Exercise & Brain Aging

Despite decades of advice to increase physical activity for the purpose of “burning calories” to aid in weight loss, millions of people conducting their own “n=1” experiments have found that exercise does not result in magical body fat loss. Lack of expected results from faithful efforts dedicating hours upon hours—for years—in gyms, on biking and running trails, and in swimming pools, only to be at the same weight as when they started, is downright demoralizing. Adding insult to injury, perhaps, is emerging data showing that exercise cannot counteract a poor diet. As they say, “abs are made in the kitchen,” and you cannot outrun a bad diet.   

Nevertheless, while the effects of exercise on fat loss, specifically, may be disappointing, exercise is quite important for overall health and wellbeing. It strengthens the cardiovascular system, and the endorphin rush induced by intense exercise may serve as a natural anti-depressant. (Side-effects may include sweating, stronger muscles, and increased self-esteem!) Additionally, muscular contractions from physical activity are crucial for aiding the flow of lymph, which, unlike blood, has no dedicated pump, and only moves when we do.

One specific area of health exercise is proving beneficial for is cognitive function. With the baby boomer generation entering their golden years, and Alzheimer’s disease statistics growing ever more grim, concerns about healthy brain aging are coming to the forefront. Generally speaking, what’s good for the body is good for the brain, and exercise is no exception. Any type of activity may be beneficial, but according to recent research, moderate and higher intensity efforts may have a greater impact than light activity.

In a study that assessed the effects of exercise on cognitive performance, researchers determined that subjects with self-reported low levels of physical activity experienced greater declines in cognitive performance over time compared to subjects with self-reported higher levels of greater intensity exercise. A standard neuropsychological examination (NPE) was performed, with a repeat examination five years later. At the baseline NPE, low levels of physical activity were associated with worse executive function, semantic memory, and processing speed. (However, after adjusting for vascular risk factors, those associations became slightly attenuated and were no longer significant. Of course, vascular risk factors may be intimately tied to habitual exercise.) Compared to study participants who reported higher levels of physical activity, those who were cognitively unimpaired but reported low to no exercise at baseline declined more over time in processing speed and episodic memory, after adjusting for sociodemographic and vascular risk factors.

This shouldn’t come as a surprise. Exercise may help increase insulin sensitivity, and also aids in non-insulin mediated glucose disposal. A strong body of evidence indicates that Alzheimer’s disease and mild cognitive impairment are disorders of insulin resistance, so any intervention that increases insulin sensitivity may have the added effect of protecting and preserving cognitive function. The insulin-sensitive glucose transporters, GLUT4s, are expressed in brain regions involved in memory and cognition, such as the hippocampus. In particular, physical activity aimed at increasing and/or preserving skeletal muscle mass may be especially beneficial for facilitating healthy brain aging. According to a leading researcher in brain fuel metabolism and Alzheimer’s disease, “Skeletal muscle is the main site of insulin-mediated glucose utilization in the body and so declining muscle mass (sarcopenia) in the elderly may be a factor contributing to the increased risk of insulin resistance associated with aging.”

Moreover, exercise may help increase brain derived neurotrophic factor (BDNF), a protein associated with strong long-term memory and overall cognitive function. Higher expression of BDNF in the brain is associated with slower rates of cognitive decline in older adults. Beyond BDNF, one of the most significant effects of exercise is an increase in mitochondrial density. This was long known to occur in skeletal muscle, but it has also been confirmed to occur in the brain. The insulin signaling and glucose metabolism problems that underlie Alzheimer’s disease may be the end result of brain mitochondrial dysfunction. Therefore, interventions that improve mitochondrial efficiency, particularly in the brain, may be one way to target cognitive decline.

Exercise may not be a one-way ticket to an ideal body weight, but there are plenty of other reasons to lace up a pair of tennis shoes and get moving.

Original article @Designs for Health

Peptides, SARMs, & Prohormones: Where it Starts

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GHRP 2, 6
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Ipamorelin MK677

Superdrol (Methasterone)
1AD (1-Androstenediol)
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The effect of 6 days of Alpha-GPC on isometric strength


Ergogenic aides are widely used by fitness enthusiasts and athletes to increase performance. Alpha glycerylphosphorylcholine (A-GPC) has demonstrated some initial promise in changing explosive performance. The purpose of the present investigation was to determine if 6 days of supplementation with A-GPC would augment isometric force production compared to a placebo.

Thirteen college-aged males (Means ± SD; Age: 21.9 ± 2.2 years, Height: 180.3 ± 7.7 cm, Weight: 87.6 ± 15.6 kg; VO2 max: 40.08 ± 7.23 ml O2*Kg−1*min−1, Body Fat: 17.5 ± 4.6 %) gave written informed consent to participate in the study. The study was a double blind, placebo controlled, cross-over design. The participants reported to the lab for an initial visit where they were familiarized with the isometric mid thigh pull in a custom squat cage on a force platform and upper body isometric test against a high frequency load cell, and baseline measurements were taken for both. The participant then consumed either 600 mg per day of A-GPC or placebo and at the end of 6 days performed isometric mid thigh pulls and an upper body isometric test. A one-week washout period was used before the participants’ baseline was re-measured and crossed over to the other treatment.

The A-GPC treatment resulted in significantly greater isometric mid thigh pull peak force change from baseline (t = 1.76, p = 0.044) compared with placebo (A-GPC: 98.8. ± 236.9 N vs Placebo: −39.0 ± 170.9 N). For the upper body test the A-GPC treatment trended towards greater change from baseline force production (A-GPC: 50.9 ± 167.2 N Placebo: −14.9 ± 114.9 N) but failed to obtain statistical significance (t = 1.16, p = 0.127).

A-GPC is effective at increasing lower body force production after 6 days of supplementation. Sport performance coaches can consider adding A-GPC to the diet of speed and power athletes to enhance muscle performance.

Keywords: Alpha glycerylphosphorylcholine, Strength, Human performance, Sport supplements


Performance in sport is often determined by moments of extreme force production and power output [1]. While much of this can be attributed to muscular strength [23], some adaptations to training can be neural in nature [4]. A study by Pensini, Martin and Maffiuletti [5] demonstrated that increases in torque associated with 4 weeks of eccentric exercise were likely the result of central (or neural) adaptation. Based upon current knowledge it appears that both central and peripheral adaptations are necessary to enhance performance in athletes. Therefore, it is important to study nutritional interventions that have the potential to augment either potential site of adaptation.

α Glycerylphosphorylcholine (A-GPC) is a substance that could potentially augment human performance by facilitiating neuro-muscular interaction. A-GPC has been shown to augment acetylcholine levels in neurons in rat CNS [6], and has been shown to maintain reaction time in humans following exhaustive exercise [7]. Additionally A-GPC is generally considered safe for consumption in moderate to high doses [89]. Ingested A-GPC is converted to phosphatidylcholine, a source of choline [10]. Dietary choline levels are linked to the rate of biosynthesis of acetylcholine [11]. Given that cholinergic nerves trigger muscle contraction, and that choline availability is linked to acetylcholine synthesis substances that could augment choline availability might have the potential to influence muscular performance. To date some work has been done examining the ability of phospholipids to restore choline levels after exercise, but there is a dearth of information regarding the ability of compounds like A-GPC to acutely enhance performance [11]. The purpose of this study was to examine the effects of 6 days of supplementation with A-GPC on measures of isometric force production in the upper and lower body.


The Institutional Review Board at the University of Louisiana at Lafayette reviewed the present investigation for ethics. The study was a double-blind, placebo-controlled crossover with a 1-week washout period that included 13 healthy, college-aged males (Means ± SD; Age: 21.9 ± 2.2 years, Height: 180.3 ± 7.7 cm, Weight: 87.6 ± 15.6 kg; VO2 max: 40.08 ± 7.23 ml O2*Kg−1*min−1, Body Fat: 17.5 ± 4.6 %). Subjects reported to the lab and give informed consent, which included consent to publish, prior to baseline assessments which included height and weight, an assessment of maximum aerobic capacity via a COSMED CPET system (COSMED, Rome ITL) with integrated electronically braked cycle ergometer as outlined in previous studies [12], and body fat percentage via air displacement plethysmography (Bod Pod Gold Standard System, COSMED Rome, ITL) . The following week trial one (random order: either placebo or 600 mg of A-GPC) began. For the trials baseline performance testing was done and they were given an initial dose (placebo or A-GPC) while in the lab, 1 h later the performance testing (isometric mid thigh pull, upperbody isometric test) was repeated. The subjects were then given 6 days of additional pre-packaged supplement to take (morning and evening). The subjects reported back on day 6 of this period to repeat performance testing after the final dose of supplement. After a 1-week washout period, the subjects repeated the trial with the other treatment. (see Fig. 1).

Flowchart of Experimental Procedures

The treatments consisted of 600 mg daily of A-GPC (AlphaSize®, ChemiNutra, Austin, TX) or a placebo. Both treatments were administered in the same capsules (gel caps) and were the same color (white). The A-GPC capsules were supplied with a certificate of analysis from a third party lab confirming the amount of active ingredient. The placebo capsule consisted of microcrystalline cellulose and magnesium stearate (Nature’s Supplements, Carlsbad, CA USA). Both the participant and researcher were unaware of the identity of either treatment until the end of the study.

The participants were instructed to take doses in the morning and evening that would deliver a total of 600 mg of A-GPC per day and were given the pills in a non-distinct plastic bottle marked only with a code. The participants returned the bottles at the end of the study. The participants reported 100 % compliance with taking the required doses.

Upper body isometric test (UBIST)

The participants were positioned on three elevated platforms with the chest directly suspended over a load cell anchored into the concrete floor of the lab (iLoad Pro, Loadstar Sensors, Fremont CA). The load cell had a capacity of greater than 5000 N and a listed accuracy of 0.25 % for the full scale of measurement. The participants were placed in a push-up style position, with the hands at 150 % of biacromial width, and the elbows at 90° of extension (measured via a goniometer). A thick, non-elastic strap was run over one shoulder and under the opposite shoulder and connected with metal rings to a chain that was tethered to the load cell.

The participants were instructed to keep their backs flat, and push with their hands maximally until told to stop by the researcher. Prior to data capture the load cell was tared to ensure the weight of the load cell and apparatus were accounted for. The researcher started data collection and verbally instructed the participant to “push as hard as possible”. The participants were verbally encouraged during data collection, which was terminated when the force production declined by 50 N from the peak value registered. The load cell was set to capture data at maximum rate (150Hz) and the data was exported and analyzed in JMP 11.0 (SAS Institute Inc, Cary NC). Peak force values were isolated from the data and used for subsequent analysis. The test was performed three times with 5 min rest between assessments. The validity and reliability of this test have been reported in the literature [14].

Statistical analysis
Reliability was assessed for the isometric tests via Intra Class Correlation Coefficients (ICC). Repeated measures Ancovas were used to examine acute (baseline and 1 h post) and chronic (baseline and day 6) changes in performance between treatments. Order of administration (Placebo first, A-GPC first) was entered into the model as a covariate. G*Power software [15] was used to determine effect size (Cohen’s d), all other analyses were performed using a modern statistical software package (JMP, version 11.0 SAS Institute Inc., Cary, NC). Magnitude based inferences were calculated to assist with interpretation of results [16]. The use of magnitude based inference is an attempt to expand the interpretation of findings to include harmful, trivial and beneficial as interpretations, rather than just significant, non-significant [17]. This interpretations in not without controversy [18], as such the authors have chosen to include it alongside a more traditional statistical approach.


Reliability of isometric tests
The isometric tests demonstrated reliability when the triplicate measurements were examined via ICC (range: 0.969–0.984). Measurements were not different at any time points (p > 0.05). Therefore in subsequent analysis the peak value from the set of three measures was used.

Treatment effects—acute
Repeated measures Anova did not reveal any main effects (F = 0.003, p = 0.9584) nor interaction effects of treatment*time (F = 0.114, p = 0.738) for IMTP performance 1 h after the initial dose of A-GPC or Placebo. Similar results were revealed when UBIST performance was analyzed.

Treatment effects—chronic
Repeated measures Anova revealed a significant interaction effect for treatment (A-GPC vs Placebo) by time (baseline, day 6) for IMTP peak performance (F = 3.12, p = 0.04; change from baseline A-GPC: 98.8. ± 236.9 N vs Placebo: −39.0 ± 170.9 N, ES = 0.961). See Fig. 2.

Mean change in Isometric Mid Thigh Pull Peak force after 6 days of supplementation with A-GPC. Error bars represent +/− 1 SEM

For the upper body test the A-GPC treatment trended towards greater change from baseline force production (A-GPC: 50.9 ± 167.2 N Placebo: −14.9 ± 114.9 N) but the interaction effect of treatment by time failed to obtain statistical significance (F = 1.36, p = 0.127). However, this data (see Fig. 3) demonstrated a large effect size (ES = 0.714). This suggests that the variability of the subject’s upper body strength limited the statistical power, however, it if likely that a real effect exists in this data. Magnitude based inferences suggest that the A-GPC was 68.3 % likely beneficial for increasing upper body isometric force and 86.5 % likely beneficial for increasing lower body isometric force production.


The results of this study support the use of A-GPC to enhance strength, particularly in the lower body after 6 days of administration of a 600 mg dose. The literature does not contain controlled experimental data regarding the effects of A-GPC on aspects of human performance directly related to isometric strength, and thus this study represents a first step in the evaluation of this product for such use. The literature does contain some evidence that choline itself is important to consider in regard to endurance performance [1920]. The current literature does contain some information about A-GPC and performance measurements. Jagim et al. [21] reported that a multi-ingredient supplement that contained A-GPC enhanced mean power during a maximal effort sprint test on a non-motorized treadmill but did not produce any changes in counter movement jumping performance peak or mean power. Parker et al. [22] reported acute supplementation with 200 mg or 400 mg of A-GPC did not statistically enhance performance, thought the authors did note a non-significant trend in vertical jump peak power. Acute supplementation with 600 mg of A-GPC has been shown to augment bench press power in a small sample of men with 2 years of training experience [23]. This study is similar in finding to the present investigation in dose of A-GPC administered (600 mg) and suggests enhancements in performance. These previously reported studies on A-GPC vary greatly in design, measurements and administrations. The lack of consistency of doses (200–600 mg) and time of administration (30–90 min prior to activity) may explain the lack of consistent findings. Given the present evidence in the literature, further studies will be needed to confirm the results reported from this experiment, the data represent a promising start and suggest alternative uses for A-GPC.

The potential mechanism by which A-GPC could confer enhanced strength and power performance involves increased bio-available choline, which may result in augmented acetylcholine synthesis in neurons. A-GPC has been shown to augment acetylcholine levels in CNS neurons [6]. Evidence suggests that when administered intramuscularly A-GPC can increase plasma choline levels [24]. A-GPC has also been shown to increase growth hormone secretion though the action of acetylcholine stimulated catecholamine release [25]. This increase in cholinergic tone and associated increased growth hormone release was also reported in old and young subjects after administration of growth hormone releasing hormone in conjunction with A-GPC [26]. In the present investigation it is unlikely a moderate increase in growth hormone over the course of 7 days would have impacted maximum strength although this evidence suggests that longer chronic studies of A-GPC may be warranted as chronic elevations in growth hormone could potentially further augment performance.

While the present study presents positive preliminary findings for A-GPC augmenting strength, it is not without limitation. The present investigation is limited by sample size. The study will need to be replicated with larger study populations and alternative measures of human performance, likely those that have the capacity to measure power not just peak force. Additionally, different does of A-GPC need to be explored to determine any potential dose-response, or lower limit for meaningful effect. We suggest that in vitro studies may also be warranted to demonstrate that A-GPC has the potential to augment neurotransmitter levels in motor neurons. These studies can help to clarify the timing of A-GPC administration, which may in turn result in studies with a more targeted and informed dosing scheme.


The results of the study suggest that A-GPC is effective at increasing lower body force production after 6 days of supplementation. A similar trend was noted in upper body isometric strength, however; this failed to attain statistical significance. Given that in many sports it is understood that a very small change in performance, often times less than 2 %, can significantly affect outcomes it is important to note that the 6 days of A-GPC resulted in greater than a 3 % increase in lower body isometric strength. Sport performance coaches can consider adding A-GPC to the diet of speed and power athletes to potentially enhance muscle performance.


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Oxandrolone, sold under the brand names Oxandrin and Anavar, among others, is an androgen and anabolic steroid (AAS) medication which is used to help promote weight gain in various situations, to help offset protein catabolism caused by long-term corticosteroid therapy, to support recovery from severe burns, to treat bone pain associated with osteoporosis, to aid in the development of girls with Turner syndrome, and for other indications.[4][5][6] It is taken by mouth.[4]

DHT Derivative

Highly anabolic – Low Androgenic/Progesteronic effects
Doesn’t aromatize

FDA-approved for treating bone pain associated with osteoporosis, aiding weight gain following surgery or physical trauma, during chronic infection, or in the context of unexplained weight loss, and counteracting the catabolic effect of long-term corticosteroid therapy.[14][15

Not metabolized in the liver, mainly metabolized in the kidney, minimal liver toxicity

Boys with good motor skills excel at problem-solving too

Boys with good motor skills are better problem-solvers than their less skillful peers, a new study from Finland shows. In contrast to previous studies, the researchers found no association between aerobic fitness or overweight and obesity with cognitive function in boys. The results are based on the Physical Activity and Nutrition in Children (PANIC) Study conducted at the University of Eastern Finland, and they were published in Medicine & Science in Sports & Exercise.

The study found that boys with better motor skills at baseline had higher cognitive scores over a two-year follow-up period than boys who had poorer motor skills. In contrast to previous cross-sectional studies, the present study shows that children with different levels of aerobic fitness or body fat percentage did not differ in cognition. In fact, boys with higher aerobic fitness at the baseline of the study had poorer cognition during the two-year follow-up than those with lower fitness.

In girls, none of the above-mentioned factors was associated with cognitive skills. This may be due to biological or sociocultural differences between boys and girls.

The results also show that boys with better motor skills at baseline had a smaller increase in their cognitive skills than those with poorer motor skills.

“It is important to remember that these results do not necessarily reflect a causal relation between motor skills and cognition. Boys with poorer motor and cognitive skills at baseline caught up with their more skilful peers during the two-year follow-up,” says Postdoctoral Researcher Eero Haapala from the University of Jyväskylä. Dr Haapala is also Adjunct Professor of Paediatric Exercise Physiology at the University of Eastern Finland.

The results suggest that motor skills and cognition are associated with one another in boys; however, it would be premature to claim that motor skills boost cognition. Furthermore, the study found no association between aerobic fitness or overweight and obesity with cognition.

The study investigated the longitudinal associations of motor skills, aerobic fitness, and body fat percentage with cognition in 371 children who were 6-8-years old at baseline. Motor skills were evaluated by agility, balance and manual dexterity tests, aerobic fitness by a maximal cycle ergometer test, and body fat percentage by a DXA-device. Cognition was assessed by the Raven’s Matrices Test. Several confounding factors such as parental education and annual household income were controlled for in the analyses.

Story Source

Materials provided by University of Eastern FinlandNote: Content may be edited for style and length.


  1. Eero A. Haapala, Niina Lintu, Juuso Väistö, Tuomo Tompuri, Sonja Soininen, Anna Viitasalo, Aino-Maija Eloranta, Taisa Venäläinen, Arja Sääkslahti, Tomi Laitinen, Timo A. Lakka. Longitudinal Associations of Fitness, Motor Competence, and Adiposity with CognitionMedicine & Science in Sports & Exercise, 2018; 1 DOI: 10.1249/MSS.0000000000001826

Men’s testosterone levels largely determined by where they grow up

Men who grow up in more challenging conditions where there is potential of exposure to infectious diseases, for example, are likely to have lower testosterone levels in later life than those who spend their childhood in healthier environments, according to new research.

Men’s testosterone levels are largely determined by their environment during childhood, according to new research.

The Durham University-led study suggests that men who grow up in more challenging conditions where there are lots of infectious diseases, for example, are likely to have lower testosterone levels in later life than those who spend their childhood in healthier environments.

The study, published in Nature Ecology and Evolution, challenges the theory that testosterone levels are controlled by genetics or race.

As high testosterone levels potentially lead to an increased risk of prostate enlargement and cancer, the researchers suggest that any screening for risk profiles may need to take a man’s childhood environment into account.

The study found that Bangladeshi men who grew up and lived as adults in the UK had significantly higher levels of testosterone compared to relatively well-off men who grew up and lived in Bangladesh as adults. Bangladeshis in Britain also reached puberty at a younger age and were taller than men who lived in Bangladesh throughout their childhood.

The researchers say the differences are linked to energy investment as it may only be possible to have high testosterone levels if there are not many other demands placed on the body such as fighting off infections.?In environments where people are more exposed to disease or poor nutrition, developing males direct energy towards survival at the cost of testosterone.

The researchers collected data from 359 men on height, weight, age of puberty and other health information along with saliva samples to examine their testosterone levels. They compared the following groups: men born and still resident in Bangladesh; Bangladeshi men who moved to the UK (London) as children; Bangladeshi men who moved to the UK as adults; second-generation, UK-born men whose parents were Bangladeshi migrants; and UK-born ethnic Europeans.

Lead author of the study, Dr Kesson Magid from Durham University’s Department of Anthropology (UK), said: “A man’s absolute levels of testosterone are unlikely to relate to their ethnicity or where they live as adults but instead reflect their surroundings when they were children.”

Men with higher levels of testosterone are at greater risk of potentially adverse effects of this hormone on health and ageing. Very high levels can mean increased muscle mass, increased risk of prostate diseases and have been linked to higher aggression. Very low testosterone levels in men can include lack of energy, loss of libido and erectile dysfunction. The testosterone levels of the men in the study were, however, all in a range that would unlikely have an impact on their fertility.

Co-author Professor Gillian Bentley from Durham University, commented: “Very high and very low testosterone levels can have implications for men’s health and it could be important to know more about men’s childhood circumstances to build a fuller picture of their risk factors for certain conditions or diseases.”

Aspects of male reproductive function remain changeable into adolescence, up to the age of 19 and are more flexible in early rather than late childhood, according to the research. However, the study suggests that, in adulthood, men’s testosterone levels are no longer heavily influenced by their surroundings.

Senior co-author Gillian Bentley and colleagues have also previously found that the environment in which girls grow up can affect their hormone levels, fertility and risk levels for reproductive cancers as adults.

The research was funded by the Economic and Social Research Council (ESRC), the Royal Society and Prostate Cancer UK, and involved researchers from the University of Chittagong (Bangladesh), Durham University (UK), and Northwestern University (USA).

Story Source

Materials provided by Durham UniversityNote: Content may be edited for style and length.


  1. Kesson Magid, Robert T. Chatterton, Farid Uddin Ahamed, Gillian R. Bentley. Childhood ecology influences salivary testosterone, pubertal age and stature of Bangladeshi UK migrant menNature Ecology & Evolution, 2018; DOI: 10.1038/s41559-018-0567-6

How to stretch your pecs without wrecking your shoulders

Don’t Do This

Sorry if this bursts your prehab bubble, but the use of “banded distraction” techniques has got to be debunked. It’s become popular to grab the thickest elastic band you can find, wrap it around a chosen joint (usually the shoulders, hips, or ankles) and stretch at extended end ranges under tension.

While this technique may work for some, most of the time the aggressive banded distraction plus end-range stretch does more harm than good.

The idea that a piece of rubber is strong enough to mobilize and alter the position of joints is a bit insane. Joints are encapsulated by thick and rigid non-contractile tissue, stabilized by more wire-like ligaments, and surrounded by multiple articulating layers of muscles and tendons, in addition to a dense fascial sheath lying above all of these structures.

And then there’s the three layers of dermal tissue and adipose tissue that exponentially decrease the transferability of a band to even reach, let alone alter, the joint’s movement.

This is the reason it may work for a select few. Band contact on skin may actually be the reason for many positive responses. Nerve roots that distribute from the spine run to both areas of the skin (dermotomes) and specific musculature (myotomes). The cool thing about the nervous system is that we can see cross linking between sensory and motor pathways, and use one to manipulate the other.

By the band touching dermotomes that correlate with underlying myotomes, contractile musculature (and dare I say fascia) can actually reduce tone, improving movement capacity. But again, this will NOT work for everyone.

I’m not saying never to mobilize and stretch with a band, but be smart about it. Structures like the hip and ankle are more resilient due to the size and stabilizing structural components to these regions. But when it comes to the shoulder, the most mobile joint in the body, there are better ways to unlock neural tightness and improve positions.

Do This

Reciprocal Eccentric/Concentric Pec Mobilization

  1. Place your hand and forearm in contact with a rack or immovable object. Elevate the shoulder to just above 90 degrees.
  2. From here, stagger your stance with your opposite foot from the elevated arm out in front. You’ll keep your shoulder, forearm, and hand in the same position throughout this drill using your body to generate the movement.
  3. Start by contracting your pecs to drive your body into rotation towards that elevated arm. Move slowly under maximal internal tension and control.
  4. Once you’ve hit end range, reciprocate the movement and move back in the opposite direction. The key here is to keep tension in the pec, and grade it back slightly so you’re stretching against your own tension, never getting into forced end ranges without control. Do this repeatedly for 45-75 seconds per side using a controlled breath.

The Details

Many lifters are correct: their chests are tight and need some attention. Where they miss the mark is the unlocking of the neural tone that’s prevalent in the front side of the shoulders after they’ve already addressed other postural regions like the thoracic spine and cage that respond extremely well when mobilized into extension and rotation.

Once the thoracic spine, cage, and shoulder blade show some semblance of function, the next region to address to combat chronic forward shoulders, dumped over scapulae, and even forward head posture is to address the pectoralis group.

A majority of injuries occur in ranges of motion that an athlete has access to, yet cannot actively stabilize. This is called the “motor control gap” and is a powerful way to objectify otherwise subjective practices like foam rolling, stretching, and corrective exercises.

For the pecs, that range of motion tends to be elevation above 90 degrees plus external rotation. This instable extended range of motion is the one most closely associated with front-sided shoulder pain. So instead of placing your shoulders into an inherently unstable position to stretch the pecs, you can create active tension around the shoulder and use a reciprocal tension technique.

This will improve positions of external rotation and horizontal abduction while keeping the shoulders in a safe and stabilized position.

by Dr John Rusin @t-nation

Tip: Don’t Cut Your Rest Periods Short

Short on time? Don’t rest less between sets or you’ll interfere with your gains. Try this instead.

Rest Periods and Gains

When you’re pressed for time, you’ll be tempted to cut your rest intervals short. Resist the urge! While it may seem like a time-saver, it’s actually a results-killer.

Consider that research shows that 3 minutes between sets is optimal for gaining strength and size (1), so when you short-change your rest times, you reduce the amount of weight you can lift and/or reps for your subsequent sets. As a result, you lower your volume load and decrease your gains.

But I’m Busy and Need a Faster Workout!

Instead of using insufficient rest intervals, try the late Charles Poliquin’s method of alternating between non-competing exercises. This system has been around for a long time, yet few people use it. That’s too bad, because when done correctly, you can cut your training time in half.

Instead of doing a set of bench press and then playing around on your phone for 3 or 4 or more minutes, place a heavy dumbbell next to the bench press. Then do this:

  • A1. Bench Press: Rest 45 seconds
  • A2. 1-Arm Dumbbell Row: Rest 45 seconds

Repeat for your desired number of rounds

If you prefer whole body training, you can also pair lower body hinge movements with upper body movements:

Hinge and Push Example

  • A1. Trap Bar Deadlift: Rest 60 seconds
  • A2. Dips: Rest 45 seconds

Squat and Pull Example

  • B1. Front Squat: Rest 60 seconds
  • B2. Chin-Up: Rest 45 seconds

This style of training only gives you time to record your set in your training journal, grab a quick swig of water, and get ready for your next set. This keeps you off your phone, which will improve your mental focus and create a better flow to your training session.


  1. Schoenfeld, BJ., et al. Longer inter-set rest periods enhance muscle strength and hypertrophy in resistance-trained men. Journal of Strength & Conditioning Research, 2015, 30(7):1805-12. doi: 10.1519/JSC.0000000000001272.

Original article @T-nation

Weightlifting is good for your heart and it doesn’t take much


Lifting weights for less than an hour a week may reduce your risk for a heart attack or stroke by 40 to 70 percent, according to a new Iowa State University study. Spending more than an hour in the weight room did not yield any additional benefit, the researchers found.

“People may think they need to spend a lot of time lifting weights, but just two sets of bench presses that take less than 5 minutes could be effective,” said DC (Duck-chul) Lee, associate professor of kinesiology.

The results — some of the first to look at resistance exercise and cardiovascular disease — show benefits of strength training are independent of running, walking or other aerobic activity. In other words, you do not have to meet the recommended guidelines for aerobic physical activity to lower your risk; weight training alone is enough. The study is published in Medicine and Science in Sports and Exercise.

Lee and his colleagues analyzed data of nearly 13,000 adults in the Aerobics Center Longitudinal Study. They measured three health outcomes: cardiovascular events such as heart attack and stroke that did not result in death, all cardiovascular events including death and any type of death. Lee says resistance exercise reduced the risk for all three.

“The results are encouraging, but will people make weightlifting part of their lifestyle? Will they do it and stick with it? That’s the million-dollar question,” Lee said.


Barriers to resistance training

The researchers recognize that unlike aerobic activity, resistance exercise is not as easy to incorporate into our daily routine. Lee says people can move more by walking or biking to the office or taking the steps, but there are few natural activities associated with lifting. And while people may have a treadmill or stationary bike at home, they likely do not have access to a variety of weight machines.

For these reasons, Lee says a gym membership may be beneficial. Not only does it offer more options for resistance exercise, but in a previous study Lee found people with a gym membership exercised more. While this latest study looked specifically at use of free weights and weight machines, Lee says people will still benefit from other resistance exercises or any muscle-strengthening activities.

“Lifting any weight that increases resistance on your muscles is the key,” Lee said. “My muscle doesn’t know the difference if I’m digging in the yard, carrying heavy shopping bags or lifting a dumbbell.”


Other benefits of strength training

Much of the research on strength training has focused on bone health, physical function and quality of life in older adults. When it comes to reducing the risk for cardiovascular disease, most people think of running or other cardio activity. Lee says weight lifting is just as good for your heart, and there are other benefits.

Using the same dataset, Lee and his colleagues looked at the relationship between resistance exercise and diabetes as well as hypercholesterolemia, or high cholesterol. The two studies, published in Mayo Clinic Proceedings, found resistance exercise lowered the risk for both.

Less than an hour of weekly resistance exercise (compared with no resistance exercise) was associated with a 29 percent lower risk of developing metabolic syndrome, which increases risk of heart disease, stroke and diabetes. The risk of hypercholesterolemia was 32 percent lower. The results for both studies also were independent of aerobic exercise.

“Muscle is the power plant to burn calories. Building muscle helps move your joints and bones, but also there are metabolic benefits. I don’t think this is well appreciated,” Lee said. “If you build muscle, even if you’re not aerobically active, you burn more energy because you have more muscle. This also helps prevent obesity and provide long-term benefits on various health outcomes.”




  1. Yanghui Liu, Duck-chul Lee, Yehua Li, Weicheng Zhu, Riquan Zhang, Xuemei Sui, Carl J. Lavie, Steven N. Blair. Associations of Resistance Exercise with Cardiovascular Disease Morbidity and Mortality. Medicine & Science in Sports & Exercise, 2018; 1 DOI: 10.1249/MSS.0000000000001822

How sleep loss may contribute to adverse weight gain



In a new study, researchers at Uppsala University now demonstrate that one night of sleep loss has a tissue-specific impact on the regulation of gene expression and metabolism in humans. This may explain how shift work and chronic sleep loss impairs our metabolism and adversely affects our body composition. The study is published in the scientific journal Science Advances.

Epidemiological studies have shown that the risk for obesity and type 2 diabetes is elevated in those who suffer from chronic sleep loss or who carry out shift work. Other studies have shown an association between disrupted sleep and adverse weight gain, in which fat accumulation is increased at the same time as the muscle mass is reduced — a combination that in and of itself has been associated with numerous adverse health consequences. Researchers from Uppsala and other groups have in earlier studies shown that metabolic functions that are regulated by e.g. skeletal muscle and adipose tissue are adversely affected by disrupted sleep and circadian rhythms. However, until now it has remained unknown whether sleep loss per se can cause molecular changes at the tissue level that can confer an increased risk of adverse weight gain.

In the new study, the researchers studied 15 healthy normal-weight individuals who participated in two in-lab sessions in which activity and meal patterns were highly standardised. In randomised order, the participants slept a normal night of sleep (over eight hours) during one session, and were instead kept awake the entire night during the other session. The morning after each night-time intervention, small tissue samples (biopsies) were taken from the participants’ subcutaneous fat and skeletal muscle. These two tissues often exhibit disrupted metabolism in conditions such as obesity and diabetes. At the same time in the morning, blood samples were also taken to enable a comparison across tissue compartments of a number of metabolites. These metabolites comprise sugar molecules, as well as different fatty and amino acids.

The tissue samples were used for multiple molecular analyses, which first of all revealed that the sleep loss condition resulted in a tissue-specific change in DNA methylation, one form of mechanism that regulates gene expression. DNA methylation is a so-called epigenetic modification that is involved in regulating how the genes of each cell in the body are turned on or off, and is impacted by both hereditary as well as environmental factors, such as physical exercise.

“Our research group were the first to demonstrate that acute sleep loss in and of itself results in epigenetic changes in the so-called clock genes that within each tissue regulate its circadian rhythm. Our new findings indicate that sleep loss causes tissue-specific changes to the degree of DNA methylation in genes spread throughout the human genome. Our parallel analysis of both muscle and adipose tissue further enabled us to reveal that DNA methylation is not regulated similarly in these tissues in response to acute sleep loss,” says Jonathan Cedernaes who led the study.

“It is interesting that we saw changes in DNA methylation only in adipose tissue, and specifically for genes that have also been shown to be altered at the DNA methylation level in metabolic conditions such as obesity and type 2 diabetes. Epigenetic modifications are thought to be able to confer a sort of metabolic “memory” that can regulate how metabolic programmes operate over longer time periods. We therefore think that the changes we have observed in our new study can constitute another piece of the puzzle of how chronic disruption of sleep and circadian rhythms may impact the risk of developing for example obesity,” notes Jonathan Cedernaes.

Further analyses of e.g. gene and protein expression demonstrated that the response as a result of wakefulness differed between skeletal muscle and adipose tissue. The researchers say that the period of wakefulness simulates the overnight wakefulness period of many shift workers assigned to nightwork. A possible explanation for why the two tissues respond in the observed manner could be that overnight wakefulness periods exert a tissue-specific effect on tissues’ circadian rhythm, resulting in misalignment between these rhythms. This is something that the researchers found preliminary support for also in this study, as well as in an earlier similar but smaller study.

“In the present study we observed molecular signatures of increased inflammation across tissues in response to sleep loss. However, we also saw specific molecular signatures that indicate that the adipose tissue is attempting to increase its capacity to store fat following sleep loss, whereas we instead observed signs indicating concomitant breakdown of skeletal muscle proteins in the skeletal muscle, in what’s also known as catabolism. We also noted changes in skeletal muscle levels of proteins involved handling blood glucose, and this could help explain why the participants’ glucose sensitivity was impaired following sleep loss. Taken together, these observations may provide at least partial mechanistic insight as to why chronic sleep loss and shift work can increase the risk of adverse weight gain as well as the risk of type 2 diabetes,” says Jonathan Cedernaes.

The researchers have only studied the effect of one night of sleep loss, and therefore do not know how other forms of sleep or disruption of circadian misalignment would have affected the participants’ tissue metabolism.

“It will be interesting to investigate to what extent one or more nights of recovery sleep can normalise the metabolic changes that we observe at the tissue level as a result of sleep loss. Diet and exercise are factors that can also alter DNA methylation, and these factors can thus possibly be used to counteract adverse metabolic effects of sleep loss,” says Jonathan Cedernaes.




  1. Jonathan Cedernaes, Milena Schönke, Jakub Orzechowski Westholm, Jia Mi, Alexander Chibalin, Sarah Voisin, Megan Osler, Heike Vogel, Katarina Hörnaeus, Suzanne L. Dickson, Sara Bergström Lind, Jonas Bergquist, Helgi B Schiöth, Juleen R. Zierath, Christian Benedict. Acute sleep loss results in tissue-specific alterations in genome-wide DNA methylation state and metabolic fuel utilization in humans. Science Advances, 2018; 4 (8): eaar8590 DOI: 10.1126/sciadv.aar8590