Review for Sambazon Energy

It’s 5:00 in the evening.  I’ve just finished taking an advanced human anatomy test followed by an organic chemistry test.  Next up is a calculus quiz.  I’m wandering aimlessly through the store, my eyes glazed over and a vacant expression on my face.  I am completely worn out.

I need something.  Not just anything, though.  Your run-of-the-mill energy drinks are probably out of the question, just because I can’t afford a crash should it come.  No…I need something that will energize me, yes, but I need the sort of energy that will revive me, something that will keep me going long enough to finish everything up and then go home and go to bed.

Wait, what’s this?  Another Sambazon energy beverage?  Yes, right here with the other fruit smoothies!  Could this be it?  The beverage I’m looking for?  The one that will brush away the fatigue and lift me up upon the blessed wings of functionality?

Let’s find out…


50 mg (yeah…you read that right.)


Found most everywhere that fruit smoothies are sold.  Local chains of intermediate size tend to be the best place to look.


This is a nice-looking bottle—about what you’d expect from an organic foods company.  It’s clean, it’s straightforward…and, of course, it’s purple.  My only complaint with regards to it is this: if you’re going to make an energy smoothie with a relatively low concentration of caffeine, why wouldn’t you make it big?  That would completely resolve the low energy/dinky smoothie problem.


Tastes pretty good, certainly better than either of their Amazon Energy drinks.  The açaí is front and center (as one would anticipate) with subtle nuances of the other berries in the blend.  Only problem is the prominent earthiness of the açaí, which offsets the whole experience by just a bit.  Other than that, it’s something I wouldn’t mind drinking regularly.


I wasn’t looking for a huge kick when I bought Sambazon Energy, and yes, I know it only had 50 mg of caffeine in it, but I was still a bit disenchanted by the minimal nature of its perceptible effects.  I didn’t really feel any more functional or awake or any less brain dead than I did before—even though I have to say I did feel slightly better as a whole than I did previously.


There were hardly any effects to note—how am I supposed to gauge its longevity?


As far as an energizing beverage is concerned, Sambazon Energy falls short of what I like to get out of a drink.  Still, it tastes good, and does have potential.  Here’s my advice, Sambazon—discontinue the Amazon Energy drinks, up the size of this bottle (say to 20 ounces), and up the guarana and yerba mate.  You’d trim some of the fat off of your lineup and give us a better energy drink in place of the others.

Also, if there’s anything you can do to down the price, do it.  $3.50 is a bit spendy for a 10.5 oz. bottle of juice, even if it is tasty.


KEYWORDS: Sambazon Energy review, organic, yerba mate, guarana

The Female(?) Athlete Triad - Part II/III: LH, GH, IGF1, Insulin, Ghrelin, Leptin & Co Form a Self-Perpetuating Vicious Cycle

I usually rant against pizza and beer, but once the athlete triad has struck, they can be an occasional part of the "healing protocol".
In last Sunday's first installment of this series we have taken a look at the prevalence, etiology and fundamental cause of an entity that is, and I am repeating myself here, profoundly mislabeled as the "female athlete triad". In fact, it is, as we have learned in the last installment, neither an exclusively female thing, nor a triad. If anything, it is a quintet or sextet. To make that clear, and give you guys, who make the same mistakes, but usually with less detrimental consequences, I will once more refer to it as "athlete triad" = AT,  in this second part of the Female(?) Athlete Triad Series in which we will take a look at the endocrine underpinnings of the previously described consequences of the temporary and long-term energy deficiency we have identified as the single most important causative factor of the onset of the "triad" last Sunday.

Which endocrine factors are figuring, here?

Instead of overwhelming you with the details right from the start, I decided to compile a list based on a cross-section of the dozens of articles I have read in the course of my eventually futile quest for a single definitive answer to the question, "Which hormonal or metabolic consequence of restrictive eating and excessive training is to blame for the fatigue, the low sex hormones concentration,the  bone resorption, the anemia, the absence of menses / lack of libido, the performance decreases and the whole string of pathological features, we have explored in the last installment?"
"Refeeding is not an option, because you will only become fat!" FALSE! Yet another myth without substantial scientific foundation that probably arises from the disturbed self-perception of those affected by AT and AN. In fact, the fat stores are the last thing that will be restored (Golden. 2004). This is probably also one of the reasons why "refeeding" often does not appear to work, because the basal energy requirements will increase with every pound of lean tissue you add back to your frame, so that athletes suffering from the "triad" will have to continuously increase their energy consumption. Unfortunately, most athletes will fail to do the former (also because exercise & stress can blunt hunger) and instead react with an increase in workout intensity, now that they are finally able to work out, again. This, in turn, will restore or even exacerbate the energy deficit and thus worsen not improve their physiological problems, even if their scale shows that they have already gained 5-10kg. If you take a look at figure 1 you will also realize that, at least in women, a baseline level of total (not relative!) body fat appears to be necessary to maintain regular menses (in men to maintain normal total testosterone & SHBG, but not so much free testosterone levels or reproductive function).
  • low luteinizing levels are unquestionably among the elemental features and causally responsible for the occurance of menstrual disorders / lack of libido and the correspondingly low estrogen and testosterone levels in women and men
  • TSH levels are not a valid / reliable indicator for the presence of absence of AT, because they can be both slightly increased or normal in the presence of low T4 and low T3 levels, as  - and this is far more often the case - TSH can be low despite low free thyroid hormone levels (usually in the presence of a low T3/rt3 ratio; if anything this would be a good indicator of beginning or full-blown AT)
  • the circadian cortisol rhythm is whacked in men and women, alike; characteristic are the absence of an appropriate cortisol spike in the morning as well as the normal decline in cortisol levels  in the course of the day; metaphorically speaking, as the athletes triad progresses, the "mountain range" turns into mesa and eventually into a plane lowland
  • the quartet of (mostly) sub-clinical hypogylcemia, low insulin, extreme high / or totally blunted insulin sensitivity, low IGF-1 and high catecholamine levels cannot be seen in isolation, most detrimental are yet probably the first and last of these four glucose-related players in the AT concert, as the former entails the constant risk to run out of "brain fuel" (in the absence of alternative fuel sources) and can - in the absence of adequate corticosteroid expression - become potentially life-threatening and the latter, i.e. low IGF-1 levels and very low IGF-1 to IGF1 binding protein 4 being one of the, if not the central factor involved in the the long-term physical decline of muscle, bone, organ and even brain mass.
As I have repeatedly emphasized in the last installment, the underlying cause, the trigger, maintaining factor and thus most important setscrew of the athlete triad (female or male) is an over-exaggerated and / or  long-lasting (weeks to months, in the worst case years; see Sundgot-Borgen. 2000) discrepancy between energy intake and expenditure, your body will initially try, but eventually fail to compensate by
  • tapping into its energy stores in form of body fat, muscle and organ mass, the insulating fat around nerves and organs, etc.,
  • continuously decreasing its metabolic activity (esp. thyroid metabolism),
  • shutting down non-vital, but energy-intensive (e.g. immune and reproductive system) bodily functions, to prioritize short term survival of the individual over long-term survival and the conservation of the species
Therefore it is an indispensable and in many cases even sufficient prerequisite to restore an adequate supply of nutrients, and abolish temporarily better reverse the discrepancy between "energy in" and  "energy out" (please read the information in the red box next to the list of the previous paragraph, as well).

And what about leptin, ghrelin, adiponectin ... ?

Figure 1: In female athletes, only total fat mass, not body fat % or BMI are associated w/ AT (here identified by amenorrhea; top, left); the correspondingly low pulsatile (not baseline, see lower left) of LH correlate negatively with ghrelin and positively with leptin (top, right); while LH and leptin show a lack of pulsality, the ghrelin levels are not simply elevated, they also have a higher pulse size, amplitude and total polsatile secretion compared to control and eumenorrhetic athletes (bottom; LH, ghrelin, leptin expressed relative to non-athletic control; based on Ackerman. 2012)
Similar to the facilitative effects of the "hunger high", the "evolutionary advantage" that's turning its ugly face on everyone, who's willing to dig a deep enough whole (see Part I), the endocrine imbalances, as well as the reduced leptin) or over-pronounced (adiponectin) release of adipokines and the disturbances of the glucose, fatty acid and cholesterol metabolism start to take on a life of their own.

And as if that alone would not already make it difficult enough to separate cause and effect, it does actually appear likely that the order may even be reversed over time - not unlike the chicken that will hatch and eventually lay an egg. 

As discussed in the last installment, the combination of over-exercising and fasting, which may at time-point T0 actually have been the root cause of the problem will often turn into a strategy to stave off the impeding total breakdown. It becomes sort of a conditioned response to the constant starvation, which  will then no longer manifest itself in the form of hunger, but as anxiety and an almost compulsive urge to exercise (this is particularly well-established for anorexics; Teufel. 2008). And while the latter can be motivated by the desire to increase athletic performance and/or lose even more body fat, it does have a very real, often under-appreciated, physiological underpinning.

If you like, you could argue that the urge of the starved athlete to exercise is yet another "evolutionary conserved" automatism that mirrors the well-known food-seeking behavior rodents display  in periods of food deprivation and in response to the stimulatory effects of ghrelin on the orexin neurons in the brain (Yamanaka. 2003).

From ghrelin to growth hormone to IGF-1 and back

At the same time, the combination of exercise, low triglyceride, low free fatty acid and exuberant levels of the "hunger hormone" ghrelin leads to an overexpression of growth hormone (Scacci. 2003), subsequent increases in adiponectin (Wölfing. 2008), which will in turn decrease progesterone and androstenedione production and LH receptor expression in ovarian cells (Lagaly. 2008) and GnRH and LH release in the pituitary (Rodriguez-Pacheco. 2007; Lu. 2008). The surprisingly high adiponectin levels (surprisingly in view of the often dangerously low levels of adipokine producing body fat) will further increase the borderline pathological insulin sensitivity and thus lower the already rock bottom blood glucose and basal, as well as (post-)prandial insulin levels even further.
Figure 2: Illustration of the self-perpetuating vicious cycle of the athlete's triad (AT)
With their suppressive effect on leptin (Böni-Schnetzler. 1999), the high growth hormone levels and low body fat reserves are probably the most important contributers to the pathologically low, in fact quasi non-existent basal leptin secretion (see figure 1). And the low insulin levels don't just compromise the normal food-induced prandial suppression of ghrelin (Murdolo. 2003), they also hamper the production of IGF-1 (especially in the liver), so that athletes who suffer from the "triad" cannot derive any anabolic benefits from their high growth hormone levels, since the latter are largely mediated by the stimulatory effect of growth hormone on the production of IGF-1... what you are seeing here is thus a self-perpetuating vicious circle, you can extricate yourself from only by a multi-faceted approach the pillars of which are an..
* in view of the insulinogenic effects of whey and the pro-IGF-1 effects of casein (Hoppe. 2009), and the anti-catabolic effects of CLA & omega-3 you should - if by any means possible - incorporate dairy products from preferably grass fed dairy (butter, milk, cheese, yoghurt, quark / curd cheese, fermented dairy and if you want protein powders) in your diet regularly, better daily.
  1. adequate and continuous energy supply to control ghrelin levels and help stabilize blood sugar (and thus glucocorticoid) levels and restore normal leptin and adiponectin expression,
  2. increased low GI (to avoid reactive hypoglycemia) carbohydrate and protein intakes to normalize glucose levels, suppress ghrelin, increase insulin and IGF-1 levels* (Foster-Schubert. 2008; suggested read: "Carbohydrate Shortage in Paleo Land"),
  3. balanced intakes of all types of natural fats, with an emphasis on long-chain PUFAs from food including a reasonable amount of "bad" omega-6 fatty acids and w/out fish oil or other omega-3 supplements, which would further blunt the already compromised glucocorticoid response and the leptin secretion (Kratz. 2002; suggested read "Omega-3 and Low Cortisol"), and
  4. profound reductions in training volume to lower GH, cortisol, catecholamin and energy requirements and a (temporary) reorientation towards low volume strength training that will help increase bone density and IGF-1 expression (Davee. 1990)
Now, this may sound hilarious, but for the time being, laziness, pizza and beer - in moderation - are actually your friends. In that, I am not suggesting that you have to copy the patient, Chris Kresser mentioned several times on the old "Healthy Skeptic" podcasts (now RHR) about a client, who "cured" his longstanding physiological, and as I suspect psychological problems with pizza and beer, but the third pillar of this guy's regimen is actually a must: Go out with friends and start to enjoy your life again! Without thinking about food and exercise and sticking to whatever form of restrictive "diet" all the time.

Figure 3: Development of BMI (blue), leptin (red), adiponectin (green) levels in 8 female adolescent malnourished AN patients (based on Modan-Moses. 2007)
Apropos, third pillar. I have already had my short intense workout for the day, I have eaten well, but I have not hung out with friends. In other words, I will postpone the in-depth discussion of the energy and nutrient requirements, useful and detrimental supplements and medications, as well as necessary and facilitative tweaks to your workout routine to the next week, add another Roman "I" to the second "II" in "Part II/II" in the preliminary headline of this post and leave you (hopefully not too frustrated) with the graphical illustration of the effects re-feeding, alone, and a normalization of the body weight from a BMI of 16kg/m² to ~19kg/m² can have on the skewed basal leptin and adiponectin in figure 3.

In view of the fact that other studies have shown that this increase in weight, which must not be confused with a mere increase in adiposity, i.e. body fat percentage (go back to figure 1 if you already forgot that the absolute not the relative fat mass counts and please remember that the latter includes the fat in the myelin sheaths of your nerves, the protective fat around the organs, the fat in your brain etc.), does help with the normalization of both insulin and ghrelin (Otto. 2001), growth hormone and IGF-1 (Argente. 1997) and is in some cases even sufficient to restore most of the endocrine abnormalities (Scheid. 2010), many of the lessons we will learn in the next (and according to my current plans last ;-) installment can also be applied to a lean bulk - and that goes irrespective of your gender and your whether or not you have already fallen victim to the athlete triad!

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Just another sufferfest

The QLD State Champs XC was held yesterday, after it almost failed to perform at all. John Pinnell, trail builder extraordinare and race organiser stepped up with The Riders Club in order to offer an alternative venue and race for state champs, when the original organisers scrapped the race less than two weeks out.

Sound familiar? Yes, this happened only two years ago, with Kenmore Club putting on the big day in that case. It leaves many of us with a strong investment in our sport (albeit only via emotion and membership and the blood, sweat and tears we shed when preparing for events!) scratching our heads as to how to make it better for QLD mountain bikers.

But, I digress, the intricacies of attempting to patch up our sport can be left for another post. This one is about the race that almost wasn't.

Coming off a bout of illness post Epic, I was in two minds as whether to even race State Champs. Towards the end of the working week I was feeling a bit more jovial so I signed up. I'm not going to lie, I almost felt like signing up to this race and the local state series this year was a bit of a duty—I haven't been fighting fit or even training for these races, however in order to add just another number, and because I want the sport to grow, I sign up everytime. Plus, time on bike is good for the soul and the best training for racing is racing, right?

So it was with this sense of duty that I signed up, hoping that more than thirty people in total would turn up at the Adare race track come Saturday.

Well, expectations were exceeded, with around 120 people racing on the day. Not bad at all for a race that almost didn't happen, and for the organisers to get everything mobilised in a mere ten days!

Driving out I felt physically ill. I was not sure if it was the coffee (I hope not, we know what that meant last time it made me sick...) but there was something making my stomach a bit like a whirlpool washing machine. Maybe it was even nerves. I don't know.

Mum and Dad were once again babysitter extraordinares, and when we arrived at the race site I realised that I had once again got a blocked duct.

The glamours of motherhood and bike racing—squatting beside your car in a field 15 minutes before your race, massaging out a blocked duct and giving the grass a good drink of milk. Weird? I'm sure it's been weirder. Maybe...

We got to rock out in the BRAND SPANKING NEW Cyclinic kit too, which is super sweet (as seen below).

You can't see the heat, but I was feeling it.
So the gun goes and the small but strong field of Elite women are off. It's a quick start so thanks goodness for the coffee. I felt really comfortable, sitting behind Jodie, she gradually gained time throughout the first lap but was visible throughout. Winning! The legs are feeling good, but it's damn hot.

"If I can keep riding like this, it will be awesome" I think. "It's like those days when I had power in the old pegs".

Yeah well that lasted about a lap and a half, at which point my body politely let me know that I was melting from the inside out. Seriously it was SO HOT. I had busted myself up in the heat, and towards the end of the second lap Kylie and I were tousling down a grassy straight. It was a max effort before a climb. Clever. I knew she was going to get around me, she had been gaining on me for most of the second lap, but I made her work for it! Oh the things we do to ourselves!

This was a pic someone snapped of me sometime during lap 2.

A bit diappointed to not have the legs to go with her, my third lap was a deep lull. I was about as busted as you can get, and without coffee or coke that whole lap was just appalingly painful. I was feeling the chills between my shoulder blades, usually that's reserved for some pretty dark places of dehydration. Bike racing is supposed to hurt, I know, and the hurt was well and truly a good sort at the start of the race, then descended into the maelstrom of overexterional, dehydrated, not-quite-enough-sugar desolation.

I had the Icona Pop song in my head, well at least one line "I don't care, I love it" going around and around on repeat. It helped me through. I had thoughts throughout the race, I wasn't sure if I was not sure where I was because I was feeling 'zen', because the course was so confusing, or because I was in such a box that I could only comprehend what was happening in front of me. Like a gormless zombie.

Surprisingly, I rode the techy climb each lap except the first, which doesn't really make sense—maybe as I breathed a little better and spun up rather than tried to stomp up frothing at the mouth and running into stuff.

My fourth lap I recieved a gift from the gods—coke in my bottle—and I managed to somehow pull my shit together and finish on a reasonable lap time. Kylie had her fastest lap for her fourth (nutter!) which is testament to her increasing fitness and proof all those long km's are paying off. She had a couple of minutes on me by the end. Jodie was a couple more in first.

Heading up the long, hot grassy straight for the final time, I don't think I quite realised how deep I had gone; as soon as I stepped off my bike I leaned over to vomit, dry reaching, then got a case of the headspins. It was very nasty, but it was testament to doing all I could out there on the track.

So, in third. It seems to be my place for this series, but we'll be clawing time back for future races i'm sure. The gap is narrowing, and i'm getting little tastes of feeling strong again. I just have to polish the things I struggle with (hairpin corners anyone?) and work on the whole uphill battle and she'll be apples!
L–R: Kylie, Jodie and ABee (+Little Pea). Not standing on the plank as it was somewhat
unstable, as was I after that race.

The best thing, other than drinking about 3L of water and consuming some carbohydrates after the race, was the prizes. We got some bike lube, grips, the usual stuff, but then we got the most awesome homemade baked goods. Aiden won the Elite male race so we had TWICE the amount of baked goods. Needless to say that much fat and sugar is a little dangerous in our house, so the babysitter extraordinares got one lot of them.

Just a huge thanks to those who put on the race, and hopefully it will mobilise more proactive-ness (? that a word?) for our sport in the future.

Today, on very, very little sleep (aren't children AWESOME for that?) I decided to head out for a 4 hour singlespeed ride, because I am a glutton for punishment. The whole thing was just awful, exhausted, I crawled home at three hours, 61km and 1300m of elevation later. But it was an exercise in making me tough. We're getting there.

At least i'm earning the beers lately.

Caffeine Protects Brain Function Against Stress & SAD Diet; Coffee Withdrawal, Anxiety & More; Giardia, Messy Subtenant W/ Gusto For Arginine; Vit B6 & n6:n3 PUFA Ratio

19 Billion Euro that's the estimated 2011 financial burden due to lung cancer, alone, here in Europe and the On Short Notice figure of the week (information based on ESMO2012 press release)
Those of you who are also following the SuppVersity facebook news, will probably recognize the figure on the right: 16,000,000,000€ or $24,419,000,000, that's the estimated economical burden due to lung cancer, alone, here in Europe (cf. "Who cares if people are dying as long as the economy is thriving?"). An enormous financial loss, and still not the reason that this is my figure of the week. Rather than the financial damage, itself, it is the tragic fact that only the latter, yet not the fate of the patients and their families, would make a valid argument, when policy makers were debating a long overdue, total and all-encompassing public smoking ban... but now for a couple of more sciency, yet not less intriguing news from the past week.

Problems thinking straight? Guess what: 3-4 cups of coffee could help :-) According to a soon-to-be-published paper by scientists from the Jordan University of Science and Technology in Irbid, Jordan, the ingestion of the human equivalent of approximately 3.8mg caffeine per kg body weight or 3-4 cups of coffee per day, can inhibit both, the stress, related as well as diet induced (we are talking of the "typical" Western diet (WD), that's both high in carbohydrates and fat) cognitive impairments (Alzoubi. 2012)... well, at least in the researchers 3-months rodent study it worked like a charm
  • learning trial: animals in the caffeine/stress, caffeine/WD, and caffeine/stress/WD groups made fewer errors, than non-supplemented stressed or WD animals; overall their performance was comparable to those of the control
  • memory tests: treatment reduced the number of error and restored short-term memory and long-term memory during chronic stress and/or WD (P < 0.05) to normal levels
With respect to the underlying mechanisms the scientists speculate that caffeine may "act mainly by inhibiting adenosine receptors" (Alroubi. 2012), which has in turn been shown to to inhibit long term potentiation (LTP) in rat hippocampal slices and disrupt the process of learning and memory at the synaptic level by blocking release of glutamate (de Mendonca. 1994).

Additionally, caffeine has also been shown to increases the expression of hippocampal brain-derived neurotrophic factor (BDNF) and its receptor, which is impaired in response to chronic stress and a hypercaloric Western diet (Aleisa. 2006; Molteni. 2004) and leads to deteriorations in cognitive performance. In the long run those effects could also contribute to the anti-dementia and anti-Parkinson's effects, I mentioned in the recent SuppVersity post on the insulin sensitizing effects of coffee.

Figure 1: While the Hedonic tone and alertness reduced to baseline on day 5 of caffeine withdrawal, the habitual caffeine consumers had >15% higher anxiety scores on day 7 after giving up on their daily dose of methylxanthine (data calculated based on Smith. 2012).
Don't worry, caffeine will also work for humans. And what's best, upon short-term withdrawl (8 days) your cognitive performance is not going to suck - at least not as much as when you are stressed or living on pizza and French fries, only. All that and a couple of interesting other results have been published ahead of print in the online version of the Journal of Pharmacology (Smith. 2012).

To probe the effects of acute caffeine ingestion on cognitive performance and the influence of previous caffeine consumption and withdrawal, Andrew P Smith, Gary Christopher and David Sutherland recruited 70 volunteers (25 male, 45 female; mean age 22.8 years). The 35 consumers (>100mg caffeine /day, mean 300mg; range 110–600 mg) were put on withdrawal and tested on day 2, alone and without caffeine, and day 8 together with the non-consumers in a double-blind placebo-controlled fashion. During the caffeine challenge, the cognitive performance was tested twice, once before and once 30min after the provision of the caffeinated beverages.

Anxious, but smart: Caffeine gives you the edge

The results of the trial clearly indicate that the ingestion of 2 mg/kg of caffeine, which were served in decaffeinated coffee or tea 30min before the testing procedures, were associated with faster simple reaction times, fewer long responses, greater detection of targets in the cognitive vigilance task, and faster encoding of new information.
"The results confirmed previous findings, with ingestion of caffeine being associated with a faster simple reaction time, fewer long responses, more targets detected and faster encoding of new information. There were no main effects of consumer status, nor were there any significant interactions between caffeine and consumer status." (Smith. 2012)
Notwithstanding, I believe that many of you will probably be more interested in the effects of caffeine withdrawal on overall withdrawal symptoms (figure 1, top), as well as the alertness, hedonic tone and anxiety (figure 1, bottom) and the cognitive performance on day 2 of the withdrawal period (figure 2, left), than in any of the well-established performance cognitive performance boost, right?
Figure 2: Performance on day 2 of withdrawal phase (w/out caffeine) and on day 8 before (w/out caffeine) and after (w/ caffeine)the ingestion of decaffeinated tea or coffee with 2mg/kg caffeine in it (data based on Smith. 2012)
As you can see on the left-hand side of figure 2 there was a minimal performance decline on day 2 of the withdrawal phase, but the latter was statistically not significant and all measured markers of cognitive function had returned to normal on day 8 (remember longer response times = worse performance!), when the resumption or first time provision of caffeine spiked the reaction times and lowered the mistakes in all tests, irrespective of whether the subjects were former habitual consumers on withdrawal, or not.

Outside of controlled experiments "real" coffee and tea do at least as well

Since a large cup of coffee contains about the same amount of caffeine the scientists simply added to decaffeinated beverages, to ensure that the drinks could not be distinguished (by their smell for example), you can simply stick to your regular coffee and if you want to enjoy similar benefits. And to be honest, in view of the plethora of benefits of chronic low dose coffee consumption, I would not even think for a second about whether or not you may be missing out on the occasional boost, when you are not "going on withdrawal" from time to time...

Figure 3: W/out arginine (Arg-) intestinal epithelial cells can't proliferate (graph based on Stadelmann. 2012)
Giardia eats away your guts arginine supply and makes itself at home within an increasingly morbid digestive tract! As a group of scientists from Sweden and Argentina reports in their latest paper, the protozoan parasite, Giardia intestinalis, feasts on the arginine your gut cells need to proliferate (Stadelmann. 2012). This will lead to reduced polyamine levels and upregulated cell cycle inhibitory genes, which will eventually disrupt the the cell cycle of the intestinal epithelial cells. The reduced intestinal epithelial cell proliferation, on the other hand, allows the gut pathogen to thrive and will, in the long run, disrupt the intestinal tissue homeostasis and thus initiate the decay of the intestinal epithelium  - a central feature of so many of the wide-spread gut pathologies.

Provision of additional arginine + citrulline can help ... in the short run

Now, the good news about all that is that the in-vitro data in figure 3 clearly suggests and anecdotal, as well as the effective therapy of diarrhea patients with arginine/citrulline actually confirm that the provision of supplemental arginine (or citrulline) constitutes a cheap and readily available way to ameliorate the decay, until the bugs have been eradicated by antimicrobial drugs.

A pros pos, antimocrobial drugs, with regard to latter, Noa Tejman-Yarden and Lars Eckmann write in a recent review of the latest drug innovations, that despite the fact that metronidazole and other antimicrobials are usually effective, "treatment failures are common and antimicrobia resistance occurs" (Tejman-Yarden. 2011), so that it would appear as if complex derivatives of 5-nitroimidazole and benzimidazole, which form the core structure of the most widely used antigiardial drugs, will replace them in the short-run. At least for so long, until several new classes of antigiardial drug candidates that have already been identity by high-throughput screening of large compound libraries, will eventually hit the market (Tejman.Yarden. 2011)

More about vitamin B6: Helps with neurotransmitters synthesis; is involved in nerve function and necessary for normal brain development & function; influences mood, and melatonin production; effects circadian clock; is needed for B12 absorption and thus red blood cell production
When low: "Pins and needles" in extremities, mental disorders, seborrheic dermatitis, estrogenic PMS, dizziness, irritability, kidney stones, abnormal EEG, anemia, convulsions, edema (water retention), hypothyroidism, migraine-headaches, glossitis, lymphopenia
When high: Depression, suicidal tendencies, severe fatigue, mood swings, low blood sugar, migraine-headaches, heart palpitations, thyroid abnormalities (hyper- in the short, hypo in the long term), numbness in hands and/or feet, spinal / nerve degeneration, muscle spasms / cramps, osteoporosis, arthritis, higher blood pressure (short-term suppl.), lower blood pressure (long-term suppl.), mineral imbalances (high phosphor & magnesium vs. low sodium & calcium), restlessness, insomnia, vivid dreams, decreased estrogen & prolactin, depressive PMS.
RDA (adults): 1.3 mg*
*higher for pregnant women & >50y
Upper tolerable limit: 30-100mg*
*depending on the source of information
Food sources: chicken, turkey, tuna, salmon, shrimp, beef liver, milk, cheese, lentils, beans, spinach, carrots, brown rice, bran, sunflower seeds, wheat germ, and whole-grain flour
n6:n3 ratio does not depend on dietary intake alone: A marginal deficiency in vitamin B6 will skew your serum PUFA levels towards the N6-side That's the long and short of the results of a study that's going to be published in the October issue of the Journal of Nutrition.

Mei Zhao and her colleagues analyzed the fatty acid profiles in plasma, erythrocytes, and peripheral blood mononuclear cells (PBMC) of healthy men and women who had been fed a low-vitamin B-6 (pyridoxine) diet for 28 days and observed that contrary to the plasma HDL and LDL cholesterol concentrations, the amount of free fatty acids (FFA) in the blood and the erythrocyte and PBMC membrane fatty acid compositions, neither of which showed any statistically significant changes, the amount of all long-chain polyunsaturated fatty acids, i.e. arachidonic acid (n6) and EPA and DHA (n3) decreased from 548 ± 96 to 490 ± 94 μmol/L, 37 ± 13 to 32 ± 13 μmol/L, and 121 ± 28 to 109 ± 28 μmol/L, respectively.

The subsequent 8% increase in the total n6:n3 PUFA ratio from 15.4 to 16.6 is not alarming, but if this trend would continue linearly, it would certainly become problematic, in the long run. Moreover, the decrease in both n6 and n3 long-chain PUFAs (of which people tend to forget that the "inflammatory" arachidonic acid is as vitally important as its "anti-inflammatory" omega-3 counterparts) could provide an alternative / complementary mechanistic explanation for the increased cardiovascular disease risk that has been associated with vitamin B-6 deficiency.

In view of the fact that the RDA is not exactly high and can easily be achieved from dietary sources, along (as long as you follow a diversified whole foods diet), and considering the fact that high levels of B6 have been associated with more negative side-effects than B6 deficiency (see infobox on the right; please note that I collected the information on a couple of trustworthy websites on RDAs & co and did not verify the research on each of them!), I would however caution against the typical Western "more helps more" supplementation mentality.

Figure 4: Easy come, easy go - the mass you gain and the fat you lose by doing nothing than simply injecting testosterone is lost / regained within 6 months after discontinuation of the "testosterone therapy" (Forbes. 1992); read more about the role of testosterone in skeletal muscle hypertrophy in the Intermittent Thoughts on Building Muscle
In view of the fact that (a) today's short news items are pretty long(ish) and you still got a couple of interesting facebook news to check out, such as...
... and a plethora of additional gems from the realms of health, exercise, nutrition & supplementation, I will call it a day for today and save the exercise and a couple of other exciting On Short Notice items for later next week.

  • Aleisa AM, Alzoubi KH, Gerges NZ, Alkadhi KA. Chronic psychosocial stress-induced impairment of hippocampal LTP: possible role of BDNF. Neurobiology of Disease 2006;22:453–62. 
  • Alzoubi KH, Abdul-Razzak KK, Khabour OF, Al-Tuweiq GM, Alzubi MA, Alkadhi KA. Caffeine prevents cognitive impairment induced by chronic psychosocial stress and/or high fat-high carbohydrate diet. Behav Brain Res. 2012 Sep 20.
  • ESMO. Press releases related to the ESMO 2012 Congress of the European Society for Medical Oncology in Vienna.
  • Forbes GB, Porta CR, Herr BE, Griggs RC. Sequence of changes in body composition induced by testosterone and reversal of changes after drug is stopped. JAMA. 1992 Jan 15;267(3):397-9.
  • de Mendonca A, Ribeiro JA. Endogenous adenosine modulates long-term potentiation in the hippocampus. Neuroscience 1994;62:385–90.
  • Molteni R, Wu A, Vaynman S, Ying Z, Barnard RJ, Gomez-Pinilla F. Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor. Neuroscience 2004;123:429–40.
  • Smith AP, Christopher G, Sutherland D. Acute effects of caffeine on attention: a comparison of non-consumers and withdrawn consumers. J Psychopharmacol. 2012 Sep 19.
  • Stadelmann B, Merino MC, Persson L, Svaerd SG. Arginine Consumption by the Intestinal Parasite Giardia intestinalis Reduces Proliferation of Intestinal Epithelial Cells. PLoS ONE. 2012; 7(9): e45325. 
  • Tejman-Yarden N, Eckmann L. New approaches to the treatment of giardiasis. Curr Opin Infect Dis. 2011 Oct;24(5):451-6.

The Latest on Sodium Bicarbonate: Serial Loading Almost as Effective as Acute Loading and Free of Gastrointestinal Side Effects. Plus: Can You Use Potassium Bicarbonate Instead?

NaHCO3 loading has been most successful in events lasting from 1 to 7 minutes (Linderman. 1994) - so either track sprints or volume training
Do you remember my last post on sodium bicarbonate and what I said about the SuppVersity being the place, where you would read about the latest studies on the wonders of baking soda, first? Well, at least I have not seen today's SuppVersity news being covered anywhere else, so I guess for the vast majority I am about to deliver on yet another promise, when I briefly summarizing the latest findings on the "effects of serial and actue NaHCO3 loading in well-trained cyclists" from University of Tasmania and the Tasmanian Institute of Sport in Lanceston, Australia (Driller. 2012; study will be published in the October issue of the Journal of Strength and Conditioning Research).

Why don't we just "load" on NaHCO3 over a longer timespan?

Interestingly, Matthew W. Driller, John R. Gregory, Andrew D. Williams and James W. Fell must have asked themselves a very similar question as I did a couple of weeks ago:  
How come, that there is "limited research describing the use of serial NaHCO3 loading?"
Or put simply: Wouldn't it be likely that we would see similar, in the long haul even superior, results from the chronic ingestion / slow loading of NaHCO3 with less side effects compared to the standard practice of downing 30-50g at once?

Figure 1: The doses on day 1-3 were taken with breakfast, lunch and dinner, the 5 doses on the day of the test (day 5) within 90min before the test; placebo capsules contained microcrystalline cellulose
To answer this question Driller et al. came up with a double-blind placebo controlled, randomized design in which each cyclist underwent 3 experimental trials over a 3-week timeframe:
  • AL - acute NaHCO3 loading
  • SL - serial NaHCO3 loading 
  • P - placebo loading condition 
You can see the "exact" protocol in figure 1 to the right. The main performance variable was a 4-minute cycling test (TT), a choice the scientists explain by referring to it as an approximation (at least duration-wise) of a "complete a 4,000-m individual pursuit in track cycling" and refer to previous research by Lindermann & Gosselink from 1994, which confirms that "NaHCO3 loading has been most successful in events lasting from 1 to 7 minutes" (Driller. 2012).

If you do the math on the figures, you'll see that the respective absolute amounts, i.e. P = 0mg, AL = 0.3mg/kg and SL = 0.9mg/kg were not identical.

You could also argue that the SL group should at least have stuck do their regular protocol on the day of the test, but (1) the higher total dosage in the serial loading trial seems reasonable - after all, your body uses the NaHCO3 also, when you don't work out so you got to build an even greater buffer, and (2) it would have been hard to distinguish the "chronic" from the acute effects if the SL protocol had involved supplementation on the day of the test.

The exercise protocol: A time trial simulates a 4k race

Can I use potassium bicarbonate instead? NO! You can combine both, but from a physiological standpoint it does not makes sense to increase your serum potassium levels before a workout, because especially strength training will leech potassium from the cells into the blood anyways. Moreover your body conserves potassium pretty well during a workout, while you lose a comparably large amount of sodium in your sweat. In other words, you risk offsetting the peculiar balance of the extra-cellular sodium ions and the intracellular potassium ions. While weakness or skeletal muscle hyperexcitability would be rather harmless, but certainly ergolytic consequences, this can - in the worst case - lead to bradycardia (=abnormally slow heartbeats), arrhythmias and even sudden cardiac arrest as it was observed in the two "salt-phobic" bodybuilders in the case report I already cited in the comments on the "Sodium Bicarbonate for High Volume Strength Training" post (cf. John. 2011; there were probably confounding factors at play, here, but still, the risk of developing hyperkalemia is nothing you can totally exclude, if you ingest tons of potassium within a couple of minutes).
If you feel that you don't get enough potassium in your diet, anyway, I'd suggest you mix them at a 3:1 ratio as you usually see it for "normal" sodium and potassium in electrolyte products.
A pros pos "day of the test", on the latter, the participants, 8 well-trained male cyclists (age = 28y; height = 181cm; mass = 73.5 +/- 8.5 kg; VO2peak =66.8 +/- 8.4ml/ kg/min), who were all cyclists currently competing at the state or national level and in their on-season, ingested the placebo or bicarbonate capsules with a tightly controlled amount of water (10 ml /kg body mass) 90 minutes before they hopped onto an air-braked cycling ergometer to perform their time-trial test.
"All the cyclists performed a standardized warm-up before the test, which was replicated before each TT. The warm-up consisted of 3 set intensities relative to the cyclists’ body mass, each lasting 4 minutes. [...] During the exercise test, each cyclist was encouraged to give a maximal effort during the TT. The investigators providing the encouragement were blinded to the trial each cyclist was undertaking. The VO2peak was taken as the highest VO2 value recorded over a 30-second period during the TT." (Driller. 2012)
After the test the cyclists were provided with a modified gastrointestinal side-effects questionnaire which allowed them to quantify the side effects on 10-point Likert scale ranging from 1 = "none" to 10 = "unbearable".

The results: Serial loading with accute effects, but less side effects

Blood samples were taken before and after the trials, the subjects performed in a rested and hydrated state after fasting for at least 2h. They also filled 3-day food and training diaries for the days before the experiment. Since the scientists don't mention those in the FT to the study, I assume there were no significant intrapersonal differences between the trials), so that the results I summarized in figure 2 are not distorted by 3-days of overtraining or 3-days of McDonalds dieting ;-)
Figure 2: Relative power (W/kg), peak blood lactate (mmol/l), HCO3 post loading and post test (mmol/l), pH post loading and post test, VO2 peak (l/min); p < 0.05 for all but the HCO3 post test value - the figures above the bars indicate the percentage of participants which did see practically relevant improvements in the respective parameter (vs. those with improvements that were trivial or even negative; based on Dreher. 2012)
As you can see both the acute, as well as the alternative serial loading protocol yielded the desired improvements in exercise performance. On average, the alkalizing effects, as well as the increases in VO2max were yet more pronounced in the acute compared to the serial loading test... but let's be honest: What's that worth if you get the runs during a race or workout? To be fair, in the study at hand no athlete developed diarrhea, but three felt bloated after the AL protocol, whereas not a single study participant experienced any side effects from the serial loading.

Why not simply stay "on" sodium bicarbonate?

In view of what I have said before about the experimental necessity of not providing any NaHCO3 to the study participants on day 4 of the SL trial, the logical next step in the "evolution of bicarbonate science" would be to probe my previous suggestion to administer the baking soda chronically and keep the study participants "on" NaHCO3 for a week or two during their regular training, without dropping the dose (alternatively even escalating it) on the day of the exercise test / training days.

Figure 3: Latent acidoses can set you up to become obese and prevent your hamper your fat loss (Berkemeyer. 2009)
I would speculate that this would also allow them to exploit the previously cited plethora metabolic benefits of being in a more or less alkaline state (see figure 3 and "How Bicarbonate Could Help You Lose Fat & Build Muscle") and would thus turn something as "profane" as an ergogenic aid into a weight loss and health supplement. This appears even more likely in view of the fact that the study at hand clearly shows that it does not matter whether you use a bicarbonate buffer before your workout, or not, when you're done with it, your HCO3 levels will be rock bottom (assuming that you have trained with maximal intensity). That being said, it appears only prudent not to restrict the use of the buffer to the pre workout window, only, but to use it to re-alkalize your body immediately post workout, as well.

And while I doubt that we will see that study being done in the near future, you know that there is no better place to check for the latest news on sodium bicarbonate, aka baking soda or NaHCO3 than right here, at the SuppVersity ;-)
Update => Dr. Andro's Bicarbonate Protein Pudding: Since Spencer asked me on Facebook how / when I use baking soda and I already betrayed my "secret protein pudding recipe" *lol* I thought I'd post it here, as well.

How it's done: You take some quark (this is a German dairy product you US guys usually know as curd cheese; depending on how hungry you are you use ~100-300g), add water maybe 100ml and stir it, you will soon notice that it does not become a smooth pudding, no matter what you do. So, next you add a scoop of casein or protein powder for the flavor you like best, e.g. chocolate, (casein works best, because it also adds to the creaminess). Mix the protein with the white "soup" and then add 1-2 teaspoons of sodium bicarbonate. You will soon realize that what happens now verifies the term "baking soda": your pudding-to-be is going to start raising like dough, keep the water and some stevia at hand and add water + stevia until the stuff has the consistency and sweetness you like best.  

Voila! Dr. Andro's Quark Based Protein Laden Alkalizing Bicarbonate Pudding is Ready! Makes an excellent last meal of the day, as well... but watch out it is really filling ;-)

  • Berkemeyer S. Acid-base balance and weight gain: are there crucial links via protein and organic acids in understanding obesity? Med Hypotheses. 2009 Sep;73(3):347-56. 
  • Driller MW, Gregory JR, Williams AD, Fell JW. The Effects of Serial and Acute NaHCO3 Loading in Well-Trained Cyclists. J Strength Cond Res. 2012 Oct;26(10):2791-7.
  • John SK, Rangan Y, Block CA, Koff MD. Life-threatening hyperkalemia from nutritional supplements: uncommon or undiagnosed? Am J Emerg Med. 2011 Nov;29(9):1237.e1-2.
  • Linderman, JK,Gosselink, KL. The effects of sodium bicarbonate ingestion on exercise performance. Sports Med 18: 75, 1994.

Adelfo Cerame - Three Months Bulk Wrap-Up + My Three Bulking Guidelines For Pre-, Post and Wendy's ;-)

Adelfo takes measure...  as an aside: This picture goes to show you that the right (or wrong) light and posing can do much more (in this case harm, on the photos I usually post of Adelfo however good!) to your physique than any anabolic steroids and it works in minutes!
I guess I'll make it brief today and won't promise too much for the SuppVersity Science Roundup which starts, as usual, at 1PM (EST) live on Super Human Radio (click here to listen live). It's always a show you don't want to miss, but if you are by any means interested in gyno, prostate and men's health, I am pretty sure we will tackle all that. Not so sure about pseudo-ephedrine being no alternative to the "real deal" and a bunch of other stuff on training, nutrition and supplementation... best you tune in life or check out the Super Human RSS Feed (see navigation on the right where it says "Listen to Physical Culture") for the podcast that will be available ~2h after the show ends.

So much for the self-promotion part and now for something that will segue right into Adelfo's post.

I have been contemplating, whether or not I should address this, but I felt it was necessary to let all people who have not seen the (who wonders) anonymous commenter who indirectly accused Adelfo of being on gear last Friday (click here to be taken right to the comment). I won't repeat what I said about the whole issue in that very post - if you are interested you can read it up, but I do want to quote part of Adelfo's reply or at least parts of it, because I feel that it tells much about the difference between "unknown" on the one hand and my friend Adelfo, on the other hand:
"To be honest; I don't really mind the steroid accusations. [...] With regards to you accusing me of being a lier? Yes that upset me a bit, but everyone is entitled to their own opinion and this is an open forum where people can comment and say what they want so I have no qualms with that but in my defense, I'm a physical culture enthusiast and a student of the game just like all the subscribers on here. I don't claim or ever will claim to know everything, I'm no genius, i'm no guru, I'm a nobody. I was just fortunate enough to be invited by Dr. Andro on a weekly basis to share my experiences with nutrition and fitness as a disabled athlete, and how I apply them to my circumstances. That's all I do; share my experiences, and give advice and pointers based on my experiences." - Adelfo Cerame, September 22, 2012 9:43 AM
Adelfo followed this up with an offer to help "unkown" to identify, where he may improve on his training, nutrition and supplementation regimen, which "unkown" did not accept... so, just in case you just missed it, "unkown", the offer is still valid... I guess you all have heard enough of me (Dr. Andro) for now, so I better hand over to Adelfo and his thursdaily progress updates!

3-month bulk wrap-up: Where I came from, am now and how I got from then to now

It’s final week of my bulk before I start my prep next week, so just thought I’d give you guys a brief final update of how everything went…

Progress facts*
Weight: 140  => 155lbs
Chest: 40 => 41"
Arms: 17.5 => 17.5"
Shoulders: 48.5 => 49"
Waist: 29 => 33"
*  (July 2 => now)
Bottom line: Chest grew about an inch- Shoulders grew ½ an inch- gut grew 4.5 inches (Lol) – but my arms stayed fairly the same. It’s kind of hard to measure the arms yourself it may have grew a tad but not to any significance to where you can noticeably see the measure tape budge.
Kind of tough to measure yourself but this is how I did it in the beginning of my bulk, so hopefully I measured right
Macros for last month: 
  • PRO: 150-180g
  • CHO: 250-300g
  • FAT: 80-100g
Total Energy: 2300-2500kcal
Overall, I feel the whole 3-month bulk went pretty well, much better than my previous attempts at bulking. I was able to stay much leaner this year, while at the same time being able to pack on a tad bit of lean muscle for the short time I had. 
Front pose – Rear Double Bi- Relaxed back pose
I felt I could’ve made a better effort to stay leaner, but it’s really hard when it’s the off-season and you don’t have a show to prepare for in a while. Particularly in the last month, I've been sort of sloppy and got lazy with tracking my macros. I eventually just started eyeballing my food and guesstimating my portions based on my total calories and daily macronutrient goals. It was a very flexible last month.

You can see the "exact" (actually I should say estimate) numbers for the last month in the overview on the right. These are the numbers where I sort of fluctuated around, and most of the days I was on the higher end of my macros and maybe have gone a little over from time to time due to my many PWO meal rendezvous at Wendy’s located right across the street from my gym.

How I tackled the bulk - Three simple dietary guidelines
  • Two 4 oz bison steaks, 2-3 cups of rice, 2 cage free eggs, 1 small whole papaya! This is how my PWO meals look like when I’m not being a fat ass eating my PWO meals at Wendy’s which has the advantage of being able make up for the calories I would otherwise miss later on ;-)
    eat a light protein + fat pre workout meal  - sometimes I even trained fasted just w/ BCAA’s and creatine if I was in a rush or on the go
  • have 2 big meals after you trained (not including PWO shake) - I just ate until I got full and I used a lot of rice to make up for the carbs, if I felt like I didn’t hit my intake. 1 cup of cooked rice is about 50g of carbs so 2 cups easily will get you 100g of carbs; it goes down pretty easily, so exercise caution ;-)
  • make sure not to miss your last meal - I have been real busy and on the go as of late, so it has been really tough to get my last meal in at times, so after my workouts I would just go to Wendy’s (which is right across the street from my gym) - Lol; and when I got home I would just pound a protein shake before bed just to make sure I got enough protein for the day just increase I didn’t.

And as far as training goes... for the first half of my bulk I did a 5x5 strength training and hypertrophy training split, but towards the home stretch I started doing Jim Wendlers 5/3/1 strength training with the same hypertrophy training split. If you want more details, just refer back to my past blogs to check the training regimen I’ve been using for the past 6 weeks using Jim Wendlers 5/3/1 - I could outline it all over again, but don't want to bore you with that.

That’s all I have for now, but stay tuned for next week for my first week of prep!

Coffee, saviour or masked enemy? Riding, racing and other things.

It's been almost a week and a half since the Epic, and I have finally (I think) kicked the lurgy which was evidently incubating during that race, and came out in full force the days after. I've been full cycle, but now it seems that health is in the house again. I knew that feeling that...dead...throughout the Epic was for a reason. Though to be fair, my hills need work regardless!

It's a funny thing, how coffee is so good but can be so bad. For instance, when one is feeling terrible, perhaps a bit sick and tired from the lack of zzz's thanks to the bout of virus one is getting about with? Have a coffee, feel AMAZING for about 40 minutes, but then feel worse than before. The strangest thing (ok, it's a bit gross if facial virus eruptions freak you out...) is when downing i'm a short black, that I know I probably shouldn't be having because i'm sick, soon after when I can feel that liquid gold pumping through my veins it makes manky cold sores throb.
A personal favourite of mine. Ah, so true!

Ideas? Excess sympathetic innervation? I don't know, but it makes me very aware that i'm doing something I shouldn't. Even though it feels so good at the time.

Addicted much?

Anyway, it's State Champs this weekend at Adare. I am in two minds about it. I'll probably go, race around, hurt a lot and feel unfit. But i'm kind of sick of being underdone at races. Theoretically it should help get me fitter, but racing as a training exercise sucks. Why? Because I don't like riding slowly, and that what ends up happening.

Aiden gets mad and says 'you're not unfit, gawsh' in a Napoleon Dynamite-esqe manner. And I guess I am not, but not being fast—as fast as I know I can go, sucks. It's all part of the long road back, and really, the need to get out for x amount of hours per week has been quelled since Elva. I still need to get out, but to obsess about getting 15 hours of training in, or whatever, just doesn't work with a kiddo. It makes the time had out there better, i'm sure.

The toughest thing is not knowing what i'm working for. The Victorian National series is really, really inconvenient for XC riders in SEQ, even moreso with a baby. Nope, don't really fancy travelling by air, followed by an epic roadtrip with a 1 year old, to go race what will no doubt be a diminished field of elite women. It doesn't make sense!

So, National Champs are in, but what else?

A near-entry in the Highland Fling 112km race on a singlespeed was quashed by rising airfares, and it was my fault for being a master procrastinator so when I went to commit to doing it, fares were $100 more expensive.

There are some cool stage races to be had, including the Hellfire Cup, Ingkerreke MTB Enduro and Wildside (which is biannual, which gives me plenty of time! Plus there is the Cape to Cape but i'm not organised enough for that i'm still feeding Elva, like, ALL the time so will have to sort that out in time too).

Meanwhile, the Chariot is being rocked out as much as possible (apart from a week's hiatus corresponding to aforementioned lurgy), and I have even got some new MTB shoes, replacing the ones with the absent buckle which was ripped off during my first race post-Elva.


I tried for an action shot, but failed. Here's the best attempt;
Handheld iPhone shoe-while-cycling photo attempt: Fail.

And here's a picture of my child trying to escape the (convenient) confines of the baby bouncinette:

We call it baby alcatraz, but no doubt one day we'll be doing something and look at her and she will have successfully escaped its buckled confines.

So, that's it! See you on the trails!