Metabolic Flexibility: A Literature Review

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

Metabolic Flexibility: You Need to Burn that Fat Off!

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 95^th 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.

References

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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
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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

Mike T Nelson

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4 Stupid Fitness Things that Need To End

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

4 Stupid Fitness Things that Need To End

1) Seeking More Sensation During Training.

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

2) Don’t Learn a New Exercise Until You Can Do It Correctly

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.

“The first rep is the worst rep!” -Frankie Faires

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!

3) Perfect Nutrition 100% of the Time

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.

4) Isolated Exericse Cues

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.

Comments
What do you think on these?  Have I lost it completely?  Let me know either way!

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.

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Dave Barr: Exclusive Interview About Supplements, Testosterone, Growth Hormone, and Exercise

One of the things that I love doing is hanging out, talking shop about exercise, nutrition, and movement.    I feel so honored to be able to pick the brains of many of the top people in the industry.

Movement, Movement, Movement

A few weeks ago, Cal Dietz from the U of MN left me a message that Neil Rampe, the therapist for the AZ Diamondbacks was going ot be in town, so I should stop down for a movement pow wow.   I was sooooo stoked and it was a great meeting.

Three hours there flew by like it was 20 minutes.  Movement of all forms was discussed from cranial work for more internal rotation (like 30 degrees more in minutes), breathing patterns, asymmetries, soft tissue work (a great local soft tissue expert was present too), and how to extract maximal performance from athletes.  Great, great time.

More This Weekend

Just last night I was hanging out with Dave, Brad Nelson, Adam T Glass and Frankie Faires and will be with them and many more today too.  Aaron S from UND (great strength coach at Univ of North Dakota) will be sleeping on my couch for 2 nights (check out his blog HERE) and a few others are scheduled to be in town also.  The amount of information I will be able to pick up and use after just a few days is going to be insane, and I am so excited about it.  I am like a kid in a candy store.  Whooo ha.

Conferences for Vacation?

I am a huge geek and I go to conferences on exercise physiology for fun.  This past May Jodie and I flew out to Seattle for a vacation and I attended the American College of Sports Medicine’s Annual conference for 3 days.  I decided to not present this year, so I just got to hang out with much less stress and absorb as much as I could (read, pester people at posters about their research).

I had a blast and learned tons of new things, although some of the presentations can be a bit dry.  Ok, a bit dry is an understatement, but I endure this all to bring you just a few worthwhile tidbit of info to have you set another PR.

Enter the Barr

Good thing there are other geeks (albeit with much bigger arms) than me there like my good buddy Dave Barr.   Dave is a very bright guy and has a great background in exercise physiology and nutrition.  He currently works for Muscle and Fitness, so be sure to check out his blog there below

David Barr’s blog at Muscle and Fitness

I was able to corner him and got to pick his brain.  Luckily for you I have it on tape here!

Sit back as Dave Barr drops knowledge bombs from the ACSM 2009 Annual Conference.

Note this was previously released as a special bonus, but now I am making it available to everyone.  The conference was this past May, but many time oral presentations have data that is not published for many months to even years after it was presented (if it gets published); so this info is still cutting edge.

Enjoy!

Thanks Dave!!

Let me know what you think about this in the comments section!

Rock on
Mike T Nelson

PS

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Cooking in the Lab: Low Carb Egg Nog Super Shake

Happy Holidays and time we do some cooking the lab!

I’ve tried it a few times after and I like it a little better now without the vanilla, but feel free to adjust to your taste. I have not added too many veggies to it yet, but I was thinking a few figs may be interesting.

Let me know what you think and if you have any other great super shake recipes to share in the comments.

Rock on
Mike T Nelson

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3 Tasty Tips for More Muscle Mass

In this video

• Find out my 3 favorite foods to gain muscle (the answer may surprise you)

• Can you eat “bad” foods and gain muscle?

• Do calories matter? (a hint, YES!)

Let me know what you think by posting a comment.   Let me know if you like video format or more written format too.   I love comments!!

Rock on

Mike T Nelson

PS

If you are looking for high quality protein at rock bottom prices, check out Protein Factory HERE (note, I do make 4% on each sale, but this is the same protein I have personally used for the past 5+ years).

Ranting on Exercise, Nutrition and Lifestyle

Hang on to your hats as I smell a rant brewing. Here we go.

My good friend David and I had a good chat about nutrition and exercise this past summer while we were hanging out his cabin.  Huge shout out to him and his wife Lisa for having Jodie and I come up there this summer to see everyone else too. I was so desperate to kiteboard, that I brought all my gear and there was no wind. So we did the next logical thing and I kiteboarded behind the pontoon boat! Whoo ha.

Oh, I got carried away there and back to the topic on hand. David said his blood pressure was high and he decided it was time to change his nutrition and exercise.

Fast forward to this email I got the other day.

I just wanted to tell you that my diet has pushed my blood pressure back to normal! I have been eating

2 bananas every morning and lots of apples, no carbs basically. I went in 4 weeks ago and they put me on the machine that takes 3 readings and averages them, 121/73!!!! 6 months ago it was 153/98 and I was in taking excessive Diet Dew also.

– David Timmersman

Sales and Marketing Manager, Plymouth, MN

Massive Action

Huge CONGRATS to David for taking massive ACTION. You would be amazed at how many people I talk with about nutrition and exercise and how many still don’t take any action. While there are many reasons for that, some just don’t believe that nutrition and exercise have that big of an effect and they need drugs for the rest of their life.

Really?

Last time I checked, I have yet to find one person with a statin deficiency. While drugs are needed at times, the long term goal should be to work with your doc and a consult a qualified trainer/ nutritionist. Note, I said “qualified”, not some bone head that you pay lots of money to who just counts your reps for you and just passed their 2 hour open book online certification. You can hire a chimp to count reps for you and just pay them in bananas.

You need someone who has a background in exercise and nutrition and they should work with you to meet YOUR goals. This include nutrition advice, a program custom designed for your needs with exercises, sets and reps, mobility work and accountability. Progress is key as the old Mel Siff line goes “Any monkey can make you sweat” Maybe that is the same monkey that is counting reps. Hmmmmm

Massive Action + Knowledge = Results

Who is going to make some massive change next? Let me know by placing a comment below!

The time is now.

Rock on

Mike T Nelson

Nutrition Chat : Cholesterol, Protein, Muscle Growth and More!

Here I talk about the latest research on how to maximize muscle growth through nutrition based on a phone chat I had with Dr. Lonnie Lowery.

You probably know Dr. Lowery from his writings at TMuscle.com (may not be uber work friendly and also Iron Radio.  I encourage you to check out both.

Here we go!

Here I yap about

• Cholesterol -  Is it that Evil?

• mTOR – What the heck is that?  Why do I give a crap?

• Calories Are King!

• How Much Protein?

• Diabetics and Carbs

• Metabolic Flexibility

Let me know what you think and what questions you have!  Post away in the comments!

Rock on
Mike T Nelson

Greetings!

I trust everyone had a killer weekend.  Jodie and I were off to South Dakota for her family reunion.  I will have an update in the next day or so and some tips on how you can survive a 12 hour one way car trip.

Here is an interview I did with Rick from Exercise for Injuries.  We chatted about everything from Z-Health, to athletic performance, to corrective exercises.  Topics covered are:

I. Movement

• How I got my first client
• Rehab and prehab work for shoulder issues
• “Traditional” corrective exercise work vs “Non traditional” (Z-Health, neurology)
• Neuroplasticity.  What is that?  Why should I care?
• Can we grow more brain cells?  (Is there hope for me?)
• How does the brain get its information?
• Movement maps- Why are they important and how do they affect athletic performance.
• If you have a chronic shoulder issue, is the shoulder always the SOURCE of the issue? (Hint, nope)
• The ultimate assessment that is really really fast
• Can you get instant pain relief? Is that possible?
• What the heck is an arthrokinetic reflex?
• How can you get an instant increase in strength in seconds

II) Nutrition (starts at 12:47)

Metabolic Flexibility

• What is it?
• How can it help you?
• What happens with energy drinks like Monster, Red Bull, etc

Notes:
This was done back in June
Blog has been updated to this one at http://www.ExtremeHumanPerformance.com
I am hoping (fingers crossed) to graduate later this Oct

Special thanks to Rick at Exercises for Injuries for doing the interview.
Check out his site at

Exercises For Injuries

Any questions or clarifications, drop me some comment love.  Feel free to download this MP3 and pass it around to your friend and enemies.

Rock on
Mike T Nelson

Play Now:

 Interview with Mike T Nelson Extreme Human Performance [19:56m]: Play Now | Play in Popup | Download

Have you heard this before?

• I am too busy to eat well
• I just don’t have time
• I travel a lot and don’t have time or access to good nutritious food
• Taco Bell needs my support!

Nutrition is very important for athletic performance, both in the gym and on the playing field.  The key is to be CONSITENT.

The wind was up here recently, so I decided to take some time off and go kiteboarding with my friend Rob.  Do you have to let your nutrition slip just to have fun with your friends?  Find out below

What are other tips that work well for you?  Post them in the comments!

Rock on

Mike T Nelson

Play Now:

 Nutrition on the Go [5:34m]: Play Now | Play in Popup | Download