In the video above, you can watch me do my first Vitamin D test. Yes, I am a huge pussy and I HATE needles, even though the needles used (as I found out) are really really small. Stay tuned to this article, as I will reveal how you can get your levels tested for better than free–they may pay YOU to have it done. Read on….
I am sure you have heard of Vitamin D by now, and for good reason. Currently there is an epidemic of low Vitamin D level almost everywhere!
Just like Omega 3 status, it is critical to know your Vit D status, especially if you live in a more northern climate. Even if you are not, there is a good chance that you are low since many people in states like Arizona, Texas, etc do not go outside much during the day since it is so hot!
At the ISSN conference I went to a great presentation on the vitamin D and the presenter (Rikki Keen) has tested athletes from all over and has found that even track athletes in FL were low, since due to heat, most of their practices were later in the day when the rays from the sun were too low to allow sufficient vitamin D production.
Vitamin D is a group of fat-soluble “steroid.” Yes a steroid! Aaaaah. Call the FDA right now.
This is using the formal classification of the term steroid as cholesterol is technically a steroid too. These compounds are naturally occurring in the body and different from anabolic steroids that athletes may use (which are illegal here in the US unless under supervision for hormone replacement under a physician).
The two major forms of which are vitamin D2 (also known as ergocalciferol) and vitamin D3 (known as cholecalciferol). Vitamin D3 is produced in the skin after exposure to ultraviolet B light from the sun or artificial sources. Ultraviolet A (UVA) does not seem to raise vitamin D levels.
We can get some from food sources such as milk, fatty fish like salmon, cod liver oil, and a few other foods that are artificially fortified with vitamin D.
The sun is still the best source, and it is also available as a supplement in pill form. If you supplement, the D3 form is going to be best and is also very cheap.
From the Vitamin D Council’s website, it states
“25(OH)D levels should be between 50–80 ng/ml (125–200 nmol/L), year-round.”
Vitamin D is measured by 25(OH)D levels and can be done by a simple blood test as shown in my video above.
When you go in for your physical, you can request a Vitamin D test and most of the time your insurance will pay for it (check to make sure). Make sure it is the 25(OH)D test though NOT 1-25(OH)D test. As Rikki Keen pointed out in her presentation at the ISSN in FL recently, she stated that there still are some docs that will request the wrong test. She writes it down for her clients and has them bring in the piece of paper to give to them to make sure they get it right.
If you order the test from the Vitamin D Council’s website, it is a few buck cheaper and you may be able to get paid to get your levels checked!
Check out these links
Vitamin D Council: Vit D testing
Make Money Getting Your Vitamin D Tested?
I was at the American College of Sports Medicine (ACSM) Annual conference last year and did a short interview with Dr. John Cannell of the Vitamin D council. Check it out.
If people are interested in more info on vitamin D, drop a comment below and in part 2 I will tell you
What do I do now?
Get your vitamin D levels tested via a lab or your doc’s office
Leave a comment below if you want to see part 2
15 comments by this Sunday at 7pm EST for part 2
Rock on
Department of Nutritional Sciences, University of Toronto, Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada M5G 1X5. heather.hanwell@gmail.com
Abstract
INTRODUCTION: Recent sun exposure should correlate with circulating 25-hydroxyvitamin D [25(OH)D] due to ultraviolet B (UVB)-catalyzed cutaneous synthesis of vitamin D. METHODS: A Sun Exposure Score was calculated for healthy adults using a recall questionnaire assessing daily Time in Sun (<5 min, 5-30 min, >30 min) and Skin Exposure (face/hands; face/hands and arms; face/hands and legs; and “bathing suit”) for 1 week in each of the winter and summer (n=47 and 23, respectively; n=18 participated in both). Concentrations of 25(OH)D were measured by DiaSorin RIA on end-of-week sera. RESULTS: Mean serum 25(OH)D was higher in summer than winter (58.6+/-16.5 nmol/L vs. 38.8+/-29.0 nmol/L, respectively, P=0.003 unpaired). The calculated Sun Exposure Score correlated strongly with serum 25(OH)D during summer (Spearman’s rho=0.59, P=0.003); based on the Pearson coefficient of determination, summer Sun Exposure Score explained 38% of the variability in summer serum 25(OH)D. The Sun Exposure Score did not correlate with 25(OH)D in the winter (rho=0.19, P=0.210). The summer correlation was largely explained by the Time in Sun (rho=0.58, P=0.004) rather than area of Skin Exposed (rho=0.10, P=0.660). Although there was a correlation between winter and summer Sun Exposure Scores (rho=0.63, P=0.005), there was no summer vs. winter correlation in serum 25(OH)D (rho=0.08, P=0.76). CONCLUSION: This simple 1-week sun exposure recall questionnaire predicted summer serum 25(OH)D concentrations, accounting for 38% of the variability in 25(OH)D among healthy Italian adults. Copyright (c) 2010 Elsevier Ltd. All rights reserved.
Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.
Comment in:
Diabetes Care. 2010 Jul;33(7):e99; author reply e100.
Abstract
OBJECTIVE: To examine cross-sectional associations of serum vitamin D [25-hydroxyvitamin D, 25(OH)D] concentration with insulin resistance (IR) and beta-cell dysfunction in 712 subjects at risk for type 2 diabetes. RESEARCH DESIGN AND METHODS: Serum 25(OH)D was determined using a chemiluminescence immunoassay. Insulin sensitivity/resistance were measured using the Matsuda insulin sensitivity index for oral glucose tolerance tests (IS(OGTT)) and homeostasis model assessment of insulin resistance HOMA-IR. beta-Cell function was determined using both the insulinogenic index (IGI) divided by HOMA-IR (IGI/IR) and the insulin secretion sensitivity index-2 (ISSI-2). RESULTS Linear regression analyses indicated independent associations of 25(OH)D with IS(OGTT) and HOMA-IR (beta = 0.004, P = 0.0003, and beta = -0.003, P = 0.0072, respectively) and with IGI/IR and ISSI-2 (beta = 0.004, P = 0.0286, and beta = 0.003, P = 0.0011, respectively) after adjusting for sociodemographics, physical activity, supplement use, parathyroid hormone, and BMI. CONCLUSIONS: Vitamin D may play a role in the pathogenesis of type 2 diabetes, as 25(OH)D concentration was independently associated with both insulin sensitivity and beta-cell function among individuals at risk of type 2 diabetes.
Michigan State University College of Human Medicine, East Lansing, MI, USA.
Abstract
Vitamin D has an important role in skeletal muscles. Previously recognized for its effects on bone, it is now known that vitamin D has a much wider spectrum of usefulness for muscle. Studies indicate that vitamin D deficiency is pandemic. Those affected include the young and otherwise healthy members of the population, including athletes. Controversy exists regarding the amount of supplementation required to reverse deficiency and the relative effect of such a reversal on overall health. This article reviews current data on the role of vitamin D on muscle function, and explores the potential implications of its deficiency and supplementation on physical fitness and athletic performance.
ASPETAR, Qatar Orthopaedic and Sports Medicine Hospital, Doha, Qatar. bruce.hamilton@aspetar.com
Abstract
Vitamin D deficiency is an increasingly described phenomenon worldwide, with well-known impacts on calcium metabolism and bone health. Vitamin D has also been associated with chronic health problems such as bowel and colonic cancer, arthritis, diabetes and cardiovascular disease. In recent decades, there has been increased awareness of the impact of vitamin D on muscle morphology and function, but this is not well recognized in the Sports Medicine literature. In the early 20th century, athletes and coaches felt that ultraviolet rays had a positive impact on athletic performance, and increasingly, evidence is accumulating to support this view. Both cross-sectional and longitudinal studies allude to a functional role for vitamin D in muscle and more recently the discovery of the vitamin D receptor in muscle tissue provides a mechanistic understanding of the function of vitamin D within muscle. The identification of broad genomic and non-genomic roles for vitamin D within skeletal muscle has highlighted the potential impact vitamin D deficiency may have on both under-performance and the risk of injury in athletes. This review describes the current understanding of the role vitamin D plays within skeletal muscle tissue.
Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, MA 02111, USA. lisa.ceglia@tufts.edu
Abstract
PURPOSE OF REVIEW: Vitamin D is best known for its role in regulating calcium homeostasis and in strengthening bone. However, it has become increasingly clear that it also has important beneficial effects beyond the skeleton, including muscle. This review summarizes current knowledge about the role of vitamin D in skeletal muscle tissue and physical performance. RECENT FINDINGS: Molecular mechanisms of vitamin D action in muscle tissue include genomic and nongenomic effects via a receptor present in muscle cells. Knockout mouse models of the vitamin D receptor provide insight into understanding the direct effects of vitamin D on muscle tissue. Vitamin D status is positively associated with physical performance and inversely associated with risk of falling. Vitamin D supplementation has been shown to improve tests of muscle performance, reduce falls, and possibly impact on muscle fiber composition and morphology in vitamin D deficient older adults. SUMMARY: Further studies are needed to fully characterize the underlying mechanisms of vitamin D action in human muscle tissue, to understand how these actions translate into changes in muscle cell morphology and improvements in physical performance, and to define the 25-hydroxyvitamin D level at which to achieve these beneficial effects in muscle.
This is a video I took from the ISSN conference in FL recently.
Many, many people are deficient in Omega 3s and probably don’t know it.
Increasing their omega 3s in their diet is a great thing for almost anything you can think of from hearing loss, head trauma, fat loss, decreased muscle atrophy (losing muscle), etc.
Up until recently you have no way of knowing what your Omega 3 status was. Are you taking enough? Are you sure?
Omega 3 are essential fatty acids. They are ESSENTIAL and MUST be provided by your diet. Your body can not make them, so they must be consumed. The highest source of Omega 3s is primarily flax seed oil.
Fish oils (EPA and DHA) are made from Omega 3s. The rate of how fast and how much can be made is up for debate. To get around this, supplementing with the fish oils themselves directly works best.
While common doses vary, look to get around 1-4 GRAMS of combined EPA and DHA per day. As always, check with your doc to make sure this is ok, especially if you are on blood thinners (although the risk is small).
Read the label and look for EPA and DHA, not just Omega 3s.
The picture above is from Flameout by Biotest (full disclosure, I make nothing promoting it). There are many fish oil supplements on the market and the key is to know what to look for on the label.
Look in the middle and it will list the EPA and DHA right below the total free-fatty acids. Add these up for your TOTAL fish oil content. So, for one serving, it is about 3 grams (3,000 mg) of total fish oils. Note the serving size here is 4 caps. I have looked at some other fish oils and they are 10-22 caps for the SAME amount of fish oils themselves (EPA + DHA).
As Doug talked about above, the easiest way is to have it tested. Very soon there will be a cheap and economical way for you to test this at home! I am super excited about this since omega 3 status is related to sooooooooo many things. Jodie and I are doing our test this weekend and if you want more info as soon as it is available, pop your name in below and you will be the first to get the info (even before it is posted here).
Let me know what questions you have about fish oil by posting one below!
Rock on
Department of Neurosurgery, West Virginia University School of Medicine, Morgantown, West Virginia; and. Abstract Object Traumatic brain injury remains the most common cause of death in persons under 45 years of age in the Western world. Recent evidence from animal studies suggests that supplementation with omega-3 fatty acid (O3FA) (particularly eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]) improves functional outcomes following focal neural injury. The purpose of this study is to determine the benefits of O3FA supplementation following diffuse axonal injury in rats. Methods Forty adult male Sprague-Dawley rats were used. Three groups of 10 rats were subjected to an impact acceleration injury and the remaining group underwent a sham-injury procedure (surgery, but no impact injury). Two of the groups subjected to the injury were supplemented with 10 or 40 mg/kg/day of O3FA; the third injured group served as an unsupplemented control group. The sham-injured rats likewise received no O3FA supplementation. Serum fatty acid levels were determined from the isolated plasma phospholipids prior to the injury and at the end of the 30 days of supplementation. After the animals had been killed, immunohistochemical analysis of brainstem white matter tracts was performed to assess the presence of beta-amyloid precursor protein (APP), a marker of axonal injury. Immunohistochemical analyses of axonal injury mechanisms-including analysis for caspase-3, a marker of apoptosis; RMO-14, a marker of neurofilament compaction; and cytochrome c, a marker of mitochondrial injury-were performed. Results Dietary supplementation with a fish oil concentrate rich in EPA and DHA for 30 days resulted in significant increases in O3FA serum levels: 11.6% +/- 4.9% over initial levels in the 10 mg/kg/day group and 30.7% +/- 3.6% in the 40 mg/kg/day group. Immunohistochemical analysis revealed significantly (p < 0.05) decreased numbers of APP-positive axons in animals receiving O3FA supplementation: 7.7 +/- 14.4 axons per mm(2) in the 10 mg/kg/day group and 6.2 +/- 11.4 axons per mm(2) in the 40 mg/kg/day group, versus 182.2 +/- 44.6 axons per mm(2) in unsupplemented animals. Sham-injured animals had 4.1 +/- 1.3 APP-positive axons per mm(2). Similarly, immunohistochemical analysis of caspase-3 expression demonstrated significant (p < 0.05) reduction in animals receiving O3FA supplementation, 18.5 +/- 28.3 axons per mm(2) in the 10 mg/kg/day group and 13.8 +/- 18.9 axons per mm(2) in the 40 mg/kg/day group, versus 129.3 +/- 49.1 axons per mm(2) in unsupplemented animals. Conclusions Dietary supplementation with a fish oil concentrate rich in the O3FAs EPA and DHA increases serum levels of these same fatty acids in a dose-response effect. Omega-3 fatty acid supplementation significantly reduces the number of APP-positive axons at 30 days postinjury to levels similar to those in uninjured animals. Omega-3 fatty acids are safe, affordable, and readily available worldwide to potentially reduce the burden of traumatic brain injury.
Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, China. Abstract BACKGROUND: To evaluate the safety and efficacy of a fish oil-enriched parenteral nutrition regimen in patients undergoing major abdominal surgery, a meta-analysis of randomized controlled trials was conducted. METHODS: An electronic search of PubMed, MEDLINE, EMBASE, Academic Search Premier, and China National Knowledge Infrastructure databases was performed in March 2009. RevMan 5.0 was used for statistical analysis. RESULTS: The combined analysis showed that a fish oil-enriched parenteral nutrition regimen had a positive treatment effect on length of hospital stay (weighed mean difference = -2.98, P < .001), length of intensive care unit stay, postoperative infection rate (odds ratio = 0.56, P = .04), and serum levels of aspartate aminotransferase, alanine aminotransferase, and alpha-tocopherol on postoperative day 6 in these patients. The regimen increased the plasma levels of eicosapentaenoic acid (standardized mean difference = 3.11, P < .001) and docosahexaenoic acid and upregulated the leukotriene B(5) production in leukocytes on postoperative day 6. No significant differences were found between the 2 groups in postoperative mortality; incidence of postoperative cardiac complications; serum levels of bilirubin, triglyceride, or arachidonic acid; or the liberation of leukotriene B(4). No serious adverse events related to fish oil treatment were reported. CONCLUSIONS: Based on the meta-analysis, fish oil-supplemented parenteral nutrition was safe, improved clinical outcomes, and altered the fatty acid pattern as well as leukotriene synthesis. More laboratory parameters should be considered in future meta-analyses.
Division of Pulmonary and Critical Care Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. marikpe@evms.edu Abstract BACKGROUND: Immunomodulating diets (IMDs) have been demonstrated to improve immune function and modulate inflammation. However, the clinical benefit of these diets in patients undergoing elective surgery is controversial. The goal of this meta-analysis was to determine the impact of IMDs on the clinical outcomes of high-risk patients undergoing elective surgery. METHODS: The review included prospective, controlled, clinical trials that compared the clinical outcome of elective surgical patients who were randomized to receive an IMD or a control enteral diet. Studies were stratified according to the type of IMD and the timing of the initiation of the IMD. Data were abstracted on study design, study size, patient population, and IMD used. The outcomes of interest were the acquisition of new infections, wound complications, length of hospital stay (LOS), and mortality. Meta-analytic techniques were used to analyze the data. RESULTS: Twenty-one relevant studies were identified, which included a total of 1918 patients. Immunonutrition significantly reduced the risk of acquired infections, wound complications, and LOS. The mortality rate was 1% in both groups. The treatment effect was similar regardless of the timing of the commencement of the IMD. The benefits of immunonutrition required both arginine and fish oil. CONCLUSIONS: An immunomodulating enteral diet containing increased amounts of both arginine and fish oil should be considered in all high-risk patients undergoing major surgery. Although the optimal timing cannot be determined from this study, it is suggested that immunonutrition be initiated preoperatively when feasible.
Department of Diabetes-INSERM U341, Hôtel-Dieu Hospital, 75004 Paris, France. Abstract Fish oil feeding has been shown to limit visceral fat accumulation in insulin-resistant rats. Our goal was to determine whether this finding is due to increased fat mobilization or decreased lipid storage. Adipocytes were isolated from rats fed for 3 wk a diet containing 57.5 g/100 g sucrose and 14 g/100 g lipids as either fish oil (SF) or a mixture of standard oils (SC); there was also a reference group (R). Substituting fish oil for standard oils protected rats from visceral fat hypertrophy, hypertriglyceridemia and hyperglycemia. The stimulation of lipolysis was greater in adipocytes isolated from SF-fed rats than in those from SC-fed rats. Fatty acid synthase (FAS) activity was markedly lower in the liver but not in the adipose tissues of rats fed SF. Lipoprotein lipase (LPL) activity was 2.2-fold higher in the adipose tissues but not in the muscle in rats fed the SF diet than in those fed the SC diet. The decrease in visceral fat in rats fed fish oil could be attributed to decreased plasma triacylglycerol concentration and/or increased lipid mobilization rather than to reduced lipid storage.
Department of Food and Nutrition, Research Institute of Human Ecology, Seoul National University, Seoul 151-742, Korea. Abstract Reduced muscle activity leads to impaired insulin signaling, which leads to loss of contractile proteins and muscle mass via the Akt pathway. Dietary fish oil rich in long chain n-3 polyunsaturated fatty acids has been shown to prevent insulin signaling resistance in skeletal muscle. This study was conducted to elucidate the protective effect of dietary fish oil on disuse-induced perturbations in insulin signaling and soleus muscle atrophy. To accomplish this, rats were fed a corn-oil- (control) or fish-oil-based diet for 2 weeks, and then subjected to hindlimb immobilization while still receiving the same diets. After 10 days of immobilization, the soleus muscle mass and myosin heavy chain level had markedly decreased; however, these losses were significantly suppressed in rats fed dietary fish oil, compared with the control group. Dietary fish oil nearly completely attenuated the disturbances in activation of the Akt and p70 S6 kinase proteins, as well as the gene expression of muscle-specific E3 ubiquitin ligases (muscle atrophy F-box and muscle RING finger 1). However, insulin receptor substrate 1 associated with the p85 subunit of phosphoinositide 3-kinase was not altered during immobilization. Dietary fish oil also inhibited alterations in the gene expression of cyclooxygenase-2 and inducible nitric oxide synthase, with no additional observation of oxidative stress. Collectively, these findings indicate that dietary fish oil prior to and during immobilization may alleviate the immobilization-induced soleus muscle atrophy, at least in part, via the Akt pathway through E3 ubiquitin ligases and p70s6k.
Just wanted to drop you a note that I will be presenting at the Fitcom Xpo coming up in the next week or so.
There will be tons of fitness professionals presenting on topics ranging from Boot Camps, How to Gain Muscle and Drop Fat, Fitness Marketing and much more!
You will be able to log on from the comfort of your own home and pick from a huge selection.
I will be doing a presentation this year for Fitcom on
This will not be some old hat presentation as it will have cutting edge science and be VERY practical for you also. I am currently finishing up my dissertation writing on Metabolic Flexibility.
More details to come very soon! This will also be a great way to get CEUs if you are a fitness professional too.
In the interest of full disclosure, I do make a few bucks if you sign up for the expo through my site HERE.
Rock on
Mike T Nelson
Below is a shorter literature review I did as part of my PhD research. It can be on the dry side, but the take away is that as your body gets closer to a Metabolically INflexible state (e.g. diabetes) you have a much harder time process any food and turning it into a good fuel sources.
If you are very Metabolically Flexible, you can adapt to virtually any fuel source (e.g. various foods). Now this is not an argument for going crazy and eating Ho Hos and Krispy Kremes, there are limits!
The point is that every is different and perhaps there is a way to quantify how metabolically efficient each person’s body is without subjecting them to IVs and sticks in the arm for hours at a time.
Any questions, let me know and I will be happy to discuss. Big thank you to my advisor Dr. Don Dengel and Dr. George Biltz for the ideas, background, and all the support.
This ran awhile back, but since I am doing a presentation on Metabolic Flexibility for Fitcon II and some other projects, I thought I would re-run it here. Other had asked for literature that supports that theory too, so here you go. I am more than happy to answer any questions in the comment section too, so post away. It is a VERY dense post and I will have more break downs that are easy to digest in the future again.
For a simple version, see this post
Enjoy
Mike N
METABOLIC FLEXIBILITY (and also INFlexibility)
It is no secret that in the United States, the rate of obesity in children is on the rise. In fact, childhood obesity in the US has tripled over the last 40 years and doubled in the past 15 years
(32). About 40% of adolescents seen in the University of West Virginia pediatric clinic have body mass index (BMI) greater than 85% for gender and age (44). Body fat and its distribution is related to cardiovascular disease, hypertension and type 2 diabetes, all diseases that are considered to have an “incubation period” during childhood and adolescence (51). In 2003-2004 17.1% of US children and adolescents (age 2 to 19) were overweight (defined as at or above the 95th percentile of the sex specific BMI for age growth charts) (29). If the current epidemic of child and adolescent obesity continues at the same rate, life expectancy could be shortened by two to five years in the coming decades(30) and it will be the first time in recent history that life
expectancy has decreased.
LITERATURE REVIEW
Metabolic Flexibility
Due to possible discontinuities in both the supply and demand for energy, humans need a “clear capacity to utilize lipid and carbohydrate fuels and have the ability to transition between them.” (18). This capacity is a healthy state and termed “Metabolic Flexibility”. It is hypothesized that metabolic inflexibility may play a role in various disease processes such as the metabolic syndrome that may even start in childhood (3, 27, 28, 46). Location of body fat may affect
disease risk also and data from prospective studies using waist to hip ratio or waist circumference confirmed that abdominal obesity is more closely associated with disease risk than total body fatness(6, 7, 22).
A key to understanding metabolic flexibility is the vital role of insulin. In humans, insulin is a regulatory hormone synthesized in the pancreas within the beta cells (?-cells) of the islets of Langerhans. Insulin can be characterized by two phases an initial (cephalic phase) driven by the nervous system and a sustained secondary phase (1). Some data indicated that variations in prestimulatory glucose can secondarily affect the magnitude and pattern of subsequent glucose-induced insulin secretions (13). Humans in a healthy state with normal insulin
metabolism have the ability to effectively switch from primarily a fat metabolism to a carbohydrate metabolism. Also, in human subjects that reach a stage in the metabolic syndrome characterized by insulin resistance and glucose intolerance bordering on frank diabetes, there is still considerable beta-cell capacity demonstrating a clear absence of the normal initial peak of insulin secretion (5, 45). Skeletal muscle is a major player in energy balance due to its metabolic activity, storage capacity for both glycogen and lipids, and its effects on insulin sensitivity (9-11). Obesity/visceral fat, transient state of puberty, ethnicity, genetic factors, and physical inactivity all may lead to insulin resistance (2).
Elevated lipid content and intramuscular triglyceride (IMTG) are both linked to insulin
resistance (20)and thus compromise efficient lipid utilization. Perseghin et al. (31) used magnetic resonance spectroscopy (MRS) to report that lipids contained within muscle fibers were strongly correlated with the severity of insulin resistance. In metabolically inflexible subject, lipid oxidation may fail to increase with fasting and fail to suppress with hormonal insulin elevation. Lowered post-absorptive fatty acid oxidation leads to excess accumulation of IMTGs and begins a downward spiral. Interestingly, endurance trained athletes also have an increased IMTG level, but remain insulin sensitivity (perhaps from increased turnover rate) (9).
Kelley et al. (17) (as shown in Figure 1 below) showed that under basal fasting conditions glucose uptake and oxidation are normal or even increased in obese subjects compared with lean subjects. Fatty acid uptake is also normal, but fatty acid oxidation is lower and its storage is elevated in the obese group which may explain why they have a higher body fat as they are more apt to store fat.
During a hyperinsulinaemic euglycaemic clamp condition the differences between lean and obese are quite different. In lean subjects, glucose uptake increased 10 fold with both oxidation and storage primarily contributing while fatty acid uptake decreased equally dramatically. In
obese subjects however, glucose uptake, oxidation and storage are reduced; which is quite a different response from the lean group.
Figure 1 (47) shows the contributions of lipid and glucose oxidation to resting energy expenditure of the leg. Obese subjects derived relatively less energy from lipid oxidation during basal conditions; showing a blunted fat burning response. During insulin-stimulated conditions, lean subjects show a greater suppression of lipid oxidation compared to the obese group under
the same conditions.
Figure 1 from Kelley et al. 1999
In summary, Kelley et al. (17) presented data from subjects with type 2 diabetes showing metabolic inflexibility as obese subjects derived relatively less energy from lipid oxidation during basal conditions (P<0.01). Lean subjects showed a greater suppress
ion of lipid oxidation during insulin-stimulated conditions (p<0.01). As shown in Figure 2 below, lean subjects have a different response compared to obese and diabetic’s subjects as carbohydrate oxidation is increased (19).
Figure 2 from Kelley et al. (19)
Assessment of Metabolic Inflexibility
One way to assess metabolic flexibility is by the infusion of drugs (insulin, glucose, etc) to alter the metabolic environment. The downside is that this is more difficult to use in a clinic, requires more specialized training, and is not generally an option for children due to its invasive nature. Metabolic inflexibility is also dynamic in nature and the data collected are normally for acute settings and brief time periods only. An ideal method of assessment would be non invasive and able to collect dynamic data.
HRV
A noninvasive measure of a dynamic system is done currently by the collection of cardiac data via heart rate variability (HRV) (40). HRV analysis has been used extensively to assess autonomic control of the heart under various physiologic conditions. Most often linear analysis is done in both the time and frequency domain.
There are some data to suggest a difference in HRV for obese and non-obese individuals (25). It is well know that the autonomic nervous system ANS) plays an important role in regulating energy expenditure and body fat content, but to what extent is not exactly clear. Nagai, et al. (25) studied 42 non-obese and obese healthy school children where both groups were matched for age, gender, and height. ANS activity was assessed by HRV power spectral analysis. The results showed that the obese children had reduced sympathetic as well as parasympathetic nerve activity which could be a factor in preventing and treating obesity.
Activity is also known to affect HRV (26). Nagai et al. (26) presented data that lean active children demonstrated a lower resting heart rate (HR) as well as higher total power (TP), low frequency (LF), and high frequency (HF). LF reflects mixed sympathetic (SNS) and parasympathetic (PNS) activity, HF reflects PNS activity and TP evaluating the overall ANS activity. In contrast, obese-inactive group showed significantly lower TP, LF and HF. These data suggest obese children have reduced sympathetic and parasympathetic nervous activities as compared to lean children with similar physical activity levels. This autonomic reduction that is associated with the amount of body fat in inactive state may be an important factor for the onset or development of childhood obesity. The good news is that regular physical activity could contribute to enhance the ANS activity in both lean and obese children (26).
There are some data to suggest alterations in HRV in young patients with diabetes (14). Autonomic neuropathy is a common complication of diabetes mellitus (DM) and the aim of the study was to assess HRV changes during prolonged (40 minute) supine rest in 17 young patients with DM compared to an aged matched healthy control group. HRV analysis consisted of time/frequency domains, Poincare and sequence plots and sample entropy. The study found that HRV was able to distinguish cardiac dysregulation in young patients with DM from a control group. However, it did not find any significant difference in sample entropy between the groups, perhaps due to the subtle nature of the cardiovascular impairment in young DM patients (14). Data from Porta et al. (41) used SampEn and ApEn to analyze HRV during a head-up tilt test and concluded that with short duration data SampEn was significantly more reliable at producing accurate entropy scores.
HRV provides a non invasive method that is able to capture data in a dynamic fashion, but to date it has very limited data regarding its relation to metabolic inflexibility.
Sample Entropy
Entropy, in the original context of thermodynamics is a measure of system disorder and randomness. Approximate entropy was first coined by Pincus et al. (36) in 1991 as a way to quantify the dynamic control of a system (such as HR control) and possibly analyze many other “random” sequences (34). The promise of approximate entropy (ApEn) is that it can classify complex systems with only 100 data values in diverse setting that include both deterministic chaotic and stochastic processes (34). To date, ApEn has been used in the analysis of medical data (37), cardiology (16, 43) and neurohormonal responses (15, 35, 38, 49, 50).
The ApEn algorithm counts each sequence as matching itself to avoid the occurrence of ln (0) in the calculations. ApEn is heavily dependent on the record length and is uniformly lower than expected on short records (42). It is also lacking in relative consistency meaning that if ApEn for one data set is higher than another, it should but does not remain higher for all conditions tested (33).
Sample entropy (SampEn) was developed to reduce the bias of ApEn as it does not count self-matches. Richman et al. (42) defines SampleEn as “precisely the negative natural logarithm of the conditional probability that two sequences similar for m points remain similar at the next point, where self-matches are not included in calculating probability.” So a lower value of SampEn indicates more self-similarity (and thus less variability). SampEn is defined in terms (m,r, N) where m is the length of sequences to be compared, r is the tolerance for accepting matches and N is the length of the time series. Another benefit of SampEn is that it does not use a template-wise approach when estimating conditional probabilities as it is in essence an event-counting statistic (42). In a study by Richman et al. (42) SampEn agreed much better than ApEn statistics with theory for random numbers with known probabilistic character over a broad range of operating conditions and it has successful been used to calculate HRV on very short ECG mV recordings (10 to 60 seconds); so it does not appear to require long periods of data collection (4). HRV calculated by SampEn has been used in studies on recovery post exercise training (12, 24) and alterations due to disease and aging (39). Lake et al. (21)performed a sample entropy analysis of neonatal HRV in an attempt to predict sepsis and found that entropy falls before clinical signs of neonatal sepsis and also that missing data points were well tolerated.
RER
The RER is the ratio of the volume of CO2 to O2 and can be measured with a metabolic cart to collect expired gases. The RER at steady state is displayed as a ratio between 0 .7 to 1.0 where 0.7 corresponds to 100% fat metabolism, 0.85 corresponds to 50% fat and 50% carbohydrate metabol
ism and 1 corresponds to 100% carbohydrate metabolism.
RER has been found to be reproducible during exercise under standardized conditions (23), but factors such as age, gender, dietary substrate intake, insulin, and plasma free fatty can influence the selection of substrates during exercise and hence alter RER(8, 48).
IMPLICATIONS
With the rise in obesity, it will be imperative to have a method to determine which children are on the fast track to further metabolic damage. Current methods such as insulin clamps may be effective, but they require more training on the clinician side, more difficult to obtain IRB approval and many times will not be used children due to their invasive nature. Future studies may be conducted on newer non-invassive methods to determine metabolic inflexibility and potentially investigate the effects of various forms of exercise and nutrition methods to combat obesity in children and target those in high risk groups.
1. The Cell Physiology of Biphasic Insulin Secretion — Rorsman et al. 15 (2): 72 — Physiology. 2007(12/12/2007).
2. Amiel S. A., S. Caprio, R. S. Sherwin, G. Plewe, M. W. Haymond, W. V. Tamborlane. Insulin resistance of puberty: a defect restricted to peripheral glucose metabolism. J Clin Endocrinol Metab. 72(2):277-282, 1991.
3. Arslanian S., C. Suprasongsin. Insulin sensitivity, lipids, and body composition in childhood: is “syndrome X” present? J Clin Endocrinol Metab. 81(3):1058-1062, 1996.
4. Bornas X., J. Llabres, M. Noguera, A. Pez. Sample entropy of ECG time series of fearful flyers: preliminary results. Nonlinear Dynamics Psychol Life Sci. 10(3):301-318, 2006.
5. Bruce D. G., D. J. Chisholm, L. H. Storlien, E. W. Kraegen. Physiological importance of deficiency in early prandial insulin secretion in non-insulin-dependent diabetes. Diabetes. 37(6):736-744, 1988.
6. Donahue R. P., R. D. Abbott. Central obesity and coronary heart disease in men. Lancet. 2(8569):1215, 1987.
7. Ducimetiere P., J. Richard, F. Cambien. The pattern of subcutaneous fat distribution in middle-aged men and the risk of coronary heart disease: the Paris Prospective Study. Int J Obes. 10(3):229-240, 1986.
8. Goedecke J. H., A. St Clair Gibson, L. Grobler, M. Collins, T. D. Noakes, E. V. Lambert. Determinants of the variability in respiratory exchange ratio at rest and during exercise in trained athletes. Am J Physiol Endocrinol Metab. 279(6):E1325-34, 2000.
9. Goodpaster B. H., J. He, S. Watkins, D. E. Kelley. Skeletal muscle lipid content and insulin resistance: evidence for a paradox in endurance-trained athletes. J Clin Endocrinol Metab. 86(12):5755-5761, 2001.
10. Goodpaster B. H., D. E. Kelley. Skeletal muscle triglyceride: marker or mediator of obesity-induced insulin resistance in type 2 diabetes mellitus? Curr Diab Rep. 2(3):216-222, 2002.
11. Goodpaster B. H., S. Krishnaswami, H. Resnick, et al. Association between regional adipose tissue distribution and both type 2 diabetes and impaired glucose tolerance in elderly men and women. Diabetes Care. 26(2):372-379, 2003.
12. Heffernan K. S., C. A. Fahs, K. K. Shinsako, S. Y. Jae, B. Fernhall. Heart rate recovery and heart rate complexity following resistance exercise training and detraining in young men. Am J Physiol Heart Circ Physiol. 293(5):H3180-6, 2007.
13. Henquin J. C., M. Nenquin, P. Stiernet, B. Ahren. In vivo and in vitro glucose-induced biphasic insulin secretion in the mouse: pattern and role of cytoplasmic Ca2+ and amplification signals in beta-cells. Diabetes. 55(2):441-451, 2006.
14. Javorka M., J. Javorkova, I. Tonhajzerova, A. Calkovska, K. Javorka. Heart rate variability in young patients with diabetes mellitus and healthy subjects explored by Poincare and sequence plots. Clin Physiol Funct Imaging. 25(2):119-127, 2005.
15. Juhl C. B., O. Schmitz, S. Pincus, J. J. Holst, J. Veldhuis, N. Porksen. Short-term treatment with GLP-1 increases pulsatile insulin secretion in Type II diabetes with no effect on orderliness. Diabetologia. 43(5):583-588, 2000.
16. Kaplan D. T., M. I. Furman, S. M. Pincus, S. M. Ryan, L. A. Lipsitz, A. L. Goldberger. Aging and the complexity of cardiovascular dynamics. Biophys J. 59(4):945-949, 1991.
17. Kelley D. E., B. H. Goodpaster. Skeletal muscle triglyceride. An aspect of regional adiposity and insulin resistance. Diabetes Care. 24(5):933-941, 2001.
18. Kelley D. E., J. He, E. V. Menshikova, V. B. Ritov. Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes. 51(10):2944-2950, 2002.
19. Kelley D. E., L. J. Mandarino. Fuel selection in human skeletal muscle in insulin resistance: a reexamination. Diabetes. 49(5):677-683, 2000.
20. Kelley D. E., F. L. Thaete, F. Troost, T. Huwe, B. H. Goodpaster. Subdivisions of subcutaneous abdominal adipose tissue and insulin resistance. Am J Physiol Endocrinol Metab. 278(5):E941-8, 2000.
21. Lake D. E., J. S. Richman, M. P. Griffin, J. R. Moorman. Sample entropy analysis of neonatal heart rate variability. Am J Physiol Regul Integr Comp Physiol. 283(3):R789-97, 2002.
22. Lapidus L., C. Bengtsson, B. Larsson, K. Pennert, E. Rybo, L. Sjostrom. Distribution of adipose tissue and risk of cardiovascular disease and death: a 12 year follow up of participants in the population study of women in Gothenburg, Sweden. Br Med J (Clin Res Ed). 289(6454):1257-1261, 1984.
23. Laplaud D., R. Menier. Reproducibility of the instant of equality of pulmonary gas exchange and its physiological significance. J Sports Med Phys Fitness. 43(4):437-443, 2003.
24. Lewis M. J., A. L. Short. Sample entropy of electrocardiographic RR and QT time-series data during rest and exercise. Physiol Meas. 28(6):731-744, 2007.
25. Nagai N., T. Matsumoto, H. Kita, T. Moritani. Autonomic nervous system activity and the state and development of obesity in Japanese school children. Obes Res. 11(1):25-32, 2003.
26. Nagai N., T. Moritani. Effect of physical activity on autonomic nervous system function in lean and obese children. Int J Obes Relat Metab Disord. 28(1):27-33, 2004.
27. Nistala R., C. S. Stump. Skeletal muscle insulin resistance is fundamental to the cardiometabolic syndrome. J Cardiometab Syndr. 1(1):47-52, 2006
.
28. Oakes N. D., P. Thalen, E. Aasum, et al. Cardiac metabolism in mice: tracer method developments and in vivo application revealing profound metabolic inflexibility in diabetes. Am J Physiol Endocrinol Metab. 290(5):E870-81, 2006.
29. Ogden C. L., M. D. Carroll, L. R. Curtin, M. A. McDowell, C. J. Tabak, K. M. Flegal. Prevalence of overweight and obesity in the United States, 1999-2004. JAMA. 295(13):1549-1555, 2006.
30. Olshansky S. J., D. J. Passaro, R. C. Hershow, et al. A potential decline in life expectancy in the United States in the 21st century. N Engl J Med. 352(11):1138-1145, 2005.
31. Perseghin G., P. Scifo, F. De Cobelli, et al. Intramyocellular triglyceride content is a determinant of in vivo insulin resistance in humans: a 1H-13C nuclear magnetic resonance spectroscopy assessment in offspring of type 2 diabetic parents. Diabetes. 48(8):1600-1606, 1999.
32. Pietrobelli A., M. S. Faith, D. B. Allison, D. Gallagher, G. Chiumello, S. B. Heymsfield. Body mass index as a measure of adiposity among children and adolescents: a validation study. J Pediatr. 132(2):204-210, 1998.
33. Pincus S. Approximate entropy (ApEn) as a complexity measure. Chaos. 5(1):110-117, 1995.
34. Pincus S., R. E. Kalman. Not all (possibly) “random” sequences are created equal. Proc Natl Acad Sci U S A. 94(8):3513-3518, 1997.
35. Pincus S. M. Orderliness of hormone release. Novartis Found Symp. 227:82-96; discussion 96-104, 2000.
36. Pincus S. M. Approximate entropy as a measure of system complexity. Proc Natl Acad Sci U S A. 88(6):2297-2301, 1991.
37. Pincus S. M., I. M. Gladstone, R. A. Ehrenkranz. A regularity statistic for medical data analysis. J Clin Monit. 7(4):335-345, 1991.
38. Pincus S. M., J. D. Veldhuis, A. D. Rogol. Longitudinal changes in growth hormone secretory process irregularity assessed transpubertally in healthy boys. Am J Physiol Endocrinol Metab. 279(2):E417-24, 2000.
39. Platisa M. M., V. Gal. Dependence of heart rate variability on heart period in disease and aging. Physiol Meas. 27(10):989-998, 2006.
40. Platisa M. M., V. Gal. Reflection of heart rate regulation on linear and nonlinear heart rate variability measures. Physiol Meas. 27(2):145-154, 2006.
41. Porta A., T. Gnecchi-Ruscone, E. Tobaldini, S. Guzzetti, R. Furlan, N. Montano. Progressive decrease of heart period variability entropy-based complexity during graded head-up tilt. J Appl Physiol. 103(4):1143-1149, 2007.
42. Richman J. S., J. R. Moorman. Physiological time-series analysis using approximate entropy and sample entropy. Am J Physiol Heart Circ Physiol. 278(6):H2039-49, 2000.
43. Ryan S. M., A. L. Goldberger, S. M. Pincus, J. Mietus, L. A. Lipsitz. Gender- and age-related differences in heart rate dynamics: are women more complex than men? J Am Coll Cardiol. 24(7):1700-1707, 1994.
44. Someshwar J., S. Someshwar, K. C. Perkins. The obese adolescent. Pediatr Ann. 35(3):180-186, 2006.
45. Storlien L., N. D. Oakes, D. E. Kelley. Metabolic flexibility. Proc Nutr Soc. 63(2):363-368, 2004.
46. Stump C. S., E. J. Henriksen, Y. Wei, J. R. Sowers. The metabolic syndrome: role of skeletal muscle metabolism. Ann Med. 38(6):389-402, 2006.
47. Takarada Y., H. Takazawa, N. Ishii. Applications of vascular occlusion diminish disuse atrophy of knee extensor muscles. Med Sci Sports Exerc. 32(12):2035-2039, 2000.
48. Toubro S., T. I. Sorensen, C. Hindsberger, N. J. Christensen, A. Astrup. Twenty-four-hour respiratory quotient: the role of diet and familial resemblance. J Clin Endocrinol Metab. 83(8):2758-2764, 1998.
49. Veldhuis J. D., M. L. Johnson, O. L. Veldhuis, M. Straume, S. M. Pincus. Impact of pulsatility on the ensemble orderliness (approximate entropy) of neurohormone secretion. Am J Physiol Regul Integr Comp Physiol. 281(6):R1975-85, 2001.
50. Veldman R. G., M. Frolich, S. M. Pincus, J. D. Veldhuis, F. Roelfsema. Growth hormone and prolactin are secreted more irregularly in patients with Cushing’s disease. Clin Endocrinol (Oxf). 52(5):625-632, 2000.
51. Wells J. C., M. S. Fewtrell. Is body composition important for paediatricians? Arch Dis Child. , 2007.
Thanks!
Rock on
I have dream that the fitness world is under a revolution. Time to stop living by all the rules of how to train based on their rules.
I WANNA LIVE IN A FEARLESS STATE
I WANNA LIVE WITHOUT THE HATE
I WANNA BE ABLE TO DECIDE MY FATE
I WANNA BREAK OUT OF THIS CAGE
LET’S TAKE IT BACK
WELCOME TO THE FUTURE
–Welcome to the Future by Left Spine Down
Trying to actively feel everything is a recipe for chronic pain. I stole this idea from Frankie. You don’t need to actively seek it. If you screw up bad enough for your body, pain WILL find you. Trust me on this. I’ve done the experiments in my own lab. If you don’t trust me, let me know if you find it not to be true. I suggest you not test this one out.
Think of pain as an indicator light and your last line of defense. If I don’t put oil in my car ever, and my Ford pinto burns oil like at the rate of sweat running off a fat man chasing a runaway M&M, I wil have damage.
You don’t listen to pain in your body, you too will have some damage.
When the oil light comes on, I better stop the car before I destroy it (unless someone hits me from behind and I blow up anyway)
No, I am still not convinced your body will lie to you. If you can’t trust your own body, you are going to trust your body to someone else who does not trust their body either to tell you what is going on? I am all for guidance and seeking help, but their goal is to help you interpret what is going on based on your feedback.
Ford Pinto: Source
Oh boy, don’t start those dangerous deadlifts since you may just suck at them since you have never done them.
Newsflash, of course you are going to suck, you have never done them! With the exception of a few crazy athletes, you will NOT be very good at them on the first rep.
Did anyone not learn to play golf because they were afraid they were going to suck at it? Or did you want to learn to play golf, took lessons, stuck with it and became pretty good (or at least better).
The first time I learned to kiteboard, I got my a$$ handed to me over and over and over, even during a lesson! My buddy Rob had bruised his ribs earlier in the week and had to keep chasing the kite down as I floored it right into the ground. After about 20 minutes of this I hear “You suck!” The truth was I did suck, but over time, I got better. I also got a free trip across the soccer fiedl on my butt, complete with sexy grass stains as the kite powered up.
If you want to learn to kiteboard, take a lesson, but don’t NOT try it.
Did I never start because I was afraid I would suck? Nope.
Why would you not learn to do an exercise for fear you wil suck? Stupid idea that has got to go the way of the DooDoo bird.
DooDoo bird: Source
For the new readers, I am NOT saying load a bar up to 400 lbs and go ape $hit crazy with it and send your spine across my gym. I hate to clean up that kind of mess.
Test it, maybe you only do rack pulls. Maybe you can’t deadlift the standard way so you use a trap bar or even sumo style. Work around it, test it (ala Grip n Rip) and get better.
My buddy Brad Nelson has the perfect line with new clients
Brad to client “Are you a perfectionist”
Client “Yes”
Brad “Then today is not your day”
Love it.
Start today!
How demotivating is that. Sorry, you suck and you will have to eat chicken and broccoli the rest of your life, so start looking forward to that and please pay me more money so I can tell you how wonderful it is too.
I will then spend more time to tell you that broccoli has over 300 different phytonutritents and is really not the vile weed you think it is
Broccoli-A Vile Weed or Nutrient Powerhouse? Source
That is BS on a stick and you know it.
The goal of a long term program should be to eat as many “bad foods” as you can get away with WHILE keeping your body composition and health goals.
This gives the client some friggin hope. Yes, it is going to suck for awhile as your metabolism changes, but we are working towards you enjoying food long term and not making anything off limits forever.
If 4 brownies on a Saturday afternoon destroys you for the rest of the week, there are some issues to fix.
Caveat. I am not saying that you should mainline high fructose corn syrup, eat boxes of Twinkies for lunch and order more large slurpees with no ice from the 7-11 across the street that you rode your scooter to.
If your body composition and metabolism is a wreck, you have some work to do, but the body is amazingly adaptable and a vast majority of the time we can alters its ability to convert food into fuel with few “ill consequences” Hint, you NEED to exercise. This BS that exercise does not help obesity has got to stop also. Studies has shown that with exercise we can change your metabolic flexibity in a rather short period of time (1), even those who are diabetic or borderline diabetic.
Why would I cue your lat muscle during a pressing movement? Last time I checked, the lat pulls the humerous (upper arm) DOWN, which is the opposite of my goal to press the darn heavy weight up! How about I cue you based on the movement I want you to do? Hmm, I see an experiment here.
Latissimus Dorsi Muscle: Source
Why can we cue isolated movement, but argue that compound movements are better?
This makes no sense. Some rip on bodybuilders for doing “isolation work” (can we really isolate anything in the body?) and say compound movements are best; but in the same breath state that you need to work more on your VMO in your quads to stabilze your knee.
Or as above, you need to contract and pull your lat down while pressing.
How can you cue an isolated movement when you just stated isolation was bad?
How about we give ONE cue (yes ONE cue) at a time (no vomitting cues on them) on what movement we want the athlete to accomplish first. Let’s start there and see how that goes. Give their own brain a chance to fix it. Their own brain is darn smart at running their own body (it has lots of reps).
How would you know the lat was the problem or maybe it was the lower trap since I just read an article that said the lower traps are really lazy bastards and don’t like to work. Or maybe it is rhomboids, etc etc. Or maybe we need more YTWLs and more corrective work.
If you are teaching better gross (large scale) movement, let’s start there by cueing gross movement. Only get finer when needed.
Rock on
Mike T Nelson
Refernces
1) Diabetes. 2010 Mar;59(3):572-9. Epub 2009 Dec 22.
Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity.
Meex RC, Schrauwen-Hinderling VB, Moonen-Kornips E, Schaart G, Mensink M, Phielix E, van de Weijer T, Sels JP, Schrauwen P, Hesselink MK.
Abstract
OBJECTIVE: Mitochondrial dysfunction and fat accumulation in skeletal muscle (increased intramyocellular lipid [IMCL]) have been linked to development of type 2 diabetes. We examined whether exercise training could restore mitochondrial function and insulin sensitivity in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: Eighteen male type 2 diabetic and 20 healthy male control subjects of comparable body weight, BMI, age, and VO2max participated in a 12-week combined progressive training program (three times per week and 45 min per session). In vivo mitochondrial function (assessed via magnetic resonance spectroscopy), insulin sensitivity (clamp), metabolic flexibility (indirect calorimetry), and IMCL content (histochemically) were measured before and after training. RESULTS: Mitochondrial function was lower in type 2 diabetic compared with control subjects (P = 0.03), improved by training in control subjects (28% increase; P = 0.02), and
restored to control values in type 2 diabetic subjects (48% increase; P < 0.01). Insulin sensitivity tended to improve in control subjects (delta Rd 8% increase; P = 0.08) and improved significantly in type 2 diabetic subjects (delta Rd 63% increase; P < 0.01). Suppression of insulin-stimulated endogenous glucose production improved in both groups (-64%; P < 0.01 in control subjects and -52% in diabetic subjects; P < 0.01). After training, metabolic flexibility in type 2 diabetic subjects was restored (delta respiratory exchange ratio 63% increase; P = 0.01) but was unchanged in control subjects (delta respiratory exchange ratio 7% increase; P = 0.22). Starting with comparable pretraining IMCL levels, training tended to increase IMCL content in type 2 diabetic subjects (27% increase; P = 0.10), especially in type 2 muscle fibers. CONCLUSIONS: Exercise training restored in vivo mitochondrial function in type 2 diabetic subjects. Insulin-mediated glucose
disposal and metabolic flexibility improved in type 2 diabetic subjects in the face of near-significantly increased IMCL content. This indicates that increased capacity to store IMCL and restoration of improved mitochondrial function contribute to improved muscle insulin sensitivity.
Here we go again, a tip inside my brain as to what is rattling around in there. Trust me, you have been warned!
Adam T Glass just found them and was blown away. Great stuff. I prefer their earlier work with J Mann, but the new upcoming CD still sounds pretty cool. Awesome live shows if you ever get the chance to see them–go!
“The iron never lies to you..the iron will always kick you the real deal. The iron is the great reference point, the all-knowing perspective giver. Always there like a beacon in the pitch black. I have found the Iron to be my greatest friend. It never freaks out on me, never runs. Friends may come and go, but two hundred pounds is always two hundred pounds.” – Henry Rollins
It seems that loading the body axially like squats and overhead pressing seems to have a greater trigger for muscle hypertrophy (bigger muscles).
There is not any direct research that I have seen on this looking at similar loads (volume), but adding squats and kettlebell clean and jerks into your routine can pack on some mass quite fast.
I added about 3-4 lbs in the past month by adding these in. I also increased my calories again and my stress level was a bit lower too. Make sure those movement test well though (ala Grip n Rip).
I think we are making it entirely too complicated. An exercise/movement either makes you better or worse. If it makes you worse, you are not doing it correctly for YOUR body, or it is not good for you at THAT time. We are either getting better or worse. Is corrective exercise any more complicated than that?
We need to stop putting foods into categories as “good” or “bad.” Very few foods are really bad. If something is really bad it will kill you fast. That is bad. A poorly prepared puffer fish will kill you very fast. I say avoid it, but even eating twinkies for a week straight will probably not kill you. You may look similar to a twinkie by the end of the week though.
Along those lines our goal of health is backwards. People think they need to eat “clean” 100% of the time. Even the most strict, pre-competition bodybuilder types don’t need to do that 100% of the time and even then the pre contest period is short compared to the rest of their life.
Having people try to get to a goal of 100% is not realistic and will set them up for massive failure.
If you can do this at a 70% compliance vs a 90% compliance, 70% is better!
The ability to take in virtually any food item and convert it into fuel (termed Metabolic Flexibility) is key to health.
Do you want to have more freedom with your diet and eat the foods you love, or feel like you are boxed in and “never good enough”?
I knew when I start this, that it would be a long road. I had other warn me about it. I thought they were nuts. No way I was going to be in school for another 5-7 years after the 11 years I had already done. Screw that.
Well, fast forward to many years later and I am still plugging away at it. Very few things have I started that I have though long and hard about quitting and this is at the top of the list. The good part is that I am fully determined to finish, no matter how long it takes. I have decided it will not rule my life and as long as each day I am making progress, the end will come. And I can’t wait for that day. Wow. Once I graduate, all hell is going to break loose as my ability to output will go through the roof. You have been warned.
Adam mentioned this on a conference call and some are now sooooo scared of not doing an exercise correctly that they will not even TRY.
How can you get better at say a kettlebell clean and press, without ever doing one? The answer is you CAN’T.
I am NOT recommending that you go load up the bar with a max load and do your first deadlift attempt ever with it. That is just stupid. But starting with the bar and doing a few reps and measuring your range of motion (biofeedback) to see if it is good is an excellent start. Then work to make it better every time. Not starting will not help you. To get better, you can video your movements and keep testing or find a local qualified coach to help determine what is best for YOUR body; not what looks picture perfect. The goal is better, not initial perfection.
Very fun to use and easy to travel with too!
I believe that if you may fall in life (which is all of us), you need to train for falling. Special thanks to Frankie for pointing this out and covering it in the Movement Certification.
Great discuss on this at Charlie Weingrofts blog.
Joint mobility,while it can have its place and does work, is only a handful of movement the human body can do. Plus, we learn by performing large (gross) movements first and then work to refine them over time. Why would we start with the smallest movements FIRST?
If you want to learn how to squat, I want to see you friggin squat first! I don’t give a crap at that point about your ankle dorsiflexion or the ability of you to active control your pinky finger. I don’t care. If I can’t correct your squat movement, I will then start to go to more fine and fin movements. I may end up with ankle work or even thumb mobility work, but I would not START there.
You must read this post on Joint Mobility from Frankie below. It is a MUST read.
I have changed how I look at things this year once again. Here are the top things I learned in 2009 below. Can you see how I do things differently now? If so, place a comment below
If you have a weakness in one leg (most of use do) and you want to bring up your deadlift, doing a B-Stance deadlift where once foot is closer to the bar than the other (think of a very mild or shallow lunge where one leg is about 4 inches back from the bar in an asymmetric stance). Check it out at
I am still not happy with modern shoes and we would all be better off training in a pair of Vibrams, flat shoes, or no shoes at all.
I love GLC 2000 for joint issues. I have been using it for several months now and it is great. Others that recommended it to have tried it love it too. I have tried similar supplements like it in the past and they did nothing for me.
While I don’t have many joint issues, they did get a bit achy after many weeks of increased volume. I even tried to push it a bit more and still had no issues. I stopped taking it and within a few days to weeks, they got a bit touchy again.
GLC 2000 has a very high form of glucosamine and chondroitin sulfate, which are natural substances found in and around the cells of cartilage (joints). Glucosamine is an amino sugar that the body produces and distributes in cartilage and other connective tissue, and chondroitin sulfate is a complex carbohydrate that helps cartilage retain water.
I have some other theories that this should help connective tissue health, which then should help maximal strength.
If you go to the link below, you can pick up 2 for the price of 1 from Carl at Super Human Radio (which you MUST listen to).
Not sure how long the offer lasts though, so it may be gone by the time you read this.
They did not ask me to mention it at all, but I feel that if I find something that works really well I need to share it with all of you.
Try it out and let me know how it goes for you. If my theory is right, over a couple months you should see a nice strength increase too.
So there you have 10 things that have been running around in my head lately. Let me know what you think by posting a comment below
Rock on
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