High-dose vitamin D administration and resistance exercise training attenuate the progression of obesity and improve skeletal muscle function in obese p62-deficient mice.

Vitamin D (VitD) possesses antiadipogenic and ergogenic properties that could be effective to counteract obesity-related adverse health consequences. Therefore, our overall hypothesis was that VitD could ameliorate obesity-induced insulin resistance, systemic inflammation, and loss of skeletal muscle mass and function in an obesity animal model, p62-deficient mice. Furthermore, it was hypothesized that resistance exercise training (RT) could enhance the benefits of VitD by upregulating protein expression of vitamin D receptor in skeletal muscle. Forty 24-week-old male p62-deficient mice were assigned to the following 4 groups (10/group) for a 10-week intervention: control (p62C, no treatment), VitD (VD, 1000 IU vitamin D3/kg/d), RT (ladder climbing, 3 times per week), or combined treatment (VRT, VD + RT). Serum VitD levels increased in VD and VRT (P < .05). Total body mass increased in p62C, VD, and VRT, but fat mass increased only in p62C (P < .05). Loss of skeletal muscle function was reported only in p62C (P < .05). Improved blood glucose levels and lower spleen mass were reported in RT and VRT compared to p62C (P < .05). However, the hindlimb muscle wet weights; myofiber cross-sectional area; and expression levels of the regulatory proteins for insulin signaling, inflammation, and muscle growth were not changed by any intervention. In conclusion, VitD administration attenuated the progression of obesity and preserved skeletal muscle function in p62-deficient mice. However, the obese mice improved systemic insulin sensitivity and inflammation only when the intervention involved RT.

The Evolving Applications of Creatine Supplementation: Could Creatine Improve Vascular Health?

Creatine is a naturally occurring compound, functioning in conjunction with creatine kinase to play a quintessential role in both cellular energy provision and intracellular energy shuttling. An extensive body of literature solidifies the plethora of ergogenic benefits gained following dietary creatine supplementation; however, recent findings have further indicated a potential therapeutic role for creatine in several pathologies such as myopathies, neurodegenerative disorders, metabolic disturbances, chronic kidney disease and inflammatory diseases. Furthermore, creatine has been found to exhibit non-energy-related properties, such as serving as a potential antioxidant and anti-inflammatory. Despite the therapeutic success of creatine supplementation in varying clinical populations, there is scarce information regarding the potential application of creatine for combatting the current leading cause of mortality, cardiovascular disease (CVD). Taking into consideration the broad ergogenic and non-energy-related actions of creatine, we hypothesize that creatine supplementation may be a potential therapeutic strategy for improving vascular health in at-risk populations such as older adults or those with CVD. With an extensive literature search, we have found only four clinical studies that have investigated the direct effect of creatine on vascular health and function. In this review, we aim to give a short background on the pleiotropic applications of creatine, and to then summarize the current literature surrounding creatine and vascular health. Furthermore, we discuss the varying mechanisms by which creatine could benefit vascular health and function, such as the impact of creatine supplementation upon inflammation and oxidative stress.

Vitamin D and Endothelial Function.

Vitamin D is known to elicit a vasoprotective effect, while vitamin D deficiency is a risk factor for endothelial dysfunction (ED). ED is characterized by reduced bioavailability of a potent endothelium-dependent vasodilator, nitric oxide (NO), and is an early event in the development of atherosclerosis. In endothelial cells, vitamin D regulates NO synthesis by mediating the activity of the endothelial NO synthase (eNOS). Under pathogenic conditions, the oxidative stress caused by excessive production of reactive oxygen species (ROS) facilitates NO degradation and suppresses NO synthesis, consequently reducing NO bioavailability. Vitamin D, however, counteracts the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase which produces ROS, and improves antioxidant capacity by enhancing the activity of antioxidative enzymes such as superoxide dismutase. In addition to ROS, proinflammatory mediators such as TNF-α and IL-6 are risk factors for ED, restraining NO and eNOS bioactivity and upregulating the expression of various atherosclerotic factors through the NF-κB pathway. These proinflammatory activities are inhibited by vitamin D by suppressing NF-κB signaling and production of proinflammatory cytokines. In this review, we discuss the diverse activities of vitamin D in regulating NO bioavailability and endothelial function.

Resistance training during a 12-week protein supplemented VLCD treatment enhances weight-loss outcomes in obese patients.

BACKGROUND: This investigation evaluated the efficacy by which resistance training enhances body composition, metabolic, and functional outcomes for obese patients undergoing a 12-week medically supervised hypocaloric treatment. METHODS: This was a single-blind, randomized, parallel-group prospective trial. Morbidly obese patients were prescribed a 12-week proprietary very low calorie diet (VLCD) treatment (Optifast®) with supplemental protein (1120 kcals/day) and were placed in one of two groups for 14 weeks: 1) Standard Treatment Control (CON) (n = 5) or 2) Resistance Training (RT) (n = 6). Both groups underwent a pedometer-based walking program; however only RT performed resistance training 3 days/week for 12 weeks. Body composition, resting energy expenditure (REE), neuromuscular function, and serum biomarkers were measured at weeks 0, 6, and 13. RESULTS: Both groups exhibited a significant loss of total body mass (TBM) (CON: -19.4 ± 2.3 kg, p = 0.0009 vs. RT: -15.8 ± 1.5 kg, p = 0.0002) and fat mass (FM) (CON: -14.7 ± 1.8 kg, p = 0.0002 vs. RT: -15.1 ± 2.1 kg, p = 0.0002) with no group differences. CON lost 4.6 ± 0.8 kg (p = 0.004) of lean mass (LM) while RT demonstrated no changes. Group differences were found for the relative proportion of total weight-loss due to FM-loss (CON: 75.6 ± 3.4% vs. RT: 96.0 ± 6.0%, p = 0.03) and LM-loss (CON: 24.4 ± 3.2% vs. RT: 4.0 ± 6.5%, p = 0.03). CON demonstrated a 328.6 ± 72.7 kcal/day (-14.3 ± 2.4%) (p = 0.02) decrease in REE while RT exhibited a non-significant decrease of 4.6 ± 1.6% (p = 0.78). RT demonstrated greater improvements in all measures of contractile function and strength when compared to CON (p < 0.05). At post-treatment, RT exhibited greater serum free fatty acids (p = 0.01), glycerol (p = 0.003), and ß-hydroxybutyrate (p = 0.005) than CON. CONCLUSION: Resistance training was advantageous for weight-loss composition by preservation of LM without compromising overall weight- or fat-loss in morbidly obese men and women undergoing a protein supplemented VLCD. These changes accompanied positive adaptations for resting metabolism and muscular function.