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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).