Adopting low carbohydrate, ketogenic diets remains a controversial issue for individuals who resistance train given that this form of dieting has been speculated to reduce skeletal muscle glycogen levels and stifle muscle anabolism. We sought to characterize the effects of a 12-week ketogenic diet (KD) on body composition, metabolic, and performance parameters in participants who trained recreationally at a local CrossFit facility. Twelve participants (nine males and three females, 31 ± 2 years of age, 80.3 ± 5.1 kg body mass, 22.9 ± 2.3% body fat, 1.37 back squat: body mass ratio) were divided into a control group (CTL; n = 5) and a KD group (n = 7). KD participants were given dietary guidelines to follow over 12 weeks while CTL participants were instructed to continue their normal diet throughout the study, and all participants continued their CrossFit training routine for 12 weeks. Pre, 2.5-week, and 12-week anaerobic performance tests were conducted, and pre- and 12-week tests were performed for body composition using dual X-ray absorptiometry (DXA) and ultrasound, resting energy expenditure (REE), blood-serum health markers, and aerobic capacity. Additionally, blood beta hydroxybutyrate (BHB) levels were measured weekly. Blood BHB levels were 2.8- to 9.5-fold higher in KD versus CTL throughout confirming a state of nutritional ketosis. DXA fat mass decreased by 12.4% in KD (p = 0.053). DXA total lean body mass changes were not different between groups, although DXA dual-leg lean mass decreased in the KD group by 1.4% (p = 0.068), and vastus lateralis thickness values decreased in the KD group by ~8% (p = 0.065). Changes in fasting glucose, HDL cholesterol, and triglycerides were similar between groups, although LDL cholesterol increased ~35% in KD (p = 0.048). Between-group changes in REE, one-repetition maximum (1-RM) back squat, 400 m run times, and VO_2peak were similar between groups. While our n-sizes were limited, these preliminary data suggest that adopting a ketogenic diet causes marked reductions in whole-body adiposity while not impacting performance measures in recreationally-trained CrossFit trainees. Whether decrements in dual-leg muscle mass and vastus lateralis thickness in KD participants were due to fluid shifts remain unresolved, and increased LDL-C in these individuals warrants further investigation.

Increased consumption of omega-3 (ω-3) fatty acids found in cold-water fish and fish oil has been reported to protect against obesity. A potential mechanism may be through reduction in adipocyte differentiation. Stearidonic acid (SDA), a plant-based ω-3 fatty acid, has been targeted as a potential surrogate for fish-based fatty acids; however, its role in adipocyte differentiation is unknown. This study was designed to evaluate the effects of SDA on adipocyte differentiation in 3T3-L1 cells. 3T3-L1 preadipocytes were differentiated in the presence of SDA or vehicle-control. Cell viability assay was conducted to determine potential toxicity of SDA. Lipid accumulation was measured by Oil Red O staining and triglyceride (TG) quantification in differentiated 3T3-L1 adipocytes. Adipocyte differentiation was evaluated by adipogenic transcription factors and lipid accumulation gene expression by quantitative real-time polymerase chain reaction (qRT-PCR). Fatty acid analysis was conducted by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). 3T3-L1 cells treated with SDA were viable at concentrations used for all studies. SDA treatment reduced lipid accumulation in 3T3-L1 adipocytes. This anti-adipogenic effect by SDA was a result of down-regulation of mRNA levels of the adipogenic transcription factors CCAAT/enhancer-binding proteins alpha and beta (C/EBPα, C/EBPβ), peroxisome proliferator-activated receptor gamma (PPARγ), and sterol-regulatory element binding protein-1c (SREBP-1c). SDA treatment resulted in decreased expression of the lipid accumulation genes adipocyte fatty-acid binding protein (AP2), fatty acid synthase (FAS), stearoyl-CoA desaturase (SCD-1), lipoprotein lipase (LPL), glucose transporter 4 (GLUT4) and phosphoenolpyruvate carboxykinase (PEPCK). The transcriptional activity of PPARγ was found to be decreased with SDA treatment. SDA treatment led to significant EPA enrichment in 3T3-L1 adipocytes compared to vehicle-control. These results demonstrated that SDA can suppress adipocyte differentiation and lipid accumulation in 3T3-L1 cells through down-regulation of adipogenic transcription factors and genes associated with lipid accumulation. This study suggests the use of SDA as a dietary treatment for obesity.

The aim of this study was to investigate the effects of resistance training (RT) on the redox status of skeletal muscle in older adults. Thirteen males aged 64 ± 9 years performed full-body RT 2x/week for 6 weeks. Muscle biopsies were obtained from the vastus lateralis prior to and following RT. The mRNA, protein, and enzymatic activity levels of various endogenous antioxidants were determined. In addition, skeletal muscle 4-hydroxynonenal and protein carbonyls were determined as markers of oxidative damage. Protein levels of heat shock proteins (HSPs) were also quantified. RT increased mRNA levels of all assayed antioxidant genes, albeit protein levels either did not change or decreased. RT increased total antioxidant capacity, catalase, and glutathione reductase activities, and decreased glutathione peroxidase activity. Lipid peroxidation also decreased and HSP60 protein increased following RT. In summary, 6 weeks of RT decreased oxidative damage and increased antioxidant enzyme activities. Our results suggest the older adult responses to RT involve multi-level (transcriptional, post-transcriptional, and post-translational) control of the redox status of skeletal muscle.

The bacteria inhabiting the gastrointestinal tract contribute to numerous host functions and can be altered by lifestyle factors. We aimed to determine whether a 6-week training intervention altered fecal microbiome diversity and/or function in older males. Fecal samples were collected prior to and following a 6-week twice-weekly supervised resistance training intervention in 14 older Caucasian males (65 ± 10 years, 28.5 ± 3.2 kg/m²) with minimal prior training experience. Participants were randomized to receive a daily defatted peanut powder supplement providing 30 g protein (n = 8) or no supplement (n = 6) during the intervention. Bacterial DNA was isolated from pre-and post-training fecal samples, and taxa were identified using sequencing to amplify the variable region 4 (V4) of the 16S ribosomal RNA gene. Training significantly increased whole-body and lower-body lean mass (determined by dual energy X-ray absorptiometry) as well as leg extensor strength (p < 0.05) with no differences between intervention groups. Overall composition of the microbiome and a priori selected taxa were not significantly altered with training. However, MetaCYC pathway analysis indicated that metabolic capacity of the microbiome to produce mucin increased (p = 0.047); the tight junction protein, zonulin, was measured in serum and non-significantly decreased after training (p = 0.062). Our data suggest that resistance training may improve intestinal barrier integrity in older Caucasian males; further investigation is warranted.

Dietary intake of omega-3 fatty acids found in fish has been reported to reduce the risk of Alzheimer’s Disease (AD). Stearidonic acid (SDA), a plant-based omega-3 fatty acid, has been targeted as a potential surrogate for fish-based fatty acids. However, its role in neuronal degeneration is unknown. This study was designed to evaluate effects of SDA on Amyloid-β(A-β)-induced neurotoxicity in rat hippocampal cells. Results showed that SDA effectively converted to eicosapentaenoic acid (EPA) in hippocampal cells. Aβ-induced apoptosis in H19-7 cells was protected by SDA pretreatment as evidenced by its regulation on the expression of relevant pro- and anti-apoptotic genes, as well as the inhibition on caspase activation. SDA also protected H19-7 cells from Aβ-induced oxidative stress by regulating the expression of relevant pro- and anti-oxidative genes, as well as the improvement in activity of catalase. As for Aβ/LPS-induced neuronal inflammation, SDA pretreatment reduced the release of IL-1β and TNFα. Further, we found that the anti-Aβ effect of SDA involves its inhibition on the expression of amyloid precursor protein and the regulation on MAPK signaling. These results demonstrated that SDAs have neuroprotective effect in Aβ-induced H19-7 hippocampal cells. This beneficial effect of SDA was attributed to its antiapoptotic, antioxidant, and anti-inflammatory properties.