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If you want other to see your pump, you got to be ripped. If not, why care about reductions in BMR?

If you remember my posts about the first generation, arginine-based pre-workout products you will be aware that the only pump they produced was the word "pump" in their name or product description. The reason was and still is simple. The mere provision of l-arginine, which is a precursor to nitric oxide does not lead to an increase in nitric oxide production. Why? Well, think of a building a house: Just buying some concrete wont make you a proud home owner, either ;-)

The bad thing: Arginine didnt work. The good thing: This means it didnt decrease your BMR, either

Against that background its quite astonishing that arginine and citrulline based pre-workout products have dominated the top-seller lists of the big supplement vendors for decades. A fact thats probably partly due to other potential benefits of these amino acids, of which one - you as a SuppVersity reader know that - could be fat loss | learn more about the potential fat loss effects.
With more and more people openly declaring that they would no longer waste money on "good tasting, but expensive and disfunctional products", they industry was yet pressed to develop alternatives. Luckily, our body has two options it can chose from, when producing nitric oxide.

Fortunately, the industry has developed better alternatives...?

You know option #1, the arginine ? nitric oxide pathway, and - with all the hype and hyperbole that surrounded the introduction of the first nitrate supplements - I am pretty sure, you know the other one as well, the nitrate-nitrite ? nitric oxide pathway

Figure 1: The Arginine- and the Nitrate-Nitrite - NO pathway are the yin and yan of nitric oxide production (Lundberg. 2008).

As the illustration (Figure 1) I have "borrowed" from a comment by Jon. O. Lundberg et al. (2008) illustrates quite nicely, the arginine and nitrite nitric oxide pathway are the yin and yan of NO production.

With the "yan", i.e. the nitrate-nitrite ? nitric oxide pathway being a relatively "new kid on the NO block", that recycles (=reduces) inorganic anions nitrate and nitrite to form bioactive NO in blood and tissues during physiological hypoxia.

It goes without saying that there is a bottle neck to this process as well, but the rate limiting availablility of oxygen which hampers the argine-based NO generation by NOS becomes limited as oxygen levels fall is actually a signal for the nitrate–nitrite ? nitric oxide to really kick in.

There is more yin and yan, here

If you take a closer look at the results of a study in the America Journal of Clinical Nutrition (Figure 2), you will yet have to realize that there is "more yin and yan", here than youd probably hope for. According to the data scientists from the venerable Karolinska Institutet in Stockholm, Sweden, present in their paper, "[d]ietary inorganic nitrate reduces the RMR." (Larsen. 2014)

Figure 2: VO2 consumption (marker of fatty acid oxidation) and basal metabolic rate (BMR) relative to means (left), thyroid hormone (T3, T4) levels after 3-d dietary intervention with sodium nitrate (Larsen. 2014)

Whut? Yes, you read Larsen et al. right: In their randomized, double-blind, crossover study, in the course of which the Swedish scientists measured the resting metabolic rate (RMR) of 13 perfectly healthy 18–49 y olds (17 women) via indirect calorimetry after a 3-d dietary intervention with sodium nitrate (NaNO3 @ 0.1mmol/kg body weight) or a placebo (NaCl), Larsen, Schiffer, Ekblom et al. observed a statistically and (probably) physiologically significant reduction BMR reduction of 4.2% which correlated strongly to the degree of nitrate accumulation in saliva (r²= 0.71) and fits in nicely with the reduced O2 consumption of which Bailey et al. were the first to observe it in response to nitrate supplementation during exercise (Bailey. 2009).

Interestingly, these effects were not - as you may have been speculated - brought about by changes in thyroid hormone status. And the subjects insulin sensitivity, glucose uptake, plasma concentration of isoprostanes, as well as their total antioxidant capacity were unaffected, as well.
Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Hotta, Yuji, et al. "Oral l?citrulline supplementation improves erectile function and penile structure in castrated rats." International Journal of Urology (2014).
• Larsen, Filip J., et al. "Dietary inorganic nitrate improves mitochondrial efficiency in humans." Cell metabolism 13.2 (2011): 149-159.
• Lundberg, Jon O., Eddie Weitzberg, and Mark T. Gladwin. "The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics." Nature Reviews Drug Discovery 7.2 (2008): 156-167.
• Neuzillet, Y., et al. "A randomized, double?blind, crossover, placebo?controlled comparative clinical trial of arginine aspartate plus adenosine monophosphate for the intermittent treatment of male erectile dysfunction." Andrology 1.2 (2013): 223-228.

Protein before workouts "accelerates protein catabolism"? That sounds worse than it actually is (photo BSN).

Most of you will probably consume a protein shake after their workout. Probably whey, if youve read all SuppVersity articles, maybe 25g whey + 10g casein (learn why), or something like that. But what do you do before your workouts? Do you consume a protein shake 60-90 minutes before your workout? If so, you will be shocked about the conclusion of a recent study from the Tokyo University of Agriculture which says: "[...]  pre-exercise protein supplementation taken in excess may accelerate protein catabolism" (Hasegawa. 2014).

But is it actually possible that consuming more protein (albeit at the wrong time) will have a negative impact on your gains?
Before we can answer this important question it is necessary to take a look at the actual design of the randomized cross-over study.

Figure 1: Graphical overview of the experimental protocol (Hasegawa. 2014)

The participants, six healthy male university students [21.2 (±0.3) years, 173.6 (±2.8) cm, and 62.7 (±2.8)kg] with no allergies to egg white or soy, the two protein sources the effects of which the researchers initially wanted to compare, underwent three 8-day testing periods with an exercise at the end (the 8-day intervals were separated by at least seven days).

"Each  testing period began on Day-1 and ended the meat-free diet  consisting of grains, beans, and milk, and 24- hour urine sample collection on Day-8 (Figure 1). Participants were allocated into  one of three groups; egg white protein (E), soy protein (S), and mineral water control (C) group with no additive, and all were carried out this study protocol three times, and asked not to change their lifestyle behaviors." (Hasegawa. 2014). 

The result of this study should remind you of the "Protein-Wheysting" Article | more is not always better!

On Day-5, the day of the workout, the  participants arrived at the  laboratory at 8:00 AM, and had a breakfast consisting of a rice ball (energy, 355 kcal; protein, 6.7 g; carbohydrate, 78.1 g). At 9:30 AM, after the baseline blood sample collection and perceived muscle soreness (MS) measurements, the subjects received one of the three test beverages which contained

• 20 g of egg protein,
• 20g of soy protein, or
• an isoenergetic placebo without protein

that had been dissolved in 200ml of mineral water. 90 minutes later, at 11:00 AM, the previously untrained participants started a resistance training protocol that involved seated rows, flys, leg extensions, and leg presses.

The exercises were performed for three sets of 10 repetitions at ~80% of a predetermined 1-RM with one min rest between sets and two minutes between each exercise.

Figure 2: no significant difference in perceived fatique, but a significant reduction in peak muscle soreness in the soy (grey blocks) vs. the control (white triangles) group (Hasegawa. 2014).

As you can see in Figure 2, the initially mentioned negative effects of the protein supplement were not the only significant inter-trial differences the scientists observed; and whats more, the significantly decreased muscle soreness in response to both protein powders (the peak levels differed statistically significantly only for control vs. soy) stands in stark contrast the mainstream interpretation of protein breakdown (which is "protein breakdown = muscle loss").

How is that possible? Increased protein breakdown and reduced muscle soreness?

So, here we are with an obvious contradiction between the reduced muscle soreness (Figure 2) and the scientists claim that "pre-exercise protein supplementation taken in excess may accelerate protein catabolism" (Hasegawa. 2014)... you already guessed it: The contradiction depends on the false assumption that "protein catabolism" means "catabolism of muscle protein", which is not generally the case and in this specific case certainly wrong.

Figure 3: Urinary nitrogen excretion measured for 72h after the workout (Hasegawa. 2014)

The process we are talking about here is thus most likely not an increase in "mucle catabolism" but rather about the absence of a reduction in protein wasting, i.e a "protein sparing" mechanism that wont be triggered if there is plenty of protein around during the workout.
References:

• Baty, Jacob J., et al. "The effect of a carbohydrate and protein supplement on resistance exercise performance, hormonal response, and muscle damage." The Journal of Strength & Conditioning Research 21.2 (2007): 321-329.
• Hasegawa, Yuko, et al. "Effect of Egg White Protein Supplementation Prior to Acute Resistance Training on Muscle Damage Indices in Untrained Japanese Men." Monten. J. Sports Sci. Med. 3 (2014) 2: 5–12.
• Rasmussen, Blake B., et al. "An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise." Journal of Applied Physiology 88.2 (2000): 386-392.
• Wycherley, Thomas Philip, et al. "Timing of protein ingestion relative to resistance exercise training does not influence body composition, energy expenditure, glycaemic control or cardiometabolic risk factors in a hypocaloric, high protein diet in patients with type 2 diabetes." Diabetes, Obesity and Metabolism 12.12 (2010): 1097-1105.