Semah Tagougui1, Pierre Fontaine2, Erwan Leclair3, Julien Aucouturier1, Régis Matran4, Kahina Oussaidene1, Aurélien Descatoire5, Fabrice Prieur6, Patrick Mucci1, Anne Vambergue2, Georges Baquet1, Elsa Heyman7. 1. University of Lille, URePSSS, "Physical Activity, Muscle, Health" Research Team, Lille, France. 2. Department of Diabetology, Lille University Hospital, EA 4489, Lille, France. 3. School of Kinesiology and Health Science, Faculty of Health, York University, Toronto, ON, Canada. 4. Department of Physiology, EA 2689 and IFR 22, Lille, France. 5. Regional Hospital Centre of Roubaix, Roubaix, France. 6. University Paris Sud-University of Orléans, EA 4532 CIAMS, Orléans, France. 7. University of Lille, URePSSS, "Physical Activity, Muscle, Health" Research Team, Lille, France elsa.heyman@univ-lille2.fr.
Abstract
OBJECTIVE: Cerebral vasoreactivity to pharmacologically induced hypercapnia is impaired in poorly controlled patients with type 1 diabetes but otherwise free from microangiopathy. However, whether this response is also compromised during exercise, a daily-life physiological condition challenging regional cerebral hemodynamics, is unknown. We aimed to investigate prefrontal cortex hemodynamics during incremental maximal exercise in patients with uncomplicated type 1 diabetes, taking into account long-term glycemic control as well as exercise- and diabetes-influenced vasoactive stimuli. RESEARCH DESIGN AND METHODS: Two groups of patients (type 1 diabetes with adequate glycemic control [T1D-A], n = 8, HbA1c 6.8 ± 0.7% [51 ± 7.7 mmol/mol]; type 1 diabetes with inadequate glycemic control [T1D-I], n = 10, HbA1c 9.0 ± 0.7% [75 ± 7.7 mmol/mol]) were compared with 18 healthy control subjects (CON-A and CON-I) matched for physical activity and body composition. Throughout exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), and total hemoglobin (THb) in the prefrontal cortex. Venous and arterialized capillary blood was sampled during exercise to assess for factors that may alter prefrontal cortex hemodynamics and oxygenation. RESULTS: No differences were observed between T1D-A and CON-A, but VO2max was impaired (P < 0.05) and cerebral blood volume (THb) increase blunted (P < 0.05) in T1D-I compared with CON-I. Nonetheless, O2Hb appeared unaltered in T1D-I probably partly due to blunting of simultaneous neuronal oxygen extraction (i.e., a lower HHb increase; P < 0.05). There were no intergroup differences in arterial oxygen content, Paco2, pH, [K(+)], and free insulin levels. CONCLUSIONS: Maximal exercise highlights subtle disorders of both hemodynamics and neuronal oxygenation in the prefrontal cortex of poorly controlled patients with type 1 diabetes. These findings may warn clinicians of brain endothelial dysfunction occurring even before overt microangiopathy during exercise.
OBJECTIVE: Cerebral vasoreactivity to pharmacologically induced hypercapnia is impaired in poorly controlled patients with type 1 diabetes but otherwise free from microangiopathy. However, whether this response is also compromised during exercise, a daily-life physiological condition challenging regional cerebral hemodynamics, is unknown. We aimed to investigate prefrontal cortex hemodynamics during incremental maximal exercise in patients with uncomplicated type 1 diabetes, taking into account long-term glycemic control as well as exercise- and diabetes-influenced vasoactive stimuli. RESEARCH DESIGN AND METHODS: Two groups of patients (type 1 diabetes with adequate glycemic control [T1D-A], n = 8, HbA1c 6.8 ± 0.7% [51 ± 7.7 mmol/mol]; type 1 diabetes with inadequate glycemic control [T1D-I], n = 10, HbA1c 9.0 ± 0.7% [75 ± 7.7 mmol/mol]) were compared with 18 healthy control subjects (CON-A and CON-I) matched for physical activity and body composition. Throughout exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin (O2Hb), deoxyhemoglobin (HHb), and total hemoglobin (THb) in the prefrontal cortex. Venous and arterialized capillary blood was sampled during exercise to assess for factors that may alter prefrontal cortex hemodynamics and oxygenation. RESULTS: No differences were observed between T1D-A and CON-A, but VO2max was impaired (P < 0.05) and cerebral blood volume (THb) increase blunted (P < 0.05) in T1D-I compared with CON-I. Nonetheless, O2Hb appeared unaltered in T1D-I probably partly due to blunting of simultaneous neuronal oxygen extraction (i.e., a lower HHb increase; P < 0.05). There were no intergroup differences in arterial oxygen content, Paco2, pH, [K(+)], and free insulin levels. CONCLUSIONS: Maximal exercise highlights subtle disorders of both hemodynamics and neuronal oxygenation in the prefrontal cortex of poorly controlled patients with type 1 diabetes. These findings may warn clinicians of brain endothelial dysfunction occurring even before overt microangiopathy during exercise.
Authors: Anna L Emanuel; Eelco van Duinkerken; Mike P Wattjes; Martin Klein; Frederik Barkhof; Frank J Snoek; Michaela Diamant; Etto C Eringa; Richard G IJzerman; Erik H Serné Journal: Microcirculation Date: 2019-02-22 Impact factor: 2.628