Volume #34

Dear Geeks of the fitness world, here is another HOT edition of GEEKY FRIDAY.

Listed below are abstracts from the freshest research on intermittent fasting, calorie restirtion mimetics, weight loss, vitamin C and and much more.

Enjoy and share!

Oh, and I almost forgot – HAVE AN AWESOME WEEKEND you all!

BK

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Randomized cross-over trial of short-term water-only fasting: Metabolic and cardiovascular consequences.

Nutr Metab Cardiovasc Dis. 2012 Dec 7;

Authors: Horne BD, Muhlestein JB, Lappé DL, May HT, Carlquist JF, Galenko O, Brunisholz KD, Anderson JL

Abstract: BACKGROUND AND AIMS: Routine, periodic fasting is associated with a lower prevalence of coronary artery disease (CAD). Animal studies show that fasting may increase longevity and alter biological parameters related to longevity. We evaluated whether fasting initiates acute changes in biomarker expression in humans that may impact short- and long-term health. METHODS AND RESULTS: Apparently-healthy volunteers (N = 30) without a recent history of fasting were enrolled in a randomized cross-over trial. A one-day water-only fast was the intervention and changes in biomarkers were the study endpoints. Bonferroni correction required p ≤ 0.00167 for significance (p < 0.05 was a trend that was only suggestively significant). The one-day fasting intervention acutely increased human growth hormone (p = 1.1 × 10(-4)), hemoglobin (p = 4.8 × 10(-7)), red blood cell count (p = 2.5 × 10(-6)), hematocrit (p = 3.0 × 10(-6)), total cholesterol (p = 5.8 × 10(-5)), and high-density lipoprotein cholesterol (p = 0.0015), and decreased triglycerides (p = 1.3 × 10(-4)), bicarbonate (p = 3.9 × 10(-4)), and weight (p = 1.0 × 10(-7)), compared to a day of usual eating. For those randomized to fast the first day (n = 16), most factors including human growth hormone and cholesterol returned to baseline after the full 48 h, with the exception of weight (p = 2.5 × 10(-4)) and (suggestively significant) triglycerides (p = 0.028). CONCLUSION: Fasting induced acute changes in biomarkers of metabolic, cardiovascular, and general health. The long-term consequences of these short-term changes are unknown but repeated episodes of periodic short-term fasting should be evaluated as a preventive treatment with the potential to reduce metabolic disease risk. Clinical trial registration (ClinicalTrials.gov): NCT01059760 (Expression of Longevity Genes in Response to Extended Fasting [The Fasting and Expression of Longevity Genes during Food abstinence {FEELGOOD} Trial]).

FGF21 is a promising dietary restriction mimetic.

Rejuvenation Res. 2012 Nov 22;

Authors: Mendelsohn AR, Larrick J

Abstract: Dietary or caloric restriction (DR or CR), typically a 30-40% reduction in ad libitum or “normal” nutritional energy levels, has been reported to extend lifespan and healthspan in diverse organisms, including mammals. Although the lifespan benefit of DR in primates and humans is unproven, preliminary evidence suggests that DR confers healthspan benefits. A serious effort is underway to discover or engineer DR mimetics. The most straightforward path to a DR mimetic requires a detailed understanding of the molecular mechanisms that underlie DR and related lifespan-enhancing protocols. Increased expression of FGF21, a putative mammalian starvation master regulator, promotes many of the same beneficial physiological changes seen in DR animals, including decreased glucose levels, increased insulin sensitivity, and improved fatty acid/lipid profiles. Ectopic over-expression of FGF21 in transgenic mice (FGF21-Tg) extends lifespan to a similar extent as DR in a recent study. FGF21 may achieve these effects by attenuating GH/IGF1 signaling. Although FGF21 expression does not increase during DR, and therefore is unlikely to mediate DR, it does increase during short-term starvation in rodents which is a critical component of alternate day fasting, a DR-like protocol that also increases lifespan and healthspan in mammals. Various drugs have been reported to induce FGF21, including PPARa agonists such as fenofibrate, the histone deacetylase inhibitor sodium butyrate, and AMP kinase activators metformin and AICAR. Of these, only metformin has been reported to extend lifespan in mammals, and the extent of benefit is less than that seen with ectopic FGF21 expression. Perhaps the most parsimonious explanation is that high, possibly unphysiological, levels of FGF21 are needed to achieve maximum life- and healthspan benefits and that sufficiently high levels are not achieved by the identified FGF21 inducers. More in-depth studies of the effects of FGF21 and its inducers on longevity and healthspan are warranted.

Weight loss on stimulant medication: how does it affect body composition and bone metabolism? — A prospective longitudinal study.

Int J Pediatr Endocrinol. 2012 Dec 5;2012(1):30

Authors: Poulton A, Briody J, McCorquodale T, Melzer E, Herrmann M, Baur LA, Duque G

ABSTRACT: OBJECTIVE: Children treated with stimulant medication for attention deficit hyperactivity disorder (ADHD) often lose weight. It is important to understand the implications of this during growth. This prospective study was designed to quantify the changes in body composition and markers of bone metabolism on starting treatment. METHODS: 34 children (29 boys) aged 4.7 to 9.1 years newly diagnosed with ADHD were treated with dexamphetamine or methylphenidate, titrating the dose to optimise the therapeutic response. Medication was continued for as long as clinically indicated. Body composition and bone density (dual-energy X-ray absorptiometry) were measured at baseline, 6 months and 3 years; changes were analysed in Z-scores based on data from 241 healthy, local children. Markers of bone turnover were measured at baseline, 3 months and 3 years. RESULTS: Fat loss of 1.4+/-0.96kg (total fat 5.7+/-3.6 to 4.3+/-3.1kg, p<0.001) occurred in the first 6 months. There were significant reductions over 3 years in the sex and height corrected Z-scores for lean tissue, bone mineral content, bone mineral density and ratio of central to total fat (-0.84+/-0.86, p=0.003; -0.55+/-0.31, p<0.0001; -0.41+/-0.28, p<0.0001 and -0.55+/-0.62, p=0.006 respectively). Propeptide of type I collagen indicated a significant reduction in bone turnover after 3 months (564+/-202 to 458+/-96ng/ml, p=0.019), which was fully recovered after 3 years (619+/-276ng/ml). CONCLUSIONS: Stimulant medication was associated with early fat loss and reduced bone turnover. Lean tissue including bone increased more slowly over 3 years of continuous treatment than would be expected for growth in height. There was long-term improvement in the proportion of central fat for height.This study shows that relatively minor reductions in weight on stimulant medication can be associated with long-term changes in body composition. Further study is required to determine the effects of these changes on adult health.

Impact of different resistance training protocols on muscular oxidative stress parameters.

Appl Physiol Nutr Metab. 2012 Dec;37(6):1239-46

Authors: Scheffer DL, Silva LA, Tromm CB, da Rosa GL, Silveira PC, de Souza CT, Latini A, Pinho RA

Abstract: This study analyzes oxidative stress in skeletal muscle using different resisted training protocols. We hypothesize that different types of training produce different specifics. To test our hypothesis, we defined 3 resistance training protocols and investigated the respective biochemical responses in muscle. Twenty-four male Wistar rats were distributed in 4 groups: untrained (UT), muscular resistance training (RT), hypertrophy training (HT), and strength training (ST). After 12 weeks of training on alternate days, the red portion of the brachioradialis was removed and the following parameters were assessed: lactate and glycogen content, superoxide production, antioxidant enzyme content, and activities (superoxide dismutase, SOD; catalase, CAT; GPx, glutathione peroxidase). Thiobarbituric acid-reactive substances (TBARS), carbonyl, and thiol groups were also measured. Results showed increased superoxide production (UT = 5.348 ± 0.889; RT = 5.117 ± 0,651; HT = 8.412 ± 0.431; ST = 6.354 ± 0.552), SOD (UT = 0.078 ± 0.0163; RT = 0.101 ± 0.013; HT = 0.533 ± 0.109; ST = 0.388 ± 0.058), GPx (UT = 0.290 ± 0.023; RT = 0.348 ± 0.014; HT = 0.529 ± 0.049; ST = 0.384 ± 0.038) activities, and content of GPx (HT = 3.8 times; ST = 3.0 times) compared with the UT group. CAT activity was lower (UT = 3.966 ± 0.670; RT = 3.474 ± 0.583; HT = 2.276 ± 0.302; ST = 2.028 ± 0.471) in HT and ST groups. Oxidative damage was observed in the HT group (TBARS = 0.082 ± 0.009; carbonyl = 0.73 ± 0.053; thiol = 12.78 ± 0.917) compared with the UT group. These findings indicate that HT causes an imbalance in oxidative parameters in favor of pro-oxidants, causing oxidative stress in skeletal muscle.

Vitamin C administration attenuates overload-induced skeletal muscle hypertrophy in rats.

Acta Physiol (Oxf). 2012 Nov 26;

Authors: Makanae Y, Kawada S, Sasaki K, Nakazato K, Ishii N

Abstract: AIM: This study aimed to investigate the effects of vitamin C administration on skeletal muscle hypertrophy induced by mechanical overload in rats. METHODS: Male Wistar rats were randomly assigned to 3 groups: 1) sham-operated group (n = 8), 2) placebo-administered group (n = 8), and 3) vitamin C-administered group (n = 8). In the placebo-administered and vitamin C-administered groups, the gastrocnemius and soleus muscles of the right hindlimb were surgically removed to overload the plantaris muscle. Vitamin C (500 mg·kg(-1) ) was orally administered to the vitamin C-administered group once a day for 14 days. RESULTS: Synergist muscle ablation caused significant increases in wet weight and protein concentration of the plantaris muscle in both the placebo-administered (P < 0.01) and vitamin C-administered groups (P < 0.01) compared with the sham-operated group. However, the magnitude of plantaris muscle hypertrophy (expressed as a percentage of the contralateral plantaris muscle) was significantly smaller (P < 0.01) in the vitamin C-administered group (141%) than in the placebo-administered group (152%). Compared with the sham-operated group, only the placebo-administered group showed higher expressions of phosphorylated p70s6k and Erk1/2 (positive regulators of muscle protein synthesis), and a lower expression of atrogin-1 (a muscle atrophy marker). Concentrations of vitamin C and oxidative stress markers in the overloaded muscle were similar between the placebo-administered and vitamin C-administered groups. CONCLUSION: Oral vitamin C administration can attenuate overload-induced skeletal muscle hypertrophy, which may have implications for antioxidant supplementation during exercise training

Activation of calcium signaling through Trpv1 by nNOS and peroxynitrite as a key trigger of skeletal muscle hypertrophy.

Nat Med. 2012 Dec 2;

Authors: Ito N, Ruegg UT, Kudo A, Miyagoe-Suzuki Y, Takeda S

Abstract: Skeletal muscle atrophy occurs in aging and pathological conditions, including cancer, diabetes and AIDS. Treatment of atrophy is based on either preventing protein-degradation pathways, which are activated during atrophy, or activating protein-synthesis pathways, which induce muscle hypertrophy. Here we show that neuronal nitric oxide synthase (nNOS) regulates load-induced hypertrophy by activating transient receptor potential cation channel, subfamily V, member 1 (TRPV1). The overload-induced hypertrophy was prevented in nNOS-null mice. nNOS was transiently activated within 3 min after overload. This activation promoted formation of peroxynitrite, a reaction product of nitric oxide with superoxide, which was derived from NADPH oxidase 4 (Nox4). Nitric oxide and peroxynitrite then activated Trpv1, resulting in an increase of intracellular Ca(2+) concentration ([Ca(2+)](i)) that subsequently triggered activation of mammalian target of rapamycin (mTOR). Notably, administration of the TRPV1 agonist capsaicin induced hypertrophy without overload and alleviated unloading- or denervation-induced atrophy. These findings identify nitric oxide, peroxynitrite and [Ca(2+)](i) as the crucial mediators that convert a mechanical load into an intracellular signaling pathway and lead us to suggest that TRPV1 could be a new therapeutic target for treating muscle atrophy.

The effects of 6 weeks of preseason skill-based conditioning on physical performance in male volleyball players.

J Strength Cond Res. 2012 Jun;26(6):1475-80

Authors: Trajković N, Milanović Z, Sporis G, Milić V, Stanković R

Abstract: The purpose of this study was to determine the changes in physical performance after a 6-week skill-based conditioning training program in male competitive volleyball players. Sixteen male volleyball players (mean ± SD: age 22.3 ± 3.7 years, body height 190.7 ± 4.2 cm, and body mass 78.4 ± 4.5 kg) participated in this study. The players were tested for sprinting (5- and 10-m sprint), agility, and jumping performance (the vertical-jump test, the spike-jump test, and the standing broad jump [SBJ]). Compared with pretraining, there was a significant improvement in the 5- and 10-m speed. There were no significant differences between pretraining and posttraining for lower-body muscular power (vertical-jump height, spike-jump height, and SBJ) and agility. Based on our results, it could be concluded that a preseason skill-based conditioning program does not offer a sufficient stimulus for volleyball players. Therefore, a general conditioning and hypertrophy training along with specific volleyball conditioning is necessary in the preseason period for the development of the lower-body strength, agility and speed performance in volleyball players.

Resistance exercise load does not determine training-mediated hypertrophic gains in young men.

J Appl Physiol. 2012 Jul;113(1):71-7

Authors: Mitchell CJ, Churchward-Venne TA, West DW, Burd NA, Breen L, Baker SK, Phillips SM

Abstract: We have reported that the acute postexercise increases in muscle protein synthesis rates, with differing nutritional support, are predictive of longer-term training-induced muscle hypertrophy. Here, we aimed to test whether the same was true with acute exercise-mediated changes in muscle protein synthesis. Eighteen men (21 ± 1 yr, 22.6 ± 2.1 kg/m(2); means ± SE) had their legs randomly assigned to two of three training conditions that differed in contraction intensity [% of maximal strength (1 repetition maximum)] or contraction volume (1 or 3 sets of repetitions): 30%-3, 80%-1, and 80%-3. Subjects trained each leg with their assigned regime for a period of 10 wk, 3 times/wk. We made pre- and posttraining measures of strength, muscle volume by magnetic resonance (MR) scans, as well as pre- and posttraining biopsies of the vastus lateralis, and a single postexercise (1 h) biopsy following the first bout of exercise, to measure signaling proteins. Training-induced increases in MR-measured muscle volume were significant (P < 0.01), with no difference between groups: 30%-3 = 6.8 ± 1.8%, 80%-1 = 3.2 ± 0.8%, and 80%-3= 7.2 ± 1.9%, P = 0.18. Isotonic maximal strength gains were not different between 80%-1 and 80%-3, but were greater than 30%-3 (P = 0.04), whereas training-induced isometric strength gains were significant but not different between conditions (P = 0.92). Biopsies taken 1 h following the initial resistance exercise bout showed increased phosphorylation (P < 0.05) of p70S6K only in the 80%-1 and 80%-3 conditions. There was no correlation between phosphorylation of any signaling protein and hypertrophy. In accordance with our previous acute measurements of muscle protein synthetic rates a lower load lifted to failure resulted in similar hypertrophy as a heavy load lifted to failure.

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