted by the stress of exercise, we compared the resulting LH pulsatilities to those previously reported in women with similar controlled energy availability who had not exercised. In the exercising women, low energy availability reduced LH pulse frequency by 10% (P < 0.01) during the waking hours and increased LH pulse amplitude by 36% (P = 0.05) during waking and sleeping hours, but this reduction in LH pulse frequency was blunted by 60% (P = 0.03) compared with that in the previously studied nonexercising women whose low energy availability was caused by dietary restriction. The stress of exercise neither reduced LH pulse frequency nor increased LH pulse amplitude (all P > 0.4). During exercise, the proportion of energy derived from carbohydrate oxidation was reduced from 73% while A = 45 kcal.kg LBM-1.day-1 to 49% while A = 10 kcal.kg LBM-1.day-1 (P < 0.0001). These results contradict the hypothesis that LH pulsatility is disrupted by exercise stress and suggest that LH pulsatility in women depends on energy availability.

To investigate whether measurements of cortisol responses to exercise are confounded by neglect of the hormone's circadian rhythm, we measured the serum and salivary cortisol responses of eight women to 40 min of 70% maximal oxygen consumption treadmill exercise beginning at 0800 and 2000. Responses were calculated relative to the usually employed preexercise concentrations and also to concentrations at the same times of another day while subjects were at rest. Compared with areas under response curves (AUCs) calculated relative to their circadian baselines, AUCs for serum and salivary cortisol calculated by reference to preexercise concentrations were underestimated (serum, P < 0.001; salivary, P < 0.01) by 93 and 84% in the morning and by 37 and 35% in the evening, respectively. Calculated by the usual preexercise baseline method, rises in serum and salivary cortisol were similarly underestimated. More accurately calculated relative to their circadian baselines, serum and salivary cortisol AUCs were similar (P = 0.63 and P = 0.37, respectively) in the morning and evening, as were their rises (P = 0.23 and P = 0.70, respectively). In future investigations of the existence and magnitude of cortisol responses, those responses must be calculated relative to the hormone's circadian baseline.

In other energy-restricted mammals, a single large meal restores luteinizing hormone (LH) pulsatility within a few hours. To determine whether this is so in women, we measured LH pulsatility during the 5th day of low energy availability [dietary energy intake − exercise energy expenditure = 10 kcal ⋅ kg lean body mass (LBM)−1 ⋅ day−1] and during a 6th day of aggressive refeeding (90 kcal ⋅ kg LBM−1 ⋅ day−1) in 15 meals providing 4,100 kcal for an energy availability of 75 kcal ⋅ kg LBM−1 ⋅ day−1. Low energy availability raised β-hydroxybutyrate 1,000% ( P < 0.001) and reduced plasma glucose 15% ( P < 0.01), insulin 63% ( P < 0.001), and triiodothyronine 22% ( P < 0.005). In five of eight subjects, low energy availability also unambiguously suppressed LH pulse frequency 57% to 8.2 ± 1.5 pulses/24 h ( P < 10−4) and raised LH pulse amplitude 94% to 3.1 ± 0.3 IU/l ( P < 10−4), levels below the 5th and above the 95th percentile, respectively, in energy-balanced women. Aggressive refeeding restored β-hydroxybutyrate, glucose, and insulin, but not triiodothyronine. In the five women with unambiguously disrupted LH pulsatility, aggressive refeeding had no effect on LH pulse amplitude ( P > 0.9) and raised LH pulse frequency only slightly (2.4 ± 0.6 pulses/24 h, P = 0.04) and not above the fifth percentile. This striking contrast between women and other mammals may be another clue to the unidentified mechanism mediating the effect of energy availability on LH pulsatility.

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