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Working out in the sun will make you lose fat, taking D3 supplements will not.

Have you been wondering why you didn't lean out magically in the past year even though you're taking a ton of vitamin D? Well, maybe it's because your previously low vitamin D levels were nothing but a symptom of your extra-pounds. One that will disappear with weight loss and one that may have mislead scientists and laymen alike to assume that vitamin D supplementation may help you lose weight.

In their latest study, scientists from the Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québe tried to get to the bottom of the relationships between changes in 25(OH)D levels and changes in adiposity volume (total and by adipose tissue compartment | Gangloff. 2015).
To do so, the researchers recruited sedentary, abdominally obese and dyslipidemic men (n=103) for a a 1-year lifestyle modification program targeted at weight loss.

Body weight, body composition, and fat distribution were assessed by dual-energy X-ray absorptiometry and computed tomography while 25(OH)D levels were measured with an automated assay. Well, the results of these assessments were interesting, to say the least.

Lowe your body fat, increase your vitamin D levels, it's as "simple as that"

Firstly, the 1-year intervention resulted in a 26% increase in circulating 25(OH)D (from 48±2 nmol/l or 19±0.8 ng/ml (±s.e.m.) to 58±2 nmol/l or 23±0.8 ng/ml, P<0.0001); and secondly, this happened alongside a 26% decrease in visceral adiposity volume (from 1947±458 cm3 to 1459±532 cm³).
Subjects were individually counselled by a kinesiologist and a nutritionist once every 2 weeks during the first 4 months with subsequent monthly visits in order to elicit a -500 kcal daily energy deficit and to increase physical activity/exercise habits.

Figure 1: Changes in serum 25OHD (vitamin D) levels and visceral fat during the 1-year lifetime intervention (left); illustration of the logical fallacy that makes people assume that popping vitamin D triggers weight loss.

Secondly and more importantly, there was a significant inverse correlation between the changes in all adiposity indices, especially Δvisceral (r=−0.36, P<0.0005) and Δtotal abdominal (r=−0.37, P<0.0005) adipose tissue volumes with the significant increases of 25(OH)D the scientists observed, when they analyzed the blood of their subjects. Now, this could certainly mean that taking vitamin D supplements will reduce your body fat, but

• well-controlled studies like Wamberg, et al. (2013), who found marginal, non-significant increases in subcutaneous fat and no change in visceral fat in response to 7,000 IU vitamin D/day in their controlled randomized trial with obese adults with low vitamin D levels, or 
• meta-analyses like the most recent one by Pathak et al. which found that "[v]itamin D supplementation d[oes] not influence the standardized mean difference (SMD) for body weight, FM, %FM or LBM" (Pathak. 2014) 

make it hard to believe that the results of singular studies that were published in smaller open-access or pay-for-publishing journals like the one Salehpour et al. did in 2012 are more than outliers (note: different rules may apply if vitamin D is administered alongside other dietary or lifestyle interventions).

What remains unquestionable, though, is the correlation between high body fat levels and low vitamin D levels that is consistent over almost all observational (Wortsman. 2000; Arunabh. 2003; Kremer. 2009; Lagunova. 2009; Lenders. 2009; Forney. 2014) and experimental studies (Blum. 2008; Lee. 2009) in both sexes and across all age-groups. To interpret this as evidence in favor of potential body-fat reducing effects of vitamin D supplements is yet totally unwarranted.
References:

• Arunabh, Sonia, et al. "Body fat content and 25-hydroxyvitamin D levels in healthy women." The Journal of Clinical Endocrinology & Metabolism 88.1 (2003): 157-161.
• Bashir, Mina, et al. "Effects of high doses of vitamin D3 on mucosa-associated gut microbiome vary between regions of the human gastrointestinal tract." European Journal of Nutrition (2015): 1-11.
• Blum, Miriam, Gerard E. Dallal, and Bess Dawson-Hughes. "Body size and serum 25 hydroxy vitamin D response to oral supplements in healthy older adults." Journal of the American College of Nutrition 27.2 (2008): 274-279.
• Forney, Laura A., et al. "Vitamin D status, body composition, and fitness measures in college-aged students." The Journal of Strength & Conditioning Research 28.3 (2014): 814-824.
• Gangloff, A., et al. "Effect of adipose tissue volume loss on circulating 25-hydroxyvitamin D levels: results from a 1-year lifestyle intervention in viscerally obese men." International journal of obesity (2005) (2015).
• Kremer, Richard, et al. "Vitamin D status and its relationship to body fat, final height, and peak bone mass in young women." The Journal of Clinical Endocrinology & Metabolism 94.1 (2009): 67-73.
• Lagunova, Zoya, et al. "The dependency of vitamin D status on body mass index, gender, age and season." Anticancer research 29.9 (2009): 3713-3720.
• Lenders, Carine M., et al. "Relation of body fat indexes to vitamin D status and deficiency among obese adolescents." The American journal of clinical nutrition 90.3 (2009): 459-467.
• Lee, Paul, et al. "Adequacy of vitamin D replacement in severe deficiency is dependent on body mass index." The American journal of medicine 122.11 (2009): 1056-1060.
• Nimitphong H, Holick MF, Fried SK, Lee MJ. 25-hydroxyvitamin d(3) and 1,25-dihydroxyvitamin d(3) promote the differentiation of human subcutaneous preadipocytes. PLoS One. 2012; 7(12):e52171.
• Pathak, K., et al. "Vitamin D supplementation and body weight status: a systematic review and meta‐analysis of randomized controlled trials." Obesity Reviews 15.6 (2014): 528-537.
• Rosenstreich, Saul J., Clayton Rich, and Wade Volwiler. "Deposition in and release of vitamin D3 from body fat: evidence for a storage site in the rat." Journal of Clinical Investigation 50.3 (1971): 679.
• Salehpour, Amin, et al. "A 12-week double-blind randomized clinical trial of vitamin D3 supplementation on body fat mass in healthy overweight and obese women." Nutr J 11.1 (2012): 78.
• Sneve, M., Y. Figenschau, and R. Jorde. "Supplementation with cholecalciferol does not result in weight reduction in overweight and obese subjects." European Journal of Endocrinology 159.6 (2008): 675-684.
• Waldron, Jenna Louise, et al. "Vitamin D: a negative acute phase reactant." Journal of clinical pathology (2013): jclinpath-2012.
• Wamberg, L., et al. "Effects of vitamin D supplementation on body fat accumulation, inflammation, and metabolic risk factors in obese adults with low vitamin D levels—results from a randomized trial." European journal of internal medicine 24.7 (2013): 644-649.
• Wortsman, Jacobo, et al. "Decreased bioavailability of vitamin D in obesity." The American journal of clinical nutrition 72.3 (2000): 690-693.

Is it worth to replete vitamin D, but not to train super-slow, right?

No, I haven't dug up a study that deals with vitamin D and super-slow training at once, but I've found two very recent studies that are in one way or another related to muscle regeneration and hypertrophy and the way/s vitamin D and different training methods affect these outcomes. More specifically, the researchers investigated the effects of vitamin D (20OHD) repletion and the use of higher times-under-tension (TUT) and super-slow training.

Before I go ahead, though, I would like to point out that the long-term implications of some of the results are not totally obvious - a fact I will therefore (re-)address in the bottom line.

• (Super-)slow training and its inferior effects on early-phase satellite cell and myonuclear domain adaptation (Herman-Montemayor. 2015) -- The purpose of one of the latest studies from the Rocky Vista University was to identify adaptations in satellite cell (SC) content and myonuclear domain (MND) after 6-week slow-speed vs. “normal-speed” resistance training programs.
  
  To this ends, thirty-four untrained women were divided into slow speed (SS), traditional strength (TS), traditional muscular endurance (TE), and nontraining control (C) groups. The ladies performed a leg work consisting of three sets of each of the following exercises twice per week in the first and thrice per week in the fifth week: Leg press, squat, and knee extensions. To investigate how the way these workouts were performed would affect the adaptive response, the scientists randomly assigned their subjects to four different groups:
  • The Super-Slow (SS) group performed 6– 10 repetition maximum (6–10RM) for each set with 10-second concentric (con) and 4-second eccentric (ecc) contractions for each repetition.
  • The Traditional Strength (TS) group and the Traditional Muscular Endurance (TE) group who performed 6–10RM and 20–30RM, respectively, at “normal” speed (1–2 seconds per con and ecc contractions).
  • The sedentary control group (C) which did not work out at all.
  To allow for a similar number of reps in the TS and SS group, the intensity (=weight used) in the SS group was reduced to the same 40–60% of the 1RM that was also used in the TE group. The TS group, on the other hand trained at 80–85% 1RM.

• I know that this is not ideal, but there's no way you do 6-10 reps with a time-under-tension (TUT) of 10-0-4 with the same weight you'd do 6-10 reps at a normal TUT of 1-0-1 or 2-0-2, accordingly, the results the scientists' analysis of the pretraining and posttraining muscle biopsies the authors analyzed for fiber cross-sectional area, fiber type, SC content, myonuclear number, and MND still have practical relevance.
  

  Figure 1: Percentage change (%) in mean fiber cross-sectional area, myonuclear domain size (domain), and number of myonuclei per fiber cross-section (myonuclear number) from pretraining to posttraining for each group (TS, SS, TE, and C). *Significant increase after training, p , 0.001. §Significant increase after training, p # 0.05. #Significantly greater increase after training compared with all other groups (SS, TE, C), p , 0.01. TS = traditional strength (Herman-Montemayor. 2015).

  And what does the scientists' analysis tell us? Well, along with the data in Figure 1, the exclusive increase in satellite cell content of type I, IIA, fibers (IIX and IIAX increased in both SS and TS, but not TE or control) that was observed in the traditional strength (TS) training group appears to confirm the superiority of this way of training when it comes to lying the foundations of further myonuclear domain growth (learn more in the "Muscle Hypertrophy 101").
  
  The fact that myonuclear domain increases of type I, IIAX, and IIX fibers occurred exclusively in the TS, yet not in the SS group, where only the domains of the type IIA fibers increased, does still appear to confirm the common prejudice that - for the average trainee - training at higher times under tension (TUTs) does not offer benefits that suggest faster or more robust size gains. Compared to strength-endurance training, however, super-slow training is still the better option. On a "per load basis" it is thus more effective to do fewer reps slower vs. more reps at a normal speed if your goal is to "grow" muscle.
• Vitamin D affects muscle recovery directly (Owen. 2015) -- We already know that vitamin D figures in one way or another in (a) the adaptive response to exercise and (b) the recovery process after strenuous workouts. Unfortunately our "knowledge" is based mostly on correlations and associations and can thus hardly be considered reliable evidence. That's something researchers from the Liverpool John Moores University, the Charité in Berlin, the Norwich Medical School and other European labs weren't happy with, either. Accordingly, they designed a randomised, placebo-controlled trial that involved twenty males with low serum 25[OH]D (45 ± 25 nmol.L-1) who performed 20×10 damaging eccentric contractions of the knee extensors with peak torque measured over the following 7 days of recovery prior to and following 6-weeks of supplemental Vitamin D3 (4,000 IU.day-1) or placebo (50 mg cellulose).
  
  To complement the results of this human trial, the authors conducted a parallel experimentation using isolated human skeletal muscle derived myoblast cells from biopsies of 14 males with insufficient serum 25[OH]D (37 ± 11 nmol.L-1) that were subjected to mechanical wound injury. Thus, the scientists tried to emulate the process of muscle repair, regeneration and hypertrophy in the presence and absence of 10 nmol or 100 nmol 1α,25[OH]2D3 in the petri dish.
  

  Figure 2: In view of the fact that the scientists used active vitamin D3 (calcitriol) in the in-vitro study, the improved recovery in the human trial is all the more the more relevant results of the study. It does yet pose the question whether similar or any effects had been observed in subjects with sufficient vitamin D levels in whom the provision of extra vitamin D3 may have increased 25OHD, but not the systemic calcitriol levels of which the scientists' in-vitro dta shows that it is responsible for the effects (Owens. 2015).

  What the results of both studies have in common is that they support the previously claimed role of vitamin D in muscle repair and regeneration. How's that? Well, the supplemental Vitamin D3 the D-ficient human subjects received didn't just increase the serum 25[OH]D levels. It also lead to measurable improvements of the recovery of peak torque at 48 hours and 7 days post-exercise. In conjunction with the observation that 10 nmol 1α,25[OH]2D3 aka calcitriol (=active vitamin D3, not the supplement you consume) improved muscle cell migration dynamics and resulted in improved myotube fusion/differentiation at the biochemical, morphological and molecular level in the cell study, where it also increased the myotube hypertrophy at 7 and 10 days post-damage, these preliminary data do just as the scientists say "characterise a role for Vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25[OH]D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy" (Owens. 2015).

Old or young, who is going to benefit and who is going to benefit most from vitamin D supplementation during a 12-week resistance training regimen. That was the question the study at hand sought to answer and this was a question it didn't find an unambiguous answer to.

Ok, I have to admit, I could have kept up the suspense by not giving away the main result of Jakob Agergaard's and colleagues' latest study in the headline, already. On the other hand, by giving away the most relevant information in the headline, I can make sure that future google searchers will immediately refute the claim that "vitamin D is a powerful muscle builder" - it is not. What it may very well be, is a vitamin that is necessary for your long-term success.

This is still much different from what you may conclude solely based on the associations that exist between low vitamin D and all sorts of ailments, though. Evidence that vitamin D(3) supplements are able to reduce the risk of bone fractures, diabetes, cardiovascular diseases, cancer, depression, osteoarthritis, multiple sclerosis, and other immune related diseases is still preliminary. Very unfortunate in view of big research dollars that have been spend without yielding D-finite results and hundreds of more or less practically useless observational studies.
I was thus very happy to see that the scientists from the University of Copenhagen did not content themselves with correlating the individual gains of their young and old subjects with the corresponding vitamin D levels. Instead, they designed a randomized controlled trial in which they "investigate[d] whether vitamin-D intake during 12 weeks of resistance training has an additive effect on muscle hypertrophy and strength"  (Agergaard. 2015) in Healthy, sedentary young (aged 20–30 years) and elderly (aged 60–75 years) Caucasian men living within the local community in Copenhagen:

"We hypothesized that intake of vitamin-D plus calcium would improve the outcome of three months of resistance training in healthy untrained individuals resulting in greater muscle strength and hypertrophy compared to a training control-group supplemented with calcium alone (placebo). Moreover, we hypothesized that resistance exercise would increase the mRNA expression of VDR and CYP27B1. The study included a group of young and a group of elderly individuals to elucidate a possible blunted hypertrophic response in the aging muscle"  (Agergaard. 2015).

The study took place at Bispebjerg Hospital, Copenhagen, Denmark (latitude of 56°N). Inclusion was continuous from November 17, 2010 to December 21, 2010 and the last subject completed the study on April 25, 2011. Thus, the study was conducted in a period of low UVB irradiation from sunlight. The risk of interference by uncontrolled sun-exposure was thus low. About as low as I suppose some of you will say the supplementation dose was. The latter consisted of either

• placebo supplementation with 800mg of calcium per day, or
• vitamin D + calcium at a dosage of 48µg (1920 IU) vitamin-D 3 + 800 mg calcium/day

that was administered in two servings, with one tablet containing 10 μg vitamin-D 3  + 400 mg calcium and one tablet containing 38 μg vitamin-D 3  + 400 mg calcium and had to be taken with meals (this increases absorption | learn more).
The scientists probably would have dosed higher, but since the maximum advisable daily dose according to the Danish Health and Medicines Authority is 50 μg, i.e. 2000 IU, they probably felt that their hands were tied.

Figure 1: Flowchart showing a young and b elderly subjects from first contact to end of study (Agergaard. 2015)

All subjects who had been randomly (double-blind) assigned to the respective group had to follow the same standardized workout routine consisting of a total of 36 training sessions (12 weeks with 3 sessions/week) with 5–10 min warm-up on cycle ergometers followed by resistance training exercises of the lower extremities (only!) performed in commercial knee extension and leg press devices (Technogym, Super Executive Line, Gambettola, Italy) in each session. All sessions were supervised. Progressive loading levels were monitored continuously and adjusted throughout the entire training period to maintain muscle loading at the intended values.

• During the first 6 training sessions, participants completed 3 sets of 12–15 repetitions at 65–70 % of 1RM. 
• During session 7–12, participants performed 3 sets of 10–12 repetitions at 70–75 % of 1RM, increasing to 4 sets at 70–75 % of 1RM during session 13–18. 
• From session 19 and onwards, participants performed 5 sets with training load progressing from 8–10 repetitions at 75–80 % of 1RM in session 19–27 to 6–8 repetitions at 80–85 % of 1RM in session 28–36 [38]. 

The exercises were performed in a moderate slow, controlled manner with 1–2 s in the concentric- and eccentric phase with a rest of 1–3 min between sets. Exercise compliance (sets, repetitions, and load) was calculated from daily exercise records completed by the instructors at each training session. Participants were informed that a mean attendance of less than 2 training sessions per week resulted in exclusion. All adverse events associated with the training intervention were recorded.
The outcome variables the scientists choose were skeletal muscle hypertrophy, isometric muscle strength, serum vitamin D levels, and a muscle biopsy that was used (a) to analyze several markers of muscle hypertrophy, metabolism & co, as well as (b) to determine whether training or treatment had triggered measurable or even significant changes in the fiber type composition of the subjects.

Figure 2: Serum vitamin D levels at all time-points during the study (I added the markups for the zones to the original figure from Agergaard to make it easier for you to interpret the data).

Of these, I deliberately chose the 25OHD serum levels to start with. Why? Well if you look at the small increase in the young subjects and the still existing gap between their 25OHD (=serum vitamin D) levels and the allegedly "optimal" zone for lower body strength gains (cf. Bischoff-Ferrari. 2006), you may feel reassured that the dosages were too low. This is yet only the case, if the goal was to get the levels into the "magic" 90-100nmol/L of which Bischoff-Ferrari estimated in 2006 that it was optimal for muscle function and health. Whether the effects would have been more pronounced if the subjects had reached this level is yet mere speculation and, if you look at the correlation analysis further down, even highly unlikely (see Figure 5 and respective explanations).

Figure 3: Cross sectional area (CSA), Isometric strength and strength/CSA of Quadriceps muscle. Change in a CSA, b isometric strength and c strength/CSA of quadriceps muscle for young and elderly vitamin-D and placebo groups, respectively. Data shown as mean percentage change from week 0 ± SEM. * different from week 0 (p < 0.05)

Now, as arbitrary as these ranges may be (things like the influence of the vitamin D binding protein levels and genotypes for example, are taken into account, at all | Chun. 2014; Koplin. 2015), we must not and will not ignore the fact that the young, unlike the old(er) subjects, didn't make it into 90-100 nmol/L zone of "magic gains" when we are looking at the data in Figure 3:

• No group effects - The first thing you should realize is that there were no significant inter-group differences and thus no group effects in response to the provision of vitamin D3 vs. placebo. This does imply that neither the increased size gains (A) in the vitamin D group in the young nor the decreased gains in the vitamin D group in the old subjects was statistically significant. The same can be said, albeit in the opposite directions for the strength increases (B) and the relative strength increases (C) in the young subjects.
• Significant time effects - Since subjects in both groups still gained significant amounts of muscle and strength, the one thing the study does confirm is the efficacy of resistance training as strength and mass builder in young and old.
• Significant group effect on relative strength in the elderly - Due to the reversal of the observations compared to the young group (lower size gains + higher strength gains in the older, higher size + lower strength gains in the younger subjects), the relative strength of the older subjects has improved by vitamin D supplementation (p = 0.008, not correctly indicated in Figure 3) - a result that stands in line with previous research like Moreira-Pfrimer et al. (2009) where the provision of 150,000 IU once a month during the first 2 months, followed by 90,000 IU once a month for another 4 months enhanced both, the 25(OH)D levels and the lower limb muscle strength of the > or =60 year old subjects, even in the absence of any regular physical exercise practice.

Now, I would be inclined to ignore the lack of statistical significance for the initially mentioned parameters and jump on the significant increase in the older subjects and the trends we may extrapolate from the rest of the data, if it were not for the results of the extra correlation analysis the scientists did. If higher levels of vitamin D3 (90-100nmol/L as they were achieved in the older subjects) could, as Bischoff-Ferrari et al. assume based on observations Guralnik, et al. (1995) and Seeman et al. made in elderly individuals, ameliorate exercise-induced strength gains in the young subjects, there should at least be a correlation between vitamin 25OHD levels and muscle size and strength similar to the one Bischoff-Ferrari et al. report for the 8-foot-walk and sit-to-stand test:

Figure 4: The optimal ranges, Bischoff-Ferrari et al. estimated are based on the above observational data from a 8-foot-walk and sit-to-stand test done in the elderly. That's super reliable and just like you, right? No? Well, that's why I believe those "optimal values" have no relevance for the young and low relevance for the old subjects (Bischoff-Ferrari. 2006)

If the trends you may believe to see in Figure 3 a-c remained trends, because the 25OHD levels didn't rise high enough, the graphs in Figure 5 would look much different: They would firstly show increasing, not no or decreasing slopes and would second of all provide evidence for a practically relevant correlation between the 25OHD levels, the muscle size, strength and relative strength.

Figure 5: Correlation between Quadriceps ΔCSA, ΔIsometric strength, Δstrength/CSA and 25(OH)D (Agergaard. 2015)

In practice, however, the correlation analysis yielded nothing: No correlation between 25OHD and size gains (A), no correlation between 25OHD and strength gains (B), and no correlation between 25OHD and relative strength gains (C). While this does not neglect the possibility that the vitamin D supplement still affected the increase in strength/size ratio of the elderly, the result warrants the conclusion that there was "[n]o additive effect of vitamin-D intake during 12 weeks of resistance training [...] on either whole muscle hypertrophy or muscle strength" (Agergaard. 2015).

• Agergaard, Jakob, et al. "Does vitamin-D intake during resistance training improve the skeletal muscle hypertrophic and strength response in young and elderly men?–a randomized controlled trial." Nutrition & metabolism 12.1 (2015): 32.
• Bischoff-Ferrari, Heike A., et al. "Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes." The American journal of clinical nutrition 84.1 (2006): 18-28.
• Chun, Rene F., et al. "Vitamin D and DBP: the free hormone hypothesis revisited." The Journal of steroid biochemistry and molecular biology 144 (2014): 132-137.
• Garcia, Leah A., et al. "1, 25 (OH) 2 vitamin D 3 enhances myogenic differentiation by modulating the expression of key angiogenic growth factors and angiogenic inhibitors in C 2 C 12 skeletal muscle cells." The Journal of steroid biochemistry and molecular biology 133 (2013): 1-11.
• Garcia, Leah A., et al. "1, 25 (OH) 2vitamin D3 stimulates myogenic differentiation by inhibiting cell proliferation and modulating the expression of promyogenic growth factors and myostatin in C2C12 skeletal muscle cells." Endocrinology 152.8 (2011): 2976-2986.
• Glendenning, Paul, et al. "Calculated free and bioavailable vitamin D metabolite concentrations in vitamin D-deficient hip fracture patients after supplementation with cholecalciferol and ergocalciferol." Bone 56.2 (2013): 271-275.
• Guralnik, Jack M., et al. "Lower-extremity function in persons over the age of 70 years as a predictor of subsequent disability." New England Journal of Medicine 332.9 (1995): 556-562.
• Jia et al. "Vitamin D Receptor Genetic Polymorphism Is Significantly Associated with Risk of Type 2 Diabetes Mellitus in Chinese Han Population." Arch Med Res. (2015): Ahead of print. 
• Ko, Min Jung, et al. "Relation of serum 25-hydroxyvitamin D status with skeletal muscle mass by sex and age group among Korean adults." British Journal of Nutrition (2015): 1-7.
• Koplin, Jennifer J., et al. "Polymorphisms affecting vitamin D–binding protein modify the relationship between serum vitamin D (25 [OH] D 3) and food allergy." Journal of Allergy and Clinical Immunology (2015).
• Makanae, Yuhei, et al. "Acute bout of resistance exercise increases vitamin D receptor protein expression in rat skeletal muscle." Experimental physiology 100.10 (2015): 1168-1176.
• Moreira-Pfrimer, Linda DF, et al. "Treatment of vitamin D deficiency increases lower limb muscle strength in institutionalized older people independently of regular physical activity: a randomized double-blind controlled trial." Annals of Nutrition and Metabolism 54.4 (2009): 291-300.