Power Up Kale Soup Author: Vince Del Monte…

Power Up Kale Soup

 

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Author: Vince Del Monte

Ingredients

• 1 medium onion (chopped)
• 4 cloves organic garlic (chopped)
• 5 cups organic chicken or vegetable broth
• 1 cup diced carrot
• 1 cup diced celery
• 2 red potatoes (diced)
• 3 cups kale (stems removed and chopped fine)
• 2 tsp dried thyme
• 2 tsp dried sage
• sea salt and pepper to taste

Instructions

1. In a frying pan, fry onion and garlic to brown. (you can do this in soup pot by using a small amount of the broth to saute them in.)
2. In soup pot add in broth, potatoes, carrots and celery.
3. Bring to boil on high
4. Lower heat
5. Add thyme, sage, salt and pepper
6. Let sit on low heat to simmer for about 15 to 30minutes.
7. Add kale at 5 minutes before taking pot off heat.

3.2.1275

 

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Block Periodization for Resistance Trainees: 3x Higher Strength Gains on the Bench vs. Zero Benefits for Legs

The deadlift probably won’t benefit from blocked periodization either… at least if you do it only once a week anyway.

I hope you all remember my recent article about the beneficial effects of block periodization on the training outcome of trained cyclists (if you don’t I’d suggest you read up on it: “Block Periodization – Impressive Performance Gains in Pro-Athletes“) and the hypothesis that the mechanism behind the beneficial effects Rønnestad et al. report in the corresponding paper are not actually a consequence of this specific periodization scheme. Rather than that, the benefits the researchers have observed may well have been a mere consequences of the “change”, of “breaking out of the rut” and the provision of a new challenge that’s absolutely essential to induce what everyone, from housewife to Olympian athlete is training for: adaptation.

Let’s discard the mechanism for a moment, though and let’s rather focus on the hard facts – hard facts that are complemented by the results of a soon-to-be-published paper by researchers from the University of Bologna and the University of Central Florida.

What’s so interesting about this paper is …

….that it looks at the effects of block periodization in trained strength athletes and could thus help us answer a question that may have been preying on your mind, ever since I published the previously cited article about the beneficial effects of block periodization in endurance athletes: “Do Different Rules Apply for Strength vs. Endurance Athletes?” Or, put simply: Would a weight lifter benefit to a similar extend from block periodizing his training regimen as a cyclist – irrespective of what the underlying mechanisms may be?

Figure 1: The subjects trained 4x per week – identical training plans in both groups (Bartolomei. 2014)

The answer is “yes and no” – Yes, if we are talking about the upper body, no – and that’s interesting because cycling obviously involves the same muscle groups – when we are looking at the lower body performance gains in Figure 2:

Figure 2: Changes in max. strength (1RM in kg), mean power (in % of baseline) and jump height (in cm) in the 24 study particpants in response to traditional linear or block periodization (Bartolomei. 2014)

As you can see, the gains in lower body power was identical – irrespective of the type of periodization (see overview in Figure 1). For the upper body, on the other hand, the subjects who did not simply ramp up the intensity continuously from 5 sets of 8-10 reps at 65-75% of  1RM  with  less  than  2  minutes  of  recovery  between  sets to 5 sets of 3 – 4 reps at 85 -95% of 1RM with 3 minutes of recovery from week 1 to week 12 (TP group), the …

“[p]articipants  in  BP  were  more  likely  (79.8%)  to increase the area under the force-power curve than TP. Participants in BP also demonstrated a likely positive (92.76%) decrease in the load corresponding to maximal power at the bench  press compared to TP group, and a possible improvement (~ 60%) in maximal strength and power in the bench press.” (Bartolomei. 2014)

Whether that’s muscle-specific reaction to the three 5-week mesocycles, instead of one 15-week mesocycle is yet highly questionable – or do you think the legs respond less to the periodization program that’s depicted in Figure 3, than chest, back, arms & co?

Figure 3: Illustration of the interplay between intensity and volume of the n=14 24-year-old male, resistance trained (>3 years, >3 sessions per week) subjects in the block periodization group (Bartolomei. 2014)

Personally, I would rather come back to the “novelty approach”. It goes without saying that we can assume that the abrupt changes on a blocked periodization regimen favor “growth promoting overloads”. In the case of the musculature of the lower body, the simple fact that it was trained just once a week may yet have provided a similarly “novel” or at least less accustomed stimulus on every leg-day.

“Periodize Appropriately and Cut 12% Body Fat in 12 Weeks!” | more

Bottom line: Again, it’s difficult to tell, whether there is any special magic in block periodization. What can be said, though, is that we can again (see “Block Periodization – Impressive Performance Gains in Pro-Athletes: Revolutionary Training Concept, Or Just a Good Way to Eventually Break Out of the Comfort Zone?” | read more) make an argument for the “breaking out of the rut” hypothesis… in this case, however, in an ostensibly muscle-specific manner that’s eventually not “muscle-“, but actually “training-frequency-specific”.

In the end, it does not matter, if my ad-hoc explanation is or isn’t accurate. For you as a practicioner who is probably training the muscles of his upper body thrice a week, the results of this study are significant – no matter what the underlying mechanisms are. In other words: The results of the A classic HST-oriented training program that is eventually “block periodized” will yield better training results than one, where you train in the same rep ranger 365 days a year. But let’s be honest: That’s not surprising, is it?

References

• Bartolomei, Sandro, et al. “A Comparison of Traditional And Block Periodized Strength Training Programs in Trained Athletes.” Journal of Strength and Conditioning Research (2014). [ahead of print]
• Rønnestad, B. R., J. Hansen, and S. Ellefsen. “Block periodization of high‐intensity aerobic intervals provides superior training effects in trained cyclists.” Scand J Med Sci Sports 24 (2014): 34–42.

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True or False? Butter, Ghee, Lard & Tallow – Are Saturated Animals Fats the Kings and Queens of the Frying Pan?

Even if animal fats were the best frying fats, this wouldn’t turn  doughnuts into “health food” and french fries into raw carrot sticks.

If you “liked” the SuppVersity on Facebook (http://ift.tt/NQiPkk) you will probably already have seen the controversies and questions my post “Scientists on the Quest for the Perfect Frying Oil” (read more) has triggered. Eventually, it all revolves about yet another of those nutritional wisdoms that’s circulating on the Internet: “Ghee, tallow, lard, … saturated animal fats and the coconut micacle, of course, are the best and only frying oils you should use.” (next best Internet source)

How on earth could F. Aladedunye, and R. Przybylski, the authors of the previously cited study even dare stating that high-oleic low-linolenic rapeseed, high-oleic sunflower oils are good frying oils?

But enough of the sarcasm: In today’s installment of “True or False” (read previous installments) we will focus solely on the cholesterol-containing animal fats, and save the one and only “coconut miracle” (Coconut oil – virgin, of course – must be good for everything, right? There have after all (E)-Books been written about it 😉 for another installment of this series. So, where do we start then? I guess, we could start by rendering down a big packet of butter in my frying pan… but *wtf* what’s that? It’s turning tar black!? Can that really be the ideal frying fat? Probably not, but if regular butter sucks, what about clarified butter aka “ghee”, then? It’s easier to process and there are not tarry clouds floating in the pan, when you heat it.

“But don’t we all know that cholestrol ain’t bad for us?”

Unfortunately, there are other problems with ghee;  problems that are related to the heat-induced oxidation of cholesterol and the presence of large amounts of cholesterol oxides in commercially available “clarified butter” even before you even start heating it as it was reported by Kubow et al. in 1993 (12.3% w/w of total sterols).

If rancid fish full of oxidized PUFA ain’t bad for us (read previous article), why would we want to use saturated animal fats for frying then? Please note that the overwhelming evidence says that oxidize PUFAs are bad for you.

Not a problem? We all know the whole cholesterol thing is a hoax that was made up just to put everyone on statins? Well, even if that were the case, the “whole cholesterol thing” is about the effects of intact, not oxidized cholesterol on heart health. The oxidized sterols in your “healthy” clarified butter, on the other hand, don’t just make it into the bloodstream (Staprans. 1994 & 2003), they will also be incorporated in various tissues (Vine. 1997) and lead to a rapid (+100%) increase the formation of fatty streak lesions in the aorta of lab animals (Staprans. 2000) and have been linked to the unexplained high risk of atherosclerosis in Indian immigrant populations in the US (Jacobson. 1987) as well as the occurrence and progression of atherosclerosis in general (Leonarduzzi. 2002; Gargiulo. 2011).

As mentioned before, butter is unfortunately, not the only high cholesterol item on the Internet’s list of “best, because highly saturated, frying oils”. Next to butter (215mg of cholesterol / 100g) you will also find lard (95mg of cholesterol / 100mg) or tallow (109mg of cholesterol / 100mg) on these lists.

“I always pour away the oil! I am safe, right?” If I had not heard this argument before I would certainly not mention that the oxidized cholesterol do make it into the fried products. In a study from 1991, Zhang et al. report that the average content of the measured forms of oxidized cholesterol in french fries that had been fried in fresh, previously unoxidized tallow at a fast food restaurant ranged from 1.6-3.8 mg/100g and thus 3-8x more than Pie et al. found in a rare steak (>0.5mg /100g after 3 minutes of cooking) or cooked pork (>0.56mg /100g) in 1991 or those reported by Al-Saghir et al. for cooked farmed salmon (0.33-0.9mg/100g; cf. Al-Saghir. 2004 — the table on the left is a fully referenced overview of COP levels in various foods from Otaegui-Arrazola. 2010).

Needless to say that neither tallow nor lard or any other of these animal fats contain enough antioxidants to protect their cholesterol from being oxidized (Ryan. 1981; Park. 1986a,b).

Figure 1: Even if you believed that cholesterol was bad for you, the ~50% reduction in intact cholesterol that occurs, when you heat tallow at temperatures of 155°C and 190°C should not be a reason to celebrate (Park. 1986a)

Interestingly, Park et al. have been able to show that this process starts at temperatures as low as 135°C (the recommended frying temperature for most products is 160°C+) and does not increase with higher temperatures. For pure cholesterol Osada et al. determined 120°C as the lowest temperature that induces oxidative changes (Osada. 1993).

In 1986, a group of researchers who conducted research for the French government found that 78% of the total cholesterol that was lost (23% of total cholesterol) from beef tallow during deep frying was recovered in form of the four best known forms of oxidized cholesterol, i.e. Triol-, 7a-, 7/3-, and 7-Oxo-cholesterol (Bascoul. 1986).

The latter have been shown to decreases barrier function of cultured endothelial cell monolayers (induce leaky gut; Hennig. 1987) and smooth muscle cells (Zwijsen. 1992).

Aside from their previously mentioned effect on the progression of atherosclerosis and their direct effect no the gut lining and other protective barriers in your body. These cholesterol oxidation products (COPs) have also been shown to promote the growth of colon (Kendall. 1992) and other forms of cancer (Sevanian. 1986; Gabitova. 2014), figure in the development of type II diabetes (Mol. 1997), block the production and blood pressure lowering effects of nitric oxide (Brown. 1999) and have been implicated in the development and progression of Alzheimer’s disease (AD) and vascular dementia, as well as kidney failure (Sottero. 2009)

Total amounts of COPs (mg/100g) in the extracted fat of raw, fried w/out and w/ corn, olive and partially hydroge- nated vegetable oil, and steamed salmon (Al-Saghir. 2004).

Surprising interactions between frying oils and fried foods: I already mentioned that (a) oxidized cholesterol from frying oils migrate into the fried foods, and (b) the cholesterol in the foods is oxidized, as well. Now, the previously cited study by Al-Saghir et al. (2004) happened to compare the amount of oxidized cholesterol (COPs) in cooked farmed salmon for different cooking oils and found that the salmon that had been fried in partially hydrogenated vegetable oils had the lowest, the steamed salmon the highest content of oxidized cholesterol (0.98mg/100g) – luckily, frying with olive oil can protect you from both, the transfats in partially hydrogenated veg. oils and the COPs in steamed salmon.

And while all the non-enzymatically produced COPs in fried (and other) foods are  “bad guys”, the enzymatic conversion of cholesterol in the body (see Figure 2, bottom) can produce compounds of which Otaegui-Arrazola, Menéndez-Carreño, and Ansorena write in their 2010 review that they play important biological role.

Figure 2: Not all oxysterols are created equal. Those your body creates by enzymatic reactions figure in cholesterol homeostasis (Otaegui-Arrazola. 2010)

In fact, certain oxysterols can suppress the activation of the master transcriptional regulators of lipid homeostasis (SREBPs) by binding to an oxysterol sensing protein in the Endoplasmic Reticulum, while others accelerate the degradation of the key cholesterol biosynthetic enzyme, HMG-CoA reductase, and/or serve as natural ligand activators of a nuclear receptor (LXR) involved in coordinating many aspects of reverse cholesterol transport (Gill. 2008).

These “good oxysterols” do thus appear(!) to play a subtle but important role in the control of cholesterol homeostasis. In the context of this true or false question, their existence, functions and benefits are however irrelevant. Apropos, question! What’s the answer to our question, after all?

The best advice I can give you is to stop consuming fried foods.

We may not be able to trace obesity, diabetes, heart disease, cancer and dementia back to a specific frying oil – what we can do, though, is to draw the links between these and the general consumption of fried foods.

So, no more fried Big Macs or Snickers Bars, and all the other delicious “all American style” foods, folks!

Note: You may or may not have realized this, but at least with respect to the formation of oxidized cholesterol products, the “healthy” steaming turned out to be even worse than frying in Al-Saghir’s 2004 study (see light-blue infobox)

Are butter, ghee, lard & tallow the best or the worst frying fats? While it stands out of question that the cholesterol oxidation products (COPs) are bad for you, we don’t have a study that proves that the amount you’d consume if you were frying your eggs in butter in the morning will cause all sorts of ailments from “A” as “Alzheimer’s” to “Z” as in “diabeteZ” 😉

The previously cited animal studies have – as usual – been conducted with very high amounts of oxidized cholesterol in the diet and the “Ghee is the reason for increased heart disease in British Indians” hypothesis Jacobson et al. proposed in their 1982 article in The Lancet would not explain, why Indians who live in India didn’t have a similarly high heart disease risk at that time… that being said, from 1960 to 1995 the prevalence of heart disease in urban areas of India increased from a meager 1% to almost 10% (Gupta. 1995; compare that to “only” 8.7% in US citizens aged 50years or older; Alexander. 2003). Moreover, US Indians who use >1kg of ghee to fry their foods have a record-breaking 4x increase in atherosclerosis risk compared to their non-ghee eating peers (Gupta. 1997).

You see, we can go back and forth on this and still won’t make any progress. Personally, I would not use ghee, tallow or lard for frying; and whether coconut oil, or maybe olive oil, of which you know that it is cholesterol-free and learned that it reduces the rate of cholesterol oxidation (Al-Saghir. 2004) are better alternatives is going to be a topic for another installment of True or False – so stay tuned for more!

Reference:

• Al-Saghir, Sabri, et al. “Effects of different cooking procedures on lipid quality and cholesterol oxidation of farmed salmon fish (Salmo salar).” Journal of Agricultural and Food Chemistry 52.16 (2004): 5290-5296. 
• Alexander, Charles M., et al. “NCEP-defined metabolic syndrome, diabetes, and prevalence of coronary heart disease among NHANES III participants age 50 years and older.” Diabetes 52.5 (2003): 1210-1214.
• Bascoul, J., et al. “Autoxidation of cholesterol in tallows heated under deep frying conditions: evaluation of oxysterols by GLC and TLC-FID.” Lipids 21.6 (1986): 383-387. 
• Brown, Andrew J., and Wendy Jessup. “Oxysterols and atherosclerosis.” Atherosclerosis 142.1 (1999): 1-28.
• Gabitova, Linara, Andrey Gorin, and Igor Astsaturov. “Molecular Pathways: Sterols and receptor signaling in cancer.” Clinical Cancer Research 20.1 (2014): 28-34.
• Gargiulo, Simona, et al. “Plaque oxysterols induce unbalanced up-regulation of matrix metalloproteinase-9 in macrophagic cells through redox-sensitive signaling pathways: Implications regarding the vulnerability of atherosclerotic lesions.” Free Radical Biology and Medicine 51.4 (2011): 844-855.
• Gill, Saloni, Renee Chow, and Andrew J. Brown. “Sterol regulators of cholesterol homeostasis and beyond: the oxysterol hypothesis revisited and revised.” Progress in lipid research 47.6 (2008): 391-404. 
• Gupta, R., and V. P. Gupta. “Meta-analysis of coronary heart disease prevalence in India.” Indian heart journal 48.3 (1995): 241-245.
• Hennig, Bernhard, and Gilbert A. Boissonneault. “Cholestan-3gb, 5α, 6β-triol decreases barrier function of cultured endothelial cell monolayers.” Atherosclerosis 68.3 (1987): 255-261.
• Jacobson, MarcS. “Cholesterol oxides in Indian ghee: possible cause of unexplained high risk of atherosclerosis in Indian immigrant populations.” The Lancet 330.8560 (1987): 656-658. 
• Kendall, Cyril W., et al. “Effect of dietary oxidized cholesterol on azoxymethane-induced colonic preneoplasia in mice.” Cancer letters 66.3 (1992): 241-248.
• Kubow, Stan. “Lipid oxidation products in food and atherogenesis.” Nutrition reviews 51.2 (1993): 33-40.
• Leonarduzzi, Gabriella, Barbara Sottero, and Giuseppe Poli. “Oxidized products of cholesterol: dietary and metabolic origin, and proatherosclerotic effects (review).” The Journal of nutritional biochemistry 13.12 (2002): 700-710.
• Mol, Marc JTM, et al. “Plasma levels of lipid and cholesterol oxidation products and cytokines in diabetes mellitus and cigarette smoking: effects of vitamin E treatment.” Atherosclerosis 129.2 (1997): 169-176. 
• Osada, Kyoichi, et al. “Oxidation of cholesterol by heating.” Journal of Agricultural and Food Chemistry 41.8 (1993): 1198-1202. 
• Otaegui-Arrazola, A., et al. “Oxysterols: a world to explore.” Food and Chemical Toxicology 48.12 (2010): 3289-3303.
• Park, S. Won, and Paul B. Addis. “Identification and quantitative estimation of oxidized cholesterol derivatives in heated tallow.” Journal of agricultural and food chemistry 34.4 (1986a): 653-659. 
• Park, S., and P. B. Addis. “Further investigation of oxidized cholesterol derivatives in heated fats.” Journal of Food Science 51.5 (1986b): 1380-1381.
• Pie, Jae Eun, Khira Spahis, and Christine Seillan. “Cholesterol oxidation in meat products during cooking and frozen storage.” Journal of agricultural and food chemistry 39.2 (1991): 250-254.
• Ryan, Thomas C., J. Ian Gray, and Tan D. Morton. “Oxidation of cholesterol in heated tallow.” Journal of the Science of Food and Agriculture 32.3 (1981): 305-308. 
• Sottero, Barbara, et al. “Cholesterol oxidation products and disease: an emerging topic of interest in medicinal chemistry.” Current medicinal chemistry 16.6 (2009): 685-705.
• Sevanian, A., and A. R. Peterson. “The cytotoxic and mutagenic properties of cholesterol oxidation products.” Food and Chemical Toxicology 24.10 (1986): 1103-1110.
• Staprans, Ilona, et al. “Oxidized lipids in the diet are a source of oxidized lipid in chylomicrons of human serum.” Arteriosclerosis, Thrombosis, and Vascular Biology 14.12 (1994): 1900-1905. 
• Staprans, Ilona, et al. “Oxidized cholesterol in the diet accelerates the development of atherosclerosis in LDL receptor–and apolipoprotein E–deficient mice.” Arteriosclerosis, thrombosis, and vascular biology 20.3 (2000): 708-714.
• Staprans, Ilona, et al. “Oxidized cholesterol in the diet is a source of oxidized lipoproteins in human serum.” Journal of lipid research 44.4 (2003): 705-715.
• Tsai, Lee Shin, and Carol A. Hudson. “Cholesterol oxides in commercial dry egg products: quantitation.” Journal of Food Science 50.1 (1985): 229-231.
• Vine, D. F., et al. “Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons.” Lipids 32.8 (1997): 887-893.
• Zwijsen, Renate ML, Ingeborg MJ Oudenhoven, and Laura HJ de Haan. “Effects of cholesterol and oxysterols on gap junctional communication between human smooth muscle cells.” European Journal of Pharmacology: Environmental Toxicology and Pharmacology 228.2 (1992): 115-120.

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Hydrated or Dumb: Dehydration Affects Brain, Muscle and Other Vital Organs – Plus: 15+ Causes of Dehydration + Can the Color of Your Urine Tell You if You Drink Enough?

If you want to stay smart, you should join hands w/ water!

Those of you who are following the 10+ SuppVersity Facebook news on a daily basis, will remember my post about the recent paper – co-authored by Brad Schoenfeld (Ribeiro. 2014) – about the significant “water gain” after workouts. I wrote about that myself, a couple of weeks before in “Cell Swelling Keeps Muscles “Pumped” For More Than 52h. Size Increases of Up to 16% After a Single Leg Workout!” | read more, and mentioned that the intra-muscular swelling is probably a necessary prerequisite, if not driver of skeletal muscle growth.

In today’s SuppVersity article, I will now take a step back, away from the musclehead’s only interest and peek at other health aspects that are influenced by the hydration status not just of your muscles, but of your whole body.

Hydration Tip of the Century: Many of you will accidentally (or because they read it here, at the SuppVersity, before) already follow this advice, but I still would like to emphasize that the dairy protein you’re probably consuming after your workout is not only going to boost your muscle, but also your “water” (=positive hydration) gains. In 2010 James et al. were able to show just that: A post-workout beverage with 40 g/l carbohydrate + 25 g/l milk protein are more effective at augmenting fluid retention than 65g of pure carbs carbohydrate (James, 2010).

In one of the most recent papers on this issue, Natalie A. Masento and her colleagues from the University of Reading reviewed the surprisingly profound effect of dehydration on cognition and mood, of which Masento et al. write that it is “particularly relevant for those with poor fluid regulation, such as the elderly and children” (Masento. 2014).

“With evidence to suggest that individuals are routinely at a risk of mild dehydration day to day (Greenleaf. 1965), particularly vulnerable populations such as children and older adults, there has been an increased interest in studying whether additional water consumption might benefit cognitive performance. The small collection of published water intervention studies involving either young adults or school children report consistent positive effects of water intervention on particular cognitive abilities” (Masento. 2014)

If you take a look at the overview, the researchers compiled (it’s too long and eventually repetitive to post it here), you will find studies everything from self-reported fatigue, tiredness and headaches to objectively measured declines in cognitive performance, eye-hand coordination, word recognition, visual attention and – as mentioned in the previously cited article physical performance markers, such as grip strength.

How come? I mean, why does dehydration have such a profound impact?

The above, probably is the question that’s preying on your mind right now and I have to admit, I have – just like the researchers from the University of Reading – no conclusive, water-tight *pun intended* answer to that question.

“Despite the expansion of this research area, we still do not have a clear understanding as to how acute water intervention may influence mental performance and its associated neural activity. Researchers have suggested psychological mechanisms related to limited attentional resources during thirst. However, evidence has also highlighted the  importance of physiological mechanisms, with findings that the expectancy of water alone does not influence cognitive performance.” (Masento. 2014)

Hitherto proposed mechanisms include references to the Global Workspace Model (Baars. 1993) and being distracted by the often subconscious thought “Where do I find water”.

Gray matter activation clusters in dehydration (Streibürger. 2012).

Of potentially greater interest (at least to me) are theories that involve physiological mechanisms, such as the already confirmed…

• shrinkage of total brain volume shrinkage (Streitbürger. 2012; Kempton. 2011) and 
• over-recruitment of specific brain areas during cognitively demanding tasks,

as well as other significant changes at the neural level which contribute to the previously mentioned decline in cognitive performance and awareness (Kempton. 2011).

Luckily, these changes can be reversed by the provision of water in minutes, as long as the subjects are only mildly dehydrated. In view of the

“lack of data related to baseline hydration states of individuals and no further published work using imaging techniques to examine hydration state” (Masento. 2014) 

We do yet once more have to acknowledge that “we know that we know nothing” or, put differently, that these proposed mechanisms are merely speculative.

Potential causes of dehydration: It’s not just working out in the heat or simply forgetting to drink (very common in the elderly), there is a multitude of other things that promote dehydration and here are a couple of examples: ✋Low sodium + chloride (can’t store water), ✋high calcium, magnesium, zinc, chromium intake, ✋ extreme high sodium or potassium intake, ✋low phosphor intake; ✋high vitamin D, pantothenic acid (B5), pyridoxine (B6) intake; ✋low adrenal output; ✋high protein intakes (esp. when protein is abused as energy source); ✋laxatives, diuretics or other meds or supps — One thing, however, does not cause dehydration: ☕ Coffee!

Another physiological mechanism that has been suggested is the albeit age-dependent reaction of the central nervous system in response to the ingestion of significant (500ml) amounts of water, of wich May & Jordan found that it causes

• a significant drop in heart rate and an increase in vasodilation in young adults (May. 2011), and the opposite effects, i.e.
• a significant increase in blood pressure in the healthy old subjects in a 2002 study by Schroeder et al. (Schroeder. 2002)

– whether this difference may be brought about by different baseline hydration status, is not clear. What is obvious, though, is that the cardiovascular reactivity promotes cerebral blood flow, which, in turn, will encourage the circulation of substances such as oxygen and glucose that are known to stimulate neural activity and associated behavioural performance (Gold. .1995) in healthy, non-diabetic individuals.

If you think about this hypothesis, i.e. the beneficial effects of water-induced increases, and the detrimental effects of reductions in glucose and oxygen availability in the brain and other organs that would occur, even upon mild dehydration, it seems perfectly logical, a mechanism similar to that has after all been proposed to account for the improved cognitive function due to physical exercise (Kashihara. 2009).

The urine color chart is a valuable tool to judge your hydration status (Wakefield. 2002)

“So how much water to I need?” — I know. I am mean… the question that’s been preying on your mind ever since the introduction. I still did not answer it – right?

Well, you can find the answer in your toilet bowel (see color chart on the right for a guide). You just have to check the color of your urine to know if you’re drinking enough… well, at least if you didn’t have beets, which will turn it red-brown or red, blackberries, which will give it a red tinge, carrots, which will produce a rusty yellow, paprika, which will make it look orange, rhubarb, which turns it re-brown, then orange, sometimes even yellow-pink, rusty or yellow-brown… and of course the nasty neon-green that’s caused by the tons of useless riboflavin (aka vitamin B2) in your urine.

References:

• Baars, Bernard J. “How does a serial, integrated and very limited stream of consciousness emerge from a nervous system that is mostly unconscious, distributed, parallel and of.” Experimental and theoretical studies of consciousness 174 (1993): 282.
• Greenleaf, John E., and Frederick Sargent. “Voluntary dehydration in man.” Journal of Applied Physiology 20.4 (1965): 719-724.
• Kempton, Matthew J., et al. “Dehydration affects brain structure and function in healthy adolescents.” Human brain mapping 32.1 (2011): 71-79. 
• Masento et al. “Effects of hydration status on cognitive performance and mood”. British Journal of Nutrition (2014) [ahead of print].
• Ribeiro, Alex S., et al. “Resistance training promotes increase in intracellular hydration in men and women.” European Journal of Sport Science ahead-of-print (2014): 1-8.
• Schroeder, Christoph, et al. “Water drinking acutely improves orthostatic tolerance in healthy subjects.” Circulation 106.22 (2002): 2806-2811.
• Streitbürger, Daniel-Paolo, et al. “Investigating structural brain changes of dehydration using voxel-based morphometry.” PloS one 7.8 (2012): e44195.
• Wakefield, Bonnie, et al. “Monitoring hydration status in elderly veterans.” Western Journal of Nursing Research 24.2 (2002): 132-142.

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16 Weeks on High Fat Diet – Weight Loss, Fat Loss, Lowered Inflammation. But is 50% Fat, 30% Carbs Really “High Fat”? Plus: SFA, MUFA & PUFA (n-6) – Doesn’t Make a Difference

This is one of the studies, where you have to look at the full-text before you celebrate or curse. Otherwise you run the risk of missing the actual research interest of the scientists and the fact that this nutritional intervention worked, although it was not particularly low carb.

It has been a while since the last SuppVersity article on high fat diets – specifically if we are talking about benefits, by the way. That being said, you may already have seen quotes from the slightly misleading abstract of a recent paper in the scientific journal Metabolism which could have led you to in the “magic” of low carb dieting more than ever (Silver. 2014). The fact that the author’s name is “Silver” and not gold, however, does already suggest that the questionable long-term effects of the “balanced high fat diet” the 245 pre-menopausal obese women, who met the inclusion criteria of being 21-50 years old, and weight stable at a BMI of 30-34kg/m² for over three months, were fed is not the only relevant information you can’t know if you don’t have access to the full-text of the study.

Beneficial, but not magical 

As I hope to be able to show in a closer analysis of the study, he provision of a diet with a high fat content is beneficial for premenpausal obese women. It is yet not the magic solution to all their health and physique problems.

• Figure 1: Macronutrient composition of the “high fat diet” (Silver. 2014)

  Caveat #1: This high fat diet, is not low in carbs — When you’re reading the words “high fat diet”, you will either think of the “fake” high fat diets (HFD) in rodent trials with carbohydrate contents of up to 40% or an (almost) Atkins-type diet with a high fat, a moderate protein and a low / very-low carbohydrate content.

  It goes without saying that you’d expect the former to be unhealthy – it does after all have a pretty similar macro-nutrient composition as the previously cited high fat diets in rodent studies.

  Consequently, you would probably not believe that the latter, i.e. a diet with max. 10% of the total energy from fat would produce results as they are listed in the “results”-section of the abstract to the paper at hand:

  “Significant improvements occurred in fat oxidation rate (↑6%), body composition (%fat: ↓2.5 ± 2.1%; %lean: ↑2.5 ± 2.1%), inflammation (↓ IL-1α, IL-1β, 1L-12, Il-17, IFNγ, TNFα, TNFβ) and vascular function (↓BP, ↓PAI-1, ↑tPA activity).”

  If I am now telling you that the exact macro composition of the diet at hand had more resemblance with the classic HFD rodent chow (see Figure 1) , than with what you’d probably expect to see, when you hear about “a balanced high fat diet” in the title of a human study, this is hopefully not going to shatter your worldview altogether. 

• Caveat #2: The high fat intake led to a significant decrease in energy intake — Despite the presence of a pretty high amount of dietary carbs in the diet, the satiety effect of the diet (or the absence of the foods that made the women obese in the first place) led to a significantly reduced energy intake of ~10%, or 200kcal.

Fat intake or energy restriction? If we make the likely assumption that the women under-reported their baseline energy intake by only 5% (cf. figure on the left – Heitmann. 1995), the following calculation would yield a predicted fat loss of exactly 4.8kg. This would mean that the macronutrient composition had – on average – no direct influence on the weight loss success.

• It goes without saying that this is not a reliable calculation, but if we still do the math, this would amount to a total energy deficit of 22,400kcal over the whole study period and should result in a fat loss of 3.2kg. In practice, the ladies lost 33% more body fat (4.8kg on average), however – an unrealiable, but at least significant indicator that the reduction in energy intake is not the only, but still a significant contributor to both the fat loss and health effects of the 16-week study intervention.

In spite of these caveats, the study at hand provides very intriguing data and compelling evidence that it is not fat in general that’s making us fat.

Something you may not have read in the short abstract-based newsposts in the blogopshere…

…is that the important information that the actual aim of the present study was to test the hypothesis that body composition, inflammation and vascular function in obese premenopausal women would improve with a high fat diet (HFD) when – and this is where the magic is – “the type of fat is balanced as 1/3 SFA, 1/3 MUFA and 1/3 PUFA.” (Silver. 2014).

In that, Silva and her colleagues from Vanderbilt University, the Northwestern University and the Tennessee Valley Healthcare System hypothesized that…

“[…]while consuming the balanced HFD, improvements in body composition, inflammation and vascular function would be greater when supplemented with 18C fatty acids – in proportion to degree of 18C fatty acid unsaturation.” (Silva. 2014)

In other words, the scientists expected to see the exact opposite of what the average low carber would propagate, i.e. greater improvements in body composition, inflammation and vascular function with a higher PUFA (omega-6, of all!) content of the diet.

To standardize the diets, the fat intake was modulated by the provision of  9 g/d of encapsulated pure stearate (18:0), oleate (18:1), linoleate (18:2) or a identically looking placebo supplement that were ingested on top of the high fat diet with the previously mentioned ratio of 50% fat,  30% carbohydrate and 20% protein. To further standardize fat  intakes, all sources of fats including oils, spreads, nuts and seeds were provided weekly in pre-portioned containers.

Figure 2: Fat intake (in % of total fat) in the four groups of this 16-week dietary intervention (Silver. 2014)

As the data in Figure 2 confirms, the scientists managed to single out the ratio of saturated to mono- and poly-unsaturated fats as their main experimental parameter, successfully. The following observations, do thus inform us about the advantages and disadvantages of three different ratios of dietary fat intake – yet not a bout the effects of a “high fat”, let alone a “high fat low carb” diet, as you may have read it elsewhere on the Internet, as of late.

Figure 3: Changes in body composition (% of baseline) after 16 weeks on different “high fat” diets (Silver, 2014)

As you can see in Figure 3 the changes in body composition were not significantly different, if anything there was a minor advantage for the placebo diet.

The only inter-group differences that did achieve statistical significance were the reduction in interferon γ (↓74%) in the HFD+placebo, and the HFD+stearate diets and the significant effect of the 
HFD+linoleate diet on the PAI-1 (↓31%) levels. The additional changes in vascular function as evidenced by an 8 mmHg reduction in systolic and a 6 mmHg reduction in diastolic blood pressure, as well as the minimal changes in the “suprisingly low” changes of the primary arterial compliance parameters, ie. the small and large artery elasticity index (SAEI/LAEI ml/mm Hg x 100) and the similarly disappointing improvements in flow-mediated dilatation (FMD) didn’t show significant inter-group differences either.

Fatty acid ratio as a modulator of inflammation: The fact that the provision of supplemental stereate, much contrary to that of palmitic acid, another saturated fatty acid led to a significant reduction in IFNƴ, a driver of macrophage activity and endothelial cell inflammation (Kofler. 2005), is as notable as the the “curious” (Silver. 2014) fact that the additional oleate did not produce the reductions in IL-1α and TNFβ, the scientists had expected based on previous studies, where oleate replaced some of the palmitic acid in the diet (Coll. 2008).

So what’s the verdict then? Eating more fat, if it is done in a controlled manner and from non-self-selected foods, can help obese pre-menopausal women lose weight – that’s not debatable.

What is debatable, though, is whether sticking to a prudent low(er) fat diet wouldn’t have elicited the same, in terms of the disappointing improvements in the main parameters of arterial compliance which have previously been reported to be compromised on otherwise “healthy” high fat diets (Keogh. 2005).

To answer this question is beyond the scope of the study at hand, which focused on the main effect of allegedly mild differences in the fatty acid composition of the diets, which affected only two of two dozen of health parameters, i.e. IFNƴ and PAI-1, which contributes to the development of  atherosclerosis (Festa. 1999).

References:

• Coll, Teresa, et al. “Oleate reverses palmitate-induced insulin resistance and inflammation in skeletal muscle cells.” Journal of Biological Chemistry 283.17 (2008): 11107-11116. 
• Festa, Andreas, et al. “Relative contribution of insulin and its precursors to fibrinogen and PAI-1 in a large population with different states of glucose tolerance the insulin resistance atherosclerosis study (IRAS).” Arteriosclerosis, thrombosis, and vascular biology 19.3 (1999): 562-568.
• Heitmann, Berit Lilienthal, and Lauren Lissner. “Dietary underreporting by obese individuals–is it specific or non-specific?.” Bmj 311.7011 (1995): 986-989. 
• Keogh, Jennifer B., et al. “Flow-Mediated Dilatation Is Impaired by a High–Saturated Fat Diet but Not by a High-Carbohydrate Diet.” Arteriosclerosis, thrombosis, and vascular biology 25.6 (2005): 1274-1279.
• Silver, Heidi J., et al. “Consuming a balanced high fat diet for 16 weeks improves body composition, inflammation and vascular function parameters in obese premenopausal women.” Metabolism (2014).

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Want to Become a Mass Monster W/Out Training for Years? Move Into a Hyperbaric Oxygen Chamber! Plus: HBO Could be Useful for Ulcer, Stroke and Cancer Treatment, As Well.

HBO > T = ? | too good to be true?

Hyperbole – you got me! I know, I have done it again. Without training and – even more importantly – proper nutrition you’re certainly not going to be a a “mass monster”. This is a particularly good thing for the ladies out there, ’cause it means that you can benefit from the recovery advantage a couple of days in a hyperbaric environment have to offer without running the risk of getting “bulky” *rofl*… ok, enough of the kiddin’ around. Let’s take a look at what today’s SuppVersity article is really about!

Actually I wasn’t too far off with the “mass monster”.

I mean, as a SuppVersity reader you know that skeletal muscle hypertrophy, i.e. the expansion of existing muscle cells is limited by a natural cap to the size of the myonuclear domains, i.e. the muscle area / volume one of the myriad of cell kernels (=nuclei) in your muscles can manage. The only solution to grow beyond these natural limits is…? Correct! To add new myonuclei (=cell kernels).

There is more to HBO than muscle: While this article focuses on thee effects of hyperbaric oxygen treatment (HBO) on skeletal muscle, it has also been used to accelerate wound healing in diabetic ulcers (Abidia. 2003), to support the bony reconstruction of the irradiated and tissue-deficient patient (Brown. 1994), to treat inflammatory bowel disease (Dulai. 2013), for stroke patients and patients with neurological conditions (Moskowitz. 2011) and even to stop the proliferation of cancer (Moen. 2012).

These new myonuclei are recruited from the satellite cell pool, a reservoir of muscle stem cells. The main purpose of this “pool”, however, is the maintenance, not the expansion of the muscle mass.

From regeneration to growth

In the real world we evolved in, “being a mass monster” was yet more of a hindrance than a help. A huge quantity of skeletal muscle is energetically costly and could – in the worst case scenario – slow you down so much that the next best sabertooth whose muscle power even the biggest “mass monster” cannot match would hunt you down.

In reality, the majority of satellite cells that move from the sarcoplasma (the “fluid” around the muscle”) into the muscle is not going to contribute to skeletal muscle growth directly. Most of them simply replace damaged / dead myonuclei to ensure that the muscle keeps functional. It is this repair process, or rather the effect of a high pressure (=hyperbaric) high oxygen environment (HBO treatment) on its evolution that intrigued Horie M, Enomoto M, Shimoda M, Okawa A, Miyakawa S, and Yagishita K.

Figure 1: HBO speeds up muscle both strength and size recovers (Gregorevic. 2002)

From previous studies they already know that three days of HBO treatment at a pressure of three atmospheres will enhance the contractile properties and recovery of muscle cross sectional are (CSA) of regenerating rat soleus muscles after myotoxic injury (cf. Figure 1; Gregorevic. 2002). Similar effects have been observed in a whole host of other studies (Gregorevic. 2000) The exact underlying cause of these improvement, on the other hand, were still unclear.

Don’t do this at home! While the scenario is completely different, papers such as Palmquist’s, Phillip’s and Barr’s case report in the British Journal of Ophthalmology, in which the authors report for the first time that the well-known, temporary and reversible lens myopia that occurs in response to prolonged hyperbaric oxygen therapy may be complemented by cataractogenic effects, when the patients are exposed to 150 or more sessions of HBO (Palmquist. 1984). The most recent review of the literature says, though, that these side effects have been observed mostly in elderly or sick patients and that “the pressure and duration of exposures used in clinical practice, ocular complications do not seem to be a problem in HBO therapies.” (Oguz. 2008) Still, the general risk of DNA through oxidative damage from the pure oxygen environment is real and should requires further investigation in realistic long(er) term scenarios (Ishii. 2005).

If you’re now asking yourselves, why this is the first time that you hear of this kind of treatment, you may want to take into consideration that the currently available human “studies have been limited due to the small sample size, lack of blinding and randomization problems” (Barato. 2011). Despite the fact that it is “promising” treatment for for injury recovery in high performance athletes, Barato et al. end their review the effects of hyperbaric oxygen therapy of sports injuries with a demand for

“larger samples, randomized, controlled, double-blinded clinical trials combined with studies using animal models so that its effects and mechanisms can be identified to confirm that it is a safe and effective therapy for the treatment of sports injuries.” (Barato. 2011)

With the publication of Horie’s paper “Hyperbaric oxygen effects on sports injuries” (Hori. 2014) we have fulfilled demand #2. What we are still lacking, though is evidence from large-scale, randomized, controlled, double-blinded clinical trials that would support that exposing injured athletes into a pressure chamber with 100% oxygen under 2.5 atmospheres absolute for 2 h/day, 5 days/wk for 2 wk will trigger the same increases in satellite cell activity (MyoD, myogenin), incorporation (increased numbers of “young” muscle cells) and IGF-1 Horie et al. observed in their latest rodent study.

You have to have a basic understan- ding of how your muscle grows to understand why the increased matu- ration and incorporation of satellite cells is so important and acute increa- ses in protein synthesis nice, but not the only thing that counts | read more

This could be more than just regeneration: If we assume that putting you into a hyperbaric environment with pure oxygen for 2h/day, 5days/week for 2 weeks, elicits the same increase in satellite cell proliferation and myofiber maturation as it was observed in the injured rat muscles, even if your “injury” is nothing but the regular wear and tear of heavy lifting, this treatment would not just accelerates your recovery, but could actually set you up for new gains.

You should after all remember from the Intermittent Thoughts on Building Muscle (learn more) that an increase in the number of myonuclei leads will decrease the average domain size. This, in turn, will losen the “hyprtrophy break” myostatin and accelerate your muscle gains… you see, in theory one of those hyperbaric oxygen chambers could be a better investment for any gym owner than another high tech sauna with solarium 😉

Reference: 

• Abidia, A., et al. “The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial.” European journal of vascular and endovascular surgery 25.6 (2003): 513-518.
• Barata, Pedro, et al. “Hyperbaric oxygen effects on sports injuries.” Therapeutic advances in musculoskeletal disease 3.2 (2011): 111-121.
• Brown, D. Ross, et al. “A multicenter review of the treatment of major truncal necrotizing infections with and without hyperbaric oxygen therapy.” The American journal of surgery 167.5 (1994): 485-489.
• Dulai, Parambir, et al. “P-135 Hyperbaric Oxygen Therapy for the Treatment of Inflammatory Bowel Disease: A Systematic Review.” Inflammatory Bowel Diseases 19 (2013): S77-S78.
• Gregorevic, Paul, Gordon S. Lynch, and David A. Williams. “Hyperbaric oxygen improves contractile function of regenerating rat skeletal muscle after myotoxic injury.” Journal of Applied Physiology 89.4 (2000): 1477-1482.
• Gregorevic, P., David A. Williams, and Gordon S. Lynch. “Hyperbaric oxygen increases the contractile function of regenerating rat slow muscles.” Medicine and science in sports and exercise 34.4 (2002): 630-636.
• Horie, Masaki, et al. “Enhancement of satellite cell differentiation and functional recovery in injured skeletal muscle by hyperbaric oxygen treatment.” Journal of applied physiology (Bethesda, Md.: 1985) (2013). 
• Ishii, Yoshimasa, et al. “Hyperbaric oxygen as an adjuvant for athletes.” Sports Medicine 35.9 (2005): 739-746.
• Moen, Ingrid, and Linda EB Stuhr. “Hyperbaric oxygen therapy and cancer—a review.” Targeted oncology 7.4 (2012): 233-242. 
• Moskowitz, Ari, Yu-Feng Yvonne Chan, and Aneesh B. Singhal. “Normobaric and Hyperbaric Oxygen Therapy for Ischemic Stroke and Other Neurological Conditions.” Chemistry and Biochemistry of Oxygen Therapeutics: From Transfusion to Artificial Blood (2011): 159.
• Oguz, Halit, and Gungor Sobaci. “The use of hyperbaric oxygen therapy in ophthalmology.” Survey of ophthalmology 53.2 (2008): 112-120.
• Palmquist, Britt-Marie, B. Philipson, and P. O. Barr. “Nuclear cataract and myopia during hyperbaric oxygen therapy.” British journal of ophthalmology 68.2 (1984): 113-117.

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3 Types Of Muscle-Building Supplements For Overall Growth

In its inaugural edition, TRAIN magazine, the newest health and fitness bible, reveals the truth about how they work and what you should be taking when.

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A New Fathers’ Guide to Building a Rock Solid Body and Life

You may recognize this guy. He stumbles out of bed feeling as though he hasn’t slept. That’s because he really hasn’t. He doesn’t have the time for a real breakfast so he hits the drive thru for a breakfast McFatty. By 3pm he’s ready to face plant on his desk. He resorts to a designer coffee or a cola from the vending machine hoping for some energy.

He plans to hit the gym after work, but by the time he leaves the office he’s exhausted and starving. His wife is just as exhausted, so he picks up some Chinese take-out and heads home.

In the last two months, he hasn’t had a shower that lasted more than five minutes or slept for more than four hours straight. He used to curl 80 pounds, but he’s down to curling 10 – however many reps it takes to change a wet diaper.

Yep, he’s a new father. You may even be him. I had no intention of being him but I narrowly escaped being him, but only because I planned ahead, took some positive steps and had a great deal of help with some of the biggest health and fitness challenges that a new father faces. I learned a lot during the process and I want to share what I’ve learned with others that are expecting a new child, whether it’s your first or your fourth.

Becoming a dad is absolutely incredible. However, nothing can prepare you for it. My B.M.W. (beautiful marvelous wife) give birth to our precious baby girl during a hot summer day last August. She is almost 5-months old and every moment with her is more magical than the last. I’m sure every parent thinks their child is the most beautiful thing ever. I’m the same and my wife and I like to say, “God must have spent extra time making our baby girl!”  I really love being a Dad and this is by far my greatest accomplishment and I wouldn’t trade her for the world. With that said, it’s time to get real.

Becoming the father of a newborn is huge game changer. Life is no longer about Vince’s workouts, Vince’s food, Vince’s business, Vince’s movies and Vince’s trips. After having a baby, it’s no longer about me, me, me.

Being the father of a newborn is incredibly challenging. If you’re also trying to gain or maintain lean muscle and eat healthfully, it’s even more so. But being a new Dad doesn’t mean you have to sacrifice your own health and physique. In fact, by incorporating these tips into your life, being a new Dad may be one of the best things that could happen to your fitness goals.

I want to share what I’ve learned with you about the five biggest challenges facing a new father: Sleep and stress, diet, focus, accountability and time.

Challenge #1 – Sleep and Stress

Shortly after my daughter was born, I had the Koenigsberg test done to check my adrenal gland function because I was eating in a caloric deficit but couldn’t lose any fat. I was exhausted and stressed and wasn’t very surprised to find that my adrenal function was at an all-time low.

Guys, stress, lack of sleep and the stress caused by lack of sleep will wreak havoc on your hormone levels and throw them completely out of whack. When that happens, you’ll be fatigued, you’ll start to gain fat (or store fat like I was) because of high cortisol levels and your testosterone levels will be too low to continue adding muscle.

Unfortunately, in the first weeks or even months after the baby is born, sleep is going to be a prize, not a guarantee. You may be one of the lucky fathers whose baby starts sleeping through the night almost immediately, but the odds are better that you’ll be getting up at least once a night to either change or help feed the baby.

We all understand the importance of getting enough rest as it relates to muscle recovery and fat loss, but lack of sleep will do a lot more damage if you don’t take steps to get more rest. At the same time, you can’t let your wife deal with the late nights on her own either or else she’ll have a mental breakdown. Accept that you’re going to have interrupted sleep and irregular sleep patterns for a while and try to counter it by getting to bed earlier, or even getting up later if your work allows it.

Because I have a business to run and because I like getting a jump on the day, I started going to bed earlier. In fact, I go to bed earlier now than I did when I was young enough to be told to go to bed. I’m in bed by 9:30 each night and wide awake at 6:00 am, it’s quite an empowering feeling. That extra time means I can still get eight hours of sleep, even if it isn’t all at once. Because my body and my health are a priority, I’m fine with missing nights in front of the TV or working late on projects. In the meantime, my adrenal glands are now functioning as they should and I have a lot more energy, burning fat and gaining muscle.

Challenge #2 – Diet

Eating a healthy diet and hitting all your macros is challenging at any time, but even more so when you have a new baby in the house. If your wife usually does most of the food shopping and cooking, she’s probably not able to do as much as she used to. She shouldn’t be expected to either. Even if you usually share the kitchen duties, time is at a premium and it’s so easy to fall into the trap of ordering out or nuking your meals. But this is a dangerous road to fat gain and poor health.

One of the best things I’ve ever done for my body and my family was to spend $2,400 on cooking lessons with one of Toronto’s top gourmet chefs. I learned how to cook meals in bulk so that I could always have healthy meals on hand that tasted good and covered all my macros. I have to say, I’ve cooked some seriously good food and the meals were easy-on-the wallet and ten times more delicious than my old “bodybuilding meals”. In fact learning how to cook in bulk had such a huge impact on my energy, health and body that I’m making it the focus of a new season of Live Large TV. In this season we’ll teach you mind-blowing recipes and how to prepare up to a weeks worth of meals in less than an hour.

This has saved my health and energy levels but it’s also saved me a huge amount of time and money. Every day after I have my first meal and get my workout in, I have an hour set aside to cook all of our meals for that day and sometimes the next. Believe me, you can cook up to a weeks worth of food in about the same time you cook a days worth of food when life is really busy. Giving my diet a makeover and having nutrient-dense foods ready to eat at any given time has saved me from the fat gain and slow muscle gains that’s typical to new fathers.

Challenge #3 – Focus

Staying focused is a constant battle for some people. For others, it’s fairly easy because they’re driven. But if you’re a new father, you’re going to have a lot of obstacles to staying focused on your personal bodybuilding goals. Things are chaotic at home, there’s a lot more to do to keep everything functioning for your family and you will be wrapped up in this incredible new baby. Staying focused is a challenge, but there are things you can do to help yourself stay on track and still get everything done.

What worked for me was to script my day. I have a set schedule that I follow each day where I perform the most important tasks first before something else has a chance to get in the way.

I can’t stress enough how essential it is to focus on the most important things first. I need to work out, I need to eat well (and make sure my wife does too) and I need to run my business so those tasks are scheduled first. I get up at 7am and eat and then work out from 8-9am. From 9-10 I cook that days meals. By 10am, I’ve taken care of working out and prepared healthy meals for the entire day. From 10-4 I work and then 4-8pm is for spending time with my wife and daughter and having a good dinner. Our daughter goes to bed at 8pm, which gives me an hour and a half to spend relaxing with my wife and doing something fun. I do my best not to go back to the computer in the evening unless there is an emergency that can’t wait.

Even if you normally hate having a set schedule, I can’t recommend it enough. We have a very limited amount of willpower, especially when we’re tired and busier than usual. Decide what you must get done each day to stay on track and take care of your family. Write a schedule that allows you to get the most important things done first. Then commit to that schedule. A lot of guys balk at following a schedule because they don’t like being told what to do at any given time, but don’t forget that you’re the one creating the schedule and it’s your goals that the schedule was created to meet.

Challenge # 4 – Accountability

On that note, let’s talk about accountability. Needing and using accountability is nothing to be embarrassed about. Some people find they do better with accountability at all times. Other people just need it during particularly challenging times. That accountability might be something as small as having a buddy at the gym to check your progress or run sprints with you.

What I chose to do was hire renowned coach Ryan Faehnle to write my workouts and write my meal plans, eliminating all guess work and giving me a structured and progressive program to follow. Hiring a coach is one of the smartest things I’ve ever done and I have never believed in being your own coach. Any time I’ve coached myself, I get worse results. Not only do I get to benefit from his incredible knowledge and unique techniques, but I get to hand over the reins to someone else so that I could focus on other priorities responsibilities. I still need to manage my business and a team of ten people. I need to support and help my wife. But I also need to have definite goals to hit and a specific program to follow. By letting Ryan create my workouts and meal plans, I freed myself up to focus on those things.

I realize that not everyone can afford to hire a great coach and I’m not saying you can’t get results on your own. But I will say that you’ll always get faster results if can find someone to help you stay accountable to your workouts and meals. Join a community, either locally or virtually. Partner up with a friend who’s interested in working together. Enter a transformation contest with a deadline. Follow a program designed by someone you look up to. Spend a few bucks on a program so that you put some money at stake. Donate money to a charity you hate if you don’t achieve your goals by a certain deadline.  There are many ways to hold yourself accountable.

Challenge #5 – Time

Time. You used to have a lot of it. Now you don’t, plain and simple. Even if your schedule was already jammed before you had a newborn, now it’s completely covered up. Aside from focusing on what’s important and creating a schedule that reflects that, the best thing you can do for you and your family is to get some help.

No matter how amazing your wife is, she’s not superwoman. Don’t expect her to be able to take care of the baby and everything having to do with your home life as well. Your wife very well may be working outside the home as well, just as you are. Do whatever you can to help each other, but don’t be afraid to get help from others.

Even if you can’t afford to pay for a cleaning service or help with the yard or whatever else, maybe you can find ways to barter for it. If you’re an accountant, maybe you know a guy who can maintain your yard in exchange for help with his taxes. Maybe your wife’s a hairstylist and knows someone who would gladly clean one morning a week in exchange for free haircuts or color. You get the idea. Let the in-laws and your parents or your friends help out when they offer. It’s temporary and it’ll save your health and your sanity and keep your marriage healthy as well.

I’d like to leave you with one last tip that has become my mantra every time the baby is pushing us to our limits – “This too shall pass, soon to be replaced by something else.”  It’s one of my favorite quotes and it’s so appropriate to the first few months of raising a newborn. It’s just for a short time, guys, although I hear the bigger the baby becomes the bigger the problems become! Take steps to make sure that you stay on track so that you don’t have to start from square one when it’s over and remember to cherish every single moment with your newborn as these are moments you’ll never get back.

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All Flavor, No Downside: 5 Simple, Healthy Marinades

Marinades are the simplest, healthiest way to take a bland diet and make it brilliant. Don't wait another day to start using these recipes!

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Ask The Protein Powder Chef: Valentine’s Day Truffles

Valentine's Day means two things: cuddles and calories. Trade in the latter for guilt-free protein truffles. Grow your love, and your gains, with this recipe!

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