Abstract: Subcutaneous adipose tissue represents about 85% of all body fat. Its major metabolic role is the regulated storage and mobilization of lipid energy. It stores lipid in the form of triacylglycerol (TG), which is mobilized, as required for use by other tissues, in the form of non-esterified fatty acids (NEFA). Neither TG nor NEFA are soluble to any extent in water, and their transport to and out of the tissue requires specialized transport mechanisms and adequate blood flow. Subcutaneous adipose tissue blood flow (ATBF) is therefore tightly linked to the tissue’s metabolic functioning. ATBF is relatively high (in the fasting state, similar to that of resting skeletal muscle, when expressed per 100 g tissue) and changes markedly in different physiological states. Those most studied are after ingestion of a meal, when there is normally a marked rise in ATBF, and exercise, when ATBF also increases. Pharmacological studies have helped to define the physiological regulation of ATBF. Adrenergic influences predominate in most situations, but nevertheless the regulation of ATBF is complex and depends on the interplay of many different systems. ATBF is downregulated in obesity (when expressed per 100 g tissue), and its responsiveness to meal intake is reduced. However, there is little evidence that this leads to adipose tissue hypoxia in human obesity, and we suggest that, like the downregulation of catecholamine-stimulated lipolysis seen in obesity, the reduction in ATBF represents an adaptation to the increased fat mass. Most information on ATBF has been obtained from studying the subcutaneous abdominal fat depot, but more limited information on lower-body fat depots suggests some similarities, but also some differences: in particular, marked alpha-adrenergic tone, which can reduce the femoral ATBF response to adrenergic stimuli.
Alex’s Notes: Whether your goal is weight-gain or weight-loss, a unique focus must be given to subcutaneous adipose tissue. It does make up roughly 85% of all body fat in most people, after all. The reason for this focus is simple: when dieting you want most the weight-loss to be from the fat covering those abs, and when looking to build muscle you want to minimize the amount of fat that is simultaneously gained. Both these goals are regulated by adipose tissue blood flow (ATBF), because if your body can’t access the fat cells, then it can’t utilize them.
The focus here is on subcutaneous white adipose tissue, not visceral fat or brown fat. This stuff is quite unique in that it is specialized in storing triglycerides (TG), with the lipid content constituting 85% of the fat cells by weight. Compare this to most other tissues which are dominated by water, then proteins. Fat cells are also rich in capillaries and clearly innervated as well.
Starting with the “fed” state, because I love eating, fat is delivered to adipocytes (fat cells) as triglycerides packaged within lipoproteins. The lipoproteins for any dietary fat are chylomicrons, while any endogenous fat is circulated within very low-density lipoproteins (VLDL).
“Chylomicron-TG is the preferred substrate for adipose tissue lipid storage, and indeed the fatty acid composition of adipose tissue (i.e., the fatty acids that make up its TG) tends to mirror the composition of an individual’s dietary fat intake.”
When you eat food, chylomicrons show up in circulation for about 2-8 hours after the meal, depending on its fat content, but they peak around three hours and this is when fat storage is greatest. Both insulin and possibly other meal-related factors up-regulate the fat-storing enzyme – lipoprotein lipase (LPL) – and also fatty acid esterification within the fat cells to ensure that their cargo can’t get out. Interestingly,
“After an overnight fast, the upregulation of LPL in adipose tissue is slower than the appearance of the chylomicrons and the well-timed blood flow response, which leads to less efficient lipid storage in adipose tissue after the first meal of the day.”
I want to break for a moment and look at the above quote. There is much discussion – at least in the world of physical culture – about meal timing and composition. Specifically, it is often claimed that you shouldn’t mix fats and carbohydrates in the same meal, at least not in huge proportions of each. Indeed, just last week we learned that saturated fat in the form of butter added to a starchy-carbohydrate meal induces acute insulin resistance. Another side of this is that with limited meals throughout the day, one is bound to break-the-fast, and you thus wonder if it should be predominantly fat or carbohydrate (with protein, obviously).
Getting back to the quote (note the hyperlink source), it appears that after an overnight fast of about 14 hours (dinner at 8pm, breakfast at 10am) leads to greater “spillover” of chylomicron triglycerides, with about only 15% of the fat content in the meal appearing to enter adipose tissue, compared to 48% in the third meal of the day (dinner). For completeness, the uptake for glucose was 12–16% of the carbohydrate content in the meal irrespective of meal order, and skeletal muscle took up 40% the fat and 45% the glucose also irrespective of meal order. I will also add that the meals were all 30g of protein, 110g of carbohydrates, and 35g of fat.
What the above should make perfectly clear is that breakfast should be a fatty meal, at least if you want to minimize fat storage. More generally, up to this point it should also be clear that adipose tissue is highly regulated, and the adipose currency is TGs and fatty acids (FA).
Moving onward to fasting and exercise, ATBF blood flow after an overnight fast is steady around 3 mL per minute per 100g of adipose tissue. This amount is regulated by numerous factors. For instance, blocking capillary nitric-oxide synthesis reduces fasting ATBF by 30-50%, blocking beta-adrenergic receptors have no effect, and blocking alpha-adrenergic receptors increased ATBF. Additionally, inhibiting cyclic-AMP (cAMP) breakdown increases ATBF in both lean and obese people. What is the common theme between all this? Exercise, which is known is increase NO synthesis and cAMP, as well as act on both adrenergic receptors through sympathetic stimulation (i.e. adrenaline).
What is interesting to note is that the exercise-induced increase in ATBF is almost entirely blocked with beta-adrenergic receptor blockage, as well as high doses of nicotinic acid (niacin), suggesting that perhaps the increased ATBF is simply an indirect effect of cardiac output and exercise itself operates directly through lipolysis. More recently, it’s been shown that only thigh-ATBF is increased with leg extensions, conflicting many studies about “spot-reduction.” Although, it could simply be that the ATBF for the thigh was lower to begin with, as gluteal fat has considerably lower fasting ATBF (67% lower) than abdominal fat. Regardless, it is clear that beta-adrenergic receptors are fat-loss “accelerators” while the alpha receptors act more like “brakes.”
As a final note, we must briefly look at obesity. Both fasting and post-prandial ATBF is markedly reduced in obese people, likely because of a diminished responsiveness to adrenaline. Alternatively, it could be that they have a greater preponderance of the lipolysis inhibiting alpha-adrenergic receptors. Or perhaps it is related to insulin resistance. Regardless, a simple calorie deficit will fix many of the issues.
And that is a brief overview of subcutaneous adipose tissue blood flow. It is a very complicated topic, and many experts and gurus alike have attempted to manipulate it for the ultimate fat-burning workouts or muscle-building with minimal fat-gain meal plans. The bottom line is that more research is needed, although some nifty takeaways can be hypothesized (i.e. fatty breakfast).