Regulation of fuel metabolism during exercise in hypopituitarism with growth hormone-deficiency (GHD). (August 2016)

• Record Type: Journal Article
• Authors: Zueger, Thomas; Loher, Hannah; Egger, Andrea; Boesch, Chris; Christ, Emanuel
• Is Part Of: Growth hormone & IGF research. Volume 29(2016)
• Page Start: 39
• Page End: 44
• Publication Date: 2016-08
• Subjects: ACTH adrenocorticotropic hormone -- AUC area under the curve -- BMI body mass index -- CI control individuals -- CV coefficient of variation -- FFA free fatty acids -- GH growth hormone -- GHD growth hormone deficiency -- GHRH growth hormone releasing hormone -- RER respiratory exchange ratio -- VCO2 carbon dioxide output -- VO2 oxygen uptake -- VO2max maximum oxygen uptake capacity; Growth hormone deficiency -- Exercise -- Endurance capacity -- Fuel metabolism -- Lipolysis; Growth regulators -- Periodicals; Growth -- Regulation -- Periodicals; Somatomedin -- Periodicals; Somatomedins -- Periodicals; Growth Hormone -- Periodicals; Growth Substances -- Periodicals; Croissance -- Régulation -- Périodiques; Croissance -- Régulateurs -- Périodiques; Somatotrophine -- Périodiques; Somatomédine -- Périodiques; Growth -- Regulation; Growth regulators; Electronic journals; Periodicals; Electronic journals; 612.4
• DOI: 10.1016/j.ghir.2016.03.007
• Languages: English
• ISSNs: 1096-6374

Abstract

Abstract: Objective: Growth hormone (GH) has a strong lipolytic action and its secretion is increased during exercise. Data on fuel metabolism and its hormonal regulation during prolonged exercise in patients with growth hormone deficiency (GHD) is scarce. This study aimed at evaluating the hormonal and metabolic response during aerobic exercise in GHD patients. Design: Ten patients with confirmed GHD and 10 healthy control individuals (CI) matched for age, sex, BMI, and waist performed a spiroergometric test to determine exercise capacity (VO2max ). Throughout a subsequent 120-minute exercise on an ergometer at 50% of individual VO2max free fatty acids (FFA), glucose, GH, cortisol, catecholamines and insulin were measured. Additionally substrate oxidation assessed by indirect calorimetry was determined at begin and end of exercise. Results: Exercise capacity was lower in GHD compared to CI (VO2max 35.5 ± 7.4 vs 41.5 ± 5.5 ml/min ∗ kg, p = 0.05). GH area under the curve (AUC-GH), peak-GH and peak-FFA were lower in GHD patients during exercise compared to CI (AUC-GH 100 ± 93.2 vs 908.6 ± 623.7 ng ∗ min/ml, p < 0.001; peak-GH 1.5 ± 1.53 vs 12.57 ± 9.36 ng/ml, p < 0.001, peak-FFA 1.01 ± 0.43 vs 1.51 ± 0.56 mmol/l, p = 0.036, respectively). There were no significant differences for insulin, cortisol, catecholamines and glucose. Fat oxidation at the end of exercise was higher in CI compared to GHD patients (295.7 ± 73.9 vs 187.82 ± 103.8 kcal/h, p = 0.025). Conclusion: A reduced availability of FFA during a 2-hour aerobic exercise and a reduced fat oxidation at the end of exercise may contribute to the decreased exercise capacity in GHD patients. Catecholamines and cortisol do not compensate for the lack of the lipolytic action of GH in patients with GHD. Highlights: Fuel metabolism and its hormonal regulation during exercise in GHD are examined. Exercise capacity is reduced in GHD patients compared to healthy individuals. During exercise FFA and fat-oxidation are lower in GHD than in healthy controls. Catecholamines do not compensate for the lack of the lipolytic action of GH.