Type II Diabetes Muscle Conspiracy

Another interesting study i read from an article from the University of Calgary suggests that muscle in obese people and Type 2 diabetics may be conspiring against them.

Extract of article...

Research by kinesiology investigator Dustin Hittel, PhD, has proven that muscle in extremely obese individuals produces large amounts of a protein called myostatin, which normally inhibits muscle growth—suggesting that for Type 2 diabetics, and the very obese, the task of getting healthy may be more difficult than initially thought.

It has been known for some years that naturally occurring mutations in the gene which controls myostatin results in double—muscling in cattle, dogs and even humans. Many in the body building community believe that blocking myostatin is a shortcut to the Arnold Schwarzenegger body.

The flipside is that producing too much myostatin has been linked with muscle wasting conditions such as HIV-AIDS, starvation and now, Type 2 diabetes.

Hittel believes this may be due to a pre-diabetic condition known as insulin resistance that “tricks” the muscles into thinking the body is starving despite the fact that blood sugar levels are skyrocketing.

“When that happens, the body reverses muscle production using myostatin,” says Hittel. “This is particularly worrisome because losing muscle mass further erodes your ability to control your blood sugar with exercise.”

One of the tell-tale signs of the transition between insulin resistance and full-blown Type 2 diabetes is a loss of muscle mass. “

Losing muscle mass makes sense from an evolutionary perspective since having large muscles during famine puts you at a serious risk for starvation,” explains Hittel. “Unfortunately, this survival mechanism has left us ill-equipped to deal with a Western lifestyle—lots of calories, little exercise—and it has laid the groundwork for the current epidemic of Type 2 diabetes.”

“The goal of my research is to understand how obesity, diet and exercise influence our metabolism and interact with our genome. This research sheds some light on an important part of the puzzle.”

So what does this mean?

Do strength training as well as training in the anaerobic zone i.e. intervals, to control Type 2 diabetes rather that the traditionally prescribed aerobic training. By doing so you also increase muscle receptor sensitivity to insulin.

My observations on man-made drugs

Man made pharmaceutical drugs always exhibit a doctor Jekyll and Mr Hyde behavior. All doctors know this and will have to decide if the benefits far out weigh the risks when prescribing them.

One of my clients happened to be on Propecia for nearly 10 years. Propecia controls male pattern alopecia (hair loss). However, side effects include loss of libido, decreased reproductivity and suspected increase in tummy fat due to the reduction in DHT which is antagonistic to estrogen production.

An excerpt of the benefits of DHT( Dihydrotestosterone) are as follows;

"How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.

Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.

Lastly, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production – testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section."

With the reduction in DHT, and corresponding icnrease in estrogen, the client had difficulty in increasing muscle density and reducing his hormonal imbalance. This resulted in less than stellar results in his weight management programme.

In conclusion, i sincerely believe that everyone should be fully aware of the consequences of being too dependent on man made drugs. There are always natural alternatives that will give you all the benefits and none of the side effects.

Research on "THORACIC STRETCHING AND MOBILIZATION"

Research in support of the influence of thoracic spine mobility, and it’s effect on shoulder range of motion. Here’s a segment of the abstract:

Title: THE EFFECT OF THORACIC STRETCHING AND MOBILIZATION ON
SHOULDER RANGE OF MOTIONAuthors: Matthew D. Ditzler, DPT, CSCS; Brian Peers, PT, OCS; Steven Adsitt, DPT

Results : Improvements in Active ROM and Passive ROM shoulder flexion, Internal Rotation, and External Rotation were demonstrated in all treatment groups with the most significant improvements being made in AROM and PROM shoulder IR. Group 1 (SS): AROM IR change in degrees=(mean ± SD) 4.2° ± 4.4°, PROM IR change in degrees= 6° ± 4° ;Group 2 (MS): AROM IR change in degrees= 8.6° ± 6.5°, PROM IR change in degrees= 8.5° ± 6.9°; Group 3 (PS): AROM IR change in degrees= 5.2° ± 7°, PROM IR change in degrees= 6.3° ± 7.4°; Group 4 (TJM): AROM IR change in degrees= 10° ± 7.6°, PROM IR change in degrees= 5.8° ± 5.1°.

Conclusions : Based on the findings above, maneuvers for addressing thoracic mobility and thoracic ROM correlate with improvements in glenohumeral ROM in each plane, with the greatest changes being made in glenohumeral IR. The most significant gains in IR ROM were made after treatment with a grade V thoracic spine mobilization. Not all changes in ROM demonstrated statistically significant changes after one treatment, however 18% average improvements in IR ROM after one treatment demonstrate clinically significant changes and the need for further research.

Clinical Relevance : Assessment and treatment of thoracic spine mobility and thoracic extension should be considered in the evaluation and treatment of decreased glenohumeral joint
ROM.

My take: Most clients you get are white collar workers with desk bound jobs. The nature of desk bound jobs encourages lumbar mobility while reducing the need for thoracic mobility. In the mobility-stability continuum, the lumbar is meant for stability while the thoracic spine is built for mobility. Getting excessive mobility from the lumbar which is built for stability will result in common injuries such as spinal spondylosis, spondylolethesis and spondylolysis (i hope i got the spelling right).

Getting the thoracic spine mobile will reduce the need for the lumbar spine to be excessively mobile. As such, including thoracic rotations and extensions in the warm up will reduce risk of injury, reduce compensatory patterns, and improve range of motion of the upper extremity.

Differentiating whether a muscle is stiff or short

In a client assessment it is important to observe if a muscle is short or if it is stiff. This helps in developing a corrective plan strategy.

Treating each case in a cookie cutter approach will only give you a 50% success rate. A short muscle lacks length. It may be that the muscle is positioned in a shortened position frequently (due to an injury) and the muscle fibers have atrophied and discarded sarcomeres in series or the connective tissues have adaptively shortened due to muscle creep in daily activities.

If you actively and/or passively stabilize the proximal attachment of the muscle and move the joint into a position to stretch the muscle, the proximal attachment will move well before reaching the end range of motion of the joint i.e. You will feel a sudden stop and the joint will start moving.

A stiff muscle has greater resistance to stretch. This may be due to muscular hypertrophy or a greater quantity of connective tissues. In the case of a stiff muscle, if you actively and/or passively stabilize the proximal attachment and move the joint into a position to stretch the muscle, The joint will move through it’s full range of motion (ROM) without movement at the proximal attachment assuming enough force is applied to stretch the muscle. You will just feel a constant resistance to stretch through full ROM.

Short muscles require repetitive, prolonged stretching (up to 10min) to encourage creep of connective tissues and the addition of sarcomeres in series to add length.

Stiff muscles can be corrected by balancing the stiffness across a joint by strengthening their antagonists and by holding the antagonists in a shortened position as they may have been adaptively lengthened over time. Stretching techniques like Active Isolated Stretching, Contract Relax Antagonist contract aids in stretching stiff muscles. Core work has also been shown to influence extensibility of stiff muscles.

Injuries from running/jogging

All the runners i have treated have at least one, and more commonly several, significant finding such as weak core musculature, poor hip range of motion, poor hip strength, lack of ankle mobility which affects dorsiflexion (and thus running mechanics), pronation issues.

The bears repeating...u don't run to be fit. You have to be fit to run. Please prepare yourself adequately for running if you don't want to suffer from overuse injuries.

A Rant on Misdiagnosed Leg Length Discrepency

95% of the cases i've seen of leg length discrepancy are misdiagnosed by unscrupulous doctors. How they normally assess patients is to compare heel to heel level in a supine position. This test normally brings up a positive result as most of us have such a differential due to posture and right/left dominance. A proper test would involve using a measuring tape to measure and compare length from ASIS (Anterior Superior Illiac Spine) to maleolus (bottom of ankle bone) on both legs.

Doctors will use the positive result to prescribe custom made insoles to the client (expensive stuff). However, using insoles can aggravate the client's condition especially if the leg length discrepancy is caused by soft tissue dysfunction i.e. tightness.

Leg length discrepancy caused by soft tissue dysfunction is normally (about 80% of the time) the result of a tight Quadratus Lumborum which causes hip hiking. Other reasons can involve motor control impairment of the soles of the foot and temporo-mandibular issues.

Usually, soft tissue work such as regular massage, self-myofascial release as well as core exercises to stabilise the hip can correct such discrepencies.