Aims/hypothesis <p>The aim of this work was to compare the cardiopulmonary, sympathoadrenal and metabolic responses to physical exercise in adults with type 1 diabetes with or without cardiovascular autonomic neuropathy (CAN).</p> Methods <p>Data collected during a graded maximal exercise test (GXT) from 24 participants with type 1 diabetes and CAN were compared against 24 matched control individuals without CAN (NO CAN). Throughout exercise, integrated cardiopulmonary variables were obtained continuously via spiroergometry. Plasma concentrations of adrenaline (epinephrine), noradrenaline (norepinephrine), glucose (PG) and lactate (PLa) were measured in 3 min intervals during exercise as well as at the peak workload. Data were assessed via independent <i>t</i> tests and two-factor ANOVAs with significance accepted at <i>p</i>≤0.05.</p> Results <p>Participants with CAN displayed a reduced <InlineEquation ID="IEq1"> <EquationSource Format="TEX">\({\dot{V}\text{O}}_{2\text{peak}}\)</EquationSource> <EquationSource Format="MATHML"><math> <msub> <mrow> <mover accent="true"> <mi>V</mi> <mo>˙</mo> </mover> <mtext>O</mtext> </mrow> <mrow> <mn>2</mn> <mtext>peak</mtext> </mrow> </msub> </math></EquationSource> </InlineEquation> (CAN 19.6&#xa0;±&#xa0;5.4 vs NO CAN 27.5&#xa0;±&#xa0;7.8 ml kg<sup>−1</sup> min<sup>−1</sup>) as well as attenuations in several other cardiopulmonary, lactate and exercise performance variables during GXT. Peak catecholamine concentrations were lower in CAN vs NO CAN (AD 0.17&#xa0;±&#xa0;0.12 vs 0.38&#xa0;±&#xa0;0.27 ng/ml, <i>p</i>=0.002; NAD 1.86&#xa0;±&#xa0;1.04 vs 2.85&#xa0;±&#xa0;1.23 ng/ml, <i>p</i>=0.007) as were the magnitudes of change in hormonal concentrations from rest to peak workloads (adrenaline Δ +0.13&#xa0;±&#xa0;0.12 vs Δ +0.32&#xa0;±&#xa0;0.24 ng/ml, <i>p</i>=0.005; noradrenaline Δ +1.33&#xa0;±&#xa0;0.89 vs Δ +2.33&#xa0;±&#xa0;1.30 ng/ml, <i>p</i>=0.005). PG concentrations throughout exercise were similar between groups and remained unchanged from rested values irrespective of CAN status.</p> Conclusions/interpretation <p>In adults with type 1 diabetes, CAN was associated with exercise intolerance characterised by impairments in various cardiopulmonary, sympathoadrenal system and metabolic responses to GXT. These data support uncovering the presence of CAN when prescribing a personalised physical training plan.</p> Graphical Abstract <p></p>

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Impact of cardiovascular autonomic neuropathy on cardiopulmonary, sympathoadrenal and metabolic responses to physical exercise in adults with type 1 diabetes

  • Olivia M. McCarthy,
  • Rasmus B. Brødsgaard,
  • Sandra Tawfik,
  • Sissel Banner Lundemose,
  • Emilie B. Lindkvist,
  • Sara H. Naaman,
  • Christian Stevns Hansen,
  • Richard M. Bracken,
  • Kirsten Nørgaard

摘要

Aims/hypothesis

The aim of this work was to compare the cardiopulmonary, sympathoadrenal and metabolic responses to physical exercise in adults with type 1 diabetes with or without cardiovascular autonomic neuropathy (CAN).

Methods

Data collected during a graded maximal exercise test (GXT) from 24 participants with type 1 diabetes and CAN were compared against 24 matched control individuals without CAN (NO CAN). Throughout exercise, integrated cardiopulmonary variables were obtained continuously via spiroergometry. Plasma concentrations of adrenaline (epinephrine), noradrenaline (norepinephrine), glucose (PG) and lactate (PLa) were measured in 3 min intervals during exercise as well as at the peak workload. Data were assessed via independent t tests and two-factor ANOVAs with significance accepted at p≤0.05.

Results

Participants with CAN displayed a reduced \({\dot{V}\text{O}}_{2\text{peak}}\) V ˙ O 2 peak (CAN 19.6 ± 5.4 vs NO CAN 27.5 ± 7.8 ml kg−1 min−1) as well as attenuations in several other cardiopulmonary, lactate and exercise performance variables during GXT. Peak catecholamine concentrations were lower in CAN vs NO CAN (AD 0.17 ± 0.12 vs 0.38 ± 0.27 ng/ml, p=0.002; NAD 1.86 ± 1.04 vs 2.85 ± 1.23 ng/ml, p=0.007) as were the magnitudes of change in hormonal concentrations from rest to peak workloads (adrenaline Δ +0.13 ± 0.12 vs Δ +0.32 ± 0.24 ng/ml, p=0.005; noradrenaline Δ +1.33 ± 0.89 vs Δ +2.33 ± 1.30 ng/ml, p=0.005). PG concentrations throughout exercise were similar between groups and remained unchanged from rested values irrespective of CAN status.

Conclusions/interpretation

In adults with type 1 diabetes, CAN was associated with exercise intolerance characterised by impairments in various cardiopulmonary, sympathoadrenal system and metabolic responses to GXT. These data support uncovering the presence of CAN when prescribing a personalised physical training plan.

Graphical Abstract