The Higher the Insulin Resistance the Lower the Cardiac Output in Men with Type 1 Diabetes During the Maximal Exercise Test

Abstract

Background:

The aim of this study was to assess the hemodynamic parameters analyzed in bioimpedance cardiography during maximal exercise in patients with type 1 diabetes differing in insulin resistance.

Methods:

The study group consisted of 40 men with type 1 diabetes. Tissue sensitivity to insulin was assessed on the basis of the glucose disposal rate (GDR) analyzed during hyperinsulinemic–euglycemic clamp. Patients were divided into groups with GDR <4.5 mg/kg/min (G1 group—lower insulin sensitivity) and GDR ≥4.5 mg/kg/min (G2 group—higher insulin sensitivity). During the exercise test, the heart rate, systolic volume, cardiac output, cardiac index were measured by the impedance meter (PhysioFlow).

Results:

Compared with the G2 group, the G1 group had a lower cardiac output (CO): during exercise 8.6 (IQR 7.7–10.0) versus 12.8 (IQR 10.8–13.7) L/min; P < 0.0001, at the maximal effort 13.1 (IQR 12.2–16.7) versus 18.6 (IQR 16.9–20.2) L/min; P = 0.001, and during observation after exercise 8.4 (IQR 6.3–9.6) versus 11.9 (IQR 10.1–13.1) L/min; P < 0.0001. We noticed a positive correlation of GDR and cardiac output: during the exercise test (r = 0.63, P = 0.0002), at the maximal effort (Rs 0.56, P = 0.001), and during observation after the exercise test (r = 0.72, P < 0.0001). In multivariate logistic regression, cardiac output during exercise and during observation was associated with high GDR, regardless of the age and duration of diabetes [OR: 1.98 (95% CI 1.10–3.56), P = 0.02 and OR: 1.91 (95% CI 1.05–3.48), P = 0.03; respectively].

Conclusion:

In nonobese subjects with type 1 diabetes, with good metabolic control, insulin resistance is associated with cardiac hemodynamic parameters assessed during and after exercise. The higher the insulin resistance the lower the cardiac output during maximal exercise in men with type 1 diabetes.

Introduction

Physical activity has clear beneficial effects on glycemic control in patients with prediabetes and type 2 diabetes, and is widely recommended in prevention and management of these conditions.¹ It is likely that regular physical activity has a positive effect on overall health in patients with type 1 diabetes through modification of concomitant risk factors. Physical activity improves cardiorespiratory fitness and psychological status.²

Physical activity plays an important role in management of diabetes. There are several benefits of physical activity. It increases physical fitness, muscle strength, improves glycemic control, reduces insulin requirement, and ameliorates lipid profile, blood pressure, and endothelial function.³ Previous studies have shown that physical activity could increase insulin sensitivity⁴ and decrease the risk of chronic complications.^5,6

In studies by Gusso et al.,⁷ patients with diabetes in comparison with nondiabetic controls had reduced aerobic capacity and reduced heart rate response to maximal exercise. Moreover, the stroke volume during submaximal exercise was lower in patients with diabetes. Patients with type 1 diabetes also have an impaired left ventricular diastolic response to acute exercise, which is associated with glycemic control.⁸ Several studies have analyzed the cardiac response to exercise in patients with diabetes, but there are no data on the association of the cardiac function and insulin sensitivity.

Several observations suggest that insulin resistance has direct effects on vascular and cardiac function. Insulin plays a role in physiologic functions of the heart and vasculature.⁹ Insulin resistance is also associated with impaired selective signaling pathways, which results in structural and functional alterations in both peripheral vessels and myocardium.¹⁰ Insulin resistance is associated with impaired endothelium-dependent vasodilation.^11,12

One of the tools that make it possible to measure hemodynamic parameters during exercise is impedance cardiography (ICG). It uses change in impedance of an alternating current applied across the thorax to determine various hemodynamic parameters, such as stroke volume, cardiac output, and cardiac index.¹³ During ICG monitoring, a low-amplitude, high-frequency electrical signal is transmitted from sensors placed on the neck and thorax, each of which has a transmitter and receiver.¹⁴ The newest generation of ICG products uses improved computer technology with faster signal processing, filtering, and better electrocardiographic triggering.¹⁵

There are observations in people with type 2 diabetes, hypertension, and subclinical vascular disease, in whom insulin resistance was not measured exactly, that cardiac output (CO) is reduced.¹⁶ It is possible that hyperglycemia can decrease CO. To explore whether insulin resistance is associated with lower CO, healthy type 1 diabetes patients, without confounders for reduced CO and without apparent insulin resistance, were included in the study.

The aim of this study was the assessment of hemodynamic parameters analyzed in bioimpedance cardiography during maximal exercise in patients with type 1 diabetes differing in insulin resistance.

Materials and Methods

The study group consisted of 40 Caucasian men with type 1 diabetes. We excluded eight patients, five due to exclusion criteria: presence of hypertension (1), chronic complications of diabetes (3), acute inflammation (hsCRP >10 mg/L), with episodes of severe hypoglycemia or diabetic ketoacidosis (DKA) within 1 month before the test (1), and three patients were excluded before clamp procedure because of hypoglycemia and ketonemia. Finally, we took into consideration a group of 32 men with type 1 diabetes. The median age was 33.5 years (IQR 28.3–38.3), median duration of diabetes 6.7 years (IQR 6.1–7.3) with median HbA1c 6.9% (IQR 6.3–7.3), and median body mass index (BMI) of 25.7 kg/m² (IQR 24.4–28.3) (Table 1). There was no significant difference in physical activity in the last 7 days before the study, as declared in the International Physical Activity Questionnaire (IPAQ). All the subjects were informed about the aim of the study and provided their written consent. The study was approved by the local ethics committee. All patients were treated with intensive insulin therapy.

Table 1.

Characteristic of Study Group, Group with Glucose Disposal Rate <4.5 mg/kg/min and with Glucose Disposal Rate ≥4.5 mg/kg/min (with Comparison of Two Subgroups)

Rated variables	Study group	Group with GDR <4.5 mg/kg/min	Group with GDR ≥4.5 mg/kg/min	P^a
N	32	17	15	—
Age [years]	33 (28–38)	35 (31–39)	31 (27–38)	0.08
Duration of diabetes [years]	6.8 (6.3–7.3)	6.6 (6.1–7.1)	6.8 (6.5–7.5)	0.09
Smoking [n] (%)	12 (37.5)	7 (43)	5 (33)	0.55
Body weight [kg]	86.5 (79.5–92.5)	88 (82.0–910)	86.0 (78.0–94.0)	0.59
BMI [kg/m²]	25.6 (24.4–28.2)	25.8 (25.2–28.4)	21.5 (19.8–23.5)	0.19
Daily insulin dose [U/kg body weight/day]	0.39 (0.31–0.49)	0.41 (0.31–0.51)	0.40 (0.33–0.48)	0.67
HbA1c [%]	6.6 (6.1–7.3)	6.4 (6.2–7.0)	7.0 (6.0–7.6)	0.39
HbA1c [mmol/mol]	48.6 (43.2–56.3)	46.4 (44.3–53.0)	53.0 (42.1–59.6)	0.39
FPG [mmol/L]	8.4 (6.2–9.9)	8.1 (6.2–10.5)	8.5 (6.2–9.4)	0.90
PPG [mmol/L]	8.6 (8.1–10.3)	8.4 (8.1–11.6)	8.7 (8.0–9.8)	0.73
hsCRP [mg/L]	0.8 (0.3–1.8)	1.3 (0.45–1.94)	0.77 (0.17–1.60)	0.18
TG [mmol/L]	0.84 (0.57–1.14)	0.86 (0.73–1.15)	0.67 (0.49–0.99)	0.10
LDL cholesterol [mmol/L]	3.15 (2.58–3.64)	3.31 (2.94–3.67)	2.71 (2.35–3.20)	0.06
HDL cholesterol [mmol/L]	1.68 (1.39–1.81)	1.57 (1.30–1.73)	1.75 (1.60–1.91)	0.15
GFR (MDRD) [mL/min/1.73 m²]	100.5 (90.6–107.7)	102.1 (92.4–105.7)	97.5 (88.2–110.2)	0.90

Median (IQR) or n (%). Mann–Whitney and chi² test.

Comparison group with GDR <4.5 mg/kg/min and with GDR ≥4.5 mg/kg/min.

BMI, body mass index; HbA1c, glycated hemoglobin; FPG, fasting glycemia; GDR, glucose disposal rate; PPG, 2-hr postprandial glycemia; hsCRP, high-sensitivity C-reactive protein; TG, triglycerides; LDL, low-density lipoproteins; HDL, high-density lipoproteins; GFR, glomerular filtration rate estimated using Modification of Diet in Renal Disease (MDRD) study equation.

Blood samples were collected in a fasting state using the S-Monovette blood collection system. Plasma glucose, serum total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride levels were measured using standard methods. Serum C-reactive protein (CRP) concentration was assessed by a highly sensitive microparticle enzyme immunoassay. The colorimetric Jaffé method was used for the measurement of creatinine. HbA1c (glycated hemoglobin) was measured using high-performance liquid chromatography with the Variant Hemoglobin A1c Program (Bio-Rad Laboratories, Hercules, CA). The glomerular filtration rate was calculated according to the Modification of Diet in Renal Disease Study Equation.¹⁷

Hyperinsulinemic–euglycemic clamp

Tissue sensitivity to insulin was assessed on the basis of the glucose disposal rate (GDR) analyzed during the hyperinsulinemic–euglycemic clamp. The study was conducted in the morning after a 12-hr period without calorie intake. During the clamp procedure, to achieve hyperinsulinemia, intravenous infusion of insulin was administered, with an infusion rate calculated as 0.06 U/kg/hr. We used a variable of 20% dextrose infusion (with an initial dose of 2 mg/kg/min) adjusted every 5 min according to the plasma glucose level to maintain target glucose (90–99 mg/dL). The rate of glucose infusion during the last 30 min of the test, after obtaining stable glucose values, determines tissue sensitivity to insulin (GDR). The total duration of clamp procedure was between 3 and 4 hr. The cutoff point of GDR used in analysis was 4.5 mg/kg/min and it was calculated from median GDR of the study group. We divided the group of patients into groups with GDR <4.5 mg/kg/min (G1 group—lower insulin sensitivity) and GDR ≥4.5 mg/kg/min (G2 group—higher insulin sensitivity).

Exercise testing

The exercise test was performed 48 hr after the hyperinsulinemic–euglycemic clamp procedure, 2 hr after the meal. Exclusion criteria were occurrence of hypoglycemia 2 hr before the exercise, hyperglycemia above 250 mg/dL, and presence of ketonemia.¹⁸

Bioelectric impedance recordings

The impedance meter used in our study is PhysioFlow PF-07 Enduro from Manatec Laboratories (Paris, France). It is a noninvasive measurement system that can be used on patients under exercise conditions. It provides hemodynamic parameters computed from the analysis of thoracic electrical bioimpedance signals. PhysioFlow measures the change in impedance by injecting a high-frequency alternating electrical current (66 kHz) of low magnitude (3.8 mA) toward the thorax between a pair of electrodes positioned on the neck and another pair positioned on the xiphoid process. Two electrodes for electrocardiogram were added to have a time base for the impedance signal.

PhysioFlow measures the heart rate [HR (bpm)], systolic volume [SV (mL)–amount of blood pumped by the left ventricle per heartbeat], cardiac output [CO (L/min)–amount of blood pumped by the left ventricle per minute], and cardiac index [CI (L/min/m²)–cardiac output normalized for body surface area].

The test was performed in a half-sitting position on the ergometer (Ergoselect 200P; Ergoline, GmbH). Before each test, the calibration procedure was performed (24 consecutive heartbeats recorded by PhysioFlow with the subject at rest in a half-seated position on the ergometer).

Each exercise test was preceded by 3 min of resting recordings with the subject seated on the ergometer. The initial work rate of 0 W lasted 1 min. The participant pedals at a constant rate of 60 rpm while the work load is increased by 20 W every minute. Participants reported their perceived exertion on the Borg scale (0–10 scale) every minute. The maximal effort was attested as the subjects reached the following criteria: (1) HR higher than 90% of age-predicted maximal heart rate and (2) 9 or 10 in the Borg scale. After the exercise, the patient was observed in a sitting position for 10 min. Each test was conducted and analyzed by the same person.

Statistical analyses

Statistical analyses were performed using Statistica 8.0 (StatSoft, Tulsa). After testing for data distribution normality and variances homogeneity, nonparametric tests were used for further analyses. The Mann–Whitney test was used for comparison of groups (with higher and lower insulin sensitivity). Spearman correlation of hemodynamic parameters and GDR was performed. Multivariate logistic regression was used to determine an independent relationship of cardiac output with occurrence of high GDR (≥4.5 mg/kg/min). Multivariate regression was performed to analyze influence of selected factors on cardiac output. P < 0.05 was considered as statistically significant. All results were expressed as median and IQR (interquartile range) and n (%).

Results

In statistical analyses, we compared groups with GDR above and below 4.5 mg/kg/min. We did not observe statistically significant differences between groups for age, duration of diabetes, BMI, daily insulin dose, HbA1c, lipid profile, and smoking status (Table 2). Groups also did not differ in physical activity in the last 7 days before the study, as declared in the IPAQ. During the exercise test, the analyzed groups had similar glycemia before and after exercise.

Table 2.

Comparison Group with Glucose Disposal Rate <4.5 mg/kg/min and with Glucose Disposal Rate ≥4.5 mg/kg/min—Parameters Analyzed During Exercise Test

	Group with GDR <4.5 mg/kg/min	Group with GDR ≥4.5 mg/kg/min	P
Duration of exercise [min]	11.1 (9.7–12.0)	12.3 (9.7–14.0)	0.15
Glycemia before exercise [mmol/L]	7.7 (6.3–11.0)	8.9 (7.2–11.0)	0.46
Glycemia after exercise [mmol/L]	7.7 (6.1–8.6)	9.0 (7.1–9.6)	0.43
Maximum watt	200 (180–220)	240 (200–260)	0.007
HR (heart rate) [bpm]
Before exercise	91 (88–95)	79 (74–86)	0.02
At maximal effort	172 (158–180)	177 (169–187)	0.14
Net difference from exercise	78 (70–87)	93 (81–103)	0.02
Mean from exercise	124 (117–130)	125 (121–131)	0.46
Mean from observation	123 (113–133)	124 (116–130)	0.66
SV (stroke volume) [mL]
Before exercise	52 (45–66)	73 (65–83)	0.001
At maximal effort	81 (70–96)	103 (98–122)	0.002
Net difference from exercise	27 (25–36)	35 (26–41)	0.30
Mean from exercise	69 (59–82)	96 (86–102)	0.0008
Mean from observation	68 (55–74)	86 (81–107)	<0.0001
CO (cardiac output) [L/min]
Before exercise	4.9 (4.2–5.5)	5.9 (5.1–6.4)	0.03
At maximal effort	13.1 (12.2–16.7)	18.6 (16.9–20.2)	0.001
Net difference from exercise	8.7 (7.5–10.9)	12.5 (11.1–14.0)	<0.0001
Mean from exercise	8.6 (7.7–10.0)	12.8 (10.8–13.7)	<0.0001
Mean from observation	8.4 (6.3–9.6)	11.9 (10.1–13.1)	<0.0001
CI (cardiac index) [L/min/m²]
Before exercise	2.3 (2.0–2.6)	2.9 (2.7–3.1)	0.009
At maximal effort	6.5 (5.6–7.7)	9.7 (8.3–10.5)	0.0002
Net difference from exercise	4.1 (3.5–5.3)	6.2 (5.4–6.6)	0.001
Mean from exercise	4.3 (3.7–4.6)	6.4 (5.6–6.6)	<0.0001
Mean from observation	4.0 (3.0–4.5)	6.0 (5.1–6.3)	<0.0001

Median (IQR). Mann–Whitney Test.

Mean from exercise—average of all measurements performed during exercise test.

Mean from observation—average of all measurements performed during observation period.

The analyzed groups achieved maximal exhaustion after 11.7 min of exercise, in G1 after 12.3 min (IQR 9.7–14.0) and in G2 after 11.1 min (IQR 9.7–12.0), P = 0.12. G1 group achieved maximal load of 240 watt (IQR 200–260) and G2 group achieved 200 watt (IQR 180–220), P = 0.007. The maximal heart rate in G1 group was 177/min (IQR 169–187) and in G2 was 172/min (IQR 158–180), P = 0.12.

Compared to G2, group G1 was characterized by a lower cardiac output (CO): during exercise, 8.6 (IQR 7.7–10.0) versus 12.8 (IQR 10.8–13.7) L/min, P < 0.0001; at the maximal effort, 13.1 (IQR 12.2–16.7) versus 18.6 (IQR 16.9–20.2) L/min, P = 0.001; and during observation, after exercise 8.4 (IQR 6.3–9.6) versus 11.9 (10.1–13.1) L/min, P < 0.0001.

Stroke volume was significantly higher in a group with GDR ≥4.5 mg/kg/min: before exercise: 73 (IQR 65–83) versus 52 (IQR 45–66) mL, P = 0.001; during exercise: 96 (IQR 86–102) versus 69 (IQR 59–82) mL, P = 0.0008; at the maximal effort: 103 (IQR 98–122) versus 81 (IQR 70–96) mL, P = 0.002; and during observation: 86 (IQR 81–107) versus 68 (IQR 55–74) mL, P < 0.0001.

Cardiac index was higher in the insulin sensitive group before exercise: 2.9 (2.7–3.1) versus 2.3 (2.0–2.6) L/min/m², P = 0.009; during exercise: 6.4 (5.6–6.6) versus 4.3 (3.7–4.6) L/min/m², P < 0.0001; at the maximal effort: 9.7 (8.3–10.5) versus 6.5 (5.6–7.7) L/min/m², P = 0.0002; and during observation: 6.0 (5.1–6.3) versus 4.0 (3.0–4.5) L/min/m², P < 0.0001. All the results are shown in Table 2.

Also, a significant positive correlation between GDR and stroke volume was observed: before exercise (Rs 0.58, P = 0.001), during the exercise test (Rs 0.67, P < 0.0001), at the maximal effort (Rs 0.58, P = 0.001), and during observation after the exercise test (Rs 0.72, P < 0.0001). We noticed a positive correlation of GDR and cardiac output: during the exercise test (Rs 0.63, P = 0.0002), at the maximal effort (Rs 0.56, P = 0.001), and during observation after the exercise test (Rs 0.72, P < 0.0001). The cardiac index was correlated positively with GDR: before exercise (Rs 0.41, P = 0.02), during the exercise test (Rs 0.69, P < 0.0001), at the maximal effort (Rs 0.66, P < 0.0001), and during observation (Rs 0.70, P < 0.0001) (Table 3).

Table 3.

Correlation of Glucose Disposal Rate with Heart Rate, Stroke Volume, Cardiac Output, and Cardiac Index Assessed During Exercise Test (Spearman Correlation)

	Spearman correlation coefficient	P
HR (heart rate) [bpm]
Before exercise	−0.57	0.001
At maximal effort	0.14	0.45
Mean from exercise	−0.02	0.89
Mean from observation	−0.03	0.86
SV (stroke volume) [mL]
Before exercise	0.58	0.001
At maximal effort	0.58	0.001
Mean from exercise	0.67	<0.0001
Mean from observation	0.72	<0.0001
CO (cardiac output) [L/min]
Before exercise	0.33	0.08
At maximal effort	0.56	0.001
Mean from exercise	0.63	0.0002
Mean from observation	0.66	0.0001
CI (cardiac index) [L/min/m²]
before exercise	0.41	0.02
At maximal effort	0.66	<0.0001
Mean from exercise	0.69	<0.0001
Mean from observation	0.70	<0.0001

Mean from exercise—average of all measurements performed during exercise test.

Mean from observation—average of all measurements performed during observation period.

In multivariate logistic regression, cardiac output during exercise and during observation was associated with high GDR (≥4.5 mg/kg/min), regardless of age and duration of diabetes [OR: 1.98 (95% CI 1.10–3.56), P = 0.02 and OR: 1.91 (95% CI 1.05–3.48), P = 0.03; respectively].

Analysis of selected predictors of cardiac output such as age, BMI, duration of diabetes, and HbA1c was performed in a multivariate regression model. It shows independent influence of GDR on cardiac output during exercise and observation period (Table 4).

Table 4.

Multivariate Analysis of Factors Influencing on Cardiac Output

	Beta	P
Age [years]	−0.17	0.10
Duration of diabetes [years]	0.16	0.86
BMI [kg/m²]	0.05	0.75
HbA1c [%]	−0.33	0.44
GDR [mg/kg/min]	0.66	0.02

BMI, body mass index; HbA1c, glycated hemoglobin.

Discussion

Our study has shown that there are important changes in the hemodynamic variables during exercise according to different insulin sensitivities in patients with type 1 diabetes.

An important question is how insulin resistance influences parameters analyzed during the exercise and how it interferes with cardiovascular fitness. In our study, we did not measure changes in daily physical activity and its influence on insulin sensitivity. However, a very important fact is that compared groups did not differ in declared physical activity. In our study, we focused on measurement of insulin resistance with a clamp technique and parameters from cardiac bioimpedance during the exercise test.

There are numerous proposed mechanisms underlying impaired exercise response in patients with diabetes. These include endothelial dysfunction, altered sympathetic activity, abnormal insulin signaling, and proinflammatory effects of advanced glycation.

Insulin increases skeletal muscle glucose uptake and whole-body oxygen consumption. It was first demonstrated in dogs that insulin has direct effects on the vasculature.¹⁹ It took several years to establish that insulin also exhibits vascular effects in humans. Insulin action plays an important role in redistribution of glucose in tissues. Insulin may change systemic vascular resistance and influence increased blood flow in the muscles.²⁰ Insulin helps in redistribution of cardiac output to insulin-sensitive tissues. All these changes are more effective in insulin-sensitive than in insulin-resistant subjects.²¹

Insulin has important vascular actions by stimulating endothelial production of nitric oxide. This leads to capillary recruitment, vasodilation, and increased blood flow. In insulin-resistant states, there is a shift in balance from the vasodilator to the vasoconstrictor actions of insulin. Vasodilator actions of insulin are mediated by phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathways that stimulate production of nitric oxide from vascular endothelium. Glucotoxicity, lipotoxicity, and inflammation selectively impair PI3K-dependent insulin signaling pathways that contribute to reciprocal relationships between insulin resistance and endothelial dysfunction.¹⁰ In insulin-resistant states, insulin could stimulate secretion of the vasoconstrictor ET-1 (ET-endothelin peptide) from the vascular endothelium.⁹ In a hypertensive rat model, insulin resistance was associated with endothelial dysfunction characterized by imbalance between NO (NO-nitric oxide) and ET-1 production.²²

Insulin resistance may also increase cardiac dysfunction even in the absence of structural heart disease. In animal models, where insulin resistance was induced by a high-cholesterol/fructose diet, rats exhibited a reduction in cardiac output, ejection fraction, stroke volume, and end-diastolic volume.²³ The effect of insulin on stroke volume was also reported by Maaten et al.²⁴ This study suggested that positive inotropic effects of insulin were not related to its vasodilatory effects and might therefore contribute to blood pressure elevation if these effects persist in insulin-resistant conditions.

It has been shown that insulin increases sympathetic nervous system activity.^9,25 Acute physiological and pharmacological euglycemic–hyperinsulinemia increases sympathetic nerve activity as determined by measurements of venous plasma catecholamine concentration²⁶ or direct microneurographic recordings of sympathetic nerve action potentials targeted at the skeletal muscle vasculature.²⁵ Therefore, insulin resistance is associated with an increased sympathetic drive. It was observed that adrenergic activity and heart rate were increased in patients with metabolic syndrome.²⁷ Chronic activation of the sympathetic nervous system may be a pathogenetic mechanism by which hyperinsulinemia induces cardiovascular damage in patients with type 1 diabetes. In our study, we observed a higher heart rate before exercise in a group with lower insulin sensitivity. Also, a negative correlation of the heart rate at the beginning of the exercise test and GDR was noticed. The lower the GDR the higher the pulse at the beginning of exercise.

Our study has some limitations. Association of insulin resistance and hemodynamic variables does not indicate a causal relationship. Measurement of changes in the fitness status or daily physical activity may help in better explanation of the connection of physical activity and insulin sensitivity. Bioimpedance is a noninvasive tool with a large number of subjects already studied in published research,^28
–30 but for better correlation with GDR, repeated hemodynamic measurements in the same individuals would be of value.

In many publications it is emphasized that insulin resistance is connected with type 2 diabetes, metabolic syndrome, and atherosclerosis-related diseases and may ignore independent pathophysiologic contributions of insulin resistance to cardiac function. Our study shows that in nonobese subjects with type 1 diabetes, with good metabolic control, insulin resistance is associated with cardiac hemodynamic parameters assessed during and after exercise. The higher the insulin resistance the lower the cardiac output during maximal exercise in men with type 1 diabetes.

Highlights

• The assessment of hemodynamic parameters during maximal exercise in patients with type 1 diabetes differing in insulin resistance was performed.

• Insulin resistance was assessed by the clamp technique.

• Noninvasive measurement system, the PhysioFlow Enduro, was used to analyze hemodynamic parameters computed from the analysis of thoracic electrical bioimpedance signals.

• In nonobese subjects with type 1 diabetes, insulin resistance is associated with cardiac hemodynamic parameters assessed during and after exercise.

• The higher the insulin resistance the lower the cardiac output during maximal exercise in men with type 1 diabetes.

Footnotes

Acknowledgment

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author Disclosure Statement

No competing financial interests exist.

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