Hormonal and Metabolic Adjustment in Patients with Central Cushing's Disease After Adrenalectomy

Abstract

In ten adrenalectomized patients with central Cushing's syndrome, the hormonal and metabolic regulation during moderate long-term exercise was investigated. In a vita maxima bicycle ergometer test, V̇O₂max and the anaerobic threshold fixed arbitrarily at 3 mmol serum lactate were determined. The maximal work load of 2.03 ± 0.05 W/kg body weight (BW), and the anaerobic threshold of 1.5 ± 0.2 W/kg BW were lower than in the age- and sex-matched control group (3.5 ± 0.2 W/kg BW and 2.0 ± 0.1 W/kg BW, respectively). The moderate long-term ergometer test was performed during a second session, and the concentrations of hormones and substrates were assayed in the venous blood drawn at rest, immediately after, and 30 and 60 min after exercise. Patients and controls accomplished both tests without failure during work and recovery periods. In patients, epinephrine was neither detectable at rest nor after exercise.

After exercise, ACTH (0.360 ± 0.190 ng/ml) and norepinephrine (0.56 ± 0.16 ng/ml) were significantly higher in patients than in controls (P < 0.05). The changes of HGH and glucagon showed no differences between the two groups. The exercise-induced insulin decline was less pronounced in patients. Immediately after exercise, Cortisol increased only in controls (118 ng/ml, P < 0.01). FFA (2.38 ± 0.66 mmol/l) and glycerol (5.18 ± 1.36 mmol/l) were significantly higher in patients than in controls, and in patients the FFA (1.4 ± 0.6 mmol/l) increase was positively correlated with the ACTH elevation (r = 0.59, P < 0.04). After exercise and during recovery, the ketone body concentration was lower. The blood glucose decline did not differ between patients and controls, but after work the lactate level was higher in patients. After work, the gluco-blastic amino acids, especially alanine, increased similarly in both groups.

Since there was no evidence of a disturbed glucose homeostasis during work despite impaired hepatic glycogenosis as a result of the complete absence of epinephrine stimulation, one may conclude that during exercise an enhanced tatty acid liberation and metabolization compensated for the reduced hepatic glucose production in the patients.

Key words

central Cushing's syndrome - adrenalectomy - moderate long-term exercise - hormones - substrate regulation