Cardiovascular and autonomic nervous system response to graded exercise in adolescents with type 1 diabetes.

Abstract

Introduction: Type 1 diabetes (T1D) is associated with an increased risk of cardiovascular and autonomic complications. Although cardiopulmonary exercise testing (CPET) is a valuable tool for assessing cardiorespiratory function, data on physiological response to maximal exertion in adolescents with T1D remain limited and inconsistent. This study aimed to compare cardiovascular, respiratory, metabolic, and microvascular responses to CPET in adolescents with T1D and healthy peers.

Methods: Sixteen participants aged 11-16 years (eight with T1D and eight healthy controls), matched for anthropometric characteristics, underwent CPET on a cycle ergometer. Respiratory gas exchange, heart rate, heart rate variability, blood pressure, blood glucose, lactate concentration, skin blood flow, skin temperature, and cutaneous vascular conductance were measured at predefined time points during rest, exercise, and recovery. Blood glucose, lactate concentration, and skin microvascular variables were assessed at rest and during recovery.

Results: Adolescents with T1D demonstrated a significantly lower V̇O₂/power output slope and a higher ventilatory equivalent for oxygen at maximal effort, suggesting altered oxygen uptake efficiency. Maximal power output and maximal oxygen consumption did not differ between groups. Heart rate responses and heart rate variability were similar throughout testing. However, finger skin blood flow and cutaneous vascular conductance were significantly lower in the T1D group at rest and during recovery.

Conclusion: Adolescents with T1D showed preserved cardiovascular function and comparable overall exercise capacity to healthy peers, despite subtle impairments in oxygen utilization and reduced skin microvascular function. These findings indicate that even at a young age, T1D is associated with altered metabolic, respiratory, and microvascular responses to maximal exercise. The results suggest that peripheral, rather than central mechanisms may underlie these differences, potentially involving glucose levels or synthetic insulin effects on vascular endothelium.