Step By Step Guide to Your Own Workout Routine - Part III: Understanding the Role of Workload, Density and Intensity

Image 1: Simply copying Arnold's routine would probably be a bad idea, but copying the way he played with workload and density to achieve maximal intensity would be.
After reading Part I and Part II of the "Step By Step Guide to Your Own Workout Routine" on the last weekend and a whole week to think about your first / new own workout program, you should by now know
  • how often and on which days you train (cf. part I), and
  • what type of workout you perform on a given day (cf. part II)
Those of you who have not already done that may want to check out Adelfo's latest "own" workout plan, the details of which he explained in the last installment of his weekly guest-posts here at the SuppVersity, so that you get an idea of what I have already hinted at in the last installment: Despite that the number of possible workout regimen you could come up with is literally endless, your knowledge about your goals, your past training experiences and your personal preferences should always be reflected in your program design.

The logical next step: Set and rep prescriptions for your workouts

It goes without saying certain decisions you may have made in the last week will make at least part of the considerations regarding the total number of sets, the number of repetitions per set, the time-under-tension (TUT), the rest times between sets and many of the related, less important parameters obsolete. If, for example, you decided on a similar routine as Adelfo's week 1 EDT + 5x5 combo, you would not have to care about either the number of sets or reps, because both "workouts" (in this case the term refers to a the whole concept) include detailed prescriptions, i.e.
  • "perform your superset for 20min with as many reps as you can" (EDT), and
  • "do 5 sets of 5 reps to failure" (5x5)
While it would certainly be possible to modify these prescriptions that would leave you with something I like to call an XY-esque, as in EDT-esque or 5x5-esque workout. In the end, though, it does not even matter if you want to modify an existing routine to suit your current goals or come up with a new one, without at least a cursory understanding of the implications the number of exercises, sets, reps, TUT and weights you use will have on your results, it is pretty likely that the latter will at least be suboptimal - if not completely absent.
Tip #1: It is very well possible to modify any detailed workout prescription to suit your individual needs. Whenever you do that, you should yet keep in mind that whoever came up with the original workout probably had his reasons to incorporate for example 10 sets of 10 reps and not 10 sets of 3 reps. Or put more simply, if you change fundamental variables of a given routine - in the example at hand this would be using a strength specific rep-range in a workout routine that was designed primarily for hypertrophy gains - it usually is more prudent to start building your own routine from scratch instead of making one modification after the other to end up with an at best "suboptimal" routine (in many cases you will end up with a non-functional mutant, though).

Learning from the bros and checking with the pros

I guess, many of you will already be familiar with the most commonly cited principles of workout programing and in case you were expecting me to come up with revolutionary insights into what you may call the "workout 101", you have obviously overlooked that they were and still are the ones 90% of the successful weight lifters and bodybuilders adhere to.

Image 2: Unlikely that you won't find the information on the left somewhere in this incarnation of the Encyclopedia of Bodybuilding (img MuscleMag International). Why? The answer is simple: They work - as long as you choose and combine them correctly.
If you take a look at the inferior and oftentimes non-existent results many of the trainees have, although they know many of these "fundamentals"
  • in and out of the gym in <60min
  • less than 18-20 sets total
  • 10-15 sets for the back and leg muscles*
  • 6-9 sets for chest and shoulders*
  • 4-8 sets for arms*
    *the numbers apply to bodypart split training
  • 3-5 reps for strength
  • 6-12 reps for hypertrophy
  • 12-25 reps for strength endurance (+conditioning)
it does yet become obvious that there is more to getting stronger, building muscle and improve your conditioning than the knowledge of these simple rules.

And as awkward as it may seem, my personal experience tells me that in 75% of the cases, where trainees are not satisfied with the results their workout programs are generating, the underlying reasons is not following the rules. In that, I have found that the "in and out of the gym in <60min" rule and the "less than 18-20 sets total" rule, as well as the "6-9 set for chest and arms" and "4-8 sets for arms" rules appear to be among the favorite "does not apply to me" rules for the average trainee
Tip #2: Even though the most fundamental contributer to continuous progress is having a sound workout program, sticking to the plan is a very close second. And both, coming up with a new plan every week and just doing more than your plan prescribes are the worst enemies of your progress.

Pull the trigger and leave!

The reason for the widespread ignorance towards these rules is the very human misconception that more was always better. To understand why this is not the case, it may be useful to read up on the underlying physiological processes of skeletal muscle hypertrophy and increases in contractile force in the respective parts of the Intermittent Thoughts on Building Muscle series, here at the SuppVersity.
Figure 1: The intricacies of skeletal muscle hypertrophy. For all the details check out the preliminary summary of the Intermittent Thoughts on Building Muscle (click here to be redirected)
If you take a closer at figure 1 and remember what you have learned in the course of the series, it should be obvious that working is at the heart of all those processes that will make you stronger and more muscular, but its role is not that of a driving force, but that of a trigger.And just as you probably do not push the "on" button on your computer ten times to accelerate the time it takes for the system to boot, you should leave the gym at the very moment, where the signaling cascade has kicked in.

The primacy of intensity and how it relates to workload and density

Of the many factors which will determine how "long" it will take to initiate this cascade, the training workload (often also referred to as "volume"), the density and the intensity are not only the most important ones, they are also the ones you can deliberately control. "Optimal" results thusly requite that you align these factors with the ones you cannot manipulate directly, such as your age, your overall health, your current training status, the time you have to spare, etc. to match your current goals.
    Image 3: German Olympic lifter Julia Rohde - do you still believe lifting heavy will make you "bulky"? (img
  • Workload: Of these three variables the training "volume" is probably the most straight forward one, as it can be measured simply by the workload. Even if you are no physicist you should be aware that the work (w) is the total amount of force applied to the weith (F = mass x acceleration) times the way (S) you are moving it (W = F x S). In other words, if you carry a 50lbs stone 100m exerting the force of F = 50lbs * 10m/s² (where 10m/s² is the acceleration due to gravity), you have performed the same amount of work as someone who carries a 5lbs stone in his pocket while walking 1km. It should be obvious that this measure alone is of little value and I do still see people training set after set, staying in the gym for 2 hours, performing twice or thrice the amount of "work" I do and still stagnate in terms of strength and size gains.
  • Density: If we use the previous example of carrying a stone, and think of ten steps you take as one rep, then the density of your "workout", i.e. carrying the 50lbs stone for 100m would be 10x higher than the one of the other person, because - if we assume that you walk at the same pace - you will be ready in 10x shorter timespan than the person who carries the 5lbs stone for 1000m.
  • Intensity: Contrary to what you often see in the "intensity" column of many workout programs, the weight (often expressed relative to your one-repetition max, the 1RM; or as the maximal amount of weight you can lift for X repetitions, the 12RM, 6RM, etc.) is not the single determinant of the intensity of your workouts. A workout with little to no rest periods, light weights, high reps and a medium amount of sets can be as "intense" as one of Metzner's HIT workouts where you warm up for two sets perform one all out set and head home. 
The last example, which revolved around the notion that a Metzner HIT workout could be as intense as a more medium workload, high density workout actually brings up an important point: Regardless of what your goal may be - you must always train intense!
Tip #3: Planned periods of light lifting after likewise planned periods of deliberate overreaching (we will get to the issue of periodization in a future installment), aside, you should always try to do the one rep more or add another of those ridiculous 2.5lbs plate to the bar. If you do not push yourself, you cannot expect to push the envelope on the way you look and perform.

Science says: Many roads lead to Rome

With "intensity" being a prerequisite and goal-specificity (re-)emerges as the fundamental determinant particularly in view of the number of reps and sets to perform. Against that background it is also less confusing that you will find scientific evidence to support almost every of the initially mentioned pieces of common wisdom. In 1999, for example, Weiss et al. confirmed the common wisdom that a low (=4x 3-5RM) rep-scheme produces favorable increases in squat performance (strength) compared to 4x 13-15RM or 4x 23-25RM routines. Now, was this a result of the heavier weight alone? No, it was the mere consequence of the specificity of the program - after all, the performance on slowly performed leg-extensions was slow-velocity (~1-2s concentric and 1-2s eccentric phase) was maximal in the 13-15RM group (Weiss. 1999). 
Tip #4: Although this is somewhat of an anticipation, the intensity principle and its dependence on volume and density do also explain why most trainees see success with higher rep work in their ab routines. While you can argue that this is a consequence of the physiology of the rectus abdominis (click here to read about the most effective exercises in the SuppVersity EMG series) and the way it is used in the exercise most trainees perform, i.e. the crunch. With the minimal range of movement and the low weight, density, i.e. short to non-existent rest periods and high reps (like walking 1km vs. just 100m in our previous example) are a must to achieve the intensity that is necessary to pull the "growth trigger".
In tomorrows direct follow up to this third part of the "Step By Step Guide to Your Own Workout Routine" we will take a look at three concrete incarnations of this principles with some guidelines how to adapt total workload and density to allow you to train, recover and grow at full intensity ;-)

High or Low Protein? Milk, Whey, Casein or Soy? In the End It Could Make Less of a Difference Than You Thought!

Image 1: All macronutrient ratios aside, my gut tells me that I cannot go wrong with something as delicious as a piece of steak (img. - I don't know if that is what scientists call the "gut brain axis", though *lol*
At least those of you who make sure, they get their daily dose of SuppVersity news should actually remember the "Bray study" (cf. "A Tale of Macro- and Micronutrient Modifications"), i.e. the methodologically exemplary, yet with respect to the underlying research question "What happens if you add 40% of additional calories in form of protein, fat or carbs to a high carb diet?" somewhat questionable overfeeding study the results of which caused quite a stir within the blogosphere and even mainstream media.

And contrary to what you may have read elsewhere, the fundamental message of the study, and I am not growing tired of repeating that, was a) "Consume more energy (not calories) than you need (not expend ;-) and you will get fat" and b) "Consume it from protein and you will get just as fat, but still gain some muscle."

Now, if we take these results and try to predict the results of a complementary experiment, in which people would be fed -40% less than their regular diet with either high or normal protein content, we would expect that a) the fat loss would be identical (remember! we use the results of the Bray study, not common wisdom as the basis of our predictions) and b) the high protein group should be able to maintain more muscle mass - right?

Caloric deficit determines weight loss in obese rodents, irrespective of protein intake

Although a pertinent (similarly well-controlled!) human study is still not available, a study that has just been published in the International Journal of Obesity does suggest that - at least in obese rodents - the above prediction does not apply (Chevalier. 2012). Although the 56 male Wistar rats in Chevalier et al.'s trial did lose identical amounts of body weight on a 3-week dietary intervention with a -40% reduced energy intake, they did not retain more muscle mass, when the diet contained 33% instead of only 12% of protein (cf. figure 1)!
Figure 1: Muscle and body fat mass of the rodents after 5 weeks on a obesogenic diet  and another three weeks on the same diet (obesity induction, ad libitum), or a diet with a -40% reduced energy content and identical macronutrient composition (OI-R) or a +20% greater protein content from either milk protein, whey protein, casein, casein + whey (50/50) or soy; the data is expressed relative to animals who were maintained on the ad libitum obesity induction = energy dense diet (blue bars = 100%; data calculated based on Chevalier. 2012)
And, as you can infer from the legend in figure 1, the major source (milk, whey, whey + casein, casein or soy) of the dietary protein in the diets did not exert any statistically significant influence on the total or relative (subcutaneous vs. visceral) body fat loss and the mass of the gastrocnemius or soleus muscles of the rodents, either.

When protein supply is low "protein recycling" kicks in

If you take a closer look at the data in figure 1 you  may notice another unexpected result (figure 1, red arrow). Not only were the rodents on the calorie reduced 12% protein diet able to maintain just as much muscle mass as their peers on the obesogenic ad-libitum diet (dark blue, left reference bar in figure 1), it does even appear that they experienced the same statistically yet non-significant "muscle growth" in the soleus as the rodents in the high protein groups.
Figure 2: Relative macronutrient (left) and absolute (in g/100g) main ingredient (right) composition of the experimental diets (data calculated based on Chevalier. 2012)
While there are probably a whole host of explanations for this, from a statistical point of view, non-existent phenomenon, I personally would assume that it is a combined result of an increase in food-seeking behavior (and a subsequent "training" effect which would obviously be more pronounced in the soleus, an "endurance" muscle, than the gastrocnemius) and an increase in "protein recycling".
Figure 3: Total protein content, fraction (FSR) and absolute (ASR) protein synthesis in liver, muscle and kidney tissue of the animals in the diet groups (data expressed relative to ad-libitum group, left) and ubqituitin mRNA expression in skeletal muscle of the rodents in all groups (right; data calculated / adapted from Chevalier. 2012)
Both the (within statistical margins) identical total protein contents, fraction and absolute protein synthesis rates in liver, muscle and kidney of the rodents (cf. figure 3, left), as well as the profound upregulation of the ubiquitin protein mRNA expression which showed a similar pattern in liver, kidney and muscle tissue (figure 3, right shows the data from the muscle samples) are indicative of the existence of protein sparing mechanisms which are triggered in response to a low(ish) protein intake. Despite its overall proteolytic activity, the physiological function of ubiquitin is after all to degrade and recycle unnecessary protein in the cell and has consequently received some attention as a potential target for cancer therapy (and prevention) in the last couple of years (Hoeller. 2009).

Bulking or dieting, lean or obese - different rules apply and generalizations are not advisable

Aside from the fact that this obviously is another rodent study and whenever the results of these studies do not conform with someones current dietary paradigm, the main argument will be that "rodents are no little human beings" (I don't know if you did notice that the same people usually rely on rodent studies to support their own argumentation ;-), there are a few other things to consider, before you flush your protein shakes down the toilette.
  1. The rodents were obese: It does make a huge difference if you have more than enough body fat to get you through a 3-week phase of relative profound (-40%) caloric restriction, or if you are already lean and want to shed the last pounds of body fat that cover your perfectly sculpted six-pack. If the former is the case - and I have pointed that out in previous blogposts, e.g. "Goal Setting and Stock Taking on a Diet" - your energy intake will be the main determinant of your weight loss. Modulated, if anything by your carbohydrate intake, which can hinder weight loss as long as you are pathologically insulin resistant (when you have achieved a decent degree of leanness, on the other hand, the exact opposite will be the case!)
  2. Rodents are in fact no small human beings: While it is simply stupid to discard all rodent data (that is not to your liking) with the argument that "rodents are no small human beings", there still is the issue of compliance, which - as we have seen in "High Carb vs. High Fat for Obese Type II Diabetics and What Really Happens, When Science Meets Real Life" - still is one, if not the major obstacle to successful weight loss and maintenance, where the satiating effects of a high protein intake and milk proteins, in particular (Lorenzen. 2012), will certainly come handy - assuming that the dieters actually adhere to their high-protein diet and don't simply return to their regular dietary habits, as it was the case in the Krebs study. Whether soy is or is not an option to achieve this "high" protein intake, is yet probably a question of faith and the potential risks you want to take (no soy for me, though).
  3. The caloric reduction (-40%) was very pronounced: I have likewise pointed out in various previous posts related to successful long-term weight loss that both scientific evidence, as well as practical experience suggest that energy restrictions >30% are of no use, if the goal is sustainable long-term weight loss (they may yet very well be indicated in morbidly obese persons). And while sustainability is of little importance in the context of the study at hand, the -40% reduction in energy intake also masked the small, yet still beneficial effects a high(er = not >50%!) protein intake exerts on the resting energy expenditure of dieters (Keller. 2011)
  4. Update - Not enough protein in one sitting: A few lines further down I wrote that I would suspect that you, my dear (and smart) readers would probably be able to come up with at least three additional confounding factors - and what shall I say? Proud Daddy just came up with #4! In view of the fact that the protein synthetic effect of protein depends largely on the size of an individual meal (in humans >20g of quality protein, or 10g+ of EAAs; cf. "Never Sip Your Whey!"), confounding factor #4 is that rodents usually don't eat just  2-3 large meals and thusly probably consumed relatively low amounts of protein per meal, even in the high protein group.
I guess, if you spent some more time thinking about possible confounding factors, you would come up with at least another three points that speak in favor of a reasonably high protein intake. One I personally would not measure in percentages, but rather in grams: Starting with a baseline protein intake of ~1.5g/kg body weight and building the rest of your diet around that, a 1,600kcal high protein diet for a 200lbs person could consist of ~150g protein, 50-100g fat and 50-150g carbs (the leaner, the more active and the less insulin resistant you are the more carbs). And please remember: This is just a sample calculation, so please deny yourself comments like "but is that not way too little protein?" - specifically, because this kind of "if high is good, higher must be even better" and "protein is the only save nutrient" logic could well be the reason why your weight loss is stalling.

Miracles & Nature.

The Czar once came to visit a group of soldiers, when suddenly one of them pointed his gun at the Czar. Instantly, a quick thinking and fast acting soldier, leaped on this criminal and saved the Czar. The Czar, thanked this fellow and said he could ask for anything in appreciation. The soldier said, “Can you please speak to my superior and ask him not to be so tough on me.” The Czar thought for a moment and responded, “Fool, you could have asked me to make you the superior, and he would have become your underling.”

We are granted auspicious times throughout the year, when G-d is listening more than other times. One such time is during this month, at the Passover table. We are told, that when we open the door for Elijah the prophet, at that time, similar to the words in the Bible, “their prayers went up to heaven”, this is an exceptional time to pray and be heard by G-d for anything we ask for. We need to be sure, we are at the Passover Seder table, and we don’t waste this opportunity on trivial matters.

The Bible identifies this month as the first of all the months of the year. In Hebrew the name of this month is Nissan – which means miracles. This is a month of miracles, and therefore, the great Exodus from Egypt and the splitting of the reed sea took place.

However, we all know that the New Year, is celebrated at Rosh Hashanah which is the seventh month of the year – Tishrei. This usually falls out some time in the autumn. How do we say that this is the first of all twelve months, as we begin the spring, while on the seventh month, we commemorate the creation of the universe, and the count of the calendar year is renewed then?

In the Ten Commandments, the first one begins with, “I am G-d who took you out of Egypt.” The question is asked. If G-d wanted to impress us, wouldn’t it have been greater to say, who created the heavens and earth?

Here we come to a seminal realization.

The bible speaks of two beginnings, two cycles. One is the creation of nature, and one is the onset of miracles. Although nature is also a miraculous event, to make a world out of pure nothingness, which is how G-d created the universe, is something pretty extraordinary and only G-d can pull off. The problem however, is that this miracle is programmed by G-d to follow a regular pattern, and the regular routine and predictability of this creation, has the unfortunate tendency to cause a person to overlook the miraculous and astonishing side of creation.

In order to make the universe that appears like it was always here, and is independent of any other causes, and is self existing, a very deep dimension of G-d, which was always, and depends on nothing for its survival must be employed. Notwithstanding this very powerful side of G-d that made the universe and nature, this leads people, to making a very grave error when looking at the world, that there is no G-d. Because it was the side of G-d that is not dependant on anything for its survival that created nature, people when looking at the world and see this trait, can forget at times that nothing can exist without Him.

Miracles are those occurrences which happen only occasionally and because they are not routine they can shake us out of our complacency, and force us to think and notice the influence of the unexpected even in our daily lives. Miracles make us realize and remind us that there is more to life than just the laws of nature.

Because miracles make the realization of G-d more genuine and authentic it was mentioned in the Ten Commandments. This month, the month of miracles, becomes realized with the holiday of Passover. Passover puts into motion a different parallel possibility and reality, that of miracles. Open awareness of outstanding occurrences in our lives. Miracles exist and they are also part of our calendar. We must merely open our eyes to see, and live, as well, this reality.

Adelfo Cerame - Back on the Grind! Introducing the World's First Hypertrophy-EDT-5x5 Alternate Cross-Over Regimen!

Image 1: A classic physique, but a novel routine.
I guess, I don't have to tell you that our mutual friend Adelfo is fired up to get back to the gym. I guess if it had not been for the intermediate famine phase after the post-contest binge, he would hardly have endured the one week without drudgery, but alas, the time of laziness is over now and Adelfo is about to return to the gym. Yet not without a detailed plan of attack, not as "voluminous" (in the literal sense) as he had intended before our conversation, last weekend, but still a ton of grindingly hard work - exactly the kind of thing Adelfo loves and what helped him build, what may not be the most muscular, but certainly the most aesthetic physique I have ever seen on a wheelchair bodybuilder (let alone other athlete). But I guess, I will just let him tell you how he is planning to take this superlative to yet another level.

Back on the grind! But not without a few tweaks

"After taking a week off, your boy is back at it again for another 14 weeks!" *lol* Today is training day. No food, just weights - or put more simply: I will focus on the exercise part of my plan of attack for the next show. As Adel, aka Dr. Andro, already gave away in Part II of his "Step by Step Guide To Your Own Workout Routine" series (click here for Part I) I will give you the run-down on the training protocol we have workout out on the last weekend. It's more or less a work in progress, with a tried and proven workout-base, which has worked for me in the past, and some additions that are intended to make it even better. If that sounds confusing, just bear with me, you will soon understand, what I mean.

Image 2: If you have not seen them already, you better make sure to go to either or Adelfo's Facebook page to check out the pics Dave Palumbo's crew shot at the 2012 Sunshine Classics
Those of you, who have been following the "Road to Wheelchair Nationals" series, here at the SuppVersity, know that I have found some success in increasing my strength and lean muscle utilizing an EDT and 5x5 training type regimen even though I was on a caloric deficit for the most part of my prep. Up to now, I have never used this regimen on a "bulk", i.e. in a phase, where I consumed at least slightly more calories than I needed, but judged by my previous results, the results should be scary - obviously, in a positive sense ;-) For now, this will yet have to wait to the off-season. After all, the time to my next competition (~15 weeks) is not that long that I could afford to go really overboard calorie-wise.

Given my past experiences with this regimen, I would yet be a fool to skip the EDT + 5x5 regimen completely. So, I decided that it would be prudent to stick to what has worked and try to come up with a set of modification that would make it even more efficient. 

The thing I have come up with is basically a "cross-over regimen" (sounds funky, right? I guess I should patent the training system and sell it, then ;-) with a two-day 5x5 strength core that is combined alternately with two-day escalating density regimen or a newly developed three-day hypertophy protocol.

The key points and main changes of / in my new regimen:
  • I threw out the static holds and added another EDT exercise to make it a total of 3 EDT exercises in 1 workout session, equaling 60 minutes total. I did this, because I felt the cost-benefit, in terms of the time I spent doing the statics and the results strength and size-wise were not worth, given that at this point of my prep I will still be consuming enough food to cope with a third escalating density superset, which would otherwise have extended my workouts into the 70min+ realm.
  • I wanted to add hypertrophy-type workout into my regimen. Something I could alternate with the EDT workouts every other week. Firstly, to avoid overtraining on the metabolically demanding 2x60 min EDT sessions per week and secondly to add another unfamiliar growth stimulus. It has been some time that I did a "normal" bodybuilding split) and as much as I love low reps and lifting heavy, I feel that hypertrophy style training also has its benefits. When I’m lifting real heavy, my intensity and focus is just on strength and moving the weight. It’s really hard to focus on the mind to muscle connection, and the stretch and squeeze, when you’re trying to lift a lot of weight. This is where a hypertrophy style training excels. It allows you to focus on good form, the mind to muscle connection, and the stretch and the squeeze. I also feel that it’s a good confidence builder, because it allows you to appreciate the strength gains you make, from lifting heavy all the time - well, at least that is what it is for me: The way the weight suddenly feel so light, when you transition from the low reps with heavy weight, to a high(er) rep protocol with moderately heavy weight just makes me feel good.
  • I wanted to work on my "new" problem area, the shoulders, which I have decided were the body part, where Neil beat me in Florida. I must admit that just doing the classic push movements, I may have neglected my rear and side delts and the results were particularly visible, when I hit the rear double biceps pose. 
In fact my decision to add additional shoulder work was part of the reason to a) add another EDT superset and b) (re-)incorporate a "classic" hypertophy split into my regimen, the first rudimentary incarnation of which looks as follows:
Figure 1: Week A of my new alternate cross-over training regimen (2x EDT + 2x 5x5)
Basically, in the first the first week, I’m sticking to my bread and butter regimen, which is EDT & 5x5. Call it a strength and conditioning phase, if you will. In the subsequent week, I will then replace the two EDT days on Monday and Wednesday with a classic three-day bodybuilding split, so that week B is slightly more hypertrophy-oriented, and will look like that:
Figure 2: Week B of my new alternate cross-over training regimen (3x Bodybuilding Split + 2x 5x5)
Overall this regimen is - and this should apply to any of your new regimen, as well (don't forget to check out the past and future installments of the "Step By Step Guide to Your Own Workout Routine") - a "work in progress". I will stick to it for these first two weeks and think about adjustments, on either the training or the nutrition side of things, afterwards. Apropos, nutrition: If you are curious about what my intermediate "maximal muscle, minimal fat gain diet" is going to look like, I suggest you do not miss the next installment of my ongoing series, here at the SuppVersity!

How to Mitigate Anonymous' Internet Shutdown March 31

In case you haven't heard, Anonymous plans to shutdown the internet March 31 to protest a multitude of issues which I'm not going to bother to get into right now.

The plan is to attack all 13 root DNS servers with Denial of Service (DoS) attacks.

By shutting down all 13 root DNS servers, a domino effect will be felt throughout the internet and eventually all DNS queries will begin to time out.

Their plan is pretty bold, and will require a tremendous number of computer systems attacking at once.

While it is unknown if Anonymous' plan can succeed, there are a few things you can do to mitigate this threat from affecting your organization.

1) Don't panic. This shutdown is on a Saturday, so the number of employees this affects will be minimal.  If your organization isn't even open on Saturdays, then this won't affect your organization at all.

2) If you are open on Saturday, consider putting one of your local DNS servers in caching mode if it isn't already, and increase the DNS caching time to live (TTL) to 86400 seconds (24 hours).  Any commonly used sites should remain cached throughout the attack.  It's a good idea to revert to your original settings Monday morning.

3) Finally, if you absolutely must have access to certain websites with static IP addresses, such as business partners or suppliers, consider making available to your on-call support staff a hosts file with critical domain names and IP addresses pre-loaded, so that they can drop this file on any organizational systems which start to have DNS problems.  Once again, revert to your original settings Monday morning.

These three simple tips should help keep your organization up and running, should Anonymous actually succeed in taking down one or more root DNS servers.

For home users, I would recommend checking your local weekend weather forecast Friday evening.  If it's going to be nice out, be ready to go outside for a change, get some exercise and have some fun.  If not, consider breaking out some board games for the kids, or find yourself a nice book to read.  It's only one day, if it even happens, and it's not the end of the world.

Executable and Linkable Format (ELF) Guide

Yesterday I found a very handy guide for understanding Linux ELF files.  Great for malware analysis!

Thought I would share it with everyone else.

Eight Weeks on Moderate Doses of Erythropoietin (EPO) Build a Bigger Mitochondrial Engine and Shed Some Body Fat, but is That Really Worth Taking the Risk?

Image 1: These EPO containing Recormon vials are highly popular in the French Pyrenees ;-)
Fatty acid oxidation is certainly one of the buzzwords in the supplement industry. Interestingly enough, it is mostly used very indiscriminately for all sorts of physiological processes which are sometime more, sometimes less related to the actual process of β-oxidation, in the course of which the acetyl CoA are liberated from their original molecular bond. In fact, the majority of the currently available "fat burners" (those neat little pills with tons of fat liberating, but not burning stimulants in them) has no effect on the efficacy of this process. In previous posts, as the one on irisin and the utility of exercise induced increases of PGC1-alpha,  I have already hinted at the importance of "building a bigger engine", or, more formally, increasing the oxidative capacity of your mitochondria in your individual battle against your love handles and the global battle against obesity. Today, we are going to have a look at a not exactly kosher, but tried and proven drug everyone who has not deliberately ignored the media coverage of the Tour de France over the past couple of years will have heard of: Erythropoietin - short, EPO!

More red blood cells transport more oxygen to larger mitochondria

About two years ago, a group of researchers from the Duke University Medical Center discovered that the "blood-building" drug Erythropoietin had an unexpected yet not exactly undesirable side-effect: It activated cardiac mitochondrial biogenesis - or, to stick to the previously introduced "terminology" it tuned the lab rats engines (Carraway. 2010). Now, in the latest issue of Frontiers in Physiology a group of European researchers reproduced these results in a group of six healthy young men (21 ± 2 years, 180 ± 1 cm, weight 73± 2 kg) who participated voluntarily (no, the study does not state that those were Tour de France competitors ;-) in an 8-week trial. Over the course of the study period received an additional iron supplement (100mg; was in fact started 2 weeks prior) which, obviously in conjunction with the EPO treatment,
  • 1st week: daily subcutaneous injections of 5,000IU of rhEPO
  • 2nd-7th week: weekly subcutaneous injections of either 0, 2500, or 5000 IU, depending on the subjects' Hct level
was intended to raise their blood hematocrit (Hct) to ∼50% (which is considered still save, i.e. the risk of developing thrombosis is low, and the maximum allowed value in sports!) and to maintain that value throughout the study period. The Hct levels were controlled on a weekly basis and the rhEPO doses were adjusted appropriately:
After the 8 week intervention period, the mean Hct for the whole group was increased significantly to 51 ± 1%. Three of the six subjects received full treatment dosage with a total of 70.000 IU rhEpo over 8 weeks, while two subjects were administered 67.500 and 62.500 IU, respectively. The remaining subject exhibited a strong response to the rhEpo injections, and received a total of 50.000 IU. 
The maximal oxygen consumption of the study participants, which was measured during a standardized exercise protocol (+35W increase in resistance every 60s) on a braked cycle ergometer, increased regardless of the dosage that was required to keep the hematocrit values from 54 to 58ml/kg per minute (cf. figure 1).
Figure 1: Changes in body composition and measures of oxidative capacity in the course of the 8-week treatment period (data calculated based on Plenge. 2012)
Contrary to these 8.3% (+/- 2%) increases in VO2max, the changes in body composition, the scientists had expected based on previous rodent studies (Hojman. 2009) did not reach statistical significance, something I personally would yet not mind if my body fat percentage dropped by 2% after 8 weeks of doing nothing would set me up to shed even more fat. That is all the more true, because the statistical more than significant +22% increase in mitochondrial oxidative phosphorylation and electron transport capacity in the muscle fibers of my vastus lateralis, which are indicative of a profound increase in mitochondrial respiratory capacity, or, the aforementioned tuning of your mitochondrial engines, would set me up for further fat loss in the future.

"Cool, bro! Where can I get this EPO?"

Image 2: You better take their bikes than their drugs.
Yet although all this certainly sounds formidable and "exercise in a pill" always sells way better than real workouts, I guess I better put these results into perspective before you jump to any conclusions. After all, the 4-weeks intervention trial Jennifer L. Trilk and her colleagues from the Department of Kinesiology at the University of Georgia conducted in 2010, is only one out of many examples, which show that "artificial enhancements" like these may be highly beneficial for people performing at already superhuman levels, but comparably ineffective for the average, let alone the formerly sedentary human being (Trilk. 2010).

After all, the overweight women in the Trilk study achieved a +12% increase in VO2Max after no more than 12 HIIT sessions consisting of 4-7 30s all-out sprints on an cycle ergometer, which were seperated by four minutes rest. And let's be honest, if you'd rather take a highly expensive, potentially dangerous drug from the gray market than invest ~90min of your precious weekly TV time into some HIIT exercise, you should not wonder if you are sick and obese.

Back in the game.

Well, sort of. I went for a ride and was pleasantly surprised at how I didn't actually feel crap! I felt a whole lot better than any pregnancy ride!

Had to put my seat up after months of running everything pretty low for comfort!
But it's hard to judge future fitness on an hour of riding, but it was still awesome, and then I got to come home to a hungry baby that fed like a machine. All is well with the world!

Dietary Thyroid Treatment: Beef, Green Vegetables, Full-Fat Milk & Butter Normalize TSH in Subclinical Hypothyroidism

Image 1: "Nutritional thyroid medication" - Sirloin of beef in smoked butter (
"Hypo- what?" This is probably the answer your grandparents would have gotten, if they had told one of their friends that they suspected to be hypothyroid, or, put simply, had an "underactive" thyroid gland. What used to be medicinal rarity, though, has become more and more of a plague in the course of the last decades. And while "full-blown" hypothyrodism, which is (quite ridiculously) defined by TSH values of >10mU/l, is still pretty rare, the number of people with oftentimes undiagnosed "subclinical hypothyrodism" who have elevated TSH levels, but remain below the more or less artificially defined upper cut-off level, or normal TSH levels, but low levels of the thyroid hormones T4 and, more importantly, T3, is on a constant rise.

"Subclinical" hypothyroidism: Not just a thread to your weight, but also to your health

Aside from the universally mourned weight problems, an inappropriate production or conversion of T4 to the active hormone T3 can have profound health consequences. Among other things it can precipitate to
Image 2: Within the hypothalamic-pituitary-thyroid-adrenal axes (HTPA), the thyroid is involved in almost all  physiological processes in your body (Rhyszard. 2010)
...and many minor health complications. Nevertheless, treatment with levothyroxin (T4; synthyroid) does not consistently resolve all / any of these problems. This is particularly true for the metabolic derangements, such as the persistent hyperlipidemia, of which a recently published review by a reasearcher from the renowned Harvard Medical School states that "trials to date have not consistently shown a beneficial effect of levothyroxine treatment on serum lipid levels in subclinically hypothyroid patients" (Pearce. 2012).

Why would you take medication, when all you need is a whole foods diet?

Against that background the latest results of a case-controlled 3-months small scale (n=54) dietary intervention trial by Marjolein W. J. Kuiper and Ellen J. van der Gaag, the results of which have been published in the latest issue of the Journal of Food and Nutrition Sciences could be of paramount importance (Kuiper. 2012). After all, this is - at least to my knowledge - the first experiment to investigate the (as it turned out) profound effects of a simple dietary intervention, which prescribed the inclusion of
  1. three servings of beef per week,
  2. green vegetables on at least 5 days of the week, and a
  3. daily portion of full fat milk and butter
into the habitual dietary regimen of 54 children with subclinical hypothyroidism, on the plasma levels of thyroid stimulating hormone (TSH), free T4 and BMI.
Figure 1: Vitamin A, iron and iodine content of the foods in the experimental diet and comparable foodstuff; data expressed for 100mg relative to the RDA for children (calculated based on Kuiper. 2012)
In view of the age of the children (1-14 years) the already statistically non-significant changes in BMI, are pretty irrelevant. The restoration of the eleveated TSH levels into the normal range in 74.1% of the patients in the active arm of the study (compared to 25.9% in the patients from the control goup), on the other hand, underlines the role of a well-balanced, nutrient-dense, whole-foods diet that is rich in iron, iodine, vitamin A and the (saturated) fat that facilitates the uptake of the latter.

Eat a whole foods diet now and avoid thyroid problems in the first place

Image 3: If you care about your (thyroid) health you better run, whenever you see this symbol ;-)
And while it is important not to fall for the idea that your diet should consist of nothing else, but the above mentioned foods, the results of this study appear to confirm what many of you probably have long suspected: The current dietary guidelines, according to which red meat must not be consumed more than once a week (better not at all), full-fat milk, cheese and other dairy products should be replaced with their low- to no-fat varieties and those "bad saturated fats" in butter and meats have to be avoided at all costs, could be one of the various dietary and environmental factors which contribute to the initially invoked increase in "subclinical" thyroid disorders within the allegedly "iodine sufficient", iron-toxic and beta-carotene orange (yet retinol deficient) Western world.

Facebook Location Sharing Enabled by Default - Another Threat to your Privacy and Safety

I noticed something disturbing today.  Ever since about the 15th of March (noticed this on some of my Friends posts going back to the 13th), my Facebook posts have started including my location.  That's pretty disturbing, because I never enabled Facebook to share my location.  It would seem Facebook has enabled this setting by default.

In fact, if I wanted everyone to know where I am, I would have typed my location in my Facebook post.

This really becomes problematic if I were to use Facebook while on vacation.  Suddenly my posts will tell everyone I'm not home, and depending on my privacy settings, that's pretty much telling the world "hey, he's on vacation, go steal stuff from his house!".

I've noticed most of my friends posts are including this information as well.

Facebook does provide instructions on disabling location sharing ( but it's not very clear if these settings stick.

I urge you the next time you post on Facebook, check to see if there is a small gray box below your post which includes your approximate location.  If there is, click the X inside that box to disable location sharing.

Share this message with your friends and family on Facebook, and help them be safe online too!

Set to Be Obese? Epigenetic Programing in Utero - The Roles of Over- & Undernutrition, High & Low Protein, Fruits, Veggies, Zinc, Magnesium, Chromium, Vitamins & More

Image 1: Your mother's diet is not the sole cause of your love handles and health problems, but it could well have tipped the scale to your fat disadvantage. Don't be resentful, but don't repeat the same mistakes, either!
While it is certainly false to assume that anyone can't help but to get obese, it's similarly hard to deny that some people just have to cut back on the coke and sweets they eat to get back in shape, while others struggle with shedding superfluous weight (=fat) and regaining their health even if they are in a reasonable caloric deficit, eat a whole foods diet and exercise regularly. "It must be in my genes!" is what you will usually hear from people on both ends of the spectrum and while the former will smile at you and grab the next best snickers bar, just "to make sure that they don't lose too much weight", the unfortunate people on the other end of the spectrum are clutching to each and every straw, or, in these days of Internet quackery, "expert" advice to finally solve their life-long misery.

In today's blogpost I want to take a brief look at the leatest research into the epigenetic realities of obesity and how those nasty love-handles you have been carrying around for years, now, may actually have been "programmed" when what is now your body was still a bunch of constantly differentiating cells.

A fetus needs more than just adequate folate (let alone folic acid)

We have known for decades, that the consequences of fetal malnurishment, i.e. the insufficient provision of macro- and micronutrients, go well beyond an increase in infant morbidity and mortality. Van Assche et al. report as early as in 1977 that fetal growth retardation (due to malnurishment or other causes) was associated with reductions in both the size and the function of the pancreas (Assche. 1977); reductions, of which Hales et al. were able to show that they can lead to glucose intolerance and hypertension later in life (Hales. 1991).
Image 2: No, no, no! Juicing your fruits and downing 5-6 apples, oranges, peaches, lemons, grapefruits or whatever in one sitting is not healthy! Neither for you, nor for your offspring!
What can you do? As I said data from human studies is scarce and mostly observational, but if you are concerned about the beta-cell autoimmunity and subsequent increases in diabetes risk of your offspring, a study from the University of Tampare suggests that it may be a good idea to eat more berries (-10% risk) and to drink more coffee (-38% risk; Virtanen. 2011). If you are afraid that your offspring may be too small, you better eat fruit and veggies instead of pills, as the consumption of the former and not the total amount of micronutrients correlates with the size of a newborn (Loy. 2011). Thusly avoiding low intakes of (leafy) vegetables and (malaceous) fruits, all you need to reduce the incidence of allergic wheeze in your offspring is to make sure you get enough chocolate (low chocolate consumption = +36% increase; Erkkola. 2012) and avoid fruit and berry juices (+40% risk increase) and and you should be good to go ;-)

The overall message should yet be: Don't stuff or starve yourself and stick to the principles of healthy living I have been trying to piece together like a puzzle in the past 727 posts and the countless comments here at the SuppVersity. This will be good for you and for your offspring!
In the last decade more and more scientists have tried to elucidate the exact mechanisms behind this metabolic deteriorations. And while the increased awareness of the importance of dietary folate is probably the most prominent results of these efforts, vitamin B9 is by far not the only (micro-)nutrient in your diet which can exert far-reaching long-term effects on your offspring. And though much of the information we have is based on rodent or epidemiological human data, I believe that it is worth considering how what you eat today, may influence the health of your children in the future:
  • Micronutrient deficiency and body fat % of the offspring: In a series of studies, Rao et al. were able to show that total (-50%) micronutrient deficiency, as well as an insufficient supply of magnesium, manganese, chromium, zinc, folic acid or vitamin B12 (summary in Rao. 2012) led to statistically significant increases in body fat levels in the offspring of rats. And while the effects of maternal chromium and manganese deficiency could be corrected later in life, those that were induced by a lack magnesium, zinc and vitamin A (Ribot. 2001) in the diet of the pregnant rat dams, were permanent.
  • Exaggerated cortisol release due to high fat diet and insufficient chromium: Both a diet insufficient in the trace element chromium (Padmavathi. 2010), as well as one of the standard "high fat diets" (30% fat; 16% protein; 37% carbs; Bullo-Cioca. 2010) increased the corticosteroid (cortisol) response to stress and thusly increased the diabetes and obesity risk of the offspring of chromium deficient or HFD significantly. Unpublished results by Roa et al. suggest that a similar increase in 11-beta-HSD (the enzyme responsible for the formation of cortisol) exist for folate and vitamin B12, as well (Rao. 2012).
  • Cholesterol, triglycerides and other lipids: While an insufficient intake of manganese during pregnancy appears to make the offspring more susceptible to diabetes, obesity and low-grade inflammation, a profound lack of magnesium and zinc reduced the levels of cholesterol and cholesterol and triglycerides, respectively (Venu. 2008; Padmavathi. 2009).
  • Iron deficiency results in growth retardation and brain chemistry: Pubs born to rats on an iron-deficient diet were not only smaller and had altered lipid metabolisms, they also exhibited disturbances in brain dopamine metabolism and defects in the brain myelin (fatty layer that protects the neurons) fatty acid composition (Kwik-Uribe. 2000)
  • Reduced and exaggerated salt intake predispose to hypertension: As of late the FDA has been going back on their recommendation to avoid salt like a plague and while their reasoning was a different one, the results of a 2011 study by Kaleganova et al. confirm that both a high and a low sodium intake during pregnancy can lead to pathological changes in the kidney morpholgy of the offspring and, subsequently, to hypertension (Kaleganova. 2011)
  • Increased susceptibility to obesity in response to high-dose multi-vitamin supplementation: Although the overall message of the above effects of nutrient-depended epigenetic programming appears to be that you better make sure not to be deficient in any nutrient, the results of a 2009 study by scientists from the University of Toronto (Szeto. 2009), suggests doubling your already high-dose multivitamin "just to make sure", is probably the worst "prophylactic" measure you could resort to. After all the pubs that were born to rats who received the high dose (10x RDA) vitamin supplement in the Szeto study, were profoundly insulin resistance, hyperphagic and obese.
While some of these negative consequences of maternal and subsequent fetal mal-nutrishment are either reversible (by replenishing respective nutrients) or induced by developmental changes and consequent malfunction of organs or organ systems, it becomes increasingly clear that some of the changes are of epigenetic nature, which means that certain DNA strains are activated or deactivated via methylation in response to dietary restrictions or, as in the case of overall malnurishment or the so-called "high fat diet", an under-, respectively overabundance of energy.

Protein (mal-)nutrition during pregnancy and epigenetic consequences

Image 3: The effects of protein malnutrition on pediatric health are profound, at any age!
Of the macronutrients, dietary protein appears to exert the most profound epigenetic effects during the fetal period. The offspring of protein malnurished rats in a 2005 study from the University of Southhampton in the UK (Lillycrop. 2005), for example, had ~20% lower PPAR-alpha and glucocorticoid receptor methylation status than that of rats on a protein sufficient diet. The subsequent >10x higher PPAR-gamma and 2x higher glucocorticoid receptor mRNA expression render provide a "mechanistical" (obviously it is a physiological one, but if we think of the body as a epigenetically controlled machine, the expression "mechanistic" would be adequate) explanation for the increased susceptibility to dietary induced obesity in later life - an effect, by the way, which has only recently been shown to be sex-depended and more pronounced in female than male offspring of mice (van Straten. 2012).

A high protein content of an overall energy deficient diet, on the other hand, has recently been shown to correct the increased cardiovascular disease risk subsequent to fetal malnutrition in mouse offspring (Kavamura. 2012), which could in fact be related to a correction, or rather aversion of the detoriations in glucocorticoid receptor expression observed in the Lillycrop study (see above).
Note: A 2011 study from the Department of Nutritional Sciences at the University of Toronto suggests that even though soy may be less of a problem for women than men, you would be ill-advised to eat (or feed your pregnant wife) larger amounts of soy protein. After all, the scientists comparison of soy vs. casein based diets showed that the offspring of the soy-fed rodents exhibited increased body and fat pad weights and a statistically highly significant increase in systolic blood pressure - an effect that was, in this case, more pronounced in the male, than in the female pubs (Jahan-Milan. 2011).
Interestingly, we see very different effects with postnatal protein restrictions, only recently, a group of researchers from the Universidade do Estado do Rio de Janeiro, in Rio de Janeiro, Brazil (Lisboa. 2012), that the offspring of the dams received a low protein (8% vs. 23%) diet during the lactation period had lower adipocytes area, a higher leptin:visceral fat ratio, increased leptin receptor expression (and thusly sensitivity) and significantly higher levels of thyroid hormones (T3 and T4) at lower TSH levels than the adult offspring of mothers who had received the normal diet during lactation. These results emphasize the need for further research and confirm my repeatedly voiced concern about jumping to radical conclusions. After all, the same high protein diet that could decrease the CVD risk of your children could be one of a myriad of factors which contribute to the rampant rise of thyroid problems, these days.

Don't surrender, and outdo your well-meaning parents

If coupled with prenatal stress exposure, which has also been shown to induce profound negative effects on the glucocorticoid metabolism of the offspring (Brunton. 2010), protein malnutrition could form a "duo infernale", which would verify the initial statement that some people have an "epigenetic disadvantage" compared to others. It would yet be unfair and above all unproductive to lay the blame on your parents. After all, familial studies suggest that only 30%-50% of the weight gain could potentially be explained by (epi-)genetic factors (Lawin. 2009). This leaves a huge margin for you to intervene and still emphasizes the importance of watching your own diet - for your own, and the sake of your children and grandchildren (I guess, we forget about humanity for now ;-)

Sunsilk Hair Fashion Makeover!

Today was Sunsilk Hair Fashion makeover day! I had a great time meeting up my fellow bloggers! Kak Cindy Biantoro, Clara Devi, Kak Diana Rikasari, Pupu Paula and Sizeka Yang. Lots of laughs and of course girlie chit-chats, and we had a chance to meet & style these 10 lucky winners of Sunsilk Hair Fashion contest. Here are some snapshots and behind the scene of the photoshoots...

Meet the girls I styled head to toe for today's makeover, Irene and Yoana :D Since today was a makeover day so they need to get out of their ordinary styles, and I gave them a touch of warm ambience with brown, orange, yellow & gold *my favorite colors!*

Irene wore orange chain top, gold glitter bodycon skirt, bowler hat and studded brown heels. And I asked for a simple hair-do for Irene, side bangs & volume shaggy hairstyle complete her sophisticated uptown gal look.

Yoana wore yellow velvet top, brown leather belt, gold unique pencil skirt (I love!!), and black maryjane pumps. I seriously love the gold pencil skirt I bought for Yoana, and I think it looks good on her for special occasions, especially with her up-do hair, totally vintage & classy lady look. I'm happy with the result!

I had my outfit matched with them too! I wore black & gold vintage blazer, orange flare dress, leather belt matched with leather Jeffrey Campbell wedges & black lacey socks. So we kinda have 3 different styles with the same color scheme. I shopped for the girls yesterday and these stuffs they wore from head to toe are gonna be all theirs, so yay I hope you both like what I picked! :)

Kak Diana, Kak Cindy, me, Sizeka, Pupu Paula & Clara Devi, styling for Sunsilk with different personal styles. Interesting! :)

Now let's peek what my fellow bloggers were doing with the other 8 girls! :D

a groupshot of the winners & the stylist bloggers ends the day, the photo's taken from Kak Cindy's blog. YAY! :)

Not for the squeamish—birth story of Elva Mae

Disclaimer: don't read if you're grossed out by body stuff. There is no bike or coffee stuff in this post.

Saturday was a great day. I had picked myself up from earlier in the week, where Thursday had me seriously considering myself depressed and questioning my identity and what the hell I was doing having a baby shortly. Surely it was a hormonal sign… I literally couldn’t pull myself together all day.

Slightly better on Friday, and on Saturday Aiden and I had a really awesome day. We mooched around the house for the rainy morning, Aido did some work and he fixed my singlespeed to be ready for my ‘comeback’, having rebuilt a sweet Lefty Max with DLR internals, converted to a 29er for the Niner. It used to be called Stash, but after that crazy mish-mash of a fork I have changed it’s name to ‘Frankenstein’ (Frank).

Anyway, there was a short break in the weather and I too Frank for a burl around the bikepath. Very uncomfortable as the front end is really low. Plus we got rained on.

That night we went to the Powerhouse, watched Charlie Pickering perform as a part of Brisbane Comedy Festival. These big belly laughs were followed by a curry, some pineapple, clary-sage backrub and sexytime (sorry ‘bout that)—purely to give Mayhem a little nudge in the right direction with these natural induction methods.

We have a lazy Sunday morning and are contemplating where we go for a ride, when I get up to get into my kit and suddenly my legs are all wet, but I am not peeing. Aido checks and confirms that it appears my membranes had ruptured.

We get checked out at the hospital, and basically because I screened positive for a transient microflora that around 30% women have living in their lady bits when I had a labour scare at 32 weeks, so they weren’t very happy to give my the usual 72hrs at home to allow labour to happen naturally due to the risk of infection to me and bub.

I bargained 24hrs, having to reassess the next day should nothing eventuate.

We went home, baked some fabulous cookies and waited.

Nothing happened—I had a terrible night sleep.

Induction loomed and I was a little teary at the hospital, knowing I would be with the Birth Centre midwives but labouring in the Birth Suite instead.

Anyway, after two doctors flailing around trying to get a 16G cannula in my hand, we were off and walked through the doors to the birth suite.

Initial obs, the drips were set up and I was stuck on the CTG. Luckily it was one of the only telemetry-based ones, so at least I could walk around with my dicky IV pole. If you haven’t tried it before, it sucks. All shopping trolley wheels and very difficult to manouver.

Aido and I walked around the corridor, bounced on a fit ball and read Cycle Sport magazine. We spent about three hours and the Syntocin (induction drug) was being titrated up and up due to the lack of labour-type activity going on. We even had a nap.

Anyway, midwife was puzzled and a few hours in decided to do an internal. The forewaters hadn’t broken, just the hindwaters. So with a bit of a ‘pop’ she ruptured the forwaters and confirmed that the baby had heaps of hair. Hearing that was a highlight!
That’s when the fun began…

The very next contraction was uncomfortable. Aido and I walked up and down the corridor again in an effort to speed things along and within 20mins I was back in the room on the fit-ball, pale as a ghost, wondering if I could get through this without drugs. From the beginning contractions were relentless—about 40sec on and 40sec off, no time for recovery.

Different from the 40sec–1min on, 2min off that I was expecting during the toughest part of labour—transition. I gritted my teeth, but eventually through all the pale sweaty clamminess and moaning and nausea I said I needed something. Anne, our midwife, stripped me off and put me in the shower to use the heat for pain relief, Aido was holding two shower heads on my back and abdomen. It was only about 40mins after the examination and the water was either too hot or too cold. Never just right.

I soon started making some pretty freaky animal noises and asked to get Anne—the sensation has changed. I was worried I would poop—there was something down low. I had a couple of contractions with the Nitrous Oxide but due to the really short interval between them it just made me fuzzy, it didn’t take the pain away. I can’t really remember that bit, just heaving away on that nozzle and semi squatting in the shower.

I called Anne once again and said I was feeling weird, that I couldn’t do this, that I wanted drugs. I said I needed to poop and she asked ‘big poop or little poop’ before I answered I was in the throes of another contraction.

She stalled me, knowing my intention of not using drugs. But a few contractions later I was politely demanding them, and she said ‘alright but first I have to examine you for the doctor’.

I hop on the bed, not really aware of what’s going on or how I got there from the shower. And the next couple of contractions, between her examining me, were probably the worst—not being able to move at all is definitely not cool in labour!

I bellowed some jungle animal sound about needing drugs again, and she said ‘don’t worry about drugs, you’re fully dilated, you’re having a baby instead’. It was about an hour after the first contraction.

In hindsight, I think it changed when the animal sounds came into it, I think I may have been fully dilated from then, and more than likely I was in ‘transition’ when pale and clammy and nauseous on the fit ball.

She popped me on my knees with the head of the bed up and my upper body and arms draped over it. I didn’t care who was in the room looking at me nude. She mentioned that there would be another midwife present at the time of delivery, but I didn’t see her at all.

Aido was at the head of the bed feeding me orange powerade between contractions.

I didn’t really get the ‘urge to push’ that you hear about, just the same contractions but lower. I was instructed to push when I had one—it was a weird sensation. The bellowing continued, I would hate to hear what it sounded like—pretty otherworldly I’m sure—but Anne was getting me to focus on pushing rather than using energy for my voice. I suppose it seemed like a long time I was there.

Did I want to touch the head? Hell no, I wanted the baby out now! I remember asking several times how long it would take. I am glad I had strong pelvic floor and ab muscles, because it was about half an hour of pushing all up and I’m glad it wasn’t any longer. I was fortunate to not have her ‘crowning’ between contractions. One moment there was a bit of furry head seen, the next contraction she was out, and Aido caught her—the slimy little white and red and pink baby, with a bluey cord.

Somehow I managed to turn over. My whole body was shaking throughout the whole pushing process and I continued to shake, holding her, for about an hour.

Aido was crying (typical, such a dad!), but I was just stunned at what the hell had just come out of me. It’s pretty evident in the photos, I don’t think I smiled at all—I was just shocked.

Fresh, wet and slimy Elva.
I'm not sure what to think. I am not sure i'm thinking here at all.
Eventually the placenta came out (very cool, I would put a pic up but it tends to gross people out) and I was much more comfortable. After inspection, no tears, just a graze. I got out of the whole fiasco well.

Mum and dad were up the coast, coming home at around 4pm—we had expected not to have a baby till the middle of the night or wee hours of the morning so told them not to worry coming till we called them. Elva was born at 4.37pm—after 1hr37mins of actual labour—and Aido just texted ‘Baby born, come to hospital’.

Eventually we went upstairs to the ward, and Aido stayed as long as he could. It was a 4-bed room and it was the only negative thing I could say about the whole experience; shared maternity wards suck!

That night I couldn’t sleep, I was still processing it all as it happened so fast and with such intensity. I guess it was that night I decided that Elva Mae was actually pretty cool, staring at her in her little see-through crib next to the bed, checking she was still breathing every now and then.

I went home the next day, totally nonplussed with ward life, and had a terrible night at home. My milk was coming in super fast too (this baby is ALL kinds of fast!) and I was a mess. But we got through it.

The next few days my quads felt like I had done a thousand Coot-tha strength efforts, and my coccyx felt pretty violated too. But other than that I was ok, we managed a walk on day three and I’m trying to do that every day until I feel up to riding, hopefully next week.

And we continue to get through it, sleep is overrated, right?