ECSS Paris 2023: OP-MH42
INTRODUCTION: Reduced heart rate variability (HRV) is an early marker of cardiac autonomic impairment in type 1 diabetes (T1D)1 and has been implicated in the “dead-in-bed” hypothesis of sudden nocturnal death2. Exercise training and higher habitual physical activity (PA) improve HRV3, but single vigorous or prolonged PA bouts can transiently depress parasympathetic activity during the subsequent night3. In T1D, days included these types of bouts are often accompanied by large hypo- and hyperglycaemic excursions4. Outside of the context of PA these glycaemic fluctuations are known to acutely disturb autonomic function5. Whether, in everyday life, the combination of acute PA and glycaemic excursions reflects in altered nocturnal HRV in adults with T1D remains unstudied. METHODS: This secondary pooled analysis included adults with T1D (18-65 years) without known autonomic neuropathy monitored for 1-2 weeks in France and Belgium. Daytime PA was measured by hip-worn accelerometer, glycaemia by continuous glucose monitoring, and overnight R-R intervals by heart rate monitor. For each night, HRV was derived from a single 5-min slow-wave sleep segment. Glycaemic exposure was quantified for an upstream period (wake-up to the HRV segment) and the concomitant 5-min segment using time spent <3.9 and <3.0 mmol/L and >10 and >13.9 mmol/L. Linear mixed models with participant random intercepts tested associations of same-day moderate-to-vigorous PA (MVPA), usual MVPA, and glycaemic metrics with nocturnal HRV, adjusting for age, sex, diabetes duration, and HbA1c. RESULTS: Forty-three participants contributed 173 nights. Higher usual MVPA was associated with higher nocturnal vagal and global HRV. In contrast, higher same-day MVPA predicted lower RMSSD, HF power, SD1, and SDNN during the subsequent night. Greater upstream exposure to level 2 hyperglycaemia (>13.9 mmol/L) was associated with lower RMSSD, HF power, SD1, and SDNN. Other upstream or concomitant hyperglycaemia and hypoglycaemia measures showed no consistent associations. CONCLUSION: In adults with T1D without clinical autonomic neuropathy, higher habitual PA is associated with better nocturnal cardiac vagal modulation, whereas higher acute MVPA is followed by transient overnight reductions in parasympathetic activity and global HRV. Severe daytime hyperglycaemia is also independently associated with lower nocturnal HRV, supporting CGM-guided strategies that minimize marked hyperglycaemia on high-PA days. References: 1 Ewing DJ, et al. BMJ 1982 2 Reno CM, et al. Diabetes 2019. 3 Sandercock GRH, et al. Medicine & Science in Sports & Exercise 2005 4 Riddell MC, et al. The Lancet Diabetes & Endocrinology 2017 5 Koivikko ML, et al. Diabetes 2005
Read CV Léo DuriezECSS Paris 2023: OP-MH42
INTRODUCTION: Type 1 diabetes (T1D) is associated with microvascular and macrovascular complications; however, increasing evidence indicates that skeletal muscle impairment represents an overlooked complication [1]. Although reductions in maximum voluntary contraction (MVC) have been consistently reported, little is known about explosive muscle strength in T1D, particularly the rate of torque development (RTD), which reflects the ability to rapidly generate force [2]. Given the early neural impairments and increased fatigability observed in T1D, the assessment of RTD may provide new insights into muscular dysfunction. Therefore, this study aimed to compare knee extensor RTD between adults with T1D and healthy individuals and to investigate its association with Continuous Glucose Monitoring (CGM) metrics. METHODS: Seventy-seven individuals with T1D (T1D_G, age=40.1 ± 14.8 yrs; BMI=25.98± 4.6 kg/m²; disease duration= 20.7 ± 12.5 yrs; insulin dose= 0.60 ± 0.18 U/kg) and sixty-nine healthy individuals (Control Group, CC, 37.5 ± 13.5 yrs; BMI= 25.2 ± 4.4 kg/m²) performed three maximal isometric knee extensions (90°). RTD was calculated as the slope of the torque–time curve between 20–80% of peak torque and normalized to body mass. In T1D_G, 14-day CGM metrics were collected: Time In Range (TIR), Time Below Range (TBR), Time Above Range (TAR), and Glucose Management Indicator (GMI). Group comparisons and correlations were analysed using parametric or non-parametric tests. RESULTS: Knee extensor RTD normalized for kg of body mass was significantly lower in T1D_G compared with CG (8.37 ± 4.06 vs 9.55 ± 3.53 Nm·s⁻¹·kg⁻¹, U = 3163, p =0.047). In the T1D_G, RTD was positively correlated with TIR (Spearman’s ρ = 0.366, p = 0.001). RTD was negatively correlated with TAR (Pearson’s r = −0.363, p = 0.001) and with GMI (Spearman’s ρ = −0.441, p < 0.001). No significant correlation between TBR and RTD was observed (ρ = 0.221, p = 0.059). CONCLUSION: The lower RTD in T1D_G compared to CG may indicate possible impairment of muscular function.Furthermore, better glycemic control was associated with superior RTD performance. These findings suggest that chronic glycemic dysregulation may contribute to early muscular impairment, even in the absence of clinically evident neuropathy. Therefore, RTD may represent a sensitive functional marker of subclinical muscular dysfunction in individuals with T1D. REFERENCES: 1 Andreo-López et al. Nutrients (2023): 4914. 2 Maffiuletti et al. European journal of applied physiology. 2016: 1091-1116.
Read CV Giovanni GuarascioECSS Paris 2023: OP-MH42
INTRODUCTION: Individuals living with Type 2 diabetes mellitus (T2D) have reduced exercise tolerance and impairments in peripheral and cerebral vascular function. Increases in middle cerebral artery blood velocity (MCAv) are blunted during intermittent incremental exercise in active males with T2D. However, whether this occurs in inactive men and women with T2D, and the underlying mechanisms, is unknown. Herein, this study: 1) compared the MCAv response during ramp exercise in inactive adults with T2D compared to non-T2D controls, and 2) explored relationships between MCAv and ventilatory exercise responses. METHODS: 17 inactive adults with uncomplicated T2D (9 male) and 17 inactive healthy controls (CON) matched for sex, age (51.7±10.7 vs 51.6±9.5 y, P=0.99) and BMI (29.5±5.1 v 28.7±3.8 kg.m-2, P=0.61) participated in this study. Participants completed a ramp incremental cycle test to exhaustion, followed by supramaximal verification of maximal oxygen uptake (V̇O2max). MCAv was measured throughout by transcranial Doppler ultrasound, and end-tidal carbon dioxide (PETCO2) by a metabolic cart (Innocor, Innovision). Data were analysed during unloaded warm-up (baseline), at the gas exchange threshold (GET), respiratory compensation point (RCP) and exhaustion, and expressed in absolute terms and as relative change from baseline (Δ%). The V̇E/V̇CO2 slope was calculated using linear regression. Data were analysed using 2-way mixed model ANOVAs and Pearson correlation. RESULTS: V̇O2max was significantly lower in T2D compared to CON (25.1±4.7 vs 28.3±4.3 ml.kg-1.min-1, P=0.046), with no difference in the V̇E/V̇CO2 slope (P=0.50). Although baseline MCAv was not different between groups (P=0.72), there were effects of exercise intensity (P<0.001) and group (P=0.049) on Δ%MCAv. MCAv increased from baseline to GET in CON (+9.1±10.1%, P=0.001), but not T2D (+3.2±11.3%, P=0.23). Δ%MCAv was significantly lower at exhaustion compared to GET and RCP in both groups (all P<0.001), and fell below baseline at exhaustion in T2D (-11.3±15.2%, P=0.002), but not CON (-2.1±13.0%, P=0.55). Baseline PETCO2 did not differ between groups (P=0.07), and increased from baseline to GET in CON only (+6.9±8.7%, P<0.001, T2D: +2.9±5.4%, P=0.11), before falling below baseline at exhaustion in both groups (all P<0.001) Overall, Δ%MCAv correlated with Δ%PETCO2 and V̇E/V̇CO2 slope at GET (r=0.77, P<0.001, r=-0.45, P=0.007, respectively), RCP (r=0.81, P<0.001, r=-0.56, P<0.001) and exhaustion (r=0.71, P<0.001, r=-0.49, P=0.008), but not with V̇O2max (all r≤0.27, P≥0.12). CONCLUSION: These novel findings demonstrate that inactive adults living with T2D have a blunted MCAv response to incremental exercise. These impairments are closely associated with changes in PETCO2 and ventilatory efficiency (but not V̇O2max), potentially indicating altered CO2-mediated cerebrovascular regulation in T2D.
Read CV Max WestonECSS Paris 2023: OP-MH42