Fatty acids represent a very large source of energy reserve throughout the body. Oxidation of fatty acids during aerobic exercise can prolong physical activity and delay the onset of glycogen depletion. However, although fat deposits are relatively large, the ability to oxidize fatty acids is limited, so carbohydrates are the dominant substrate. The reason for limiting the use of fat deposits may be due to the little information available about the role of fats during exercise, which conditions the understanding of fat metabolism during physical activity. For this reason, exercise development must be supported by a solid conceptual framework, including the contributions of research in the area of Biology.
This work proposes to incorporate fundamental contributions from Biology research to rule out the use of empirical practices without scientific support.
The chosen methodology was the bibliographic search in scientific journals, which allowed to arrive at conclusions of interest. The analysis was divided into three parts:
Mobilization of fatty acids (GA) from adipose tissue.
Transport of GA to muscle.
Consumption of GA by the muscle cell.
The first part refers to the stimulant and inhibitory factors of lipolysis and their relationship with exercise. The second part is dedicated to knowing how the transport of GA towards the muscle is carried out and how it varies according to the intensities of the exercise. The third part deals with the factors involved in the consumption of fatty acids by the muscle cell. These factors should be enhanced by aerobic endurance training.
They are also considered: Other aspects to take into account in lipid metabolism and exercise, such as: age, sex and hormones.
The main objective of this review is to provide Physical Education and Sport professionals with an overview of the knowledge of fat metabolism during exercise, paying special attention to the factors that limit fat oxidation and the effects of exercise on them.
“From then on, openness to criticism and debate is totally welcome since only from it, the less likely can become a little more likely and the erroneous, which always exists in this kind of knowledge, a little less wrong” (Di Santo Mario, 1997).
They were analyzed:
Mobilization of fatty acids (GA) from adipose tissue.
Transport of GA to muscle.
Consumption of GA by muscle cell.
Mobilization of GA from adipose tissue.
1.1. Lipolysis stimulating factors
They are activators of beta adrenergic receptors. According to Horowitz JF (2003) the regulation of lipolysis can vary depending on the adrenergic receptors located in different anatomical sites of the adipose tissue layer or stratum. Variability in lipolytic rate in different adipose tissue layers is related to regional differences in density and function of beta adrenergic receptors (Horwitz, 2001):
Fat cells of intra-abdominal adipose tissue (visceral adipose tissue TAV).
Subcutaneous fat of the abdomen (TASA).
Subcutaneous gluteal and femoral fat.
Intraabdominal adipose tissue is the most lipolitically active deposit and fat accumulation in this region is associated with a wide range of clinical complications (Pasman et al, 2002). GA released from this adipose tissue are taken up by the liver and produce an increase in VLDL (Horwitz, 2001). Despite this increased lipolytic activity, intra-abdominal fat does not contribute significantly to muscle energy production.
Most of the GA released into systemic circulation are derived from subcutaneous adipose tissue (SAD), particularly abdominal subcutaneous adipose tissue because they are more sensitive to beta agonist receptors than subcutaneous buttock and femoral adipose tissue.
TGIMs (intramuscular triglycerides) are “droplets” of lipids deposited within muscle cells. A great deal of evidence suggests that TGIMs provide, at most, between 10 and 55% of total fat oxidation during exercise (Horowitz, 2003). We can also say that it is a fairly controversial point in the literature, since:
Horowitz & Klein (2000) found that total fat oxidation during endurance exercises of moderate intensity was higher in abdominal obese than in lean women, due to an increase in oxidation of non-plasma AGs presumably derived from TGIM.
Steffensen et al (2002) revealed that, despite the degree of training, resting women had a higher TGIM content than men; in addition, regardless of training status, women used higher amounts of TGIM than men during prolonged exercise.
Another potential source of exercise fuel is circulating triglycerides (TG), which are hydrolyzed by lipoprotein lipase (LPL), located in the capillary endothelium of skeletal muscles.
A. Heterogeneous lipolytic activity in different layers of adipose tissue.
Figure 1. Source: Modified graph from Horwitz, JF (2003)
The catecholamines activate the lipolytic cascade, by union with different types of beta adrenoceptors located on the plasma membrane of the adipocytes. The role of the three different adiposite receptors in lipolytic regulation is not well known. The affinity for catecholamines differs among the three adrenoceptors (Horowitz, 2001):
Beta 2 > beta1 > beta 3 for epinephrine
Beta 1 > or = beta 2 > beta 3 for norepinephrine
However, each Beta receptor differs in its resistance to desensitization:
Beta 3 > beta 2 > or = beta 1
This Beta 3 adrenoreceptor is mainly active in omental (visceral) adipocytes and is also present in mammary and subcutaneous fat in vivo.
In this respect, the heterogeneous distribution of the different types of beta receptors in several layers of adipose tissue seems to reflect an important role of these in the regional regulation of lipolysis.
A very important enzyme involved in the regulation of lipolysis in adipose tissue is the Lipase sensitive hormone (LHS), a rate limiting enzyme for the release of fatty acids from triglycerides of adipose tissue into the circulation.
B. Blood flow in adipose tissue (FSTA)
The increase in FSTA is coordinated with the increase in epinephrine produced by low to medium intensity resistance exercises (25 to 65% of maximum VO2), which improves GA lipolysis. It was also found that there is a lack of coordination between FSTA and lipolytic activity when epinephrine concentrations are equal to or greater than 1.6nM. These concentrations cause a decrease in FSTA; however, AGL Ta and Glycerol Ta continue to increase (Horowitz et al, 1999).
However, it is interesting to note that plasma AGL Ta and plasma AGL concentration increased abruptly when exercise ended to 85% and, to a lesser extent, to 65% of maximum VO2. This seems to indicate that the influx of LGA into the plasma after exercise is not associated with increased lipolysis, which may reflect the plasma entry of GA “trapped” in adipose tissue during exercise, possibly due to inadequate blood flow in adipose tissue (Mora-Rodriguez and Coyle, 2000).
The decrease in FSTA during high-intensity exercise results in a decrease in the transport of LFA into the circulation.
C. Lipase Sensitive Hormone (LHS)
LHS is a limiting rate enzyme for the release of TG AG from adipose tissue to the bloodstream. Catecholamines and insulin are the hormones that regulate lipolysis in humans.
In the post-pandrial state, despite the great response to insulin after food, normal suppression in the flow of GA is lower in obese abdominals when compared to lean or obese people in the lower extremities of the body (Berger & Barnard, 1999) (Kim, Yeon et al, 2000). However, LHS is dependent on the size of the fat cell (Berger & Barnard, 1999). Thus, a large mobilization of basal and post-pandrial GA enters circulation in people with abdominal obesity, which appears to be a direct consequence of their excessive subcutaneous abdominal fat mass. This type of people who have a high abdominal obesity also have a high basal lipolytic rate, and present a sharp increase in lipolysis during exercise, if compared with lean people, or with people with obesity in the lower body (Horowitz, 2001).
Inhibitory factors of Lipolysis
It is antagonist of catecholamines and activator of alpha 2 adrenergic receptors that inhibit the activity of the LHS and activate the LPL.
The antilipolytic effects of insulin are greatest in the fat cells of subcutaneous adipose tissue of the lower body, which seem to have higher density of alpha 2 adrenergic receptors and less amount of beta adrenergic receptors.
While prolonged exercises cause an increase in plasma catecholamine HG, they also produce a concomitant reduction in insulin, which favors the release of GA. But carbohydrate intake before or during exercise attenuates this response, raising glucose-insulin and significantly attenuating the catecholamine response to prolonged exercise. In addition, this intake increases the rate of oxidation of carbohydrates (Horowitz et al, 1997).
During low-intensity exercises, lipids are the main source of energy. With increasing exercise intensity, the proportion of energy derived from lipid oxidation decreases. The factors responsible for this reduction in LGA mobilization are:
Low availability of plasma albumin for transporting LGA.
Low blood flow in adipose tissue.
Both favor re-estirification over mobilization.
High plasma lactate, which is an alleged inhibitor of adipose tissue mobilization.
This last inhibiting factor has been called into question by research conducted by Trudeau et al (1999), who dismissed the hypothesis that lactate could exert a direct inhibitory effect on lipolysis. The study was carried out with eight male subjects of 26 years of age, with a good physical condition (59.87ml/kg/min. VO2 maximum). The result of the study suggests:
Lactate applied locally to adipocytes in subcutaneous abdominal adipose tissue does not result in a decrease in fat mobilization from these deposits during exercise.
However, given the specificity of this adipose tissue, this statement cannot be conclusive, as lactate may induce inhibition of lipolysis in other regions of fatty deposits. The suggested mechanisms by which lactate may produce lipolysis inhibition is the decrease of cAMP in adipocytes; decrease in union with adrenoreceptor (Trudeau et al 1999).
Lipopretein lipase (LPL)
LPL is a key regulator of fat accumulation in various adipose areas. It was demonstrated in men with a wide variation of body fat, that triglycerides are taken more by TAV than by TASA. This suggests that other factors – such as LPL – may be important in regulating the intake of TG in adipose tissue, such as Acylation Stimulating Protein (ASP), a strong stimulator of reestirification of AGL and synthesis of TG in human adipose tissue (Waychember, 2000).
Omental adipose tissue has, only in women, small adipocytes and less activity of the LPL than subcutaneous fatty adipocytes. Compared to men, lipid accumulation is greater in the femoral region of premenopausal women. In men, both the activity of LPL and the mRNA levels of the LPL protein were higher in the abdomen than in the fat cells of the buttock; the opposite was observed in women (Wajchenberg, 2000).
Mobilization of GA from adipose tissue during endurance exercises
During low-intensity exercises, 25% of VO2 maximum, lipolysis of adipose tissue (measured as the rate of glycerol appearance in the circulation – Ta glycerol -) increases 2 to 5 times with respect to levels of rest (Mora-Rodriguez and Coyle, 2000). During the same time, the rate of re-esterification decreases, which produces a greater amount of GA released to be oxidized in skeletal muscle. During prolonged low-intensity exercises, the lipolytic rate increases considerably after 4 hours (10 times higher than at rest levels) (Horowitz, 2001).
Although the lipolytic rate remains relatively high with increasing exercise intensity, the release of GA to the circulation declines. The mechanisms responsible for this reduction in GA mobilization are unknown; however, because concentrations increase dramatically immediately after intense exercise, it is believed that the reduction in the release of GA into the circulation may be the result of a restriction of blood flow in adipose tissue resulting from a constriction vessel caused by catecholamines (Mora-Rodriguez & Coyle, 2000).
- Transport from GA to muscle
The transport of fatty acids to the muscle is carried out by means of albumin and blood flow in adipose and muscular tissue.
The low availability of albumin in the blood, plus a reduced blood flow, favours the re-esterification of LFA.
In a study by Mora-Rodriguez and Coyle (2000), it was observed that the rate of appearance (AD) of LGA increased abruptly when exercise ended, to 85% of maximum VO2; to a lesser extent, to 65% of maximum VO2; and was low after exercise to 25% of maximum VO2. This appears to demonstrate the plasma entry of GA “trapped” in adipose tissue during exercise. But, despite a higher lipolytic rate, muscle transport and oxidation of GA is reduced due to a reduction in FSTA.
- Consumption of GA by the muscle cell
The consumption of fatty acids by the muscle cell is limited by what we will call mitochondrial factors. Since fat oxidation occurs in the mitochondria, the increased mitochondrial density, characteristic of resistance training, results in increased fat oxidation and reduced glycolytic flow of both muscle glycogen and blood glucose.
During low-intensity exercise, resistance-trained subjects have a better balance between Td AGL and total fat oxidation than distrained subjects, since the availability of AG does not limit fat oxidation. It is likely, then, that oxidation is limited by mitochondrial factors. In addition, the enzyme that regulates the entry of GA into the mitochondria – Carnitin Palmito transferase I – is considered a limiting rate step in GA oxidation (Mora-Rodriguez and Coyle, 2000).
In people with abdominal obesity, low availability of this enzyme has been found in skeletal musculature, as well as reduced activity of some key mitochondrial oxidation enzymes (Howoritz, 2001).
According to Horowitz (2001), the entry of fatty acids into the muscle is much more complex, and involves a number of transporter proteins: protein-linked plasma membrane AG, translocase fatty acid (FAT/CD36) and AG transporter proteins.
Other aspects to take into account are: age and sex, gender differences, hormones and their receptors in adipose tissue and fasting.
Age and Sex
The amount of visceral fat increases with age in both sexes, and this increase is present in both normal weight subjects (body mass index -BMI- 18.5 to 24.9 kg/m2), overweight subjects (BMI 25 to 29.9) and obese subjects (BMI greater than 30 kg/m2); in addition, it is higher in men than in women ( Wajchemberg, 2000).
It was found that in young women, obese or lean, the area of subcutaneous abdominal fat was predominant over visceral abdominal fat, which were measured by computed tomography (Wajchemberg, 2000). This fat topography was observed in young and middle-aged women; while above the age of 60, a change towards an android type fat distribution was observed. This redistribution of fat is due to a relative and absolute increase in visceral fat deposits, particularly in obese women, which appears to be with an increase in androgenic activity in post-meospáusic women.
In men, a close linear correlation between age and visceral fat volume was demonstrated, suggesting that visceral fat increases continuously with age. This correlation was present in women but with a slight inclination in the premenopausal condition.
The accumulation of fat in visceral adipose tissue explains the difference in cardiovascular risk according to sex.
Differences between sexes
We investigated differences in visceral fat mobilization in obese men and women, with equal BMI and age, who underwent elective surgeries (Wajchenberg, 2000). It was observed that the men presented a large number of fat cells, but there were no lipolytic differences in specific adrenoreceptors beta 1 and beta 2, or in the antilipolytic effect of insulin. However, the lipolytic sensitivity of beta 3 adrenoreceptor was 12 times higher in men than in women, and the sensitivity of alpha 2 antilipolytic adrenoreceptor was 17 times lower in men than in women.
These results were conclusive regarding the role of catecholamines in mobilizing visceral fat LFA to the portal venous system, being higher in men than in women. This factor may contribute to gender-specific differences observed in metabolic disturbances accompanied by obesity.
Friendlander et al (1998) suggest that training may produce better mobilization of subcutaneous abdominal lipids in women than in men due to:
Overregulation of beta adrenergic stimulation.
Low alpha-2 adrenergic inhibitory regulation.
Mobilization and oxidation of GA improved by an interaction of growth hormone and estrogens.
This study contrasts with the research presented by Romjin et al (2000), whose results indicated that metabolic substrates in women trained in endurance respond in a similar way to those of men.
In the study conducted by Mittendorfer et al (2002), the effect of sex on lipid metabolism during endurance exercises of moderate intensity was examined. Men and women with equal adiposity and aerobic condition were evaluated to rule out influences attributed to sex and its relationship with metabolic substrates. The researchers found that:
The whole-body lipolytic rate and availability of plasma LFA was higher in women than in men.
The whole-body oxidation rate of GA was similar in men and women.
The source of GA used as fuel differs between sexes: compared to men, women oxidized more plasma AGL derived from adipose tissue TG and lesser amount of AG derived from TGIM.