Lipid physiology and vascular lesions: Lipid function, lipid transport and the formation mechanism of atherosclerosis

Lipids are essential components of human tissue cells, including phospholipids, glycolipids, sterols, and sterol esters, accounting for approximately 5% of body weight. Lipids can be synthesized in the body and are relatively unaffected by activity levels. Phospholipids are mainly found in cell membranes and blood, and are one of the main components of biological membranes. The total amount of lipids accounts for more than half of membrane weight, and their physicochemical properties are closely related to membrane permeability.

Phospholipids are also surfactants that transport lipids in the body, playing an important role in the formation of lipoproteins and the transport of triglycerides. Furthermore, they are involved in the activity of certain protease enzymes and the transmission of nerve impulses. The lipid layer in the myelin sheath of nerves acts as insulation, facilitating the directional transmission of nerve impulses. Sterols include cholesterol derived from animals and phytosterols.

Cholesterol is an essential substance for the human body. It not only participates in cell membrane formation but is also a raw material for the synthesis of bile acids, steroid hormones, and vitamins. Without cholesterol, cells cannot maintain normal physiological functions. However, a long-term diet high in cholesterol can lead to the deposition of lipids on the inner walls of blood vessels, resulting in narrowing of blood vessels, increased vascular resistance, and high blood pressure.

Atherosclerosis is a vascular disease that leads to serious consequences. It is characterized by lipid deposition in the arterial intima, accompanied by smooth muscle cell proliferation, resulting in thickening and hardening of the vessel wall. It is named for the yellowish, porridge-like appearance of the accumulated lipids. It is mostly caused by lipid metabolism disorders and neurovascular dysfunction. Obesity is essentially a chronic inflammatory state, and inflammatory factors secreted by adipose tissue play a key role in plaque formation.

Obesity-induced inflammatory factors can lead to intimal thickening and endothelial dysfunction. Furthermore, insulin resistance can also induce vascular damage. During the pathological process, any lipoprotein that increases cholesterol influx (such as low-density lipoprotein) can lead to sclerosis, while high-density lipoprotein (HDL) has an anti-sclerotic effect. Therefore, the effects of exercise on weight loss in lowering LDL and increasing HDL are of great health significance.

Long-term participation in moderate-intensity running can significantly improve lipid metabolism and normalize blood lipids. This type of exercise not only burns fat but also increases the sensitivity of tissue cells to insulin. Individuals with higher levels of obesity have lower anaerobic thresholds and should choose low-intensity, long-duration exercises to ensure vascular health.

Cardiac function also improves significantly after exercise and weight loss. Obese individuals often have a large amount of fat accumulated around the heart, causing physical blockage and affecting diastolic function. Through exercise and weight loss, this fat is consumed, increasing the end-diastolic volume of the ventricles, significantly reducing resting heart rate, and increasing stroke volume. This functional morphological change is central to cardiovascular system remodeling.

Warm-up and cool-down activities before and after exercise can effectively prevent myocardial ischemia. This is especially true for obese individuals with cardiovascular insufficiency; warm-up exercises before formal exercise can accelerate blood circulation, while cool-down activities can prevent insufficient blood supply to the brain caused by blood stagnation in the lower limbs.