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Prediabetes is characterized by elevated glycated hemoglobin and plasma glucose, and its prevalence (~90 million Americans, ~38% of adults) is nearly triple that of type 2 diabetes. Unfortunately, most people with prediabetes progress to type 2 diabetes within 5 years, which is among the top five causes of mortality worldwide. Exercise and diet can prevent this progression in ~60% of people with prediabetes; however, excessive fatigability of limb muscles during exercise impairs physical function and exercise performance in these individuals. Our previous studies show that people with prediabetes have increased fatigability (greater reductions of force and power in the knee extensor muscles) during a bout of exercise due to impairments in the exercising muscle, and the effects are even greater in people with type 2 diabetes. Despite the clear clinical significance, the mechanisms for the excessive fatigability in the muscle are not known and significant knowledge gaps exist regarding the optimal intervention(s) to improve fatigability in these individuals.
Prediabetes is characterized by elevated glycated hemoglobin and plasma glucose, and its prevalence (~90 million Americans, ~38% of adults) is nearly triple that of type 2 diabetes. Unfortunately, most people with prediabetes progress to type 2 diabetes within 5 years, which is among the top five causes of mortality worldwide. Exercise and diet can prevent this progression in ~60% of people with prediabetes; however, excessive fatigability of limb muscles during exercise impairs physical function and exercise performance in these individuals. Our previous studies show that people with prediabetes have increased fatigability (greater reductions of force and power in the knee extensor muscles) during a bout of exercise due to impairments in the exercising muscle, and the effects are even greater in people with type 2 diabetes. Despite the clear clinical significance, the mechanisms for the excessive fatigability in the muscle are not known and significant knowledge gaps exist regarding the optimal intervention(s) to improve fatigability in these individuals.
Our central hypothesis is that impaired vascular function impedes blood flow and blunts subsequent oxygen delivery to skeletal muscle during exercise, resulting in excessive fatigability of the limb muscles in people with prediabetes. We include people with type 2 diabetes (without neuropathy or insulin dependence) to understand fatigability across the disease spectrum and compare them to prediabetes and controls. We will also assess fatigability, skeletal muscle metabolism, capillary density, and vascular function in people with prediabetes and type 2 diabetes before and after a novel training intervention that couples dynamic resistance training with blood flow restriction to the exercising limb. This novel intervention has been shown to improve vascular function in young and older adults but has not been investigated in people with prediabetes and type 2 diabetes.
Our central hypothesis is that impaired vascular function impedes blood flow and blunts subsequent oxygen delivery to skeletal muscle during exercise, resulting in excessive fatigability of the limb muscles in people with prediabetes. We include people with type 2 diabetes (without neuropathy or insulin dependence) to understand fatigability across the disease spectrum and compare them to prediabetes and controls. We will also assess fatigability, skeletal muscle metabolism, capillary density, and vascular function in people with prediabetes and type 2 diabetes before and after a novel training intervention that couples dynamic resistance training with blood flow restriction to the exercising limb. This novel intervention has been shown to improve vascular function in young and older adults but has not been investigated in people with prediabetes and type 2 diabetes.
Funding: National Institute of Health [R01 AG077688]
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