Another jump - 45 inch box

there is also some interesting commentary with videos of the same guy missing at 42"

Nutrient Administration and Resistance Training

Again the full text of this one is available and - if you are interested in this topic then I would suggest you read the whole thing.

Here is the summary:

The impact of resistance training on muscle hypertrophy is well known. For years, resistance training athletes have been interested in identifying which forms of nutritional supplementation will provide the greatest support in an effort to maximize the training adaptations from resistance training. Many findings and suggestions have been reported in this regard and are outlined below:

• Resistance training modestly stimulates protein synthesis and further stimulates protein breakdown resulting an overall negative protein balance after exercise.

• As the training status of an individual progresses, the magnitude of changes seen in protein synthesis and breakdown diminishes after each exercise bout as well as a diminished increase of protein synthesis after each subsequent exercise bout.

• Infusion or ingestion of amino acids is an effective way to increase amino acid concentrations at rest or after resistance exercise.

• Availability of amino acids after resistance exercise increases protein synthesis.

• Essential amino acids do appear to play a primary role in protein synthesis and adding carbohydrate to them may enhance this effect.

• Ingestion of carbohydrate alone after resistance exercise causes marginal improvements in overall protein synthesis while maintaining a negative net protein balance. No studies have found carbohydrate to be detrimental and it may be useful to enhance palatability; however the additional caloric burden may not be desired.

• A small dose of essential amino acids after resistance exercise has been found to stimulate protein synthesis to a similar degree when compared to studies that used much larger doses of both amino acids (EAA, NEAA, or both) or that were combined with carbohydrate.

• Ingestion of amino acids after resistance exercise has been shown at many different time points in several studies to stimulate increases in muscle protein synthesis, cause minimal changes in protein breakdown and increase overall protein balance. It has not been conclusively determined what time point is optimal. Similar changes have been found for studies that have administered amino acids alone or with carbohydrate immediately upon completion of an acute exercise bout, 1 h after completion, 2 h after completion and 3 h after completion. Interestingly, ingesting nutrients before the exercise bout may have the most benefit of all the time points.

• It is possible for the mechanisms involving amino acid transport and protein synthesis to be overwhelmed with extremely high, continuous levels of amino acids. The likelihood of this occurring is rare even upon considering the highest of protein intakes among individuals.

• An optimal dosage in which to ingest amino acids at this time does not exist. Studies using similar techniques while resistance training have used 6 g EAA only, 6 g EAA + 6 g NEAA, 12 g EAA only, 17.5 g whey protein, 20 g casein protein, 20 g whey protein, 40 g mixed amino acid, 40 g EAA only all with similar increases in protein synthesis and protein balance. Athletes who desire to increase muscle mass or are involved in power sports should consider consuming protein supplements that will provide amino acids in similar amounts used in these studies.

• Intact proteins or combinations of them that are commonly used in popular protein supplements appear to elicit similar increases in protein balance after resistance training as compared to other studies using free amino acids.

From these primary findings, it is our hope that athletes, coaches, nutritionists and researchers will be able to provide clearer advice and recommendations when consulting themselves, their players, clients, or research participants in regards to optimal administration of nutrients while participating in a resistance training program.

Gender Differences in Carbohydrate Metabolism

One of the things that is not discussed that often with respect to nutrition at least, is that men and women are different. (Of course they are, I've noticed) Hormonally and in terms of their broader physiology there are significant differences.

Lyle McDonald talks about this a bit in his Stubborn Fat book but I've not seen it addressed much elsewhere.

Anyway, this is an interesting study - the full text of which is available - it is mainly about carb loading for endurance events (a topic also discussed here recently strangely in the context of intermittent fasting) but there is good stuff there about how carbs are actually burned and how men and women differ in this respect.

The abstract is below

Gender differences in carbohydrate metabolism and carbohydrate loading.

Prior to endurance competition, many endurance athletes participate in a carbohydrate loading regimen in order to help delay the onset of fatigue. The "classic" regimen generally includes an intense glycogen depleting training period of approximately two days followed by a glycogen loading period for 3–4 days, ingesting approximately 60–70% of total energy intake as carbohydrates, while the newer method does not consist of an intense glycogen depletion protocol. However, recent evidence has indicated that glycogen loading does not occur in the same manner for males and females, thus affecting performance. The scope of this literature review will include a brief description of the role of estradiol in relation to metabolism and gender differences seen in carbohydrate metabolism and loading.

Fiber Type Composition and Capillary Density

I find this one pretty interesting. I'm not immediately sure what the application is but there are some intriguing issues here.

The experimenters looked at how many reps guys could do with 70% of their 1 rep max and then correlated this with different measures of the physiological make up of the muscles. Anyway, they found that the fibre type was not that important but that the capilliary density was the important factor.

There are trainers out there that make a lot out of the different fibre types. In this - admittedly specific - case that was not the important factor.

Application? If you want to maximise your reps at 70% of 1 rep max work to increase the capilliary density in the muscles. Now how do you do that?

Fiber Type Composition and Capillary Density in Relation to Submaximal Number of Repetitions in Resistance Exercise.
The purpose of this study was to investigate the relationship between skeletal muscle fiber type composition and the maximum number of repetitions performed during submaximal resistance exercise. Twelve young men performed a maximum repetitions test at 85% of 1 repetition maximum (1RM) in the leg press, which was repeated after 1 week. Seven days after the second 85% 1RM test, they performed a maximum repetitions test at 70% of 1RM in the leg press. This test, at 70% 1RM, was repeated 7 days later. One week before the initiation of the testing sessions, a biopsy sample was obtained from the vastus lateralis muscle and analyzed for fiber type distribution, fiber cross-sectional area, and capillary density (capillaries.mm). A low and nonsignificant relationship was found between the fiber type distribution or percent fiber type area and the number of repetitions performed at either 70% or 85% 1RM. Moreover, the number of repetitions performed at 70% or 85% of 1RM was not related significantly with 1RM strength. In contrast, the number of repetitions performed at 70% 1RM was significantly correlated with the number of capillaries per mm of muscle cross-sectional area (r = 0.70; p = 0.01). These results suggest that fiber type composition is not the major biological variable regulating the number of repetitions performed in submaximal resistance exercise. Rather, it seems that submaximal strength performance depends on muscle capillary density, which is linked with the endurance capacity of the muscle tissue.

Some protein research

Spotted a couple of interesting protein studies today, both of which seem to indicate that moderate protein intake is enough.......

Moderate protein intake improves total and regional body composition and insulin sensitivity in overweight adults.

A high protein intake (~40% of energy intake) combined with aerobic and resistance exercise training is more closely associated with improved body composition and cardiovascular risk profile than a traditional protein intake (~15% of intake) combined with moderate-intensity aerobic exercise. However, there is concern that such high-protein diets may adversely affect health. We therefore tested the hypothesis that moderate protein intake (~25% of energy intake) would elicit similar benefits on body composition and metabolic profile as high protein intake. Twenty-four overweight/obese men and women (body mass index [BMI] = 32.2 +/- 3.4, percentage of body fat [%BF] = 37.3 +/- 8.0) were matched for BMI and %BF and randomly assigned to one of 3 groups for a 3-month nutrition/exercise training intervention: (1) high-protein diet (~40% of energy intake) and combined high-intensity resistance and cardiovascular training (HPEx, n = 8, 5 female and 3 male), (2) moderate-protein diet (~25% of energy intake) and combined high-intensity resistance and cardiovascular training (MPEx, n = 8, 5 female and 3 male), or (3) high-protein diet only (HPNx, n = 8, 5 female and 3 male). Total and regional body composition (dual-energy x-ray absorptiometry), insulin sensitivity (insulin sensitivity index to the oral glucose tolerance test), insulin-like growth factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), IGF binding protein-3 (IGFBP-3), and blood lipids were measured at baseline and after the intervention. All groups experienced significant (P < .05) and similar losses of body weight, BMI, and total and abdominal %BF, and similar improvements in insulin sensitivity (HPEx, 6.3 +/- 1.2 vs 9.5 +/- 0.98; MPEx, 6.2 +/- 1.4 vs 8.4 +/- 1.6; HPNx, 3.7 +/- 1.1 vs 7.0 +/- 1.1; insulin sensitivity index to the oral glucose tolerance test; P < .05) and leptin levels. Furthermore, the HPEx group demonstrated decreases in total cholesterol (TC) and triglycerides, and increases in IGF-1 and IGFBP-1. The MPEx group experienced decreases in TC, whereas the HPNx group had increases in high-density lipoprotein cholesterol, TC to high-density lipoprotein, IGF-1, and IGFBP-1. In conclusion, moderate protein intake elicits similar benefits in body composition and insulin sensitivity as a high-protein diet. These findings may have practical implications for individuals interested in diets containing elevated dietary protein.

Effect of protein intake on strength, body composition and endocrine changes in strength/power athletes. FULL TEXT HERE

ABSTRACT : Comparison of protein intakes on strength, body composition and hormonal changes were examined in 23 experienced collegiate strength/power athletes participating in a 12-week resistance training program. Subjects were stratified into three groups depending upon their daily consumption of protein; below recommended levels (BL; 1.0 - 1.4 g.kg-1.day-1; n = 8), recommended levels (RL; 1.6 - 1.8 g.kg-1.day-1; n = 7) and above recommended levels (AL; > 2.0 g.kg-1.day-1; n = 8). Subjects were assessed for strength [one-repetition maximum (1-RM) bench press and squat] and body composition. Resting blood samples were analyzed for total testosterone, cortisol, growth hormone, and insulin-like growth factor. No differences were seen in energy intake (3,171 +/- 577 kcal) between the groups, and the energy intake for all groups were also below the recommended levels for strength/power athletes. No significant changes were seen in body mass, lean body mass or fat mass in any group. Significant improvements in 1-RM bench press and 1-RM squat were seen in all three groups, however no differences between the groups were observed. Subjects in AL experienced a 22% and 42% greater change in Delta 1-RM squat and Delta 1-RM bench press than subjects in RL, however these differences were not significant. No significant changes were seen in any of the resting hormonal concentrations. The results of this study do not provide support for protein intakes greater than recommended levels in collegiate strength/power athletes for body composition improvements, or alterations in resting hormonal concentrations.

Calories still matter

In all the discussion of the composition of diets - low fat or low carb etc - and the potential for "metabolic advantage" we can sometimes forget the simple fact that calories still matter.

If you are eating too much, you are not going to lose weight no matter how low your carbs are. Dr Eades had a post on this today: Low carb and calories

Although the lowered insulin and elevated glucagon open the doors to the fat cells allowing fat to come out to be burned, the fat comes out only if it’s needed. If you are meeting all your body’s energy needs with the food you eat, the body doesn’t need the fat in the fat cells. On a low-carb diet your body burns fat for energy. But it doesn’t care where this fat comes from; it can come from the diet or it can come from the fat cells or it can come from both. If you are consuming enough fat to meet all your body’s requirements, your body won’t go after the fat in the fat cells no matter how severely you restrict your carbs. You will burn dietary fat only and no body fat. And you won’t lose weight. It’s that simple.

The low-carb diet is a wonderful, healthful way to lose weight quickly, but you do have to watch your calories as well to a certain extent. If your plugging along losing away, keep doing what you’re doing. But if you quit losing, take a look at your cheese and/or nut consumption. Cut those out, and I’ll just about guarantee that your weight loss will pick up again.

Exercise and your bones

Exercise can benefit the bone mineral density which is a good thing - especially in older women who are prone to osteoporosis. However, you have to keep it up to maintain the benefits.......

The beneficial effects of exercise on BMD are lost after cessation: a 5-year follow-up in older post-menopausal women

This study investigates whether the positive effects on bone mineral density (BMD, g/cm2) and neuromuscular function following a combined weight-bearing program are sustained in older women, a longer period after cessation of training. Thirty-four women (18 exercisers and 16 controls) aged 73–88 years, who completed a 12-month randomized-controlled trial, were invited to a 5-year follow-up assessment of BMD and neuromuscular function. Both groups sustained significant losses in BMD of the femoral neck, trochanter, and Ward's triangle during the follow-up period. Significant losses were also seen in all neuromuscular function tests. The inter-group change was, however, significant only for maximal walking speed where the exercise group had a significantly greater loss. In conclusion, this study suggests that gains in bone density and neuromuscular functions achieved by training are lost after cessation of training. Continuous high-intensity weight-loading physical activity is probably necessary to preserve bone density and neuromuscular function in older women.

Obesity research 3 - Fish Oil reduces blood lipids

Fish Oil is often recommended. For example Lyle McDonald says:

Of the total fat intake, the only requirement is fish oils. A minimum of 6 X 1 grams standard capsules (180 mg EPA/120 mg DHA) should be taken daily. This can be increased to ten capsules per day for athletes who are either larger, simply want to, or have the calories to do it.

Beyond that, I don’t get overly hung up on fat intake. Source here

(I am actually a big fan of fat, like Peter)

Here is a study explaining another of their benefits.....


Inclusion of fish or fish oil in weight-loss diets for young adults: effects on blood lipids

Objective: To assess the effects of fish (lean or oily) and fish oil consumption on blood lipid concentration during weight loss.
Design: Randomized, controlled 8-week trial of energy-restricted diet varying in fish and fish oil content. Subjects, 324 men and women, aged 20–40 years, body mass index 27.5–32.5 kg m- 2, from Iceland, Spain and Ireland, were randomized to one of four groups: (1) control (sunflower oil capsules, no seafood), (2) cod diet (3 150 g week- 1), (3) salmon diet (3 150 g week- 1), (4) fish oil (DHA/EPA capsules, no seafood). The macronutrient composition of the diets was similar between the groups and the capsule groups were single-blinded.
Measurements: Total cholesterol (TC), high-density lipoprotein (HDL) and low-density lipoprotein cholesterol, triacylglycerol (TG) and anthropometrics were measured at baseline and end point.
Results: The difference in logTG lowering between the control group and the cod diet, salmon diet and fish oil from baseline to end point was - 0.036 (95% CI - 0.079 to 0.006), - 0.060 (- 0.101 to - 0.018) and - 0.037 (- 0.079 to 0.006), respectively. Reduction in TC was about 0.2 mmol l- 1 greater in the fish groups (cod and salmon) than in the control group, but only of borderline significance when adjusting for weight loss. HDL tended to decrease less in the diet groups consuming a significant amount of n-3 fatty acids (salmon and fish oil).
Conclusion: Weight-loss diet including oily fish resulted in greater TG reduction than did a diet without fish or fish oil. Controlled trials using whole fish as a test meal are encouraged to be able to elucidate the role of different constituents of fish for human health.

Obesity research 2

More from the International Journal of Obesity:


Effects of continuous versus accumulated activity patterns on postprandial triacylglycerol concentrations in obese men - Exercise reduces the level of fats in your blood after a meal.....but it doesn't matter if the exercise is one long session or several shorter ones. I wonder if several short bursts (intervals?) are actually more convenient?

Objective: There is limited information regarding the effects of short (<10 min) bouts of activity on postprandial lipaemia and no studies are available regarding the effects of short bouts of activity on postprandial lipaemia in obese men. The objective of this study was to compare the effects of accumulating ten, 3-min bouts of exercise versus one 30 min bout of exercise on postprandial serum triacylglycerol (TAG) concentrations in obese men.
Design: Each subject completed three 2-day trials at least 1 week apart in a randomized, repeated-measures design. On day 1, subjects rested (no exercise) or cycled at 60% of maximum heart rate in either ten, 3-min bouts (30 min rest between each), or one continuous 30-min bout. On day 2 of each trial, after an overnight fast, the subjects consumed a standardized test meal for breakfast. Venous blood samples were obtained in the fasted state (0 h), and 2, 4 and 6 h postprandially on day 2.
Subjects: Eight sedentary men (age: 272 years) with body mass index between 25 and 37 kg/m2.
Measurements: Postprandial TAG, non-esterified fatty acids, 3-hydroxybutyrate, insulin and glucose were determined.
Results: Total area under the postprandial serum TAG concentrations versus time curve was 18% (P=0.042) and 15% (P=0.032) lower throughout day 2 of both the accumulated exercise trial and the continuous exercise trial, respectively, compared with the control trial with little difference between exercise trials.
Conclusion: At 30 min of moderate cycling (0.87 MJ per 30 min) accumulated in short bouts is equally effective in reducing postprandial serum TAG concentrations as one continuous 30 min bout of cycling in obese men.

Obesity research 1

There were a couple of interesting studies this month in the International Journal of Obesity:

Physical activity energy expenditure has not declined since the 1980s and matches energy expenditures of wild mammals - so the fatties can't blame it all on their "sedentary lifestyle". If you want to lose fat, you are going to have to get serious with your diet - what you eat and how much of it you scoff. It reminds me a little of Taubes piece here, and Matt's comments : Food versus Exercise

Objective: Obesity results from protracted energy imbalance. Whether this comprises excessive energy intake, lowered physical activity or both, remains disputed.
Design: Physical activity energy expenditure, evaluated in three different ways from daily energy expenditure (DEE) measured using doubly labelled water, was examined for trends over time. Data included subjects in Europe (Maastricht, the Netherlands) and North America extending back to the 1980s. These data were compared with measures from the third world, and measures made on wild terrestrial mammals.
Results: Physical activity expenditure in Europe (residual of the regression of DEE on basal energy expenditure (BEE)) has slightly but significantly increased since the 1980s. There was no trend over time in physical activity level (PAL=DEE/BEE), or in the residual variance in DEE once mass, sex and age were accounted for. This latter index of physical activity expenditure also significantly increased over time in North America. DEE of individuals in Europe and North America was not significantly different from individuals measured in the third world. In wild terrestrial mammals, DEE mostly depended on body mass and ambient temperature. Predicted DEE for a 78 kg mammal living at 20 °C was 9.2 MJ per day (95% CI: 7.9–12.9 MJ per day), not significantly different from the measured DEE of modern humans (around 10.2–12.6 MJ per day).
Conclusion: As physical activity expenditure has not declined over the same period that obesity rates have increased dramatically, and daily energy expenditure of modern man is in line with energy expenditure in wild mammals, it is unlikely that decreased expenditure has fuelled the obesity epidemic.

UPDATE - Stephan has some helpful comments on this study: Exercise Didn't Keep Us From Getting Fat

Eggs - another study says they do no harm......

I love eggs and tend to eat them everyday - scrambled usually, but fried or boiled is great too as long as the yolk is nice and runny.

I am glad that lots of research keeps indicating that they are good for you.

Here is another:

Eggs used to get a bad rap for their cholesterol content, which many thought led to a build up of cholesterol in the blood. That's not necessarily true. Saturated fats and trans fats are a bigger concern than the cholesterol in eggs. However, old beliefs die hard, so here's another piece of evidence. In this Univ. of Connecticut study, researchers put a group of young, unfit subjects on a 6-week endurance training program. One group of subjects ate 12 eggs a week as part of their diet; the other group ate none. After 6 weeks, both groups had the same improved profile in the blood cholesterol levels. Their cholesterol markers moved 10 to 20 percent in "good" directions. The eggs had no effect. Source: The Journal Of Nutritional Biochemistry

Habitual consumption of eggs does not alter the beneficial effects of endurance training on plasma lipids and lipoprotein metabolism in untrained men and women.

Changes in plasma lipid and apolipoprotein profiles were evaluated in 12 healthy, unfit subjects (VO(2peak) 39.1+/-2.8 ml.kg(-1).min(-1); 5 women, 7 men) at baseline and following endurance exercise training. The exercise protocol consisted of a 6-week endurance exercise training program (4-5 days week(-1); 60 min.session(-1); >/=65% HR(max)). Subjects were randomly assigned to consume an egg- (n=6; 12 eggs.week(-1)) or no-egg (n=6; 0 eggs.week(-1))-based, eucaloric, standardized diet for 8 weeks. Both diets were macronutrient balanced [60% carbohydrate, 30% fat, 10% protein (0.8 g.kg(-1).day(-1))] and individually designed for weight maintenance. Plasma lipids were measured twice within the same week at baseline and following exercise training. At baseline, subjects were normolipidemic with values of 163.9+/-41.8, 84.8+/-36.7, 60.6+/-15.4 and 93.1+/-52 mg dl(-1) for total cholesterol, LDL cholesterol and HDL cholesterol and triglyceride concentrations, respectively. A two-way ANOVA was used to analyze diet and exercise effects and interactions. In both groups, endurance exercise training resulted in a significant 10% increase in HDL-C (P<.05), a 19% decrease in Apo B concentrations (P<.05) and reductions in plasma CETP activity (P<.05). Plasma LDL-C decreased by 21% (P=.06). No main effects of diet or interactions with plasma lipids or Apo B concentrations were observed. These data demonstrate that endurance training improved the plasma lipid profiles of previously unfit, normolipidemic subjects independent of dietary cholesterol intake from eggs.

Fasting.....and jet lag

This study popped up today:

Study identifies food-related clock in the brain Findings could help travellers, shift workers adjust to changes in time zones and overnight schedules

It is basically about another potential effect of intermittent fasting: The findings, which appear in the May 23 issue of the journal Science, help explain how animals adapt their circadian rhythms in order to avoid starvation, and suggest that by adjusting eating schedules, humans too can better cope with changes in time zones and nighttime schedules that leave them feeling groggy and jet-lagged.

If you are interested, the story was commented on elsewhere:

Fasting may starve off jet lag

Are mealtimes the answer to jet lag?

Bounding....

I've said before that I am a sucker for videos of big jumps..... (remember this one?) Anyway, Mark recently posted a good article on Plyometrics..."to make you fitter, faster and stronger"

He includes some the video above of extreme bounding:

Starting from a gentle jog, push off the ground with your left foot and bring the leg forward with knee bent and thigh parallel to the ground. Extend the right arm forward as the left leg comes through and swing back as left foot touches floor. Then the right leg drives forward, with opposite arm extending and then flexing back. By keeping foot strikes (that is, the time that your foot is in contact with the ground) to a minimum, you will execute a series of quick, long strides that attempt to cover as much distance as possible

Carbs and fat; which is the villain, which the hero?

Of course it is not as simple as that.....

Lyle McDonald has just posted a couple of good thought provoking articles on this. You may not agree with them all, but they are a good read:


Carbohydrate and Fat Controversies Part 1

Carbohydrate and Fat Controversies Part 2

Salt: good or bad?

I thought this was interesting. I do not add salt to my food in general - I don't really like it. I suppose I've also had a view that excess salt is unhealthy .

This study casts doubt on that idea....

New study casts further doubt on risk of death from higher salt intake

May 15, 2008 – (BRONX, NY) – Contrary to long-held assumptions, high-salt diets may not increase the risk of death, according to investigators from the Albert Einstein College of Medicine of Yeshiva University. They reached their conclusion after examining dietary intake among a nationally representative sample of adults in the U.S. The Einstein researchers actually observed a significantly increased risk of death from cardiovascular disease (CVD) associated with lower sodium diets. They report their findings in the advance online edition of the Journal of General Internal Medicine.

The junkfood science blog had a good post on this subject last year: Salt Shaking News

Strength training for runners

While I am not a massive fan of distance running, if it is your sport, you may find this study of interest.

I'm sure you could design a better training programme, but even 4x4 half squats improved strength, running economy and the time to exhaustion. So if you want to improve your running there is an argument for adding strength training to the mix.....



Maximal Strength Training Improves Running Economy in Distance Runners.

Purpose: The present study investigated the effect of maximal strength training on running economy (RE) at 70% of maximal oxygen consumption (V[spacing dot above]O2max) and time to exhaustion at maximal aerobic speed (MAS). Responses in one repetition maximum (1RM) and rate of force development (RFD) in half-squats, maximal oxygen consumption, RE, and time to exhaustion at MAS were examined.

Methods: Seventeen well-trained (nine male and eight female) runners were randomly assigned into either an intervention or a control group. The intervention group (four males and four females) performed half-squats, four sets of four repetitions maximum, three times per week for 8 wk, as a supplement to their normal endurance training. The control group continued their normal endurance training during the same period.

Results: The intervention manifested significant improvements in 1RM (33.2%), RFD (26.0%), RE (5.0%), and time to exhaustion at MAS (21.3%). No changes were found in V[spacing dot above]O2max or body weight. The control group exhibited no changes from pre to post values in any of the parameters.

Conclusion: Maximal strength training for 8 wk improved RE and increased time to exhaustion at MAS among well-trained, long-distance runners, without change in maximal oxygen uptake or body weight.

I'm Back Again

Just had an excellent week in the highlands. Seven new Munros climbed (223 total now, only 61 to go). The weather was surprisingly good all week. Windy, but otherwise excellent.

This photo above looking over to Ben Nevis from Aonach Beag, last Wednesday. A hard day - only about a 15km walk but over 1200m of ascent which was tough.

Back to normal posting activity now....

Gone walking.....

Back in a week

More kneeling jumps - it is all in the hips

from Scrapper

It is interesting that the key move in these - like in the kettlebell swing - is the hip drive.

how to dope a sprinter

this BBC news page has some interesting information on how Dwain Chambers managed his drug programme and avoided detection by the authorities.

There is also a video of his former Balco supplier, Victor Conte, explaining the doping regime.

I have a funny attitude towards steroids. I would never take them because I would be scared of causing myself harm. However I have known people who have taken the gear, although this was around 15-20 years ago when things were less sophisticated. The drugs worked I could see that. They grew fast and got strong.

Is it cheating though? Yes. But sometimes I think that you could argue that altitude training is cheating or that particularly streamlined swimsuits are cheating. People are never on an level playing field.

It doesn't seem right, but maybe we should not be so nieve. The world is a tough and unpleasant place. People use drugs.

What I don't like is the deception - the lies that people are clean when they are not. If they are on gear, fine admit it.


What do you think? What do we do?

600lb one arm bench press

This video is kicking around the internet at the moment, but I think it deserves a wide exposure.

At the APF/AAPF Master's Nationals held May 4 in Baton Rouge, Louisiana Mike Hummel, 242, bench pressed 600 pounds as an M1. That, in itself, is not an insignificant achievement. Even more impressive, Hummel did it with only one arm. Hummel lost his left arm a few years ago at the mid-forearm. After extensive rehabilitation, he began training again and with the help of a prosthetic is able to compete. The prosthetic features a hinge and screw clamp, allowing him to "grip" the bar. Here's video of Hummel's feat:

Amazing. Ross makes some good comments on this in the context of thinking about people's general negativity in "Life is tough, deal with it"

More Core Training......

Mark Twight says:

One-Piece
Dan John originally said that the body is one-piece, and joked that there is no core. We couldn't see how rolling around on a Swiss Ball could do any more than help stabilize muscles around one's center. However, we learned that many other exercises taught one to initiate movement from the centre without ever being recognized as "core exercises" so we filmed some.

Check out the Turkish Get ups at the end....

There is no core......The body is one piece....

More ketogenic diet reseach

I've pointed out recently that keotgenic diets are used to treat epilepsy and possibly benefit other neurological conditions. However each time this is mentioend the science will often say something like:

However, the mechanism(s) by which the Ketogenic Diet achieves neuroprotection and/or seizure control are not yet known.

Here is a study which makes a guess at what is going on. Increases in ATP - the basic fuel of cells

Are purines mediators of the anticonvulsant/neuroprotective effects of ketogenic diets?

Abnormal neuronal signaling caused by metabolic changes characterizes several neurological disorders, and in some instances metabolic interventions provide therapeutic benefits. Indeed, altering metabolism either by fasting or by maintaining a low-carbohydrate (ketogenic) diet might reduce epileptic seizures and offer neuroprotection in part because the diet increases mitochondrial biogenesis and brain energy levels. Here we focus on a novel hypothesis that a ketogenic diet-induced change in energy metabolism increases levels of ATP and adenosine, purines that are critically involved in neuron-glia interactions, neuromodulation and synaptic plasticity. Enhancing brain bioenergetics (ATP) and increasing levels of adenosine, an endogenous anticonvulsant and neuroprotective molecule, might help with understanding and treating a variety of neurological disorders.


And another one - look at the sentence I've put in bold in this abstract:



Effect of weight loss and ketosis on postprandial cholecystokinin and free fatty acid concentrations.


BACKGROUND: Weight regain after weight loss may not be due primarily to voluntary return to social habits but may be explained by changes in peripheral hormonal signals activating hunger and encouraging feeding behavior. OBJECTIVE: The objective of this study was to investigate physiologic adaptations to weight loss that may encourage weight regain. DESIGN: The study had a within-subject repeated-measure design [12 healthy, obese men, 33-64 y, body mass index (in kg/m(2)) 30-46] and was a clinical intervention investigation of circulating metabolites and hunger-satiety responses before and after weight loss. Measures included anthropometry (bioelectrical impedance, body weight, and waist circumference), concentrations of circulating hormones and metabolites [ketone bodies, free fatty acids (FFAs), insulin, leptin, glucose, and cholecystokinin (CCK)], and measures of hunger and satiety at baseline, 8 wk after weight loss with a very-low-energy diet, and 1 wk after weight maintenance. RESULTS: Weight loss led to a reduction in postprandial CCK secretion (P = 0.016). However, when subjects were ketotic (elevated circulating beta-hydroxybutyrate concentrations), CCK secretion was sustained at concentrations before weight loss. After weight loss, there were reduced postprandial FFA concentrations (P = 0.0005). The presence of ketosis sustained FFA to concentrations before weight loss (P = 0.60). CONCLUSION: Rapid weight loss of approximately 10% of initial body weight results in a reduction in postprandial CCK and FFA concentrations.

.....when subjects were ketotic (elevated circulating beta-hydroxybutyrate concentrations), CCK secretion was sustained at concentrations before weight loss.

What is CCK?

Cholecystokinin (CCK; from Greek chole, "bile"; cysto, "sac"; kinin, "move"; hence, move the bile-sac (gallbladder)) is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called pancreozymin, is synthesised by I-cells in the mucosal epithelium of the small intestine and secreted in the duodenum, the first segment of the small intestine, and causes the release of digestive enzymes and bile from the pancreas and gallbladder, respectively. It also acts as a hunger suppressant. Recent evidence has suggested that it also plays a major role in inducing drug tolerance to opioids like morphine and heroin, and is partly implicated in experiences of pain hypersensitivity during opioid withdrawal.[1][2]

So reading this abstract in the light of this it seems that the weight loss causes a reduction in CCK - and therefore an increase in hunger.....unless you are in ketosis, when hunger is suppressed?

One hand pullup

this is pretty sick....a climber doing a one handed pull up:

a ketogenic diet is good for you....

well ok it is good for rats.

It increases the level of Glutathione, an important antioxidant. So forget your 5 a day, just dump the carbs?

The Ketogenic Diet Increases Mitochondrial Glutathione Levels.

The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague-Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of beta-hydroxybutyrate (BHB). KD-fed rats showed a 2-fold increase in hippocampal mitochondrial glutathione (GSH) and GSH/GSSG ratio compared to control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity, as well as upregulated protein levels of GCL subunits in KD-fed, but not control rats, was observed. Reduced coenzyme A (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared to controls. Since GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial hydrogen peroxide (H(2)O(2)) production and H(2)O(2)-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H(2)O(2) production and mtDNA damage. Together, the results demonstrate that the KD upregulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.

UPDATE - Emma has written more about a ketogenic diet in the last couple of days here and here

more knee jumps

I'm sure this is a potential ankle breaker!

Protein, heart health and diabetes

Protein in optimal health: heart disease and type 2 diabetes


Diets with increased protein and reduced carbohydrates have been shown to improve body composition, lipid and lipoprotein profiles, and glycemic regulations associated with treatment of obesity and weight loss. Derived from these outcomes, high-protein, low-carbohydrate diets are also being examined for treatment of heart disease, metabolic syndrome, and type 2 diabetes. High-protein, low-carbohydrate diets have been found to have positive effects on reducing risk factors for heart disease, including reducing serum triacylglycerol, increasing HDL cholesterol, increasing LDL particle size, and reducing blood pressure. These diets appear particularly attractive for use with individuals exhibiting the atherogenic dyslipidemia of metabolic syndrome. High-protein, low-carbohydrate diets have also been investigated for treatment of type 2 diabetes with positive effects on glycemic regulation, including reducing fasting blood glucose, postprandial glucose and insulin responses, and the percentage of glycated hemoglobin. Specific effects of increasing protein compared with reducing carbohydrates have not been extensively investigated. Additional research is needed to determine specific levels of protein, carbohydrate, and fat for optimum health of individuals who differ in age, physical activity, and metabolic phenotypes.

the benefits of protein

Protein, weight management, and satiety

Obesity, with its comorbidities such as metabolic syndrome and cardiovascular diseases, is a major public health concern. To address this problem, it is imperative to identify treatment interventions that target a variety of short- and long-term mechanisms. Although any dietary or lifestyle change must be personalized, controlled energy intake in association with a moderately elevated protein intake may represent an effective and practical weight-loss strategy. Potential beneficial outcomes associated with protein ingestion include the following:

• 1) increased satiety—protein generally increases satiety to a greater extent than carbohydrate or fat and may facilitate a reduction in energy consumption under ad libitum dietary conditions;
• 2) increased thermogenesis—higher-protein diets are associated with increased thermogenesis, which also influences satiety and augments energy expenditure (in the longer term, increased thermogenesis contributes to the relatively low-energy efficiency of protein); and
• 3) maintenance or accretion of fat-free mass—in some individuals, a moderately higher protein diet may provide a stimulatory effect on muscle protein anabolism, favoring the retention of lean muscle mass while improving metabolic profile. Nevertheless, any potential benefits associated with a moderately elevated protein intake must be evaluated in the light of customary dietary practices and individual variability.

carbs and cancer....

I've previously pointed out some of the research stating that cancer can be treated with a ketogenic diet, starving the cancer cells of the glucose that they need to survive.

Here is a new and related study.

Carbohydrate intake, glycemic index, glycemic load, and risk of postmenopausal breast cancer in a prospective study of French women

Background: Diets high in carbohydrates may result in chronically elevated insulin concentrations and may affect breast cancer risk by stimulation of insulin receptors or through insulin-like growth factor I (IGF-I)–mediated mitogenesis. Insulin response to carbohydrate intake is increased in insulin-resistant states such as obesity.

Objective: We sought to evaluate carbohydrate intake, glycemic index (GI), and glycemic load (GL) and subsequent overall and hormone-receptor-defined breast cancer risk among postmenopausal women.

Design: A prospective cohort analysis of dietary carbohydrate and fiber intakes was conducted among 62 739 postmenopausal women from the E3N French study who had completed a validated dietary history questionnaire in 1993. During a 9-y period, 1812 cases of pathology-confirmed breast cancer were documented through follow-up questionnaires. Nutrients were categorized into quartiles and energy-adjusted with the regression-residual method. Cox model–derived relative risks (RRs) were adjusted for known determinants in breast cancer.

Results: Dietary carbohydrate and fiber intakes were not associated with overall breast cancer risk. Among overweight women, we observed an association between GI and breast cancer (RRQ1–Q4: 1.35; 95% CI: 1.00, 1.82; P for trend = 0.04). For women in the highest category of waist circumference, the RRQ1–Q4 was 1.28 (95% CI: 0.98, 1.67; P for trend = 0.10) for carbohydrates, 1.35 (95% CI: 1.04, 1.75; P for trend = 0.01) for GI, and 1.37 (95% CI: 1.05, 1.77; P for trend = 0.003) for GL. We also observed a direct association between carbohydrate intake, GL, and estrogen receptor–negative breast cancer risk.

Conclusions: Rapidly absorbed carbohydrates are associated with postmenopausal breast cancer risk among overweight women and women with large waist circumference. Carbohydrate intake may also be associated with estrogen receptor–negative breast cancer.

coffee and blood sugar.....

We have mentioned coffee before with respect to its impact on insulin. Here is another related study. Caffeine makes you insulin resistant?

Caffeinated coffee consumption impairs blood glucose homeostasis in response to high and low glycemic index meals in healthy men


Background: The ingestion of caffeine (5 mg/kg body weight) and a 75-g oral glucose load has been shown to elicit an acute insulin–insensitive environment in healthy and obese individuals and in those with type 2 diabetes.

Objective: In this study we investigated whether a similar impairment in blood glucose management exists when coffee and foods typical of a Western diet were used in a similar protocol.

Design: Ten healthy men underwent 4 trials in a randomized order. They ingested caffeinated (5 mg/kg) coffee (CC) or the same volume of decaffeinated coffee (DC) followed 1 h later by either a high or low glycemic index (GI) cereal (providing 75 g of carbohydrate) mixed meal tolerance test.

Results: CC with the high GI meal resulted in 147%, 29%, and 40% greater areas under the curve for glucose (P < 0.001), insulin (NS), and C-peptide (P < 0.001), respectively, compared with the values for DC. Similarly, with the low GI treatment, CC elicited 216%, 44%, and 36% greater areas under the curve for glucose (P < 0.001), insulin (P < 0.01), and C-peptide (P < 0.01), respectively. Insulin sensitivity was significantly reduced (40%) with the high GI treatment after CC was ingested compared with DC; with the low GI treatment, CC ingestion resulted in a 29% decrease in insulin sensitivity, although this difference was not significant.

Conclusion: The ingestion of CC with either a high or low GI meal significantly impairs acute blood glucose management and insulin sensitivity compared with ingestion of DC. Future investigations are warranted to determine whether CC is a risk factor for insulin resistance.

the number of fat cells remains constant....

........researchers determine that the number of fat cells in a human's body, whether lean or obese, is established during the teenage years. Changes in fat mass in adulthood can be attributed mainly to changes in fat cell volume, not an increase in the actual number of fat cells.

This is interesting. Read the rest here.

Knee Jumps

Nick McKinless is a British Strongman (and stuntman and grip monster) whose blog I keep an eye on.

I've noted before that I am a sucker for vertical jumps. Take a look at this video and make sure that you keep watching until the end when, at about 2:06 you will see a massive jump.....

The impact of freezing and toasting on the glycaemic response of white bread

The impact of freezing and toasting on the glycaemic response of white bread

Then again, don't eat the bread at all and the GI is even better. Of course the GI concept is not without problems

Washboard abs on a high fat diet?

You are what you eat?


That is Mark, age 54. His diet works out at about 58% of calories from fat, not as high as some.....but certainly higher than many! Otherwise there is:

2,458 calories, 58% of which was from fat; 165 grams of protein (1 gram per pound of body weight) and 114 grams of carbs. Now some might say that eating less than 2500 calories is too low for a moderately active man, but there are two points to make here. First, I am never really hungry. On this Primal Blueprint eating style, I eat when I want to and stop when I no longer feel hungry. Pretty simple. If I skip meals, I don’t get light-headed or famished. I don’t ever feel like I need more calories or that I am missing out on anything or “sacrificing” some guilty pleasure. I get plenty of protein to spare muscle and add to protein turnover. I get plenty of fat for fuel – sometimes 65% of daily calories.

Second - and this goes to the heart of the Primal concept – when you eat fewer carbs, your body readily accesses dietary and stored fat for fuel. Even at 8% body fat, I still have 46,000 calories of stored fat, at least 25,000 of which is available to use as fuel at any time. Theoretically, you could walk 250 miles on that. It’s a beautiful thing when you direct gene expression to “want” to burn fat instead of always storing it. You certainly don’t need cardio to produce the full effect (you can if you want, within guidelines). As we often say here “80% of your results come from how you eat.” Conversely, eating more carbs drives up insulin, drives carbs towards fat storage, decreases fat-burning by prompting fat cells to hold on to stored fat and makes you hungrier for more carbs. I could burn some or most of all that off again by doing tons of cardio, but that only makes me hungrier for more carbs and perpetuates the cycle. It’s like digging a hole to put the ladder in to wash the basement windows.

Sounds like what Peter is telling us here and here.....

Scientific Study of the "paleolithic" diet

Here is another study of the impact of a Paleolithic diet. The abstract is linked to below, but I also managed to get the whole paper this time. So click on the tables to see the results

Effects of a short-term intervention with a paleolithic diet in healthy volunteers



Looking at the results in the full study, there are some interesting bits.

In terms of macro nutrient ratios the diet went from 13.5% / 54.3% / 29.6% protein / carbs / fat to 23.9% / 40% / 35.8% (% of calories). Total energy intake went down from 2478 to 1584.

I suppose if you wanted to link the changes in blood lipids etc to the diet you'd have to make is iso-calorific. Otherwise all we can say is that taking in fewer calories has an effect.....


Interesting anyway and worth reading. UPDATE Br Briffa comments on this here. And of course the establishment do not like it!

This takes some grip

almost a 32kg bottoms up TGU......



from Rif

Not all fat is the same

Beneficial Effects of Subcutaneous Fat Transplantation on Metabolism

Subcutaneous (SC) and visceral (VIS) obesity are associated with different risks of diabetes and the metabolic syndrome. To elucidate whether these differences are due to anatomic location or intrinsic differences in adipose depots, we characterized mice after transplantation of SC or VIS fat from donor mice into either SC or VIS regions of recipient mice. The group with SC fat transplanted into the VIS cavity exhibited decreased body weight, total fat mass, and glucose and insulin levels. These mice also exhibited improved insulin sensitivity during hyperinsulinemic-euglycemic clamps with increased whole-body glucose uptake, glucose uptake into endogenous fat, and insulin suppression of hepatic glucose production. These effects were observed to a lesser extent with SC fat transplanted to the SC area, whereas VIS fat transplanted to the VIS area was without effect. These data suggest that SC fat is intrinsically different from VIS fat and produces substances that can act systemically to improve glucose metabolism





I'd read this in Lyle McDonald's Stubborn Bodyfat Solution where he spends chapter 3 discussing the different types of bodyfat:

• essential
• brown adipose tissue
• visceral fat
• subcutaneous fat (and stubborn fat which is a subtype of this)

and how they differ.

This press release goes over similar ground.

Not all fat created equal

Joslin researchers find certain body fat reduces insulin resistance

BOSTON -- May 6, 2008 -- It has long been known that type 2 diabetes is linked to obesity, particularly fat inside the belly. Now, researchers at the Joslin Diabetes Center have found that fat from other areas of the body can actually reduce insulin resistance and improve insulin sensitivity.

In a study published in the May issue of Cell Metabolism, a team lead by C. Ronald Kahn, M.D. found that subcutaneous fat -- fat found below the skin, usually in the hips and thighs -- is associated with reduced insulin levels and improved insulin sensitivity.

Kahn said it is possible that subcutaneous fat may be producing certain hormones, known as adipokines, which produce beneficial effects on metabolism. These effects may offset the negative effects produced by abdominal fat.

Interesting stuff

Fat - Its not what you think.....

According to the press release, this one sounds a lot like Taubes' Good Calories, Bad Calories.....

In making her argument, Leas offers some startling facts. For example:

• Overweight people live longer than those in the so-called “healthy” range of the BMI scale.
• No one has ever shown a correlation between egg consumption and cardiovascular disease.
• Doctors often prescribe statin drugs when our cholesterol level reaches 240, even though this is actually within the normal range.
• A porterhouse steak contains more unsaturated fat than saturated fat.
• Today Americans consume 15 percent less fat than we did in 1970, yet overall we are 20 percent fatter.

Leas points to a number of studies that offer convincing evidence that the over-consumption of carbohydrates and the past proliferation of synthetic transfat—a truly dangerous fat—are actually to blame for the obesity and heart disease epidemics.

Throughout the book, Leas explains the science behind fats in a manner that the layperson can easily comprehend. She also explains the terminology often used in fat discussions that most people do not really understand, such as triglycerides, polyunsaturated, omega-3, and transfat, allowing everyone to truly know what is in their foods so that they can make informed health decisions. Nina Planck, author of REAL FOOD: WHAT TO EAT AND WHY, sees the importance of this, “Americans are terrified of fat, doctors tell myths about fat, and journalists repeat them. Butter is good for you and corn oil isn’t. Don’t be the last one to know why: read this book.”

Old guys, weights and protein.....

I am sure that there are lots of clever people reading this blog that will be able to make more of this study than I can but how about:

• Resistance training still has effects on older men
• Taking protein around training in older men reduces the usual resultant levels of testosterone in the blood; but
• Taking protein around training did not affect the gene expression associated with other hormonal growth factors.
  

So in the light of this study and of this one - Protein co-ingestion stimulates muscle protein synthesis during resistance type exercise - is it a good idea to eat protein around your training? I don't know and I can't really comment since I've not tried it, but I can't help thinking that I would throw up.

Androgen receptors and testosterone in men-Effects of protein ingestion, resistance exercise and fiber type.

The purpose of this study was to examine the impact of protein ingestion on circulating testosterone and muscle androgen receptor (AR) as well as on insulin-like growth factor-I (MGF and IGF-IEa) responses to a resistance exercise (RE) bout in (57-72 year) men. Protein (15g whey) (n=9) or placebo (n=9) was consumed before and after a RE bout (5 sets of 10 repetition maximums), and vastus lateralis muscle biopsies were taken pre, 1 and 48h post-RE. The protein ingestion blunted the RE-induced increase in serum free and total testosterone while the RE bout significantly increased muscle AR mRNA levels in older men (P<0.05). However, protein ingestion did not significantly affect AR mRNA or protein expression, or MGF and IGF-IEa mRNA expression at 1 and 48h post-RE. Immunohistochemical staining of muscle cross-sections was done with antibodies specific to AR and MyHC I and II and showed that there seems to be within or near the type-I muscle fibers a greater staining of ARs than within or near the type-II fibres. In conclusion, the protein ingestion hinders RE-induced increase in serum testosterone in older men but may not significantly affect muscle AR, MGF or IGF-IEa gene expression. Furthermore, the present study shows that even older men are able to increase muscle AR mRNA expression in response to a RE bout.

Round up

Just a quick round up of things I've spotted of interest in the last couple of days:

Weight loss when it is hard - read all the comments too

Roman Gladiators were fat vegetarians!

Fat cells die and are replaced - Every year, whether you are fat or thin, whether you lose weight or gain, 10 percent of your fat cells die. And every year, those cells that die are replaced with new fat cells, researchers in Sweden reported Sunday.

Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults - In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved but that such a trend may rely on reducing caloric intake in addition to exercise training.

"You can strive for excellence without being burdened by a need for perfection" - great motivational post from Rannoch.

Plyometric training - how often?

I've had posts before on the effectiveness of plyometrics (for example here). This study looked at the optimal frequency of such training... Once or twice a week is better than 4 times per week......

Low and Moderate Plyometric Training Frequency Produces Greater Jumping and Sprinting Gains Compared With High Frequency.


The purpose of this study was to examine the effect of 3 different plyometric training frequencies (e.g., 1 day per week, 2 days per week, 4 days per week) associated with 3 different plyometric training volumes on maximal strength, vertical jump performance, and sprinting ability. Forty-two students were randomly assigned to 1 of 4 groups: control (n = 10, 7 sessions of drop jump (DJ) training, 1 day per week, 420 DJs), 14 sessions of DJ training (n = 12, 2 days per week, 840 DJs), and 28 sessions of DJ training (n = 9, 4 days per week, 1680 DJs). The training protocols included DJ from 3 different heights 20, 40, and 60 cm. Maximal strength (1 repetition maximum [1RM] and maximal isometric strength), vertical height in countermovement jumps and DJs, and 20-m sprint time tests were carried out before and after 7 weeks of plyometric training. No significant differences were observed among the groups in pre-training in any of the variables tested. No significant changes were observed in the control group in any of the variables tested at any point. Short-term plyometric training using moderate training frequency and volume of jumps (2 days per week, 840 jumps) produces similar enhancements in jumping performance, but greater training efficiency ( approximately 12% and 0.014% per jump) compared with high jumping (4 days per week, 1680 jumps) training frequency ( approximately 18% and 0.011% per jump). In addition, similar enhancements in 20-m-sprint time, jumping contact times and maximal strength were observed in both a moderate and low number of training sessions per week compared with high training frequencies, despite the fact that the average number of jumps accomplished in 7S (420 jumps) and 14S (840 jumps) was 25 and 50% of that performed in 28S (1680 jumps). These observations may have considerable practical relevance for the optimal design of plyometric training programs for athletes, given that a moderate volume is more efficient than a higher plyometric training volume.

Ketogenic diet and epilepsy

I really didn't think this was news, but it was on the radio this morning

Diet treatment call for epilepsy
A special high-fat diet helps to control fits in children with epilepsy, a UK trial suggests.
The number of seizures fell by a third in children on the "ketogenic" diet, where previously they had suffered fits every day despite medication.
The diet alters the body's metabolism by mimicking the effects of starvation, the researchers reported in the Lancet Neurology.
The researchers called for the diet to be more widely available on the NHS.

A further story gives a case of a young child who improved with the diet and an example of it.

The abstract of the study is here.

Lyle McDonald explains the history of this diet:

The ketogenic diet has been used to treat a variety of clinical conditions, the most well known of which is childhood epilepsy. Writings as early as the middle ages discuss the use of fasting as a treatment for seizures. The early 1900's saw the use of total fasting as a treatment for seizures in children. However, fasting cannot be sustained indefinitely and only controls seizures as long as the fast is continued.

Due to the problems with extended fasting, early nutrition researchers looked for a way to mimic starvation ketosis, while allowing food consumption. Research determined that a diet high in fat, low in carbohydrate and providing the minimal protein needed to sustain growth could maintain starvation ketosis for long periods of time. This led to development of the original ketogenic diet for epilepsy in 1921 by Dr. Wilder. Dr. Wilder's ketogenic diet controlled pediatric epilepsy in many cases where drugs and other treatments had failed. The ketogenic diet as developed by Dr. Wilder is essentially identical to the diet being used in 1998 to treat childhood epilepsy.

The ketogenic diet fell into obscurity during the 30's, 40's and 50's as new epilepsy drugs were discovered. The difficulty in administering the diet, especially in the face of easily prescribed drugs, caused it to all but disappear during this time.

So it has been around since 1921 and it is now rediscovered...

Metcon ramblings.....

Crossfit, circuit training, metabolic conditioning, GPP. Call it what you will it has become popular in recent years. Scott (The Modern Forager) had an excellent post on this a few days ago: Picking the Right Tool for the Job, Part 1: GPP vs SPP

I think there is something of a backlash against crossfit at the moment and it is worth reading all of Scott's post and the comments.

It does all depend on what you are training for. Crossfit is about being an all-rounder - and probably fitter than 95% of the population - which is fine. Some of the criticism I think is coming from those who are trying to excel in a specialism while using a generalist programme.

For example Mark Twight - the guy who trained the actors for 300 - has moderated his training away from pure crossfit stuff and added in a lot more endurance work. But this makes sense because he is an endurance athlete - doing bike racing. He explains here

January 2008: Every now and then someone posts an old quote of mine about Crossfit and using short-duration, high-intensity effort to improve endurance, referring to my initial experience. Those who imagine I still believe what I did then, or train the way I did when testing the validity of the method should re-read the following paragraphs:

“... it must be understood that these workouts were not undertaken in a vacuum; they were used to sharpen a 20-year endurance base gained by training and climbing at intensities specific to long endurance effort. The same results would not be produced in the athlete without a similar aerobic base ...”

Surely the meaning of “20-year endurance base” is clear.

“During the two years since that race I have learned – through personal experimentation and experience and discussion with coaches and scientists smarter than me – that recovery must be trained, and recovery adaptations occur just like the compensatory reaction to imposed athletic demands. Similarly, it is now absolutely clear that there is no such thing as a free lunch and there never was: to go long you have to go long, if you want genuine endurance and/or multi-day endurance you have to train it. Period.

A few have asked me to update my thesis on the subject and I’ll do so eventually. For now, the link below should clear up any misconceptions regarding how I think about endurance and what I am doing to train it. Endurance Revisited

Anyway......Here is a study just published. You get what you train for of course, but this is interesting in that the subjects were doing a "heavy circuit" - rather than the sort of metcon stuff on which crossfit is built - and they built and some degree of "cardio" as well as strength.

Physical Performance and Cardiovascular Responses to an Acute Bout of Heavy Resistance Circuit Training versus Traditional Strength Training.


Circuit training effectively reduces the time devoted to strength training while allowing an adequate training volume to be achieved. Nonetheless, circuit training has traditionally been performed using relatively low loads for a relatively high number of repetitions, which is not conducive to maximal muscle size and strength gain. This investigation compared physical performance parameters and cardiovascular load during heavy-resistance circuit (HRC) training to the responses during a traditional, passive rest strength training set (TS). Ten healthy subjects (age, 26 +/- 1.6 years; weight, 80.2 +/- 8.78 kg) with strength training experience volunteered for the study. Testing was performed once weekly for 3 weeks. On day 1, subjects were familiarized with the test and training exercises. On the subsequent 2 test days, subjects performed 1 of 2 strength training programs: HRC (5 sets x (bench press + leg extensions + ankle extensions); 35-second interset rest; 6 repetition maximum [6RM] loads) or TS (5 sets x bench press; 3-minute interset rest, 6RM loads). The data confirm that the maximum and average bar velocity and power and the number of repetitions performed of the bench press in the 2 conditions was the same; however, the average heart rate was significantly greater in the HRC compared to the TS condition (HRC = 129 +/- 15.6 beats.min, approximately 71% maximum heart rate (HRmax), TS = 113 +/- 13.1 beats.min, approximately 62% HRmax; P < 0.05). Thus, HRC sets are quantitatively similar to traditional strength training sets, but the cardiovascular load is substantially greater. HRC may be an effective training strategy for the promotion of both strength and cardiovascular adaptations.

Crash diets 'may reduce lifespan'

This one just bemused me, mainly due to the photo of the fish. I kept on thinking "I've never seen an obese fish!"

Scottish scientists have found that binge eating and crash dieting may significantly reduce life expectancy.

Researchers from Glasgow University observed that fish given a "binge then diet" food regime had a reduced lifespan of up to 25%.

Their study compared the growth rate, success of reproduction and lifespan of stickleback fish.

They believe the findings could have implications for teenagers and children who follow extreme patterns of dieting.

I'm really puzzled the way the researchers extrapolate from sticklebacks to humans.

Effect of exercise and calorie restriction on aging

There has been a fair bit of research and some hype about the potential for combating aging via calorie restriction.

In light of all this I thought that this study looked interesting. All the usual caveats (like this is mice not humans) but interesting that exercise did not accelerate the accumulation of oxidative damage. Even so, exercise doesn't make you live longer....which is worth bearing in mind

Effect of exercise and calorie restriction on biomarkers of aging in mice

Unlike calorie restriction, exercise fails to extend maximum life span, but the mechanisms that explain this disparate effect are unknown. We used a 24-wk protocol of treadmill running, weight matching, and pair feeding to compare the effects of exercise and calorie restriction on biomarkers related to aging. This study consisted of young controls, an ad libitum-fed sedentary group, two groups that were weight matched by exercise or 9% calorie restriction, and two groups that were weight matched by 9% calorie restriction + exercise or 18% calorie restriction. After 24 wk, ad libitum-fed sedentary mice were the heaviest and fattest. When weight-matched groups were compared, mice that exercised were leaner than calorie-restricted mice. Ad libitum-fed exercise mice tended to have lower serum IGF-1 than fully-fed controls, but no difference in fasting insulin. Mice that underwent 9% calorie restriction or 9% calorie restriction + exercise, had lower insulin levels; the lowest concentrations of serum insulin and IGF-1 were observed in 18% calorie-restricted mice. Exercise resulted in elevated levels of tissue heat shock proteins, but did not accelerate the accumulation of oxidative damage. Thus, failure of exercise to slow aging in previous studies is not likely the result of increased accrual of oxidative damage and may instead be due to an inability to fully mimic the hormonal and/or metabolic response to calorie restriction.

Amazing one arm snatch

spotted on the Bodyrecomposition forum