Exercise & Adipose Tissue ~ Part I: Adipose Tissue & General Relationship

From the great research group of Keith Frayn, Aging Hippie linked to this article recently:

PHYSICAL ACTIVITY AND EXERCISE IN THE REGULATION OF HUMAN ADIPOSE TISSUE PHYSIOLOGY

In composing this post, it started to get rather long so I'll break it up into parts.  I'm going to do a bullet-pointed summary and excerpts for you.  Direct quotes will be in italics, regular font is my paraphrased summary, and non-indented/bulleted text is my general commentary.

• Cell types in adipose tissue in addition to adipocytes:  endothelial cells and fibroblast-like adipocyte precursors, macrophages and other leukocytes (particularly in obesity)
• Adipocytes make up 80-90% of adipose tissue volme, but only 60-70% of tissue cell type
• Fat cell turnover rates are conflicting with half-lives estimated of around a year to 8 years.
• Mature adipocyte number appears to remain relatively constant in adulthood
• Blood flow through adipose tissue in the fasting state is greater than that through resting skeletal muscle
• This blood flow is highly regulated and increases rapidly with an ingested meal, especially one containing carbohydrates.
• This blood flow is regulated in fasted state by endothelial nitrous oxide, and in the postprandial state by  β -adrenergic activity (see below).  
• Adipose tissue is highly innervated for the sympathetic nervous system, with some evidence that this acts on adipocytes themselves, but definitely on the vasculature.  This innervation is not uniformally distributed.
• There is debate over the presence of parasympathetic innervation.  (For a nice description of sympathetic vs. parasympathetic mouse-over HERE or click for full reference.)  

On Adipose Tissue Regulation:

Adipose tissue triacylglycerol content reflects energy balance.  Because the body’s capacity to store glycogen is finite and relatively small, long-term imbalances between energy intake and energy expenditure are reflected in a change in the amount of triacylglycerol stored in adipocytes. Adipocyte triacylglycerol content in turn reflects the balance between the processes of fat deposition and fat mobilization. It follows that these processes must be regulated in relation to whole body energy balance. Fat mobilization is readily stimulated by β -adrenergic activation (99, 218). However, the diurnal fluctuation in fat mobilization, which is high after an overnight fast but suppressed after meals, seems to depend more on changing insulin concentrations. Local infusion of propranolol (β -adrenergic blocker) in the postabsortive state does not change lipolysis (8), although phentolamine (α -adrenergic blocker) causes a large increase, suggesting α -adrenergic inhibition of lipolysis.  However, the effect of α -adrenergic blockade may be secondary to changes in blood flow (75). Fat deposition after meals also appears largely to depend on insulin stimulation, which increases the activity of lipoprotein lipase, responsible for hydrolysis of circulating triacylglycerol (270) and increases fatty acid uptake and re-esterification in the adipocytes (69).

Given the wealth of literature on the role of ASP in chylomicron "sensing" and clearance -- e.g. dietary fat -- from circulation, I have to say I'm disappointed that it is not mentioned.  But this wasn't a paper on dietary influences on fat tissue metabolism.  I would like to point to the bolded statement above.   The figure below comes from the article.

There are more hormones than just insulin involved that can alter the balance of fat deposition/mobilization.  Adrenergic activity involves mainly the catecholamines adrenaline and noradrenaline (epinepherine and norepinepherine) on different receptors throughout the body.  Wikipedia has a pretty nice entry on all of this if you're interested.  So what causes "β -adrenergic activation"?  Exercise.  Yet a certain science journalist tells us exercise is useless to alter the balance of fatty acids in our adipose tissue.   But I digress ...

Next the paper defines some terms for exercise and physical activity and some of the problems in assessing TEE (or TDEE).  They use the term PAL for physical activity level and give four examples of how PAL is highly variable and may or may not include decided "spikes" in terms of formal exercise.

In most people, accumulated physical activity (rather than “exercise”) represents the most quantitatively important (and variable) subcomponent of physical activity energy expenditure.

They go on to discuss why moderate exercise interventions have little effect on their own due to the small number of calories involved.

Observational Relationships between Physical Activity and Adiposity:

• ... in general, there appears to be the anticipated inverse relationship between measures of physical activity and measures of fat mass and distribution. 
• Results in large studies have not been consistent
• Cross-sectional studies don't tell us the direction of causation, e.g. does sedentary behavior cause increased adiposity of vice versa?
• Longitudinal studies have been mixed in terms of activity at baseline and future adiposity.  Some have shown no relationship, a modest inverse relationship.

Exercise Interventions:

• Exercise interventions will induce a negative energy balance and consequently reduce fat mass provided dietary compensation or activity the rest of the day is not changed.
• The magnitude of the subsequent reduction in fat mass will ultimately depend on the net energy deficit. 
• Systematic reviews of the literature do demonstrate that exercise interventions do generally effect a reduction in body mass, albeit the size of the reductions are often small (likely due to the magnitude of the intervention/caloric deficit).
• There is good evidence that weight loss through exercise-induced energy deficit results in loss fat mass and retention or even increases in lean mass.
• Many interventions involving both calorie restriction and increased activity (ELMM) complicate the picture as exercise in this context does not always protect against loss of lean mass.

I note that although this article discusses hormonal regulation of fat cells, the point is repeatedly made that fat mass is *energy balance*.  

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Part II will discuss Exercise & Fat Distribution