Barker, T., Schneider, E. D., Dixon, B. M., Henriksen, V. T., & Weaver, L. K. (2013). Supplemental vitamin D enhances the recovery in peak isometric force shortly after intense exercise. Nutrition & Metabolism, 10(1), 69. doi:10.1186/1743-7075-10-69
Introduction: Vitamin D is a fat-soluble vitamin which has been examined in a number of clinical fields. Early research identified vitamin D’s role in bone health. Since this discovery, the research on vitamin D has expanded to other physiology systems. In muscle physiology, vitamin D is hypothesized to play a vital role in regulation of skeletal muscle. This hypothesis stemmed from clinical observations suggesting increasing serum 25 (OH)D concentrations results in improved muscle strength and function in subjects with osteomalacia. Further research identified vitamin D’s role in calcium handling and transport, phosphate metabolism, cytoskeletal expression, and activation of mitogen activate protein kinase signaling pathways in skeletal muscle. These results have led to the hypothesis that increasing serum 25(OH)D concentrations could be a complementary approach to improving muscle function. The authors of this article also found a positive correlation between serum 25(OH)D concentrations and strength recovery after injury. In the rat model, supplemental vitamin D restored strength after a crush injury. This increase was hypothesized to occur secondary to increased proliferation and a reduction in apoptosis of muscle cell nuclei. Human data to date has been less conclusive. Therefore, the purpose of this study was to identify the influence of supplemental vitamin D on strength recovery following intense exercise. The authors’ hypothesized vitamin D would enhance strength recovery after a damaging exercise protocol.
The authors of this paper did an excellent job going into the background details regarding vitamin D. As a reader, I got a clear picture of the significant discoveries of vitamin D, beginning from studies in bone and spreading into other areas of research. The authors also did a good job of identifying the gaps in knowledge and where their research is going to fill this gap. The purpose was also clearly stated along with a hypothesis, leaving no questions as to the intent of the study.
Purpose: The purpose of this study was to identify the influence of supplemental vitamin D on strength recovery following intense exercise.
Subject Description: Healthy and modestly active (30 minutes of continuous active at least 3 times per week) were recruited for this study. Exclusion criteria included dietary supplements, medications, history of disease requiring medical attention, lower leg injuries during the previous year, increasing/decreasing exposure to the sun or tanning bed, morbidly obese ( > 40 kg/m2), strength or power asymmetry between legs (> 5% difference in peak isometric or power output between legs), or travelling below of 37° N in latitude during the study. Asymmetry was included in the exclusion criteria because exercise and evaluation was performed unilaterally.
This section was well written, the authors did a very good job of defining their variables and exclusion criteria. This allows the reader to grasp a greater understanding of the subjects used in this study. One minor detail not accounted for was the method of the recruitment process. Otherwise, this section provided more than enough detail. Characteristics such as age and weight were provided in a table format, making it easy to interpret.
Methods: The study design was a randomized, double-blind, placebo-controlled experimental design. The subjects were randomly allocated to either a placebo (n=13) or vitamin D (cholecalciferol, 4000 IU, n=15). Supplementation occurred daily for a period of 35 days. Subjects were asked to maintain their normal diet. Seventy-two hours prior to each blood draw subjects were asked to avoid physical activity, aspirin, ibuprofen, naproxen, acetaminophen, or other anti-inflammatories. A total of 8 fasting blood samples were drawn. Time frames for blood draws were baseline, immediately before (pre), immediately after (post), and 1, 24, 48, 72, and 168 hours post. Single leg strength and muscle soreness was investigated at 7 different time frames which included baseline (bsl), pre, post, and 24, 48, 72, and 168 hours thereafter. The supplementation period initiated after the baseline blood draw. Each subject performed intense, stretch-shortening cycle (SSC) exercise on a randomly selected leg. The non-exercise limb served as a control (CON). The exercise protocol consisted to 10 sets of 10 repetitive eccentric/concentric jumps at 75% body mass with 20 s rest between sets. Participants were encouraged to produce maximal effort and to jump as high as possible through a full range of motion (90° knee flexion). If participants were unable to jump secondary to fatigue, they were allowed to perform full range of motion presses. An inability to produce two successive presses resulted in termination of the exercise protocol. This protocol took place 28 d post Bsl. The mean number of jumps and presses were not deemed statistically significant between placebo and vitamin D groups (jumps, 62 ± 9; presses 19 ± 4 vs. (jumps, 59 ± 8; presses, 30 ± 6). Six of the placebo, and 9 of the vitamin D, were able to complete the protocol. ANOVA revealed no statistically significant differences in soreness and leg strength between those who finished and those who did not or between placebo and vitamin D.
Blood samples were taken from the antecubital vein. Plasma was separated via centrifugation. Following separation, plasma samples were sent to a lab for evaluation. Serum 25 OH)D concentrations (ng/mL) were measured in duplicate (coefficient of variation (CV) = 3.90%) in each sample. A comprehensive metabolic panel was performed on Bsl plasma samples measuring plasma AST (U/L), ALT (U/L), PTH (pg/ml), and calcium (mg/dL).
Strength testing was performed on a horizontal Plyo-Press. The sled was adjusted to each subject to produce a joint angle of 90° at the knee. Subjects performed a submaximal isometric contractions as a warm-up at 50,75, and 90 % intensities. Peak isometric contractions consisted of 3 s in duration and separated by 1 minute of rest. Each subject was encouraged to produce maximal force against the mounted force platform. Peak isometric force was taken from the highest of 3 trials (N/kg). Single-leg power output were taken after isometric testing. Testing consisted of a similar setup as described above. A Plyo-press was utilized with the subject beginning in full extension (0°). Subjects then performed several warm-up submaximal jumps to gain familiarity with the procedure. Subjects then performed repetitive maximal effort single leg jumps. Jumps were instructed to be performed as fast as possible and through a full range of motion (90° of knee flexion-to-full extension). Each test consisted of 20 s duration and the weight was set to 75% body mass. Power output was calculated from the resultant force (N) and the weight-stack velocity (m/s). Peak power was defined as the highest power output obtained in the 20 s set.
Muscle soreness was assessed positioning subjects into a 90° of hip and knee squat position for 5 seconds against a wall. A perceived soreness score was obtained for the gluteus, quadriceps, hamstrings, and calves via a visual analog scale. 0 was rated as no pain and 10 was rated as the worst pain possible. A score of 5 was deemed tender to touch but not to contractions.
The methods section was very well written. Details were provided throughout in regards to the different testing positions and definitions for terms such as peak power. This avoids the readers having to make assumptions about terms. The description of the exercise protocol was particularly well done. The authors were sure to describe the joint angles and selection of the limbs. Additionally they provided all the details about instructions such as encouraging subjects to jump as high as possible. This allows readers to further grasp whether appropriate verbal encouragement was provided. The only detail missing from the methods section was a statistical power evaluation to determine study size. Without this detail, it is difficult to determine how the author’s chose to use the current study size.
Results: Average serum 25(OH)D was 30.8 (1.6) ng/mL upon enrollment and randomization. Three subjects were determined to be vitamin D deficient (serum 25(OH)D < 20 ng/mL). Ten subjects were determined to be vitamin D insufficient (serum 25(OH)D 20 to 29 ng/mL). Fifteen subjects were determined to be vitamin D sufficient (serum 25(OH)D > 30 ng/mL). Following randomization, serum 25(OH)D levels were similar between groups. In the placebo group, six subjects were vitamin D deficient (n=1) or insufficient (n=5). Seven subjects were considered vitamin D sufficient. In the vitamin D group, seven subjects were considered deficient (n=2) or insufficient (n=5). Eight subjects were considered sufficient. At conclusion of the trail, the number of vitamin D deficient, insufficient, and sufficient subjects remained constant in the placebo. Serum 25(OH)D concentrations significantly increased ((≈ 70%, range = 7 – 175%) in the vitamin D group at 168-h (47.9 (7.6) ng/mL). The % increase was inversely correlated with baseline levels. Increases in plasma calcium (≈ 4%) concentrations at Post and a decrease in PTH (≈ 26%) were noted. Peak isometric force was decreased (≈ 6%) in the CON leg immediately and 48 hours post exercise. Peak isometric force in the SSC experienced greater decreases in force (≈ 32% at Post, 17% at 24-h, 21% at 48-h, and 14% at 72 h) . Peak isometric force in the CON and SSC legs were not significantly different between placebo and vitamin D groups. Peak power outputs in the SSC leg were greater (≈ 43% at Post, 12% at 24-h, and 12%) than the CON (≈ 4 and 5% at Post and 24-h). Peak power output in the SSC leg was significantly decreased compared to the CON leg (≈ 39%). Recovery of peak isometric force Post to 24-h in the SSC leg was significantly greater in the supplemental vitamin D group (≈ 8%). A similar trend for peak power was observed (P = 0.10)( (≈ 9%). Vitamin D also appeared to blunt ALT and AST, measures of muscle damage, at 48, 72, and 168-h. No differences were found for muscle soreness between groups.
The results section was similar to the methods section, with ample amounts of details and easy to view graphs. The graphs the authors selected were easy to view and decipher (simple bar and line charts). This made tracking vitamin D levels easy, and the reading is easily able to see the inverse relationship between vitamin D supplementation and % changes. The graphs also easily display the changes in peak isometric force and peak power over the various time frames tests. One detail I found lacking was in variation statistics. The authors did not choose to report measures of variance, such as standard deviation and confidence intervals. This makes it difficult for the reader to gain a grasp of the homogeneity of the data.
Discussion: This study identified vitamin D’s ability to enhance recovery and muscle strength quickly after an intense bout of exercise. The results suggest vitamin D supplementation may play a complementary strategy for individuals requiring fast recovery following intense physical activity. The enhancement in peak isometric force relatively quickly (Post-24 h) suggest vitamin D modulates mechanisms of muscle weakness. One theory to this mechanism revolves around restoring phosphocreatine. This theory suggests vitamin D may enhance strength by altering phosphate metabolism or accumulation in muscle. An interesting finding to note was the failure of vitamin D to enhance delayed recovery in peak isometric force. It seems plausible vitamin D may enhance strength by reducing weakness attributable to fatigue, rather than muscle damage. Vitamin D did prevent increased in ALT and AST in this study, which are released following acute muscle damage. This is contradictory to the previously mentioned hypothesis. Further research is required in this area to confirm these findings. A few hypotheses have been purported to explain vitamin D’s ability to enhance recovery. Mitochondrial oxidative phosphorylation reportedly increases with vitamin D supplementation in deficient subjects, which could explain an enhanced recovery. Another proposed theory involves strength enhancement via inhibition of apoptosis and increased extracellular matrix proteins. Lastly, supplementation may increase vitamin D receptor in skeletal muscle, which may play a role in protein synthesis and calcium transport.
Conclusion/Limitations: In conclusion, this study demonstrated vitamin D enhances the recovery of force production after an acute bout of intense exercise. Additionally, vitamin D appeared to reduce markers of muscle damage. Limitations to this study include a small sample size and exercise protocol. In regards to the exercise protocol, some subjects performed exercise to volitional failure while others completed the entire program. Thus, the volume was different. There was a trend for the vitamin D group to perform less jumps and more presses, although the difference was not statistically significant. Another limitation to this study was the inability to determine if vitamin D enhanced strength by ameliorating muscle damage or fatigue.
My Thoughts: I thought the authors did an excellent job of discussing their thought processes and theories in regards to why vitamin D appears to enhance recovery. They provided a number of possible hypotheses. Additionally, I felt the authors did a good job of not over-reaching with their conclusion. This discussion was one of the best and most comprehensive pieces I have read in terms of these critiques. The authors really analyzed their findings well. Finally, the limitations section was also done well. The authors mentioned a number of obvious, and not so obvious limitations. I think bringing up the exercise protocol was an intelligent observation. Overall, this study was very thorough and well written.
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