Regional cerebral hemodynamic response to incremental exercise is blunted in poorly controlled patients with uncomplicated type 1 diabetes.

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.

Aerobic fitness influences cerebral oxygenation response to maximal exercise in healthy subjects.

The study examined whether the aerobic fitness level modifies the cerebral oxygenation response to incremental ramp exercise, and more specifically the decline in cerebral oxygenation from heavy exercise up to maximal intensities. 11 untrained (VO2max 47.3±4.0 mL min(-1) kg(-1)) and 13 endurance-trained (VO2max 61.2±8.0 mL min(-1) kg(-1)) healthy men performed a maximal ramp cycle exercise. Left prefrontal cortex oxygenation (ΔHbO2) was monitored by near-infrared spectroscopy. A cerebral oxygenation threshold decline (ThCOx) during exercise was determined. ThCox occurred in all subjects but for higher VO2 (mL min(-1) kg(-1)) in endurance-trained than in untrained subjects (P<0.01). At submaximal exercise intensity corresponding to ThCOx, ΔHbO2 was higher in endurance-trained than in untrained subjects (P<0.05). VO2 at ThCox was related to VO2 at respiratory compensation point (n=24, r=0.93, P<0.001) and to VO2max (n=24, r=0.92, P<0.001). These findings indicate that above the respiratory compensation point the prefrontal O2 demand exceeds the supply in untrained and in endurance-trained subjects. In addition, the occurrence of ThCOx was delayed to higher absolute exercise intensities in endurance-trained in relation with their higher VO2max than untrained men. These results demonstrated that aerobic fitness influences cerebral oxygenation during exercise.

Muscle oxygen supply impairment during exercise in poorly controlled type 1 diabetes.

PURPOSE: Aerobic fitness, as reflected by maximal oxygen (O2) uptake (VO2max), is impaired in poorly controlled patients with type 1 diabetes. The mechanisms underlying this impairment remain to be explored. This study sought to investigate whether type 1 diabetes and high levels of glycated hemoglobin (HbA1c) influence O2 supply including O2 delivery and release to active muscles during maximal exercise. METHODS: Two groups of patients with uncomplicated type 1 diabetes (T1D-A, n = 11, with adequate glycemic control, HbA1c <7.0%; T1D-I, n = 12 with inadequate glycemic control, HbA1c >8%) were compared with healthy controls (CON-A, n = 11; CON-I, n = 12, respectively) matched for physical activity and body composition. Subjects performed exhaustive incremental exercise to determine VO2max. Throughout the exercise, near-infrared spectroscopy allowed investigation of changes in oxyhemoglobin, deoxyhemoglobin, and total hemoglobin in the vastus lateralis. Venous and arterialized capillary blood was sampled during exercise to assess arterial O2 transport and factors able to shift the oxyhemoglobin dissociation curve. RESULTS: Arterial O2 content was comparable between groups. However, changes in total hemoglobin (i.e., muscle blood volume) was significantly lower in T1D-I compared with that in CON-I. T1D-I also had impaired changes in deoxyhemoglobin levels and increase during high-intensity exercise despite normal erythrocyte 2,3-diphosphoglycerate levels. Finally, VO2max was lower in T1D-I compared with that in CON-I. No differences were observed between T1D-A and CON-A. CONCLUSIONS: Poorly controlled patients displayed lower VO2max and blunted muscle deoxyhemoglobin increase. The latter supports the hypotheses of increase in O2 affinity induced by hemoglobin glycation and/or of a disturbed balance between nutritive and nonnutritive muscle blood flow. Furthermore, reduced exercise muscle blood volume in poorly controlled patients may warn clinicians of microvascular dysfunction occurring even before overt microangiopathy.

Cerebral oxygenation during hyperoxia-induced increase in exercise tolerance for untrained men.

This study aimed to investigate the involvement of cerebral oxygenation in limitation of maximal exercise. We hypothesized that O2 supplementation improves physical performance in relation to its effect on cerebral oxygenation during exercise. Eight untrained men (age 27 ± 6 years; VO2 max 45 ± 8 ml min(-1) kg(-1)) performed two randomized exhaustive ramp exercises on a cycle ergometer (1 W/3 s) under normoxia and hyperoxia (FIO2 = 0.3). Cerebral (ΔCOx) and muscular (ΔMOx) oxygenation responses to exercise were monitored using near-infrared spectroscopy. Power outputs corresponding to maximal exercise intensity, to threshold of ΔCOx decline (ThCOx) and to the respiratory compensation point (RCP) were determined. Power output (W max = 302 ± 20 vs. 319 ± 28 W) and arterial O2 saturation estimated by pulse oximetry (SpO2 = 95.7 ± 0.9 vs. 97.0 ± 0.5 %) at maximal exercise were increased by hyperoxia (P < 0.05). However, the ΔMOx response during exercise was not significantly modified with hyperoxia. RCP (259 ± 17 vs. 281 ± 25 W) and ThCOx (259 ± 23 vs. 288 ± 30 W) were, however, improved (P < 0.05) with hyperoxia and the ThCOx shift was related to the W max improvement with hyperoxia (r = 0.71, P < 0.05). The relationship between the change in cerebral oxygenation response to exercise and the performance improvement with hyperoxia supports that cerebral oxygenation is limiting the exercise performance in healthy young subjects.