Body fat is stored as triglycerides (TG) in the adipose tissue, the fat cells and some cells inside and abdominal viscera. Adipocyte has two enzymatic systems of control of metabolism, influenced by the neuroendocrine system, conditions of intake and physical activity. The enzyme lipase hormone sensitive (LHS) catalyzes the degradation of the TG to free fatty acids (AGL) and glycerol (Gl), this last is released into the plasma and is used as a measure of the magnitude of lipolysis, and can also be a gluconeogenico in the liver substrate; Meanwhile the enzyme endothelial lipase lipoprotein (LPL) which is optimally active at acidic ph, catalyzes the synthesis of TG from AGL and Gl. Insulin stimulates the LPL as contrainsulares hormones stimulate the reverse pathway (LHS): glucagon, adrenaline, VIVO norepinephrine and cortisol, growth hormone, the antidiuretic, the melanocitoestimulante, the adrenocorticotrophin, the parathormone (PTH) and vitro thyroid hormone have a permissive effect. On the other hand (by stimulation of Phosphodiesterase) insulin, lactate and ketone bodies inhibit the LHS.
Adipose tissue possesses both receptors stimulating adrenergic beta of lipolysis (via stimulation of Adenylate Cyclase) whose action prevails during the exercise, as also inhibitory Alpha receptors whose action modulates lipolysis during rest, regulating metabolism. There are also receptors beta 3 whose stimulation causes release of leptin from the Adipocyte, which mediates satiety response to hypothalamic level. Adiposity in the intra-abdominal area related with different clinical entities is the most active area from the point of view lipolytic and relates to the prevalence of receivers adrenergic beta. Despite mobilize a significant amount of AGL, not contribute largely to the energy used for physical activity. Most of AG that would contribute to muscle activity would be derived from abdominal subcutaneous adipose tissue and to some extent of intramuscular triglycerides (TGIM).
The AGL can be reesterificados in the Adipocyte, to form new TG in a process known as "fatty acid triglyceride cycle-". But the muscle activity in most uses as fuel rather than for the re-esterification processes. Although the available evidence points out that reesterificarse in muscles not involved can directly in the exercise or into motor units inactive muscles involved in submaximal exercise.
TG of adipose tissue sources are various: glucose, amino acids, the chylomicrons TG and lipoproteins of low density (LDL) from the diet and from liver lipoproteins of very low density (LMBD).
As the provision of skeletal muscle activity in power comes from the AG related to plasma albumin, the TG to LMBD, possibly the FA released by fat cells attached to myocytes and also the TGIM.
Some studies evidenced a contribution of up to 10% of the total energy supplied during the exercise in conditions of fasting in males, although it may be higher in women.
Adipocyte is metabolically very active, considering the cytoplasmic mass isolated content of TG constituting about 90%. Similarly the TG stored far from being metabolically inert, they experience a continuous replacement.
The AGL (in fact the more accurate term would be to call them acids not esterified fatty: AGNE) freed from the adipose tissue are transported to their destinations, mostly attached to albumin, are not truly free except in a very small amount. You can go to the liver and reesterificarse forming again TG or esterified cholesterol, rust forming carbon dioxide (CO2), forming phospholipids, or rust forming incompletely ketone bodies. They can also go to the muscle and used for the formation of ATP in the Krebs cycle in the presence of oxygen.