It is known that postprandial hyperglycemia increases the cardiometabolic risk in both diabetic and non-diabetic patients. Moreover, there is insufficient data on the effectiveness of exercise on preventing Type II diabetes mellitus in individuals with insulin resistance and prediabetes. This study aims to examine the effectiveness of resistance exercise in limiting postprandial hyperglycemia and the necessity of prescribing medication particularly in patients with beta-thalassemia and insulin resistance.
Type II diabetes mellitus is a condition characterized by chronic hyperglycemia due to insufficient insulin production and action and tissue resistance to insulin. Pre-diabetes is also characterized by elevated levels of blood glucose, but not so high as those in diabetes. Existing studies have shown that postprandial hyperglycemia is associated with an increased risk for complications of diabetes, both microvascular and macrovascular, as it contributes to the deficiency of β-pancreatic cells and endothelial dysfunction to a much greater extent than glycosylated hemoglobin (HbA1c) and fasting glucose. The main problem in glycemic control is the glucose peak 1-2 hours after the meal. Therefore, there is a need to investigate whether postprandial exercise can help solve this problem. Βeta-thalassemia is a group of heterogeneous hereditary anemias characterized by decreased or no production of beta-chain hemoglobin, resulting in inefficient erythropoiesis. The three main phenotypes are: a) major b) intermediate and c) heterozygous beta-thalassemia. Major thalassemia occurs in the first 2 years of life with severe anemia and requires systemic transfusions. The intermediate appears later and usually does not need transfusions. The heterozygote is asymptomatic, but some carriers may experience mild anemia. Beta-thalassemia is inherited in an autosomal recessive manner. Patient survival has increased significantly in recent years due to systemic transfusions and early treatment of disease complications. However, multiple transfusions result in the accumulation of large quantities of iron, which is toxic to pancreatic beta cells. Both decreased insulin production and decreased tissue sensitivity to insulin occur and result in pre-diabetes or Type II diabetes. Regarding the effect of exercise on diabetic patients, it is confirmed that it reduces both the blood glucose concentration and hyperglycemia during the day. Resistance exercise increases heat production and oxygen consumption by the muscles, thus increasing metabolic activity and glucose uptake by these muscles. In addition, resistance exercise improves glycemic control without causing hypoglycemia and without affecting fasting glucose. Thus, the aim of this study is examine the effectiveness of resistance exercise in limiting postprandial hyperglycemia in patients with beta-thalassemia and insulin resistance.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
6
2 major muscle groups (lower extremity, chest)
Exercise Biochemistry Laboratory, School of Physical Education & Sports Sciences, University of Thessaly
Trikala, Greece
Changes in blood glucose
Concentration of blood glucose will be measured in serum
Time frame: Pre-breakfast (fasting glucose), 45 min post-breakfast (before exercise), immediately post-exercise, 1 hour post-exercise, 2 hours post-exercise, 24 hours post-exercise
Changes in blood insulin
Concentration of blood insulin will be measured in serum
Time frame: Pre-breakfast (fasting glucose), 45 min post-breakfast (before exercise), immediately post-exercise, 1 hour post-exercise, 2 hours post-exercise, 24 hours post-exercise
Changes in blood triglycerides
Concentration of blood triglycerides will be measured in serum
Time frame: Pre-breakfast (fasting glucose), 45 min post-breakfast (before exercise), immediately post-exercise, 1 hour post-exercise, 2 hours post-exercise, 24 hours post-exercise
Body mass
Body mass (kg) will be measured with Beam Balance-Stadiometer (SECA, Vogel \& Halke, Hamburg, Germany)
Time frame: At the baseline and before each trial
Body height
Body height (m) will be measured with Beam Balance-Stadiometer (SECA, Vogel \& Halke, Hamburg, Germany)
Time frame: At the baseline
Body fat
Body fat (kg and percentage) will be measured with Dual-emission X-ray absorptiometry (GE Healthcare, Lunar DPX-NT)
Time frame: Before each trial
Resting heart rate
Resting heart rate (beats per minute) will be monitored using Team Polar (Polar Electro Oy, Kempele, Finland)
Time frame: At the baseline and before each trial
Heart rate during exercise
Heart rate (beats per minute) will be monitored using continuous heart rate measurements (Team Polar, Polar Electro Oy, Kempele, Finland)
Time frame: During exercise in each trial
Changes in total antioxidant capacity
Concentration of total antioxidant capacity will be measured in serum
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
Changes in reduced glutathione (GSH)
Concentration of GSH will be measured in erythrocyte lysate
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
Changes in catalase
Concentration of catalase will be measured in erythrocyte lysate
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
Changes in uric acid
Concentration of uric acid will be measured in serum
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
Changes in protein carbonyls
Concentration of protein carbonyls will be measured in plasma
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
Changes in substances that react with thiobarbituric acid (TBARS)
Concentration of TBARS will be measured in plasma
Time frame: Pre-breakfast (fasting glucose), immediately post-exercise, 24 hours post-exercise
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