title: Difference between diabetic and nondiabetic smokers in the pituitary response to physical exercise.
abstract: The growth hormone (GH), cortisol, and arginine vasopressin (AVP) responses to bicycle ergometry (with increasing workload until exhaustion) were measured in 20 patients affected by insulin-dependent diabetes mellitus (IDDM) (10 habitual smokers and 10 nonsmokers) and 20 nondiabetic subjects (normal controls) (10 habitual smokers and 10 nonsmokers). Cardiorespiratory parameters such as heart rate, blood pressure, ventilation, frequency of breathing, tidal volume, oxygen consumption (Vo(2)), carbondioxide production (Vco(2)), and respiratory exchange ratio (R) were monitored before and during exercise tests. No significant differences between groups were observed; furthermore, there were no differences in circulating somatomedin-C (SM-C) and free fatty acids (FFA) levels between groups. Blood glucose levels were similar before exercise and followed a similar pattern during tests in diabetic smokers and nonsmokers. Basal GH, cortisol, and AVP levels were similar in diabetic smokers, diabetic nonsmokers, normal smokers, and normal nonsmokers. In all groups, exercise induced a significant increase in the serum concentrations of all examined hormones. Increments were significantly higher in diabetic than in nondiabetic groups. No significant differences were observed between diabetic smokers and nonsmokers for all examined hormones. AVP responses during tests were similar in normal smokers and nonsmokers. In contrast, exercise-induced GH and cortisol increments were significantly lower in normal smokers than in normal nonsmokers. These data support the hypothesis that in normal subjects habitual nicotine consumption may attenuate both GH and cortisol responses to a releasing stimulation, such as physical exercise. This phenomenon may represent an expression of adaptation of nicotinic neurotransmission to chronic stimulation. Furthermore, the data show that the effect induced by habitual smoking is absent in diabetics, probably because of diabetes-induced neuroendocrine alterations in the central nervous system.
authors.affiliation: Department of Internal Medicine, University of Parma, Parma, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Coiro
authors.forename: G Saccani
authors.initials: GS
authors.lastname: Jotti
authors.forename: R
authors.initials: R
authors.lastname: Volpi
authors.forename: M g
authors.initials: Mg
authors.lastname: Magotti Mg
authors.forename: P
authors.initials: P
authors.lastname: Galli
authors.forename: L
authors.initials: L
authors.lastname: Finardi
authors.forename: M l
authors.initials: Ml
authors.lastname: Maffei Ml
authors.forename: P
authors.initials: P
authors.lastname: Chiodera
authors.forename: A
authors.initials: A
authors.lastname: Casti
mesh_terms: D001127:Arginine Vasopressin / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000503:physiopathology*; D003930:Diabetic Retinopathy / Q000503:physiopathology; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D019382:Human Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D010902:Pituitary Gland / Q000503:physiopathology*; D012907:Smoking / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D001127:Arginine Vasopressin; D019382:Human Growth Hormone; D006854:Hydrocortisone