Image 1: Unexpectedly ergogenic - Carthamus tinctoriusL., better known as "safflower", a highly branched, herbaceous, thistle-like annual.
As a regular visitor of the SuppVersity and/or listener of
SuperHumanRadio, you will be familiar with my skepticism towards fish oil supplementation as the "good for all" wonder-supplement in an
athletic population. You will also be familiar with studies such as Filaire et al. (2010) which showed increased MDA (malondyaldehide) levels (and thus more, not less toxic
waste) in athletes receiving 600mg of EPA and 400mg of DHA for 6 weeks. Thusly, it
may not come as a total surprise that Guihua Zhang and his colleagues
the National Food Research Institute and the National Institute of Vegetable and Tea Sciences in Japan found that 12 weeks on a diet containing 6% fish oil reduced endurance performance in aged mice by -20%. What may be more surprising, though, is that the vilified n6-pufas from safflower oil more than doubled the rodents' endurance performance.
Video 1: Not the swimming test performed in the study, but maybe an explanation why mouse-oil might be good for fish, but not vice versa - or have you ever seen a mouse eating a fish?
In view of the fact that the mice in the lard group suffered a similar
loss in endurance performance, it should be said that the overall effect
of fish oil, as well as lard, could in fact have been a null-effect. In
other words, contrary to safflower oil, fish oil and lard had no
beneficial effect on swimming endurance, so that an age-related decline
in swimming endurance would have become obvious. After all, the average
mouse-life is no longer than ~100-150 weeks, so that another 12 weeks are
quite a time-span for 52 weeks old mice. On the other hand, previous
studies such as Shimomura et al. (Shimomura. 1990) and Rustan (Rustan.
1993) would point toward an overall negative effect of high SFA+MUFA
(lard) and high N3-PUFA (fish oil) on fatty acid oxidation in skeletal
muscle and subsequently (endurance) exercise performance.
In the study, 40 male Crlj:CD-1 (ICR) mice had been randomly assigned to
one out of three groups with the 6% of fatty acids of their
experimental diet coming from either lard (n=13), safflower oil (n=13)
or fish oil (n = 14) for 12 weeks.
Figure 1: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on swimming endurance of aged mice (data calculated based on Zhang. 2011).
As the data in figure 1 goes to show, the fat content of the diet, i.e.
low PUFA (lard), high N3-PUFA (fish oil) and high N6-PUFA (safflower
oil) had a profound impact on the swimming performance of the animals.
In view of the fact that we cannot completely rule out that the
"negative effect" of lard and fish oil were simply due to an age-induced
decline in swimming performance (cf. red box above), the most important
finding of this study is however the +113% endurance increase in the safflower group, and not so much the -20% performance decreases in the other groups in swimming endurance [if you asked me, it's a pitty that there is no control group on a mixed diet]
Figure 2: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on lactate levels pre and post endurance exercise in aged mice (data calculated based on Zhang. 2011).
As Zhang et al. point out, this increase in endurance performancecannot
be explained based on increases in muscle or liver glycogen stores,
because scientists measured "[s]imilar glycogen storage and plasma
glucose levels in sedentary mice in the three diet groups suggest". A
better explanation relates to the significant differences in the
accumulation of plasma lactate following swimming (cf. figure 2), where lactate levels
were "significantly lower" in the safflower oil group than in the lard
(+57%) and non-significantly higher in the fish oil (+14%) group.
These results imply that the improved endurance associated
with dietary safflower oil may be due, at least in part, to glycogen
sparing. The working skeletal muscle is not only the major site of
lactate production but is also important for utilization of lactate,
which is mainly removed by oxidation. The decreased accumulation of
lactate observed in aged mice fed safflower oil could be due to
increased lactate oxidation and subsequent utilization as an additional
energy sourceduring swimming.
Yet the effect on accumulation or utilization of lactate was not the
only difference that may have contributed to the increase in swimming
performance that was observed in the safflower oil group. As the
researchers point out,
the significant increase in muscle and liver CPT
activities and decrease in plasma NEFA levels observed following
exhaustive swimming in mice fed safflower oil implies an upregulation of fatty acid metabolism in these mice.
The absence of these effect in the lard or fish oil fed animals suggest that "the safflower oil group may have increased fatty acid utilization for energy than the other diet groups". In that, it is particularly noteworthy that we are talking about a localized
increase in CPT activity and consequent fatty acid oxidation in muscle
tissue. The increased liver CPT in the fish oil group, on the other hand
could have contributed to an overall negative effect of fish oil
consumption on endurance performance that would have been corroborated
by the established suppressive effect of N3PUFAs on fatty acid synthesis
(Kim. 1999; Nakatani. 2004) and lipid oxidation (Rustan. 1993),
against the backdrop of which less fatty acids became available for and
subsequently oxidized in skeletal muscle.
Image 2: Biological activities of IL-6 (illustration by Prof. Dr. Heinrich)
Not directly relevant to the endurance aspect, but nevertheless interesting is another result of the study, which is the absence, respectively statistically insignificant elevation of
elevations in the inflammatory maker IL-6 in the exercised
(non-existent) and sedentary (non-significant) mice on the safflower oil
diet. A result the anti-n6-faction in the diet-guru camp will probably find
surprising and which goes against previous findings by Moon et al.
(Moon. 2003) and Garcia-Escobar (Garcia-Escobar. 2010) - on the other hand, this also means
that it was not the increase in IL6, which has in human studies been
shown to selectively stimulate lipolysis in skeletal muscle (Wolsk. 2010), that facilitated the increase in endurance performance.
If and in what extent the reduction in plasma ferritin (fe) levels in the fish oil group (-13%
sedentary; -24% exercised; both compared to lard, with slightly greater
reductions compared to safflower oil) could have been an additional
factor in a complex equation of substrate availability, usage and enzyme
activity which could eventually explain the perfomance increases and
decreases in the different groups is questionable. After all, the fe
levels in the lard and safflower oil groups were virtually identical.
So, what would be the overall lesson, we can learn from the results of
this study? Fish oil is poison, safflower oil liquid gold? Probably not. Yet, while it may still be questionable in how far the mouse metabolism is a good model for the human one, the inhibition of fatty acid synthesis and the increased
fatty acid oxidation observed in mice as a consequence of fish oil feeding is present in humans, as well. Moreover, I assume you would agree that not everything that would be beneficial for the average
sedentary borderline to morbidly obese inhabitant of the Western
Hemisphere, is equally beneficial for performance-oriented athletes - or would you suggest 200 meter sprinters start swallowing statins and blood pressure medications? So, wouldn't it be remotely possible, then that a physical culturist (as I hope you would consider yourself to be one) would be much better off with a reasonable amount
of those "nasty" n6-PUFAs in his/her diet to keep the fire in the mitochondrial furnace of his/her muscles in full blast? If you want to, ask your guru about it ;-)
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