ONLINE DRIVERS MEDIA

One study wouldnt be enough to prove that pea is superior to whey as muscle builder, anyways.

In a recent study, French scientist investigated the effects of two types of protein supplementation on muscle thickness and strength in 161 moderate physically active (2–6 hours per week) male participants (mean age 22 years). More specifically, the scientists compared the effects of vegetable Pea protein (NUTRALYS®) vs. Whey protein and Placebo on biceps brachii muscle thickness and strength after a 12-week resistance training program. And as the headline already reveals: The pea protein had the upper hand, when it comes to biceps brachii size, but the way the gains were measured and superior strength gains in the whey group raise questions about whether the results of this study are practically relevant - meaning you have to switch from whey to pea.
These values are based on measurements of arm circumference of the right arm which were taken using a constant tension tape during maximal elbow extension at rest and during a maximal voluntary contraction (with maximal elbow flexion).

Figure 1: Overview of the study design.

"All subjects followed the same training routine, three times per week with a rest day between each session. Training was based on three exercises involving the elbow flexor and extensor muscles. The exercises soliciting the flexor muscles were arm curl and lateral pulldown. In the arm curl exercise, subjects sat with weights in their hands with a ~40° trunk/arm angle. They had to flex/extend the forearm over the arm. For the lateral pull-down, subjects sat with a bar in their hands above the head. They had to flex/extend the forearm over the arm with a vertical movement. The exercise soliciting the extensors was the bench press. Subjects were lying on their backs with a bar in their hands with a 90° trunk/arm angle, arms extended, and had to flex and extend their upper limbs vertically. Throughout the training program, the number of sets was progressively increased from 2 to 5 while the number of repetitions was reduced in parallel from 15 to 5 repetitions maximum (RM). In the final week, the subjects did three sets of 5 RM in order to preclude any fatigue for the D84 tests" (Babault. 2015).

Recovery between sets was identical for all workouts: 2–3 minutes. The load used for each exercise was regularly adapted during training depending on individuals’ maximum load (1-RM, one maximum repetition, evaluated every two weeks).

Figure 2: Muscle thickness in the 3 groups at baseline after 42 and 84 days. There was only a trend (£) for increased gains in the pea protein group (Babault. 2015).

Three measurements were made (at rest and contracted) along the length of the biceps, namely ¼, ½ and ¾ of the length of the upper arm (distance between the acromion process of the scapula and the lateral epicondyle of the humerus). Averaging was performed to obtain mean values for the circumference at rest and contracted.

Faulty measurements due to messed up timing?

That sounds great, but since the time of measurement is not mentioned, it may well be that all the values are fundamentally flawed. Why?

Well, as a SuppVersity reader you know that even in leg muscles, which are muss less prone to "the pump", "Cell Swelling Keeps Muscles "Pumped" For More Than 52h. Size Increases of Up to 16% After a Single Leg Workout!" (learn more).

Practically speaking, this means that the "size measurements" in the study at hand may be worthless if the scientists didnt wait for at least 72h-96h before they measured the sleeve sizes of their subjects.
The absence of information on the time-point at which the sleeve sizes were measured (suggestive of immediately post) and the fact that the strength gains do not reflect the alleged superiority of pea protein as muscle builders (see Figure 3) put a huge question mark behind the assumption that pea protein tends to produce greater muscle gains than whey.

Figure 3: It is strange that the "superior muscle builder" triggers the lowest gains in maximal isometric contractile force. Even the placebo group had greater strength gains - despite a lack of sign. differences at baseline (Babault. 2015).

Rather than "gains", the increases could in fact be a result of increased inflammation and the reduced "gains" in the whey group a result of its anti-inflammatory effects (Buckley. 2010; Sugawara. 2012; Kerasioti. 2013). The existing evidence of anti-inflammatory properties of pea protein (Ndiaye. 2012) does yet render this assumption questionable.
References:

• Babault, et al. "Pea proteins oral supplementation promotes muscle thickness gains during resistance training: a double-blind, randomized, Placebo-controlled clinical trial vs. Whey protein." Journal of the International Society of Sports Nutrition 12:3 (2015).
• Buckley, Jonathan D., et al. "Supplementation with a whey protein hydrolysate enhances recovery of muscle force-generating capacity following eccentric exercise." Journal of Science and Medicine in Sport 13.1 (2010): 178-181. 
• Lang, Vincent, et al. "Satiating effect of proteins in healthy subjects: a comparison of egg albumin, casein, gelatin, soy protein, pea protein, and wheat gluten." The American journal of clinical nutrition 67.6 (1998): 1197-1204.
• Ndiaye, Fatou, et al. "Anti-oxidant, anti-inflammatory and immunomodulating properties of an enzymatic protein hydrolysate from yellow field pea seeds." European journal of nutrition 51.1 (2012): 29-37.
• Kerasioti, Efthalia, et al. "Anti-inflammatory effects of a special carbohydrate–whey protein cake after exhaustive cycling in humans." Food and Chemical Toxicology 61 (2013): 42-46.
• Sirtori, Cesare R., et al. "Hypocholesterolaemic effects of lupin protein and pea protein/fibre combinations in moderately hypercholesterolaemic individuals." British journal of nutrition 107.08 (2012): 1176-1183.
• Smith, Christopher E., et al. "The effect of yellow pea protein and fibre on short-term food intake, subjective appetite and glycaemic response in healthy young men." British Journal of Nutrition 108.S1 (2012): S74-S80.
• Sugawara, Keiyu, et al. "Effect of anti-inflammatory supplementation with whey peptide and exercise therapy in patients with COPD." Respiratory medicine 106.11 (2012): 1526-1534.

If you dont have ginger powder, just shred a fresh rhizome. Thats by the way what the researchers did, as well.

Yeah, we all know "Ginger is good for your glucose metabolism". We all know "there are dozens of rodent studies that support its benefits". And we also know that there is evidence from acute interventions that indicate that ginger can ameliorate the glucose response to oral glucose tolerance tests.

But do we know, whether the regular consumption of realistic amounts of pure ginger will have beneficial effects on the glucose levels of those who would benefit the most, i.e. type II aka "lifestyle" diabetics?
The results of the latest study from the Tehran University of Medical Sciences where scientists obviously dont depend on being able to produce patentable agents would suggest: There are benefits!

I have to admit, though, the ginger the 20-60 years old diabetics consumed was not provided in form of whole roots, but rather as a powder made of ginger roots.

"The under study patients were diagnosed with non-insulin dependent diabetes mellitus (NIDDM) by an endocrinologist on the basis of the results of the blood tests and met the criteria of the study. These criteria included: disease duration at least 2 years, HbA1c level of 6-8%, taking no antioxidant supplements such as selenium, zinc and beta-carotene for at least 3 months prior to the study, no smoking and drinking. Exclusion criteria of the study were insulin therapy at baseline or during the study, changes in the type or dose of medication, changes in diet or daily physical activity, any acute illnesses or some chronic diseases including kidney, liver, cardiovascular, and gastrointestinal diseases, smoking pregnancy and lactation, consumption of ginger or other botanical supplements, ginger hypersensitivity, and consumption of less than 80% of supplements during the study period." (Khandouzi. 2015)

Patients were divided randomly into two groups (experiment and control, 25 subjects in each) using computers random numbers to receive either ginger or placebo one capsule twice a day for 12 weeks. All subjects were permitted to consume their usual medications according to their physicians recommendation.

Regular ginger powder, nothing else!

The fresh rhizomes for the ginger powder purchased from local market and were ground as a fine particle after drying. The powder was delivered to a pharmaceutical lab (Tehran university of medical sciences, Iran) to prepare capsules containing 1 gram ginger in each. Lactose was also used to make placebo. Information on when the supplements were ingested is unfortunately, not available, but I assume "twice daily" means with breakfast and dinner or something like that.

Figure 1: Changes in fasting blood sugar, HbA1C, Apo-B/Apo-A1 and MDA levels (Khandouzi. 2015).

What is available, is the most relevant information, i.e. glucose, apolipoproteins and MDA levels we can use to access the effects on glucose and lipid metabolism and the peroxidation of polyunsaturated fatty acids.Parameters of which the data in Figure 1 tells you that they were significantly improved over the course of the 12-week study period. More specifically, this means:

• A 12% and 10% reduction in fasting blood glucose and HbA1c that may reduce many of the nasty chronic side effects of type II diabetes, such as its negative effects on heart health (Patel. 2008)
• A 28% reduction in the Apo B / Apo A-I ratio that signifies a significant reduction in coronary atherosclerosis risk (Van Stiphout. 1986)
• A 23% reduction in malondialdehyde (MDA) levels that signifies a reduction in coronary heart disease risk (Khan. 2000)

Overall, there is thus little question that something as simple as adding 2g of pulverized fresh Zingiber officinale rhizomes will have a significant impact on important health markers in middle-aged type II diabetics.
References:

• Khan, Mudassir Ahmad, and Abdul Baseer. "Increased malondialdehyde levels in coronary heart disease." J Pak Med Assoc 50.8 (2000): 261-264.
• Khandouzi, Nafiseh, et al. "The Effects of Ginger on Fasting Blood Sugar, Hemoglobin A1c, Apolipoprotein B, Apolipoprotein AI and Malondialdehyde in Type 2 Diabetic Patients." Iranian Journal of Pharmaceutical Research: IJPR 14.1 (2015): 131.
• Patel, Anushka, et al. "Intensive blood glucose control and vascular outcomes in patients with type 2 diabetes." (2008).
• Schweizer, A., et al. "Comparison between vildagliptin and metformin to sustain reductions in HbA1c over 1 year in drug?naïve patients with Type 2 diabetes." Diabetic Medicine 24.9 (2007): 955-961.
• Van Stiphout, W. A. H. J., et al. "Is the ratio of apo B/apo AI an early predictor of coronary atherosclerosis?." Atherosclerosis 62.2 (1986): 179-182.

Creatine, obviously monohydrate and no expensive and often impotent spinoff (Jäger. 2011) is useful for any athlete.

The number of items on the list of health and performance benefits of creatine is about as high as the number of boring articles about "the benefits of creatine" you can find all over the Internet. And even here at the SuppVersity they have been piling up in a way that has me ignore the majority of "creatine supplementation increases strength gains in XY" studies that appear on a monthly, sometimes weekly basis. Against that background I will cut todays creatine post short and get straight to the facts, Giuseppe Potrick Stefani et al. report in their latest paper in (how else could it be) the peer-reviewed Journal of the International Society of Sports Nutrition (Stefani. 2014).
In what turns out to be another rodent study Stefani et al. investigated whether creatine supplementation exerts intra and/or extracellular antioxidant effects and if it plays a synergistic role in the adaptation of antioxidant enzymes associated with resistance training. The actual aim of the study was thus

"to evaluate the effects of monohydrate creatine supplementation associated, or not, with RT on oxidative stress and antioxidant enzymatic activity in the plasma, the heart, the liver and the gastrocnemius of rats." (Stefani. 2014)

And the results were unambiguous. As you can see in Figure 1, the anti-oxidant capacity of plasma, heart and liver of all 40 male Wistar rats which had been divided into four groups, i.e.

• sedentary (SED),
• sedentary + creatine  (SED-Cr), and
• resistance training (RT) and resistance training + creatine (RT-Cr),

increased significantly in response to the provision of creatine (0.3 g/kg/day of creatine for seven days, 0.05 g/kg for the rest of the 8-week study period).

Figure 1: Oxidative stress in heart, liver and muscle after 8 weeks of intervention.Concentrations of MDA and CAT activity. Values are mean ± SD; n = 10 for all groups (Stefani. 2014).

As you can see, both treatments, creatine-only and creatine + resistance training led to significant improvements in heart, liver and muscle antioxidant status - and that, this is important, in the absense of those direct free radical scavenging abilities that turn vitamin C, vitamin E & co into highly questionably agents with potential anti-adaptational effects (learn more).

Works w/ and w/out exercise, but with the latter creatine really excels

Compared to the sedentary animals the rats in the exercise group did yet significantly increased catalase levels (=good, because it catalyzes the decomposition of hydrogen peroxide - the bad stuff - to water and oxygen - the benign stuff) in the heart and - obviously - increased strength gains.

Figure 2: Absolute and relative 1RM strength before and after the intervention (Stefani. 2014).

What is (positively) surprising, at first, is the fact that the latter, i.e. the increases in 1-RM strength in response to creatine supplementation occurred even in the absence of resistance training.

If you look closely, you will yet realize that the relative increase in strength, a much better gauge for lasting real-world strength gains, in the sedentary rodents was ZERO. So that it is very likely that they would disappear with the increased water the rats were holding, as soon as the creatine supplementation is seized.
References:

• Jäger, Ralf, et al. "Analysis of the efficacy, safety, and regulatory status of novel forms of creatine." Amino Acids 40.5 (2011): 1369-1383.
• Stefani, Giuseppe Potrick, et al. "Effects of creatine supplementation associated with resistance training on oxidative stress in different tissues of rats." Journal of the International Society of Sports Nutrition 11.1 (2014): 11.

Its nice to be lean, but is it really worth ruining your health? I dont think so, but everyone is the architect of his / her own future.

I want to say in advance that youd better not read this article if you belong to the ever-increasing number of carbophobs (people who are afraid of carbohydrates) who have been so indoctrinated by the confusing information on the Internet that they are willing to close their eyes to all objective data.

In view of the fact that you kept reading, I assume that you (a) dont belong to this group of blockheads or are (b) a blockhead who is about to scroll down to the comment section to start raving about how bad carbohydrates are, pointing out that "you just have to eat a ketogenic diet to live happily ever after" - spare me this bullshit, please!
Its scaremongering bullshit like that due to which more and more non-athletes develop what Can Zhao et al. describe in their latest paper in the peer-reviewed scientific Journal of Sport and Health Science as "exercise-associated menstrual dysfunction" aka EAMD (Zhao. 2014).

For those who have read the SuppVersity Athlete Triad Series, its no news that menstrual irregularities and amenorrhea in female athletes is closely linked to the imbalance between energy intake and exercise-associated energy requirement (Williams. 2001). Accordingly Zhao et al. wanted to investigate, ...

"[...]whether carbohydrate supplements can reverse EAMD and protect against exercise-induced impairment in ovary as an important part of HPO axis regulation and rebalances the energy intake and energy expenditure to support the reproductive function" (Zhao. 2014).

Now the bad news is that they did this in rodents. 45 healthy mature 2-month-old female Spraguee Dawley rats, to be precise. This sounds idiotic, but in view of the fact that the experimental procedure required that "subjects" are sacrificed in the course of the study its quite reasonable to use rodents, not ladies.

Figure 1:  Treadmill running schedules show the specific timeline and various treatments of each groups (Zhao. 2014)

Figure 1 shows a graphical overview of the study protocol which involved an identical initial exercise period in the course of which the speed of the treadmill was continuously increased for six weeks.

At the end of this initial 6-week study period, the female rats, the ovary epithelial cells of the rodents showed significant abnormalities. At the end of week 9, the follicular cells of the rodents in group E contained swollen mitochondria with broken cristae.

Similar exercise-induced mitochondrial damages were also observed in the EAMD rats with post-exercise rest. In the rodents in group O and G, however, Zhao et al. observed a significant recovery of exercise-induced mitochondria impairment. They showed significant reduction of swollen endoplasmic reticulum and Golgi complex, and increases in abundant organelles, irrespective of whether they had been fed a 30% glucose or 30% oligosaccharide diet.

Normalization of organ changes and hormones w/out increase in energy intake

In contrast to the previously hinted at prejudices, the addition of simple sugars to the rodent diet did not lead to an increase in energy intake - in spite of the fact that the goal was a 30% increase in energy intake from glucose / oligosaccharide supplements, the total energy intake was not higher than in the non-exercised control group (see Figure 2).

Figure 2: Changes in energy intakes in each group throughout 9 weeks study (Zhao. 2014).

In conjunction with the significant improvement in GnRH, LH, FSH and estrogen its thus more than unlikely that a comparable increase in "sugar" intake in human females would trigger the increase in body fat many women fear so much that they are willing to run around tired and infertile for years, although most of them know that reducing the exercise volume and normalizing their eating behavior would solve the problem once and for all.

Figure 3: Relative levels (% of control) of GnRH, FSH, LH, E2 and Progesterone (P) after 9 weeks (Zhao. 2014)

Interestingly, the saccharide polymers (oligosaccharides), which are also commonly found on the plasma membrane of animal cells, where they can play a role in cell–cell recognition, did a slightly better job than glucose, when it comes to the restoration of normal hormone levels (see Figure 3).
Reference:

• Qiang, Xu, Chao YongLie, and Wan QianBing. "Health benefit application of functional oligosaccharides." Carbohydrate Polymers 77.3 (2009): 435-441. 
• Tomten, S. E., and A. T. Høstmark. "Energy balance in weight stable athletes with and without menstrual disorders." Scandinavian journal of medicine & science in sports 16.2 (2006): 127-133. 
• Williams, Nancy I., et al. "Longitudinal Changes in Reproductive Hormones and Menstrual Cyclicity in Cynomolgus Monkeys during Strenuous Exercise Training: Abrupt Transition to Exercise-Induced Amenorrhea 1." Endocrinology 142.6 (2001): 2381-2389. 
• Zhao, Can, et al. "Effects of carbohydrate supplements on exercise-induced menstrual dysfunction and ovarian subcellular structural changes in rats." Journal of Sport and Health Science (2014).