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School of Anatomy and Human Biology, the University of Western Australia, Perth, Australia. School of Anatomy and Human Biology, the University of Western Australia, Perth, Australia.. The absence of functional dystrophin protein in patients with Duchenne muscular dystrophy (DMD) and dystrophic mdx mice leads to fragile myofibre membranes and cycles of myofibre necrosis and regeneration. This research is funded by the Australian National Health and Medical Research Council (MG) and Australian Postgraduate Award Scholarships (HR-C). Duchene muscular dystrophy (DMD) is characterised by progressive muscle weakness and wasting resulting from a lack of functional dystrophin that promotes increased myofibre membrane fragility, repeated cycles of myofibre necrosis and regeneration, and the eventual replacement of skeletal muscle by fatty and fibrous connective tissue. Dietary interventions in the form of various amino acids (with different biochemical effects) or other nutritional supplements have shown variable beneficial effects in both mdx mice and DMD patients [Reviewed in [7] [8] [32] [33] [34] . A comparison of sedentary mice on a control diet, high fat diet or high protein diet between 8-24 weeks of age and 24-40 weeks of age. Gastrocnemius muscle weight adjusted for bodyweight was significantly (P=0.045) heavier in mdx mice fed a control diet compared to C57 at 40 weeks of age (Figure 2C). A comparison of sedentary mice on a control diet with mice on either a high fat or high protein diet. Blood serum CK levels are always lower (approximately 10-fold) in C57 mice compared to mdx mice [18] [54] [55] and were not measured for C57 mice in this study.
Data for dietary consumption between 8-12 weeks of age is shown for both sedentary and voluntarily exercise mdx mice on either a control diet, high fat diet or a high protein diet.
Voluntary wheel exercise for 4 weeks caused no change in the body weight of 12-week-old mdx mice, and neither did consumption of a high protein or high fat diet (Figure 8A). Exercise was completely voluntary and distance run is an indirect indicator of muscle function and exercise capacity.
Voluntary exercise increased (P=0.02) myofibre necrosis (% CSA) in the quadriceps muscle from 12-week-old mdx mice approximately twofold, relative to the amount present in sedentary mice. To our knowledge, the response of adult mdx mice to a high fat diet has not been described previously.
Dystrophic mdx mice were significantly heavier than control C57 mice at both 8 and 24 weeks of age (Figure 2A), primarily due to a well described increase in muscle mass [52] [55] [59] [60] [61] [62] [63] . The muscular body composition of mdx mice (<40 weeks) is in stark contrast to DMD patients who can move between the spectra of over-nutrition (and obesity) to under-nutrition within their shortened lifespan, and who lose muscle mass at a rate of 4% per year as adults [7] [34] [64]. The 8 – 24-week-old mdx mice consumed similar amounts of food and energy compared to age-matched C57 mice across the 3 diets (Figure 1A-C). In contrast to mdx mice, after consumption of a high fat diet (for 16 weeks) C57 male mice at both 24 and 40 weeks had significantly greater body weights most likely due to a gain in epididymal fat pad weight (and presumably other body fat) (Figure 2A, B) with significant accumulation of adipocytes in the quadriceps muscle of 40-week-old mice (Figure 4B). The lack of any benefits with the high protein diet contrasts with studies in mdx mice that show mildly reduced dystropathology after dietary supplementation of creatine, taurine and glutamine (both alone and in combination with prednisolone) [8] [25] [37] [38] [40] . A prolonged positive imbalance between energy intake and expenditure resulting in obesity, is associated with chronic inflammation and may be a potential mechanism by which obesity leads to insulin resistance (in both humans and mice) [Reviewed in [44] [46] [69]. Due to the multiple systemic effects that the 3 PPARs and PGC-1? have on whole body metabolism (e.g.
In order to further examine the potential benefits of a high fat or high protein diet on dystrophic muscle, 8 – 12-week-old mdx mice were voluntarily exercised to exacerbate the dystropathology [1] [49] [50] [54] . Despite a high fat diet reducing myofibre necrosis in sedentary 24-week-old mdx mice (Figure 4), this diet had no significant benefit on myofibre necrosis or serum CK levels in voluntarily exercised mdx mice. This research clearly identifies an ‘altered’ response to a high fat diet in dystrophic muscles of mdx mice compared to C57 controls. The authors thank Mr Greg Cozens (School of Anatomy & Human Biology, UWA) for excellent technical assistance, Dr Andrew Hoey (University of Southern Queensland) for consultation regarding the preliminary studies and Mr Warren Potts (Specialty Feeds, WA) for design and manufacture of the three semi-purified diets.
CLICK HERE for PDF printable copy. Be sure hit to scale to page or fit page for print options! Blue Diamond pecan thins with cheddar cheese slices, Green valley yogurt with homemade granola (made with oats, maple syrup, oatbran as primary ingredients) My favorite snack: rice cake, spread with natural p.
Butter is not restricted on the low FODMAP diet but if you are avoiding it because of other health concerns, I bet you could substitute olive oil in many recipes. Dianna, I would encourage you meet with a dietitian to help you manage the low FODMAP diet. Stay tuned as I am now in Australia learning more on the latest on FODMAPs and will be ready to share and update the FODMAPs info via the blog very soon! I would be sure that celiac disease and small intestinal bacterial overgrowth have been ruled out which may be a contributing factors to weight loss. Sounds like you may have more than lactose intolerance as the cheeses listed are very low lactose. They say IBS and migraines are related and cheese such as cheddar is a trigger for migraines. The wrong diet foods, filled with empty calories and artificial sweeteners, could actually cause you to gain weight.
Disclaimer:The information contained in this website is provided for informational purposes only, and is not intended to convey medical advice or to substitute for advice from your own physician.
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You won't want to miss my FREE Trim Healthy Mama low carb-style recipes, tutorials, giveaways, and deals - get them delivered fresh to your inbox! You must score at least a 50 in each event in order to pass the APFT to graduate Basic Combat Training.
The Army's Basic Training Physical Fitness Test is a three-event physical performance test used to assess endurance. I am not a big fan of supplements other than some protein drinks after workouts and vitamins. Don't change anything, just eat like you normally would and count how many calories you consumed. Eat these in moderation if you are trying to lose weight, but add additional helpings if you are trying to boost your caloric intake to 2500-3000 cals per day in order to gain weight. Stew Smith is a former Navy SEAL and fitness author certified as a Strength and Conditioning Specialist (CSCS) with the National Strength and Conditioning Association. It is proposed that both DMD patients and mdx mice have an altered metabolism and impaired energy status and that nutritional supplementation may reduce the severity of dystropathology. The specific mechanism(s) responsible for myofibre necrosis are still unclear, although there are strong associations with excessive inflammation, increased intracellular calcium levels, elevated oxidative stress, and metabolic abnormalities [1] [2] [3] [4] [5] [6] [7] [8] . Studies in both DMD patients and mdx mice indicate that dystrophin defects may also lead to altered skeletal muscle metabolism and an impaired energy status. Recently completed clinical trials have examined the safety and role of specific amino acid supplementation (creatine and glutamine) in DMD patients and demonstrated some beneficial effects [35] [36] .
Diet specifications for the 3 semi-pure diets used in this study: control (AIN93g), high protein (SF00-252) and high fat (SF06-40).
The low level of muscle damage in dystrophic adult mdx mice can be exacerbated by voluntary exercise [18] .
The quadriceps muscles were dissected and immediately fixed in 4% paraformaldehyde (Sigma P6148) for 48 hours. Non-overlapping tiled images of transverse muscle sections provided a picture of the entire muscle cross section.
While under terminal anaesthesia blood from the mdx mice was collected via cardiac puncture. Consumption of the high fat diet induced many changes in the body composition of both C57 and mdx mice, whereas the high protein diet did not. There was no significant difference in the body weights of 40-week-old C57 mice and mdx mice on the control diet (Figure 2A); nor did the high protein diet have any significant effect of the body weight of either strain of mice (Figure 2A). The high protein diet had no impact on the epididymal fat pad weight in either strain of the older mice. There was no difference in the average myofibre CSA in the tibialis anterior (TA) muscle from 12-week-old C57 and mdx mice on the control diet (Figure 3). Myofibre necrosis (% CSA) was significantly (P=0.04) decreased in the quadriceps muscle of 24-week-old mdx mice fed the high fat diet and was approximately half the amount present in mice fed, the control diet (Figure 4A). There was no change in the level of myofibre necrosis in the quadriceps muscle between 24 and 40 week old mdx mice (Figure 4A) and no effect of either the high protein or high fat diet on myofibre necrosis in 40-week-old mdx mice (Figure 4A).
There were no significant changes in inflammatory cytokine mRNA levels with age in either strain of mice fed the control diet. Mdx mice were voluntarily exercised for 4 weeks to increase the low level of dystropathology in skeletal muscles [1] [50] [ 54]. Mdx mice fed the high fat diet ran approximately 50% further (P=0.003) during 4 weeks of exercise (compared to mdx mice on the control diet (Figure 9A).
The high fat diet for 4 weeks had no effect on myofibre necrosis in either voluntarily exercised or sedentary mdx mice. In contrast, 40-week-old mdx mice were the same weight as C57 mice; this equalising in bodyweight occurred at approximately 32 weeks of age (data not shown) and was most likely due to an increase in body fat in C57 mice (Figure 2B). It is important to consider that the striking loss of muscle mass in DMD patients occurs during the growth phase of the boys (approximately 20 years). Yet, there was a large difference in the way the two strains of mice responded to the high fat diet.
Consumption of either diet for 16 weeks did not reduce levels of serum CK (an indicator of myofibre leakiness), even though the high fat diet reduced by approximately 2.5-fold myofibre necrosis in the quadriceps muscle of 24-week-old mdx mice. Taurine is not a substrate for protein synthesis, but may improve dystropathology via regulation of calcium homeostasis [67] . Although the 12-week-old mdx mice were very lean, there was a further reduction in epididymal fat pad weight after 4 weeks of voluntary exercise (Figure 8B). Energy intake was significantly increased in voluntarily exercised mdx on the high fat diet compared to mdx mice on the control diet (Figure 7B). This response was pronounced in younger mdx mice<24 weeks old, but diminished with age (by 40 weeks).
Research funding from the Australian National Health and Medical Research Council (MG) and Australian Postgraduate Award Scholarships (HR-C) are gratefully acknowledged. Reduced muscle necrosis and long-term benefits in dystrophic mdx mice after cV1q (blockade of TNF) treatment.
Meeting with someone that can help you navigate the diet appropriately will ensure you are eating a healthy diet and also following the diet correctly. I try to eat several small meals a day but still it’s really hard to gain weight with IBS-D. Oz wants us to print this 99 Diet Foods Shopping List and bring it to the grocery story to avoid our biggest diet-food mistakes.


Oz wants in your shopping cart: The list includes sensible things like Kashi frozen pizza, Wholly Guacamole, Evol frozen meals, and packaged broccoli slaw. Oz does not endorse any of the brand name products in the diet foods shopping list – While the list includes specific brands, if you find a similar product with the same nutritional value, feel free to use it. This information has not been evaluated by the Food and Drug Administration and is not intended to diagnose, treat, cure or prevent any disease. CardsTrim Healthy Mama Visual Shopping ListPlanning a Frugal Family Trip to Washington, D.C. The bad news, if you are lean, you will lose muscle, so bulking up to 10-12% body fat will not hurt you.
In addition, ruck marches spanning over 15-20 miles in a day will cause you to lose significant amounts of weight in both muscle and fat. This is another important step to how to gain weight, so make sure you are doing it correctly. If you want to lose weight you have to drop your calories to 1500-1800 calories a day in addition to exercise.
But making sound decisions and remaining calm while tired and hungry adds to the true test of leadership. Corticosteroids remain the standard pharmacological treatment [9] [10] [11] [12] although promising approaches to replace the defective dystrophin gene have been extensively investigated over the last 10 years [13] [14] [15] [16] [17] . Repeated cycles of myofibre necrosis and regeneration, increased demand on the sarcoplasmic reticulum to regulate intracellular calcium, defective mitochondrial function, increases in both protein synthesis and protein degradation rates, altered oxidative stress and disruption in nNOS signalling may all contribute to an altered metabolic state [4] [22] [23] [24] [25] [26] [27] [28] [29] [30] . The dystropathology of skeletal muscles was not examined in this study, but these results led us to propose that due to their altered energy flux, a high fat diet may reduce the extent of dystropathology and may be metabolically beneficial to mdx mice. Group 1) sedentary C57 and mdx mice fed a custom diet from 8-24 weeks of age, Group 2) sedentary C57 and mdx mice fed a custom diet from 24-40 weeks of age and Group 3) voluntarily exercised mdx mice fed a custom diet from 8-12 weeks of age. Mdx mice were caged individually with free access to a voluntary running wheel for 4 weeks (from 8 to 12 weeks of age). Total body weight, epididymal fat pad weight, and gastocnemius muscle weight were recorded immediately.
Muscles were then placed into 70% ethanol, processed in a Shandon automatic tissue processor overnight, and finally paraffin embedded for sectioning. Therefore gene expression was quantified only in mice which consumed the control or high fat diet. All variables were analysed by ANOVAs (to account for diet, strain, age, and exercise) and Least Significant Difference (LSD) post-hoc tests. The high protein diet had no significant impact on epididymal fat pat weights in either strain of mice; fat pads remained heavier in C57 mice compared to mdx mice. On the high fat diet, there was a slight increase (but not significant P=0.38) in body weight-adjusted epididymal fat pad weight of C57 mice (Figure 2B). Between 12 and 24 weeks of age, myofibres in the mdx TA continued to grow (hypertrophy) and were significantly larger on average than C57 myofibres at 24 weeks of age (P=0.02) (Figure 3). The high protein diet had no effect on the adipocyte content of the quadriceps muscle in either strain of 40-week-old mice. Increasing the extent of dystropathology allowed for further evaluation of the potential beneficial effects of a high protein or high fat diet in mdx mice. There was no difference in distance run by mdx mice fed the high protein diet compared to the control diet. The high protein diet had no effect on sedentary mice, but significantly (P=0.04) increased myofibre necrosis in exercised mdx mice) (Figure 9B). The CK levels in mdx mice were not affected by a high protein or high fat diet (data not shown).
It is commonly accepted that obesity occurs when there is a chronic positive imbalance between energy intake and energy expenditure, and that long-term consumption of a high fat diet increases deposition of adipose tissue and eventually leads to obesity in both sedentary laboratory rodents and humans [Reviewed in [46] ]. The body weight of mdx mice did not increase between 24 and 40 weeks of age, nor was there a change in relative epididymal fat pad and gastrocnemius muscle weights (Figure 2A), supporting reports that there is a stabilisation of the dystrophic phenotype in adult mdx mice [18] [52] .
In contrast to the C57 mice, the mdx mice<24 weeks of age did not deposit significant body fat. It is possible that a high fat diet (and increased energy intake) assists mdx mice metabolically and thus helps them to maintain skeletal muscle structure and mass, or that increased lipid coming from the high fat diet stabilises fragile membrane lipids and prevents myofibre necrosis. These increases in gene expression were not seen in mdx mice (Figure 5A-C) which demonstrates, in addition to the lack of changes in body composition, the resistance of mdx mice (particularly<24 weeks) to a high fat diet.
However, the precise consequence(s) in dystrophic skeletal muscle, to our knowledge, are not documented.
It appears that mdx mice were able to maintain body weight and muscle mass (Figure 8A, C) over 4 weeks of voluntary exercise by increasing food consumption and energy intake (Figure 7A, B). This may have enabled the mdx mice to run further (approximately 50%) without producing further muscle damage (e.g. Therefore, it is proposed that the increased capacity for exercise in dystrophic mdx mice fed a high fat diet may be modulated, in part, via up-regulation of the 3 PPARs and PGC-1?. The high fat diet appears to have enabled the mdx mice to better meet their energy needs, and reduced the severity of their dystropathology and increased their voluntary exercise ability.
Oz wants in your shopping cart; Not all diet foods are created equal – some might even cause you to gain weight.
You just have to do it smart and NOT let the added weight affect your PT and running scores. Also rucking utilizes the bigger muscles groups of the body like legs, butt, and lower back. The Ranger Course produces a mentally hardened soldier, who possesses abilities to operate on land, air, and sea. Consumption of a high protein diet had minimal effects on the body composition or muscle morphology in both strains of mice.
Clearly, studies to identify strategies that will mitigate the muscle damage and sustain efficient repair are warranted. In addition, creatine, taurine and glutamine treatments have shown various benefits in treadmill-exercised adult mdx mice [37] [38] . All animal experiments were conducted in strict accordance with the guidelines of the National Health and Medical Research Council Code of practice for the care and use of animals for scientific purposes (2004), and the Animal Welfare act of Western Australia (2002), and were approved by the Animal Ethics committee at the University of Western Australia.
All mice were fed a standard (cereal-based) mouse chow (meat free, 5% fat, 19% protein) prior to the study. Exercise data were collected via a small magnet attached to the mouse wheel, and a sensor from a bicycle pedometer attached to the back of the cage. Blood serum was collected via cardiac puncture, the gastrocnemius muscle was snap frozen in liquid nitrogen for gene expression analysis and the quadriceps and tibialis anterior (TA) muscles were collected for histology. Blood serum creatine kinase (CK) analysis was completed at the Murdoch Veterinary Hospital, Murdoch, WA.
RNA was extracted from snap frozen gastrocnemius muscles, DNAse treated, reverse transcribed into cDNA and purified. This difference in body weight was maintained throughout the study until 24 weeks of age for mice on the control and high protein diet (Figure 2A). After consuming the high fat diet, the epididymal fat pad weight adjusted for body weight was significantly (P=0.015) higher in C57 mice compared to C57 mice fed the control diet (Figure 2B) and, at sacrifice, large amounts of adipose tissue were conspicuous around the sternum, kidneys and hip joints. Neither the high protein nor high fat diet resulted in any differences in standardised or absolute gastrocnemius muscle weight in either strain of mice. Consumption of the high fat diet also significantly (P=0.04) increased the body weight of the older mdx mice (Figure 2A). There was no change in gastrocnemius muscle weight adjusted to bodyweight in mdx mice between 24 and 40 weeks of age.
Dystrophic myofibres do not continue to hypertrophy and average myofibre CSA in 40-week-old mdx mice was significantly reduced (P=0.025) compared to 24-week-old mice and not different from the average mdx myofibre CSA at 12 weeks of age.
No significant change in standardised or absolute gastrocnemius muscle weight was seen after voluntary exercise or diet change (Figure 8C).
Obesity is associated with numerous changes in cell signalling that are believed to underlie much of the morbidity associated with the condition [Reviewed in [46] [57] [58] ].
Both 24 and 40-week-old mdx were very lean, with significantly smaller epididymal fat pads, larger gastrocnemius muscles and larger myofibres CSA compared to C57 mice (Figures 2B, 2C, 3).
We propose that the reduced myofibre size in 40-week-old mdx mice is probably due to myofibre splitting or branching. Amino acid supplementation is already widely used amongst DMD patients despite there being no conclusive supporting evidence in the literature [7] [12] . Inflammation plays a major role in myofibre necrosis and regeneration in skeletal muscle, thus the inflammatory state can be an indirect indicator of the extent of dystropathology [1] [42].The high fat diet significantly reduced PGC-1? gene expression in 24-week-old C57 mice but, apart from this, there were no other significant changes in PPAR expression caused by the high fat diet in either strain of mice. I cannot have Boost, Ensure or any other of those supplements without my stomach going crazy. Oz’s 100 foods list, that features breakfasts, meals, grains and cereals, snacks, side dishes, desserts, condiments, and beverages. To accomplish weight gain while still on a rigorous cardiovascular training cycle, you have to add more calories - plain and simple.
Break it up into days, and you only need to eat an additional 300 calories a day to gain a pound a week. Instead of eating 3 big meals a day or eating all day all the time, spread those calories out over 5-6 smaller meals.
This will spur growth to those muscles as well - this is where you should see your greatest increase in weight.
So, when you stop gaining for at least 2 weeks, it means it is time to start eating an extra 250 calories a day.
Yes, that's a lot of water, but it's water that will give you the energy you need to gain weight! A combined nutritional therapy (creatine monohydrate, conjugated linoleic acid, ?-lipoic acid, and ?-hydroxy-?-methylbutyrate) administered, in addition to prednisolone, for 8 weeks increased muscle strength and reduced the extent of dystropathology in 12-week-old treadmill-exercised mdx mice [39] . The pedometer records single wheel revolutions, allowing total distance (km) run by an individual mouse to be determined, as per [1] [49] [50] . Histological analysis was carried out on whole cross sections of the quadriceps muscle (dystropathology and adipocyte content) and the frozen TA muscle (myofibre CSA).
After consuming the high fat (HF) diet for 16 weeks, the final bodyweight of 24-week-old C57 mice was significantly greater (P=0.04) than for C57 mice on the control (C) diet. In contrast, 24-week-old mdx mice fed a high fat diet were very lean and had small epididymal fat pads, similar in weight to mdx mice fed the control or high protein diet (Figure 2B). The largest increase in body weight (group average) was seen in C57 mice on the high fat diet. There were no significant differences in adipocyte content of the quadriceps muscle in 24 week old C57 and mdx mice after consuming any of the 3 diets. The high fat diet also significantly increased adipocyte content between 24 and 40-week-old mdx mice (Figure 4B). Expression of the three PPARs was unchanged in either strain by consumption of the high fat diet. PPAR alpha mRNA was approximately twofold lower (P=0.02) in the gastrocnemius muscle of 40-week-old mdx mice compared to C57 mice (Figure 5A).


Shavlakadze et al (2010) reported no difference in myofibre CSA in the quadriceps muscle between 12 and 52 weeks due to significant myofibre splitting in 52-week-old mdx mice [52] . The older mdx mice (24-40 weeks) were susceptible to the negative effects of a high fat diet, showing significant increases in total body weight and standardised fat pad weight compared to those on the control diet (Figures 2A, B). It is important to consider possible counteracting effects when combined interventions are administered.
It has also been shown that several gene programmes linked to PGC-1? are dysregulated in dystrophic muscle (e.g. A possible interpretation is that the high fat diet was able to better meet the increased energy needs of the mdx mice thereby enabling them to run further while also maintaining myofibre integrity. This study in mdx mice raises many interesting questions about possible differences in metabolism and energy demands between dystrophic and normal muscle. Depending on your overall caloric intake, you can use this program to either lose weight or gain weight.
Gaining anymore than 1 or 2 pounds a week is unhealthy and means you are putting on way too much fat. Every time you see you haven't gained weight for at least 2 weeks, add an extra 250 calories - UNTIL you have reached your goal. Pilot trials were conducted prior to commencement of the study to ensure that all diets were palatable. In contrast, there was no difference in the bodyweight of 24-week-old mdx mice fed the high fat or control diet (Figure 2A). In the abdominal cavity, the epididymal fat pads often of mdx mice could not be seen until the testes were pulled up into the abdominal cavity. The average changes in body weight for C57 mice (% change of sample group) were 116% after control diet, 102% after high protein diet and 141% after high fat diet. The 40-week-old mdx mice were still very lean with no change in the body weight adjusted epididymal fat pad weight between 24 and 40 weeks of age for mdx mice fed a control diet (Figure 2B).
However, PGC-1? was reduced significantly (P=0.02) in 24-week-old C57 mice fed the high fat compared to the control diet. The high fat diet caused no change in the mRNA levels of the 3 PPARs or PGC-1? in either strain of 40-week-old mice. Since our study examined myofibre CSA at 24 weeks and identified significant myofibre hypertrophy in mdx mice at this age, it seems that myofibre splitting occurs sometime beyond 24 weeks, but before 40 weeks of age.
A high protein diet or supplementation with certain amino acids (such as leucine) can stimulate skeletal muscle protein synthesis in both young and adult animals, but there is a threshold of protein requirement for maximum growth and once reached, additional protein intake does not further stimulate protein synthesis in skeletal muscle [Reviewed in [66] . For example, our data from mdx mice on the high protein diet (which contains increased concentrations of the essential amino acids such as leucine and phenylalanine used in protein synthesis, but without an increase in metabolisable energy intake – Table 1) do not support such an intervention since elevated myofibre necrosis was observed in response to voluntarily wheel exercise. The extent to which this benefit of a high fat diet is due to an increased energy intake per se, or to specific benefits of increased dietary fat directly on dystrophic muscles is not yet clear: determining the precise mechanism responsible for these demonstrated benefits is an important future goal. William Li, Lisa Lillien with her Shrimp Fettuccine Alfredo recipe that’s only 195 calories per serving.
Think of weight gain as saving money - at the end of the week, if you do not spend more than you make then you have a surplus on money. Do not eliminate fat - just try to limit the amount of fat calories to protein calories you ingest. In contrast, after consuming the high fat diet for 16 weeks the mdx mice (< 24 weeks) remained lean with minimal fat deposition and were resistant to changes in body composition. Throughout the study mice were caged in groups of 4-8 and group body weights were measured weekly, mice were not tracked individually for the duration of the study. Throughout the experiment the mice were monitored daily for food consumption and distance run. The TA muscles were collected, and embedded in tragacantch gum (Sigma Aldrich G1128) mounted on a small cork block, and quenched in isopentane cooled in liquid nitrogen. The largest gain in body weight (group average) between 8 and 24 weeks of age was seen in the C57 mice fed the high fat diet. The average changes in body weight for mdx mice (% change of sample group) were 103% after control diet, 94% after high protein diet and 110% after high fat diet. The body composition of mdx mice changed between 12 and 24 weeks of age, with significant increases in body weight, absolute and standardised gastrocnemius muscle weight and individual myofibre CSA (Figures 2A, 3, 8A).
Therefore, it is possible that in well-nourished sedentary mice (with adequate protein intake), the high protein diet had no effect on muscle mass.
Overall there seems to be an association with decreased PGC-1? expression having detrimental effects in both dystrophic and normal muscle. In addition, the effects of a high fat diet on dystrophic heart function and pathology needs to be addressed in mdx mice, before considering translation to the clinical situation. You are not obligated to use these links when you make a purchase, but when you do so it helps to support this site, so thank you! Group food intake was monitored twice weekly by subtracting from a pre-weighed amount, the food that remained in the food compartment on the cage lid, and food inside the cage that could be separated from the cage bedding. The average changes in body weight for C57 mice (% change of sample group) were 130% after control diet, 140% after high protein diet and 159% after high fat diet.
There was no effect of the high fat diet on the standardised gastrocnemius muscle weight in mdx mice. Additionally, the utilization of dietary protein for anabolic processes is dependent on the adequacy of energy intake.
It is appreciated that in corticosteroid-treated inactive DMD patients, a high fat diet may contribute to obesity and thus impact on disease severity (especially since corticosteroid usage is known to contribute to obesity and Cushingoid symptoms).
If you have an additional 2000 calories at the end of the week that you did NOT expend - YOU WILL GAIN WEIGHT.
In fact, you can still do your calisthenics (PT) workouts and run and still gain weight too - as long as you eat BIG. TA sections were stained with Sirius red to distinguish myofibres (yellow) from collagenous myofibre membranes (red), and which allows for easy and accurate quantification of myofibre cross-sectional area (CSA). The average changes in body weight for mdx mice (% change of sample group) were 130% after control diet, 132% after high protein diet and 137% after high fat diet. If the energy requirements of the mdx mice were increased, and not met by a corresponding increase in intake, dietary amino acids would be preferentially oxidized for energy rather than used for protein synthesis.
In addition, the impact of a high fat diet might be different in steroid-naive DMD boys and also influenced by growth and disease severity. A 10 pounds weight gain will help as long as it does not impact your running and pull-ups and other PT tests. Additional, more mechanistically based research will be required to establish optimal dietary interventions to reduce the severity of dystropatholgy and maintain muscle function for potential application to DMD. Distinct areas of active myofibre necrosis and very early muscle regeneration (small myotubes) were not included in myofibre cross sectional area analysis.
While it is possible that a beneficial response to high protein consumption might be seen in combination with resistance exercise, such demanding exercise is usually not recommended for dystrophic boys or animal models of DMD due to additional damage to dystrophic muscles. Impaired mitochondrial oxidative phosphorylation in skeletal muscle of the dystrophin-deficient mdx mouse. Dysregulated intracellular signaling and inflammatory gene expression during initial disease onset in Duchenne muscular dystrophy.
Long-term benefits of deflazacort treatment for boys with Duchenne muscular dystrophy in their second decade. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and pharmacological and psychosocial management.
Treatments for muscular dystrophy: increased treatment options for Duchenne and related muscular dystropies. Towards developing standard operating procedures for pre-clinical testing in the mdx mouse model of Duchenne muscular dystrophy.
Creatine supplementation reduces skeletal muscle degeneration and enhances mitochondrial function in mdx mice.
Measurement of sub-membrane [Ca(2+)] in adult myofibers and cytosolic [Ca(2+)] in myotubes from normal and mdx mice using the Ca(2+) indicator FFP-18. Muscle wasting in muscular dystrophy: decreased protein synthesis or increased degradation? CINRG randomized controlled trial of creatine and glutamine in Duchenne muscular dystrophy. Creatine monohydrate enhances strength and body composition in Duchenne muscular dystrophy. Enhanced dystrophic progression in mdx mice by exercise and beneficial effects of taurine and insulin-like growth factor-1. Nutritional therapy improves function and complements corticosteroid intervention in mdx mice.
Evaluation of Potential Synergistic Action of a Combined Treatment with Alpha-Methyl-Prednisolone and Taurine on the Mdx Mouse Model of Duchenne Muscular Dystrophy. Implications of cross-talk between tumour necrosis factor and insulin-like growth factor-1 signalling in skeletal muscle. Damage and inflammation in muscular dystrophy: potential implications and relationships with autoimmune myositis.
The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity. Reduced necrosis of dystrophic muscle by depletion of host neutrophils, or blocking TNFalpha function with Etanercept in mdx mice. Cromolyn administration (to block mast cell degranulation) reduces necrosis of dystrophic muscle in mdx mice. 2011.Spurney CF, Gordish-Dressman H, Guerron AD, Sali A, Pandey GS, Rawat R, Van Der Meulen JH, Cha HJ, Pistilli EE, Partridge TA, Hoffman EP, and Nagaraju K.
Preclinical drug trials in the mdx mouse: Assessment of reliable and sensitive outcome measures. Hypertrophic response of Duchenne and limb-girdle muscular dystrophies is associated with activation of Akt pathway. Electron microscopic and autoradiographic characterization of hindlimb muscle regeneration in the mdx mouse. Of bears, frogs, meat, mice and men: complexity of factors affecting skeletal muscle mass and fat.
Regulation of skeletal muscle physiology and metabolism by peroxisome proliferator-activated receptor delta. Blockade of TNF in vivo using cV1q antibody reduces contractile dysfunction of skeletal muscle in response to eccentric exercise in dystrophic mdx and normal mice.
PGC-1alpha regulates the neuromuscular junction program and ameliorates Duchenne muscular dystrophy.



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