Question

What may be the consequences of endurance training for people with the metabolic syndrome? Describe the metabolic defects in the skeletal muscles and in the adipose tissue of people with the metabolic syndrome , and then explain how endurance training could improve these defects in the skeletal muscles and in the adipose tissue . Do not forget to explain how the communication between these 2 tissues is involved in the development of metabolic defects, and how the communication between these 2 tissues is also involved in the improved metabolism in response to endurance training.

Answer 1

Metabolic syndrome (MS) is a group of disorders that occur at the same time and increase the risk of heart disease, stroke, and type 2 diabetes. These include increased blood pressure, high blood sugar levels, excess body fat around the waist and abnormal levels of cholesterol or triglycerides.

Metabolic defects in adipose tissue
The dysfunctional energy storage of the obese people is the key point for the development of MS. Insulin resistance (IR) is a consequence of alterations in the processing and storage of fatty acids and triglycerides (TG) (basic molecules of energy reserve). The physiological trend is the storage of T6 in small peripheral adipocytes, but when the capacity of these cells is exceeded, they accumulate in the muscle and cause IR to insulin from those tissues. The increase in intra-abdominal or visceral adipose tissue causes an increase in the flow of free fatty acids (FFA) to the splanchnic circulation, while derivatives of subcutaneous tissue prevent the hepatic passage and its consequences (increased glucose production, lipid synthesis and secretion of prothrombotic proteins). Dyslipidemia in MS is characterized by elevation of TG and very-low-density lipoproteins (VLDL), decrease in small and dense high lipoprotein (HDL) and low (LDL) density, which has been called atherogenic lipoprotein phenotype The cause of hepatic steatosis could be related to the increase in abdominal and visceral fat, as these adipocytes have great activity, both in lipolysis and lipogenesis. In these patients, the production and release of fatty acids by adipocytes is increased, which contributes a large amount of AGL to the liver, which means, by competitive mechanism, poor utilization of liver glucose.

Metabolic defects in skeletal muscles
Under the action of insulin, skeletal muscle is the largest site for glucose deposition. Therefore, defects in the uptake, storage or use of muscle glucose have an important influence on the pathophysiology of RI and type 2 diabetes (DM2). The explanation lies in the inhibition of the early steps of muscle glucose metabolism: glucose transport by GLUT-4, phosphorylation by hexokinase, and glycogen deposition. In humans, there is a negative relationship between insulin-stimulated glucose metabolism and intramuscular lipid accumulation that includes triglycerides, diacylglycerol, long-chain fatty acid (or FA-CoA), and ceramides. The glucose-fatty acid cycle, in which it basically indicated that excessive lipolysis caused by obesity determined a massive entry of AGL into the muscle, with increased fat oxidation that restricted glucose oxidation by altering the redox potential of the cell and inhibit key glycolytic enzymes.

Effects of resistance training on SM

Skeletal muscle
Physical exercise should be aerobic in people with T2DM, this increases insulin sensitivity and the consumption of muscle and liver glucose favorably influences metabolic control. It should be borne in mind that the indication of the type of exercise, intensity, and duration must be personalized, in order to avoid possible risks. Furthermore, several studies show a strong association between obesity and physical inactivity, in which metabolic syndrome is associated with a sedentary lifestyle and poor cardiorespiratory fitness.
In turn, the greatest reductions in systemic inflammation and improvements in well-being, depression, and sleep have been achieved through combined exercise (strength and resistance training) in people with chronic pain related to inflammation. This is important because it is likely that individuals in a proinflammatory state due to abdominal adiposopathy may also be susceptible to chronic pain conditions. If changes in body composition are more important than the total loss of body weight, then concurrent training would produce optimal effects in improving muscle tissue.
Some direct effects to avoid MS through training are;

• Structural changes of skeletal muscle: Increase in fiber size, percentage of type II fibers and capillary density and blood flow.
• Biochemical changes in skeletal muscle: Increases insulin signaling kinetics, AMPK Activation, Increases the enzymatic machinery for glucose metabolism (hexokinase, glycogen synthetase, citrate synthase, aconitase, among others) and Increases myoglobin synthesis.
• Systemic influence: Increases oxygen uptake and functional working capacity, synthesis of lipoprotein lipase and Decreases excessive production of liver glucose and VLDL, in addition, Improves levels of counter-regulatory hormones and comorbid conditions: hypertension, visceral obesity, inflammation systemic and dyslipidemia.

Adipose tissue
Reductions in abdominal fat deposits through exercise are important because abdominal obesity is a marker of dysfunctional adipose tissue (adiposopathy). Abdominal or visceral obesity plays a central role in the development of a pro-inflammatory state that we now know is associated with MS. If there is a high proportion of fat in the muscle, it is likely that it contributes to this metabolic dysfunction since an increased circulation of free fatty acids requires increased insulin secretion to control glucose metabolism. The resulting hyperinsulinemia desensitizes insulin-sensitive tissues, predisposing people to type II diabetes. Chronic systemic inflammation increases oxidative stress and reduces metabolic flexibility, thereby perpetuating MS, leading to a vicious cycle of illness, depression, and additional inactivity.
Exercise also improves the circulation of oxygen in the body. Adipose tissue hypoxia also occurs, with poor angiogenesis being suggested to cause decreased blood flow due to reduced capillary density and excessive growth of adipose tissue. This can also be exacerbated by the sleep disturbance that is common in obese people and results in a reduction of oxygen in the tissues. In adipose tissue, hypoxia is associated with increased expression of inflammatory genes and decreased expression of adiponectin, resulting in local and systemic inflammation. The response to hypoxia of adipose tissue includes insulin sensitivity and glucose intolerance since adiponectin is associated with normal glucose and lipid metabolism.