Effects of antecedent hypoglycemia on subsequent counterregulatory responses to exercise.

Abstract

Antecedent hypoglycemia can blunt counterregulatory responses to subsequent hypoglycemia. It is uncertain, however, if prior hypoglycemia can blunt counterregulatory responses to other physiologic stresses. The aim of this study, therefore, was to determine whether antecedent hypoglycemia attenuates subsequent neuroendocrine and metabolic responses to exercise. Sixteen lean, healthy adults (eight men and eight women, ages 28+/-2 years, BMI 22+/-1 kg/m2, VO2max 43+/-3 ml x kg(-1) x min(-1)) were studied during 2-day protocols on two randomized occasions separated by 2 months. On day 1, subjects underwent morning and afternoon 2-h hyperinsulinemic (528+/-30 pmol/l) glucose clamp studies of 5.3+/-0.1 mmol/l (euglycemic control) or 2.9+/-0.1 mmol/l (hypoglycemic study). On day 2, subjects underwent 90 min of exercise on a static cycle ergometer at 80% of their anaerobic threshold (approximately 50% VO2max). Glycemia was equated during day 2 exercise studies via an exogenous glucose infusion. Day 1 hypoglycemia had significant effects on neuroendocrine and metabolic responses during day 2 exercise. The usual exercise-induced reduction in insulin, together with elevations of plasma epinephrine, norepinephrine, glucagon, growth hormone, pancreatic polypeptide, and cortisol levels, was significantly blunted after day 1 hypoglycemia (P<0.01). Commensurate with reduced neuroendocrine responses, key metabolic counterregulatory mechanisms of endogenous glucose production (EGP), lipolytic responses, and ketogenesis were also significantly attenuated (P<0.01) after day 1 hypoglycemia. Significantly greater rates of glucose infusion were required to maintain euglycemia during exercise after day 1 hypoglycemia compared with day 1 euglycemia (8.8+/-2.2 vs. 0.6+/-0.6 micromol x kg(-1) x min(-1); P<0.01). During the first 30 min of exercise, day 1 hypoglycemia had little effect on EGP, but during the latter 60 min of exercise, day 1 hypoglycemia was associated with a progressively smaller increase in EGP compared with day 1 euglycemia. Thus, by 90 min, the entire exercise-induced increment in EGP (8.8+/-1.1 micromol x kg(-1) x min(-1)) was abolished by day 1 hypoglycemia. We conclude that 1) antecedent hypoglycemia results in significant blunting of essential neuroendocrine (glucagon, insulin, catecholamines) and metabolic (endogenous glucose production, lipolysis, ketogenesis) responses to exercise; 2) antecedent hypoglycemia may play a role in the pathogenesis of exercise-related hypoglycemia in type 1 diabetic patients; and 3) antecedent hypoglycemia can blunt counterregulatory responses to other physiologic stresses in addition to hypoglycemia.

Antecedent Hypoglycemia Impairs Autonomic Cardiovascular Function

“…In one study of type 1 diabetic subjects, the epinephrine and norepinephrine responses to exercise and upright posture were intact after antecedent hypoglycemia (19). Other studies of type 1 diabetic subjects suggested that the deficit is more generalized (20,21); the epinephrine and norepinephrine responses to a cold pressor test were reduced in wellcontrolled type 1 diabetic subjects (20), and antecedent hypoglycemia reduced the normal exercise-induced rise in epinephrine, norepinephrine, glucagon, growth hormone, pancreatic polypeptide, and cortisol in healthy individuals (21). Our data are consistent with these latter studies and strongly support the view that the effects of antecedent hypoglycemia on the autonomic nervous system are more generalized and not specific to subsequent hypoglycemic stimuli.…”

Effect of prior hyperglycemia on IL-6 responses to exercise in children with type 1 diabetes

“…While the role of IL-6 and other pro-and anti-inflammatory cytokines in the evolution of diabetes is still incompletely defined, the above evidence suggests that the simultaneous presence of diabetes, hyperglycemia, and intense exercise (all independently able to increase IL-6) may result in inappropriately elevated IL-6 concentrations, with potentially negative implications on the onset and progression of diabetic complications. It is also likely that hyperglycemia need not occur simultaneously with exercise to affect exercise-induced IL-6 secretion, as numerous exercise responses can be altered by prior, rather than concurrent, glycemic fluctuations (8,16).…”

A suplementação de carboidrato maximiza o desempenho de tenistas?

“…Essa queda na concentração de glicose também foi observada em outros modelos de exercício com duração superior a 90 minutos (44,45) . Provavelmente, a redução da glicemia foi decorrente do aumento da demanda imposta pelo músculo esquelético e/ou menor liberação/produção hepática de glicose (via glicogenólise e gliconeogênese).…”