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"No sun, no diabesity protection." The evidence is equivocal and the number of studies low, but there is evidence that this statement could be true.

Ok, its November and not exactly sunny in the Northern hemisphere, but if you look back at the months June-August, how much sun exposure did you actually get, this year? Hardly any? Well, thats bad news, because a recent review of the scant scientific evidence suggests that there is "a role of recreational sun exposure in reducing odds of T2DM incidence" (Shore-Lorenti. 2014).

In view of the fact that the contemporarily available evidence is not exactly comprehensive, you should yet consider the following overview of the potential effects and mechanism as a "work in progress".
As Shore-Lorenti et al. point out, the recent International Diabetes Federation (IDF) Diabetes Atlas (6th edition) describes a snapshot of the global diabetes burden in 2013 and projects this forward to the year 2035.1 Cur rently, an estimated 382 million global citizens have diabetes, costing around $1437 USD in 2013 for each person affected by the condition. Projections based on current trends predict that 592 million people will be living with diabetes by 2035; one in ten people will be affected, with an inordinate amount of fund ing required globally to treat diabetes and manage diabetic com plications ($627 billion USD in 2035).

And while scientists are feverishly searching for a solution for the diabesity epidemic, the ongoing research into the effectiveness of vitamin D supplementation in diabetes have yielded inconsistent results (Mitri. 2011). Against that background it appears almost negligent that only few scientists have yet taken a closer look at the factors that trigger vitamin D sufficiency or rather the global low vitamin D epidemia.

Lack of sun"low vitamin D" - thats not all!

Figure 1: Australians who use sunscreen chronically have 50% reduced vitamin D levels (Matsuoka. 1988)

A lack of sufficient (unprotected) sun exposure - previous studies have shown that chronic sunscreen use decreases circulating concentrations of 25-hydroxyvitamin (Figure 1 | Matsuoka. 1988) - is one of the factors of which researchers speculate that it contributes to the development of vitamin D deficiency even in those of us who live in areas with a high annual sun-exposure.

Now, if restoring the 25-OHD (vitamin D) levels to normal does not work the anti-diabetic magic it is supposed to do and our D-levels are low due to insufficient sun-exposure, it appears only logical to assume that a lack sun-exposure and not a lack of vitamin D is one of the factors that contributes to the ever-increasing rates of diabesity - in conjunction with the usual subjects, obviously: The consumption of a junk-food diet and a lack of exercise, which is without doubt the #1 reason people in the Western Obesity Belt develop obesity, diabetes and the other characteristics of the metabolic syndrome.

Against that background its all the more surprising that evidence for an association between sun exposure and fasting serum glucose level is scarce.

"Typically, the lowest glucose levels occur during summer and levels peak in winter or early spring. One of these analyses [Shore-Lorenti et al. reviewed] went beyond simply observing trends in fasting glucose throughout the year: fasting plasma glucose was positively correlated with a measure of available sun and inversely correlated with temperature." (Shore-Lorenti. 2014)

The study, the researchers from the University of Melbourne have in mind was conducted by Suarez, L. & Barrett-Connor, E. in 1988, already.
If you look at the data Suaraez & Barret-Connor generated, you can see - even without their statistical sophisticated analysis - that there is a significant correlation between possible sun exposure (Figure 1, left) and the fasting plasma glucose levels (Figure 1, right).
Since physical activity may follow a similar circannual rhythm, its yet difficult to exclude that the effects Suarez & Barret-Connor observed were not corroborated (or corrupted?) by an increase in physical activity. However, Shore-Lorenti et al. believe that ...

"[...c]onsidering that the unadjusted analyses and three of four of the studies included in the best evidence synthesis (including the study adjusting for physical activity) are in agreement, it is possible that future research may confirm that sun exposure reduces fasting glucose" (Shore-Lorenti. 2014).

Shore-Lorenti et al. also point out that the highest level of evidence (moderate) for an association between sun exposure and T2DM outcomes in adults originates from the study by Lindqvist et al. (2010). In their paper, the researchers from the Karolinska University Hospital report a reduction in odds of developing T2DM given increased recreational (rather than occupational) sun exposure. 

Figure 2: Leisure time sun exposure is associated with a significantly reduced risk (up to 50%!) of developing T2DM in Swedish adults (Lindqvist. 2010)

In subjects with a low BMI the beneficial effect of using the tanning bed and sunbathing is even more pronounced (-60% risk). In the obese, however, it is significantly reduced (-10%) compared to the average reductions you see in Figure 2.

The fact that only leisure time, but not occupational sun exposure was linked to a significant reduced risk of developing type II diabetes may, as Shore-Lorenti et al. point out be due ...

"[...] to the frequency of sun exposure (perhaps leading to tolerance), duration, intensity and site of exposure (sun protective clothing and behaviour differences between the two settings), or perhaps selection biases for such work (for example, fair-skinned people may avoid occupational sun exposure or a less healthy lifestyle may be associated with manual labour)."

Incidentally, a similar disparity between recreational and occupational sun exposure is well described for risk of developing melanoma (Chang. 2009).

A review by Chen et al. (2008) provides low-level evidence for an association between sun exposure and fasting insulin levels; fasting serum insulin was higher in summer than in winter. Overall, the results are yet inconclusive. A fact, Shore-Lorenti et al. ascribe to "the lack of adjustments made by the included study – particularly for BMI" (Shore-Lorenti. 2014)
Overall, we are thus left with the above overview (Table 1) as a conclusion of which the mere number of "unkown"s and "inconsistent"s tell you that we are not yet at the point to draw a water-proof conclusion.
References:

• Chang, Yu-mei, et al. "Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls." International journal of epidemiology (2009): dyp166. 
• Chen, Shui-Hu, et al. "Community-based study on summer-winter difference in insulin resistance in Kin-Chen, Kinmen, Taiwan." Journal of the Chinese Medical Association 71.12 (2008): 619-627.
• Lindqvist, Pelle G., Håkan Olsson, and Mona Landin-Olsson. "Are active sun exposure habits related to lowering risk of type 2 diabetes mellitus in women, a prospective cohort study?." Diabetes research and clinical practice 90.1 (2010): 109-114.
• Mitri, J., M. D. Muraru, and A. G. Pittas. "Vitamin D and type 2 diabetes: a systematic review." European Journal of Clinical Nutrition 65.9 (2011): 1005-1015.
• Nelemans, P. J., et al. "An addition to the controversy on sunlight exposure and melanoma risk: a meta-analytical approach." Journal of clinical epidemiology 48.11 (1995): 1331-1342.
• Shore?Lorenti, Catherine, et al. "Shining the Light on Sunshine: a systematic review of the influence of sun exposure on type 2 diabetes mellitus?related outcomes." Clinical endocrinology (2014).
• Suarez, L., and E. Barrett-Connor. "Seasonal variation in fasting plasma glucose levels in man." Diabetologia 22.4 (1982): 250-253. 

Study leaves no doubt: For the biceps femoris, Romanian deadlifts rule.

I am not quite sure if some of the guys at my gym even know what the hamstrings, are... I guess if I told them that theyre also started biceps femoris, they were more likely to train it, instead of telling me that they play soccer and thus wouldnt have to train legs (I have honestly never heard something that stupid - I mean, its like, I dont train jumping, because I am a high jumper ;-).

Now, if we assume for the moment that my arguments are convincing enough to include a single hamstring exercise on their every-day-international-chest-and-biceps-day, what should it be, then?
If you look back at the SuppVersity EMG Series, it would be the lying leg curl with tighs raised from the pad or hamstring exercises on the hip pendulum. If, on the other hand, you take a look at the data Matt J. McAllister & colleagues are about to publish in the next issue of the venerable Journal of Strength and Conditioning Researchers, one of the few places, where editors actually care about the interests of muscle-headz like us, the answer would be different.

Figure 1: EMG activity of biceps femoris and semitendinosus durinc ecccentric (light) and concentric (dark) phase of the romanian deadlift, the prone leg curl, good mornings and glute-ham raises in 12 subjects w/ 9y+ training exp. (McAllister)

What? You want to know where this difference comes from? Well, the reason should be obvious, Boeckh-Behrens & Buskies who conducted the study the EMG Series is based on did not test the weighed Romanian deadlift w/ maximum weight for "security reasons".

The leg curl, on the other hand, was significantly less effective when it was done with the tighs lying on the pad (as it was done in the study at hand) - exercise selection and execution did thus both contribute to the surprisingly different study outcomes, which do yet have one thing in common: The insight that activities of similar kinematics, dont necessarily produce similar muscle activation. As McAllister et al. poin out, this revelation may...

"[...] also indicate that the kinematics are not as similar as they appear to be, especially when you consider possible variance of internal and external rotation. For instance, the ST [semitendinosus] and SM  [semimembranosus] insert at the upper medial surface of the tibia, and the BF inserts at the head of the fibula. The greater amount of activity from ST may be related to the fact that ST contributes to the internal rotation of the knee, whereas BF contributes to the external rotation of the knee. Although the potential impact is unclear, the absence of control for hip rotation (internal or external) may have obviated the identification of specific patterns of muscle recruitment. Foot position was not standardized in this study because the investigators felt that the subjects’ experience would allow foot position to be habitual and consistent. This delimitation must be considered when interpreting our results." (McAllister. 2014)

In contrast to the semitendinosus & semimembranosus, the EMG activity for the biceps femoris (BF) was similar for the concentric prone leg curl and concentric romanian deadlift. As McAllister et al. point out, "[t]hese results are consistent with a previous investigation that reported no significant difference in activity from the concentric actions of the BF between the leg curl and stiff-leg deadlift." The authors of the corresponidn study did also find that the biceps femoris was significantly more active during the eccentric portion of the leg curl in comparison with the stiff-leg deadlift - the exact opposite of the findings McAllister et al. present in the study at hand, which showed significantly greater activity from the BF during the eccentric RDL as compared with the eccentric prone leg curl.

When the satellite cells merge with the existing muscle cells to form new myonuclei this is more than muscle repair, its also the foundation for future muscle growth - beyond previous limits | more

If youve read the Intermittent Thoughts On Building Muscle (read it) you are beyond the simplistic view of muscle growth as a one-way process in the course of which muscle cells balloon up endlessly. Without the incorporation of "new" myonuclei (cell kernels) from the periphery your muscle would become dysfunctional sooner or later (learn more); and while myostatin will prevent that from happening the recruitment of new muscle cells from the satellite cell pool will provide the basis for future muscle growth.

I dont want to go into more detail, here. If you want to develop a better understanding of this process(es), I suggest you head back to the initially mentioned series about the physiological underpinnings of skeletal muscle hypertrophy.
Next to the inclusion of new myonuclei and facilitation of future muscle growth, the satellite cell pool will also provide the raw material for the repair or I should say replacement of damaged muscle cells. For strength trainees like you and me, its thus of paramount importance to ensure that our satellite cells are happy and healthy. And you know what? Thats not even difficult!

According to a recent study from the Aarhus University all it takes to  help your muscle precursor cells happily proliferating (grow, divide and mature to "real" muscle cells) is the mix of carbohydrates and whey protein youre probably consuming after each workout, anyway: A shake containing 28 g whey protein hydrolysate high in leucine (4 %) an 28 g of carbohydrate (4 %) - a 56h carbohydrate supplement served as control.

Figure 1: Overview of the experimental procedure (Farup. 2014)

As you can see in Figure 1 this supplement was not ingested once, but rather thrice a day - with the first serving being ingested immediately after the fasted subjects, 24 healthy young recreational active men,  initiated the exercise protocol, which lasted for approximately 30 min.

Its the whey that does the trick, but we dont know if we dont need CHOs as an adjunct

The provision of extra whey protein (but nor carbohydrates; white bars in Figure 2) lead to significant increases in satellite cell activity in both mixed muscle and type II fibers, but not type I fibers (not shown in Figure 2).

Figure 2: Number of satellite cells per muscle fiber (higher number = higher chance of incorporation; Farup. 2014)

Still, in view of the fact that regeneration is an energetically costly process, its not 100% certain that a certain amount of carbohydrates may be necessary to see the beneficial effects on satellite cell activity and the changes in maximal voluntary contraction force (not shown).
Reference:

• Farup, et al. "Whey protein supplementation accelerates satellite cell proliferation during recovery from eccentric exercise." Amino Acids (2014). Ahead of print.

Remember: If anything fructose from beverages (including juices), yet not fructose from whole fruit is a problem. In fact eating whole fruits will decrease your blood lipids and high sensitivity C reactive protein (hs-CRP) inflammation markers.

Fructose is bad for you, right? Right. According to the latest study from the University of Newcastle, the consumption of only one drink containing containing 50 g of either fructose or glucose or sucrose dissolved in water will have detrimental effects on the #1 indicator of whole body inflammation, which is high sensitivity C-reactive protein (hs-CRP).

Much to the researchers surprise, though, the same amount of fructose had significant beneficial effects on the plasma lipid levels of the healthy male and female adults (n = 14) between the ages of 18-60 years who were recruited by advertisement and underwent study procedures at the Nutraceuticals Research Group Clinic rooms at the University of Newcastle in Australia.
Since the exclusion criteria were: diagnosed hyperlipidaemia, diabetes, gastrointestinal disorders, currently on fructose/sugar restricted diet, vegan diet or weight loss program, undergone any surgical procedure for obesity, pregnant or lactating mother, taking lipid-lowering or anti-inflammatory drugs and BMI >30kg/m², the results may well be different in "sicker" individuals, but for the guys and gals who drank the three 50g "sugar" solutions on three different occasions after an overnight fast, the "negative effects" of fructose were far from being conclusive.

Figure 1: Changes in hs-CRP, HDL and LDL in response to the ingestion of the test drinks (Jameel. 2014).

Even if you belong to the ever-increasing numbers of brainwashed fructose haters who believe that fructose and not a general overconsumption of energy was to blame for the obesity epidemic, you will have to admit that the data in Figure 1 leaves the significance of concomitant increases in hs-CRP and significant improvements in the HDL/LDL ratio, as the scientists phrase it, "to be delineated when considering health effects of feeding fructose-rich diets" (Jameel. 2014).
Well, yes, but (a) its only an acute response and (b) while increased levels of hs-CRP have been found to be associated with heart disease (Rifai. 2001; Danesh. 2004), the same can be said for a high LDL/HDL ratio (Fernandez. 2008).

Figure 2: CRP-dependent risk levels for cardiovascular disease according to the American Hear Association.

If we also take into consideration that the baseline hs-CRP level of the subjects was 1.5mg/L and thus low to mid-range for the average Westerner (depending on his or her ethnicity | Albert. 2004), an increase of 10% to a maximal value of 1.65mg/L would not bring them to critical heights of which the Farmingham study says that they start at 3mg/L for Westerners (Wilson. 2005). Thats not ana optimal level, but considering the fact that we are talking about "average Joes and Janes" who probably dont work out, eat whatever they like and give a damn about their sleep hygiene (all three factors have previously been linked to elevated hs-CRP levels) thats not astonishing and has absolutely nothing to do with the ingestion of 50g of fructose.

Furthermore, a comparison of the predictive value of different risk markers for cardiovascular disease by Folsom, et al. (2006) indicates that the hs-CRP values did not add to the prognostic value of the standard risk factors which are age, race, sex, systolic blood pressure, smoking status, diabetes and - you guessed it - total and high density lipoprotein cholesterol, which increased by almost 7% while the amount of LDL dropped by maximally 6%. Thus the LDL/HDL ratio decreased from 1.84 to 1.62. Thats a 12% decrease that would be health relevant if the subjects LDL/HDL ratio was not far away from the danger-zone (>5 | see Manninen. 1992), already. Similarly, the total cholesterol to HDL ratio dropped by -1.97 but wasnt in the danger zone before, either.
References:

• Danesh, John, et al. "C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease." New England Journal of Medicine 350.14 (2004): 1387-1397. 
• Fernandez, Maria Luz, and Densie Webb. "The LDL to HDL cholesterol ratio as a valuable tool to evaluate coronary heart disease risk." Journal of the American College of Nutrition 27.1 (2008): 1-5.
• Folsom, Aaron R., et al. "An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study." Archives of internal medicine 166.13 (2006): 1368-1373. 
• Hermsdorff, Helen Hermana M., et al. "Research Fruit and vegetable consumption and proinflammatory gene expression from peripheral blood mononuclear cells in young adults: a translational study." (2010).
• Jameel, Faizan, et al. "Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation." Lipids in Health and Disease 13.1 (2014): 195.
• Manninen, Vesa, et al. "Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment." Circulation 85.1 (1992): 37-45.
• Oliveira, A., F. Rodriguez-Artalejo, and C. Lopes. "The association of fruits, vegetables, antioxidant vitamins and fibre intake with high-sensitivity C-reactive protein: sex and body mass index interactions." European journal of clinical nutrition 63.11 (2009): 1345-1352. 
• Ravn-Haren, Gitte, et al. "Intake of whole apples or clear apple juice has contrasting effects on plasma lipids in healthy volunteers." European journal of nutrition 52.8 (2013): 1875-1889.
• Rifai, Nader, and Paul M. Ridker. "High-sensitivity C-reactive protein: a novel and promising marker of coronary heart disease." Clinical chemistry 47.3 (2001): 403-411.
• Wilson, Peter WF, et al. "C-reactive protein and risk of cardiovascular disease in men and women from the Framingham Heart Study." Archives of internal medicine 165.21 (2005): 2473-2478.