FYI-an interpretation

[Sarah Ralston <ralston@AESOP.RUTGERS.EDU>]

Ti wrote, in response to to one of the queries regarding the abstract: 
> This concept is one of the many points made in that book I
> recommended--extended medium intensity exercise is what tunes the body to
> burn fat--not the feeding of fat. And that was the thrust of my
> "hypothesis"--presented a couple of weeks ago. And today my monthly
> database comes in and, lo and behold, here's a very convenient paper that
tends to
> support the concept. Also, it makes me feel more comfortable about only
> allowing a month of fat loading in that protocol.

Now, I have absolutely no problem with the above statements. 
Hey-I don't feed my horse a high fat feed...However, reading 
abstracts can be tricky, and there is danger of overinterpreting what is
presented.
There is always a risk in looking just at the abstract, since so much
detail is left out, plus,
since the authors are, I believe, Dutch, something may be lost in
translation), but:

>The hypothesis tested was that dietary fat, when compared with an 
>isoenergetic amount of non-structural carbohydrates, stimulates lipolysis in 
>adipose tissue and also stimulates the fatty-acid oxidative capacity in 
>skeletal muscle from horses. 

Ok, there are two hypotheses supposedly tested:

	Hypothesis 1: Feeding fat causes increased break down of lipid into
glycerol and free fatty acids.
	 No reference to exercise. Feeding of fat per se has never been reported to 
	 do this in resting horses or even suspected to do it. Why should it? If
anything
	 it will stimulate fat deposition! I don't see the earth shaking
significance of this
        hypothesis.

      Hypothesis 2: Feeding fat stimulates (increases) fatty acid oxidative
	 capacity in skeletal muscle, ie: increasing the muscle's ability to 
	 utilize fatty acids as energy sources. Now this hypothesis has been 
	 tested several times over and reported to be true if adequate time for 
	 adaptation is given in EXERCISING horses!

>Six adult horses 

Six is a pretty small sample size though not unusual for horse 
research since it's so darn expensive to keep them. No idea as to whether 
these animals were conditioned, sedentary, 6 or 26 years old, Draft horses
or arabs,
or if they all completed all phases of the experiment (see below), all of
which could impact results.

>were fed a high-fat, glucose or starch containing diet  

No mention of how high the "high fat" diet was. The horses fed the starch
and glucose
diets would be consuming much higher amounts overall if the rations were
truly equal
in calories since fat provides 2.2 times the calories as starch or glucose.
Also were they fed for maintenance only? Were they allowed outside to
exercise 
in paddocks-high starch may haveresulted in more activity than the high fat).

>according to a 3 x 3 Latin square design with feeding periods of three weeks.

This means that each horse had received each treatment once and were
allowed only three weeks
on each. In all of the work on high fat rations I've seen, the maximum
benefits with respect 
to endurance, etc have been reported after 4 to 6 weeks of adaptation.
Don't forget that since
horses normally eat only 2 to 3% fat rations, gearing up the secretion of
bile salts
and enzymes necessary for digestion and absorption nd metabolic pathways
takes time.
Horses don't have a gall bladder like we do that stores the bile salts and 
squirts them out when a high fat meal is consumed-horse's livers just dribble 
the salts in very low concentration continually, totally unresponsive to a
single meal-
it takes time to increase the rate of secretion here... (Work done by Dr.
Joe Bertone)

>The diets were formulated so that the intake of 
>soybean oil versus either glucose or corn starch were the only variables.

But what was the basal ration? Also, the corn starch also contains phosphorus,
other minerals and even a few vitamins not found in dextrose or soybean
oil. How 
did they get it into them? In my experience, horses will often refuse to
eat rations
with high glucose or oil. This often results in having full data sets on
only 3 or 4 
horses, which, in a design like this, makes data interpretations difficult,
if not 
impossible.
 
> In accordance with previous work, whole plasma triacylglycerol (TAG) 
>concentration decreased significantly by 58% following fat supplementation. 

Decreased??? Blood lipid concentrations usually increased on high fat rations 
(How many of you get your cholesterol checked?? TAG's are closely related).
I suspect this was a typo-
or, if not, that it may reflect increased fat deposition in these
supposedly sedentarty horses.
Also no mention was made of when the blood sample was taken relative to
feeding.
(Doesn't your doctor insist that you not eat before taking your
cholesterol?). If it was indeed a typo, 
a 58% increase in blood TAG could be seen easily 2 hours after feeding a 5
to 7% fat meal, but if 
the sample was taken before feeding after an overnight fast, they must have
been giving
huge amounts of fat.

>This fat effect was accompanied by a 2476% increase in lipoprotein lipase 
>(LPL) activity in post-heparin plasma. 

This is a huge increase. However all lipoprotein lipase does is break down
lipoproteins,
which are fats attached to a protein molecule, into protein and TAG-first
step in making 
lipids available for utilization in aerobic exercise OR for fat deposition.
It does nothing to the TAG's per se.

>The dietary variables did neither significantly affect the basal in vitro
lipolytic rate

This means that when they took a blood sample from the horse and subjected 
it to tests measuring the rate of fat breakdown in a test tube. There were no 
differences in the rate of breakdown of TAGs between treatments. However,
this is
outside the body and lacking the hormonal cues that would stimulate the
enzymes to go to work
on the fats.

> nor the lipolytic rate after adding noradrenaline. 

Great-they added noradrenaline (the flight or fight hormone) to the blood
in the test tube.
First of all, noradrenaline stimulates ANaerobic responses-not fat
utilization!
Second, a lot of the metabolic responses to noradrenaline depend on other
responses
from the body, which are not present in a test tube.

>There was no significant diet effect on the 
>activities of hexokinase and phosphofructokinase as indicators of glycolytic 
>flux and citrate synthase and 3-hydroxy-acyl-CoA dehydrogenase as indicators 
>of fatty-acid oxidative capacity.

These are enzymes involved in the metabolic pathways for fat
utilization.They are
usually active in the muscle cells, though the enzymes are also present in
the blood. 
Were these measured in the muscle or the blood? I'd like to see
the actual numbers-with the huge increase in LPL activity (which is much
more easily measured 
and doesn't tend to be as variable as the above enzymes) I'd bee really
surprised if there ween't
at least a trend for these to also differ. As a writer of abstracts of
papers with some shaky data myself, 
if you have numbers with huge amounts of variation (the +/- numbers after
the means) that make statistical
interpretation impossible, you don't put them in the abstract and just say
there was
no effect, hoping no one will read the whole paper, since that invalidates
a lot of the conclusions (equivalent to the "one rat" experiment-gives some
trends,
some ideas, but proves nothing). On the other hand, if I have really strong
data, you
better believe I put the numbers in the abstract. Their absence here makes
me wonder.

> The concentrations of muscle glycogen and TAG were not affected by fat
supplementation. 

Self explanatory-But these horses were apparently not exercising. Eating
French fries
or pasta, if in the same amount of calories, would not affect fitness,
muscle glycogen etc in a
couch potato either! Again, I'd also like to see the numbers.

>It is concluded that our hypothesis is not supported by the present results.

Indeed from what they have stated above, assuming the stats are correct,
in NON EXERCISING HORSES the feeding of high fat (what % though?) 
did increase blood lipid and TAG liberating enzymes concentrations but
failed to
increase lipid breakdown in the blood in a test tube, even when
noradrenaline, which stimulates
anaerobic metabolism, was added to the tube. Big deal! It apparently did not 
increase increase muscle glycogen or TAG but why should it in unconditioned
horses? 
The reported glycogen sparing effect of high fat rations has been seen only
in 
exercising horses. Again, if the animals were not exercising, why should a
lack 
of difference as to the source of calories make a difference in the
measures of fitness???

Mind you, I am not disgreeing with Ti here-just giving "reading science
abstracts 101"
and avoiding the office work I should be doing :=))

Sarah and Fling (Hey, Mom-come home, then and ride me!)