Saturday, March 8, 2008

Crossfit sums it up

It is a bit dumbed down, but the teacher here begins to explain a lot of what I am coming to believe about diet - it is ultimately a question of hormones.



I might even buy the journal to get the rest of this lecture.


I hope I am not a disciple of any particular fitness guru or school - I try to take the good bits from lots of sources, avoiding the "cultic" tunnel vision that can sometimes come with adherence to a single philosophy.

That being said I think that the Crossfit Fitness in 100 words sums up a lot of what I have come to believe about fitness and diet - especially the first 14 words about diet. (They explain more in this pdf) , and develop their ideas about nutrition a bit more here. I might argue with some bits and pieces, e.g. I might say to eat eggs (and butter and cream!), put IF in the mix and maybe add in more easy days, but I think as a 100 word summary, this is pretty good.

World-Class Fitness in 100 Words:
Eat meat and vegetables, nuts and seeds, some fruit, little starch and no sugar. Keep intake to levels that will support exercise but not body fat. Practice and train major lifts: Deadlift, clean, squat, presses, C&J, and snatch. Similarly, master the basics of gymnastics: pull-ups, dips, rope climb, push-ups, sit-ups, presses to handstand, pirouettes, flips, splits, and holds. Bike, run, swim, row, etc, hard and fast. Five or six days per week mix these elements in as many combinations and patterns as creativity will allow. Routine is the enemy. Keep workouts short and intense. Regularly learn and play new sports.

Low Carb diets - not a problem for a healthy cardiovascular system


This study came through yesterday. The researchers were looking at the effects of a very-low-carbohydrate, high-saturated-fat weight-loss diet (LC) on brachial artery flow-mediated dilatation (FMD). Reduced flow-mediated dilation, as measured in this study, is an early indicator of cardiovascular disease - the vessels are not opening up as the blood flows though - they are not "flexing".

The researchers found that this study showed that a low carb diet does not impair FMD and actually had benficial effects on most other markers of cardiovascular health.

The full abstract is copied below for you to look at.

Now that might be enough to write. However, a few days ago I put up a fairly innocuous post "Low Carb Brief" In the comments to that someone pointed me to a study reported here , the abstract of which is found here

The shock horror headline was that "Low-fat Diets More Likely To Reduce Risk Of Heart Disease Than Low-carb Diets" as those researchers found that their low carb diet diminished FMD. Stephan commented superbly on this research here:

So let me get this straight. What we're looking at is data showing that LC beat or tied LF on every relevant parameter they reported except one, and somehow that means LF diets are healthier than LC? Even though overweight and hypertension are important risk factors for cardiovascular disease? Even though trig/HDL is probably the best predictor of heart disease of any of these measures?

This article wouldn't bother me if it weren't so arrogant. If it had simply reported the facts as an interesting phenomenon, instead of tacking on a politically motivated (and incorrect) interpretation, I would have just found it interesting. But the author is bigger than his britches: "LF diets may confer greater cardiovascular protection than LC diets."

The irony isn't lost on me that the paper is published in the journal Hypertension, shows that LC diets ameliorate hypertension better than LF diets, yet somehow claims LF diets are more protective of cardiovascular disease than LC. Huh?

Unfortunately, this is typical of researchers in the diet-health field and the media that report on it.

Now there is new research that indicates that low carb diets do not affect FMD and have benefits in other areas of cardiovascular health. I wonder how Science Daily will report this one!

Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of cardiovascular disease risk in subjects with abdominal obesity

Background: The effects of a very-low-carbohydrate, high-saturated-fat weight-loss diet (LC) on brachial artery flow-mediated dilatation (FMD) and markers of endothelial function are unknown.

Objective: The effect of an LC on markers of endothelial function and cardiovascular disease (CVD) risk was compared with that of an isocaloric high-carbohydrate, low-saturated-fat diet (HC).

Design: FMD and markers of endothelial function (n = 70) and CVD risk were measured before and after 8 wk of weight loss. Ninety-nine subjects aged 50.0 ± 8.3 y with a body mass index (in kg/m2) of 33.7 ± 4.1 completed the study.

Results: Mean (±SD) FMD did not change significantly (P = 0.55) with either diet. Pulse wave velocity improved with both diets (P < 0.01). Endothelial markers, E- and P selectin, intracellular and cellular-adhesion molecule-1, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 decreased (P < 0.001), with no diet effect. Adiponectin did not change significantly. More weight (P = 0.05 for diet x time interaction) and more abdominal fat mass (P = 0.05 for diet x time interaction) were lost with the LC than with the HC. LDL cholesterol decreased more with the HC than with the LC (P < 0.05, time x diet), and C-reactive protein decreased more with the HC than with the LC (P < 0.05 for diet x time interaction). Homocysteine increased more with the LC (P < 0.01 for diet x time interaction). Folate decreased with the LC and increased with the HC (P < 0.05, time; P < 0.001 for diet x time interaction).

Conclusion: A LC does not impair FMD. We observed beneficial effects of both diets on most of the CVD risk factors measured. This trial was registered with the Australian Clinical Trials Registry as ACTR N0 12606000203550.

Thursday, March 6, 2008

"Healthy" Diet Makes You Fat?

UPDATE

Dr Eades comments in this study here


I couldn't really resist this one....it seems like a "healthy diet" - whole grains, fruits and vegetables accompanied by vegetable oil - makes people fat......

Vegetable-rich food pattern is related to obesity in China

Abstract
Objective: To investigate the association between a vegetable-rich food pattern and obesity among Chinese adults.
Design: A food pattern rich in vegetables is associated with lower risk of obesity and non-communicable chronic disease in Western countries. A similar food pattern is found in the Chinese population but the cooking method is different. A cross-sectional household survey of 2849 men and women aged 20 years and over was undertaken in 2002 in Jiangsu Province (response rate, 89.0%). Food intake was assessed by food frequency questionnaire. Factor analysis was used to identify food patterns. Nutrient intake was measured by food weighing plus consecutive individual 3-day food records. Height, weight and waist circumference were measured.
Results: The prevalence of general obesity (BMI 28 kg m-2) was 8.0% in men and 12.7% in women, central obesity was 19.5% (90 cm) and 38.2% (80 cm), respectively. A four-factor solution explained 28.5% of the total variance in food frequency intake. The vegetable-rich food pattern (whole grains, fruits and vegetables) was positively associated with vegetable oil and energy intake. Prevalence of obesity/central obesity increased across the quartiles of vegetable-rich food pattern. After adjusting for sociodemographic factors and four distinct food patterns, the vegetable-rich pattern was independently associated with obesity. Compared with the lowest quartile of vegetable-rich pattern, the highest quartile had higher risk of general obesity (men, prevalence ratio (PR): 1.82, 95% confidence interval (CI): 1.05–3.14; women, PR: 2.25, 95% CI: 1.45–3.49).
Conclusion: The vegetable-rich food pattern was associated with higher risk of obesity/central obesity in Chinese adults in both genders. This association can be linked to the high intake of energy due to generous use of oil for stir-frying the vegetables.

More Intermittent Fasting Research

It is probably obvious from this blog that I find the whole area of diet, exercise, fitness etc absolutely fascinating and reading and researching this material is a great pleasure. I'm always on the lookout for new information on these things that interest me and one of the areas of my particular interest is intermittent fasting. I recently came across another blog - Spartan Training / the way is in training - which has - among the workout records of its author a couple of interesting articles on IF.

The two blog posts are:
These are two really well thought out and well written posts that will repay some study.

The first does some thinking - based on several studies - about the similarities and differences between IF and CR and the various mechanisms that are at play.

The second looks at a study which suggests the idea that long-term intermittent fasting can lead to improved cognitive function - fasted mice exhibited improved learning and memory compared to controls.

Anyway good stuff and I like how the author throws studies like this in among his Crossfit style training records!

Wednesday, March 5, 2008

Exercise, eat less and extend your life?

While referring to rats, this is still an interesting study regarding the potential benefits of calorie restriction - of which Intermittent Fasting (IF) is a form - and exercise. Basically there is a problem that as we get older we tend to lose muscle. This study suggests that you can avoid that problem (and its consequences) through lifelong, voluntary exercise combined with mild (8%) caloric restriction.

Anyway, the relevance here is that IF has been shown to have similar results to caloric restriction (CR) which itself has been demonstrated to increase lab rat lifespans more than 20%. I often post IF studies here and am also a fan of resistance exercise. Brad Pillon's Eat Stop Eat, that I've pointed to before, also proposes IF coupled with resistance training.

Lifelong exercise and mild (8%) caloric restriction attenuate age-induced alterations in plantaris muscle morphology, oxidative stress and IGF-1 in the Fischer-344 rat

Abstract


Muscle atrophy is a highly prevalent condition among older adults, and results from reduced muscle mass and fiber cross-sectional area. Resistive exercise training and moderate (30–40%) caloric restriction may reduce the rate of sarcopenia in animal models. We tested the hypothesis that lifelong, voluntary exercise combined with mild (8%) caloric restriction would attenuate the reduction of muscle fiber cross-sectional area in the rat plantaris. Fischer-344 rats were divided into: young adults (6 mo) fed ad libitum (YAL); 24 mo old fed ad libitum (OAL); 24 mo old on 8% caloric restriction (OCR); lifelong wheel running with 8% CR (OExCR). Plantaris fiber cross-sectional area was significantly lower in OAL than YAL (−27%), but protected in OCR and OExCR, while mass/body mass ratio was preserved in OExCR only. Furthermore, 8% CR and lifelong wheel running attenuated the age-induced increases in extramyocyte space and connective tissue. Citrate synthase activity decreased with age, but was not significantly protected in OCR and OExCR. Total hydroperoxides were higher in OAL than YAL, but were not elevated in OExCR, with out a change in MnSOD. IGF-1 levels were lower in OAL (−57%) than YAL, but partially protected in the OExCR group (+51%).

Tuesday, March 4, 2008

More support for CoQ10

I have had a previous post about co enzyme Q10. Here is a new study on this supplement, which again suggests some benefits....

Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals


Background

To determine whether acute (single dose) and/or chronic (14-days) supplementation of CoQ10 will improve anaerobic and/or aerobic exercise performance by increasing plasma and muscle CoQ10 concentrations within trained and untrained individuals.

Methods

Twenty-two aerobically trained and nineteen untrained male and female subjects (26.1+/-7.6 yrs, 172+/-8.7 cm, 73.5+/-17 kg, and 21.2+/-7.0%) were randomized to ingest in a double-blind manner either 100 mg of a dextrose placebo (CON) or a fast-melt CoQ10 supplement (CoQ10) twice a day for 14-days. On the first day of supplementation, subjects donated fasting blood samples and a muscle biopsy. Subjects were then given 200 mg of the placebo or the CoQ10 supplement. Sixty minutes following supplement ingestion, subjects completed an isokinetic knee extension endurance test, a 30-second wingate anaerobic capacity test, and a maximal cardiopulmonary graded exercise test interspersed with 30-minutes of recovery. Additional blood samples were taken immediately following each exercise test and a second muscle biopsy sample was taken following the final exercise test. Subjects consumed twice daily (morning and night), 100mg of either supplement for a period of 14-days, and then returned to the lab to complete the same battery of tests. Data was analyzed using repeated measures ANOVA with an alpha of 0.05.

Results

Plasma CoQ10 levels were significantly increased following 2 weeks of CoQ10 supplementation (p<0.001); while a trend for higher muscle CoQ10 levels was observed after acute CoQ10 ingestion (p=0.098). A trend for lower serum superoxide dismutase (SOD) was observed following acute supplementation with CoQ10 (p=0.06), whereas serum malondialdehyde (MDA) tended to be significantly higher (p<0.05). Following acute ingestion of CoQ10, plasma CoQ10 levels were significantly correlated to muscle CoQ10 levels; maximal oxygen consumption; and treadmill time to exhaustion. A trend for increased time to exhaustion was observed following 2 weeks of CoQ10 supplementation (p=0.06).

Conclusions

Acute supplementation with CoQ10 resulted in higher muscle CoQ10 concentration, lower serum SOD oxidative stress, and higher MDA levels during and following exercise. Chronic CoQ10 supplementation increased plasma CoQ10 concentrations and tended to increase time to exhaustion. Results indicate that acute and chronic supplementation of CoQ10 may affect acute and/or chronic responses to various types of exercise.

Monday, March 3, 2008

Another Turkish Get Up Style

I've posted a couple of tutorials before on the Turkish Get Up (TGU) here and here.

Scott Sonnon has just posted another variation which is specifically aimed at developing speed-strength. He trains fighters, so that is a particularly useful fitness element.

The describes the move and its context in a blog post here. The video below shows the style:



I like the shin roll to the squat.

Sunday, March 2, 2008

Intermittent Fasting - another mechanism

There are quite a few of us now that have an interest in Intermittent Fasting (IF). I have just seen this abstract which looks at another mechanism associated with IF. This mechanism could add to the fat-burning effect of fasting.

You may have heard of l-carnitine - it has been sold as a supplement allegedly to increase fat burning and prevent fatigue. The description below is from Wikipedia:

Carnitine, also known as L-carnitine or levocarnitine, is a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine.[1] It helps in the consumption and disposal of fat in the body because it is responsible for the transport of fatty acids from the cytosol into the mitochondria. It is often sold as a nutritional supplement.

One of the supplement advertisements explains:

L-carnitine transfers long-chain fatty acids, such as triglycerides into mitochondria (a cell's energy powerhouse), where they may be oxidized to produce energy. L-carnitine is a very popular supplement that promotes growth and development. It is also used for fat-burning, increasing energy, and improving resistance to muscle fatigue. L-carnitine has also been shown to help build muscle. is also great in dieting, as it reduces feelings of hunger and weakness.

OK, that is the context.

Now there is this study, Fasting and Caloric Restriction Increases mRNA Concentrations of Novel Organic Cation Transporter-2 and Carnitine Concentrations in Rat Tissues.

The study shows that fasting and caloric restriction lead to an upregulation of OCTN2 in several tissues, probably mediated by activation of PPAR. Increased tissue carnitine concentrations in fasted and calorie-restricted rats might be at least in part due to increased uptake of carnitine by OCTN2.


The study identifies a particular mechanism but the key issue is that fasting and calorie restriction (CR) lead to increased carnitine concentrations.


So that which athletes and bodybuilders seek to achieve via supplementation is possible - at least in rats - via fasting or calorie restriction...



Background: Recently, we have shown that activation of peroxisome proliferator-activated receptor (PPAR)- by clofibrate leads to an upregulation of novel organic cation transporter (OCTN)-2, a carnitine transporter, and in turn increases the carnitine concentration in the liver of rats. In this study, we tested the hypothesis that fasting and caloric restriction, conditions under which PPAR activation also occurs, cause similar effects. Methods: Three groups of rats received the diet either ad libitum (control rats) or 10.5 g diet/day (70% of energy requirement for maintenance, E70 rats) or 6 g diet/day (40% of energy requirement for maintenance, E40 rats) for 10 days. A 4th group received the diet ad libitum for 9 days and was then fasted for 24 h (fasted rats). Results: Fasted and calorie-restricted rats had increased mRNA concentrations of acyl-CoA oxidase and carnitine palmitoyltransferase-1 in the liver, heart and kidneys compared to control rats (p < 0.05), indicative of activation of PPAR in these tissues. E70 rats had increased OCTN2 mRNA concentrations in liver (2.6-fold) and kidneys (1.5-fold) and increased total carnitine concentrations in these tissues compared to control rats. E40 rats had increased OCTN2 mRNA concentrations in the liver (3.3-fold), skeletal muscle (2.2-fold), heart (2.3-fold) and kidneys (3.5-fold) and increased total carnitine concentrations in these four tissues compared to control rats. Fasted rats had increased OCTN2 mRNA concentrations in the liver (4.0-fold), heart (2.1-fold) and kidneys (2.0-fold) and increased total carnitine concentrations in these three tissues (p < 0.05). Conclusion: The study shows that fasting and caloric restriction lead to an upregulation of OCTN2 in several tissues, probably mediated by activation of PPAR. Increased tissue carnitine concentrations in fasted and calorie-restricted rats might be at least in part due to increased uptake of carnitine by OCTN2.


Low carb brief...

Just to point you towards a couple of great recent posts on low carb eating:
  1. Matt points to a study about carb intake and sleepiness -"Higher fasting insulin levels were positively correlated with sleepiness. This is why refiend carbs are so deadly: they increase hunger which leads to weight gain, and they also make people more sluggish and less likely to exercise." Brad Pillon - of Eat Stop Eat fame - recently made a similar observation: "......I can't recall the last time bacon and eggs made me sleepy. But I know that anytime I have a big "sugar bomb" type of meal, I'm out like a light about 30 minutes after I'm done eating."
  2. Dr Briffa - of whom I am a huge fan - asks "Where weight loss is concerned, could it be that it’s more than calories that count?" . He reminds us that ".... that one way to lose weight is to eat a diet that tends not to get stored as fat. The fat storage hormone in the body is insulin, which is secreted primarily in response to carbohydrate consumption. " and ".....In short, there is at least some evidence suggests that when people eat more protein and less carb, less of what they eat is stored as fat, and the energy that appears to go ‘missing’ is simply burned by a more ‘efficient’ metabolism. When it comes to weight control, it might be that it’s more than just calories that count."


Research digest.....

I wanted to get a post up to point to a couple of pieces of research that I have seen in the last week, about which I've not had time to write:

  1. A study which might indicate that garlic is helpful in treating exercise induced muscle damage: Effects of allicin supplementation on plasma markers of exercise-induced muscle damage, IL-6 and antioxidant capacity.
  2. Yet another complication associated with statin use! This time it a French study confirmed previous anecdotal reports that statins seem to trigger tendinitis or even an Achilles rupture. The study is reported here and here. Statins are full of potential side effects which are swept under the carpet by physicians desperate - for some reason - to reduce cholesterol. Once again I'd encourage you to read some of the cholesterol sceptics (e.g. this essay) and think for yourself about whether or not cholesterol deserves to be so demonised!