JOURNAL OF ENDURANCE
July 2005 #7.
Kee' atta h 'atta 'ath 'attı y 'attem 'atten 'atte na h 'atte nna h 'o r nı yr
nir ne yr ne r ne ra h…
THOU SETS ON FIRE
my
LIGHT...
PSALM 18:28 a
______________________________________________
Greetings, the following questions are reviewed in this issue:
#1 What is the role of dietary fat for optimal health and performance?
#2 What is the rationale behind the performance enhancing report of the “COMPEX
SPORT” from top pro cyclists, Olympic Time Trial Champion Tyler Hamilton, 6time Tour de France top sprinter, Erik Zabel, and 3-time female winner of the Tour
de France, Joane Somarriba?
#3 Is there a genetic relationship between endurance sports, cognitive health, and
longevity?
#4 What foods chronically consumed are shown to enhance life span?
#1 What is the role of dietary fat for optimal health and performance1?
Lipids (fats) are a chemically diverse group of molecules. Some lipids are long chain
hydrocarbons with polar ends (such as fatty acids) and others are combinations of
1
By permission, courtesy of Professor David D. Kitts, Ph.D, et al., The Food, Nutrition & Health
(FNH) of the Faculty of Agricultural Sciences at The University of British Columbia, Department of
Food Science @:
http://www.agsci.ubc.ca/fnh/index.htm
or go to: Food 301 module @
http://www.agsci.ubc.ca/courses/fnh/301/carb/carb3.htm
http://www.agsci.ubc.ca/courses/fnh/301/modules.htm
porphoryin rings (such as cholesterol). Nevertheless, almost all lipids are insoluble
in water and are soluble only in organic solvents such as chloroform, benzene, and
ether. Food Scientists often differentiate fats vs oils by their physical state at room
temperature. Fats, which consist mainly of saturated fatty acids, are solid at room
temperature. These include beef tallow and lard. Oils are liquid at room
temperature. This is because they are made up of mainly long chain unsaturated
fatty acids. This unsaturation inhibits close packing and keeps the lipids form
crystallizing at room temperature.
ƒ(A) Fats – Solid
ƒ(B) Oils - Liquid
(A) Saturated fatty acids have crystallization stabilized by hydrophobic interactions.
(B) Mixtures of saturated and unsaturated fatty acids. The cis-double bonds of the
unsaturated fatty acids introduce bends in the hydrocarbon tail and inhibit close
packing.
Triacylglycerides
Fatty acids are the building blocks of triacylglyceride which is the most common
molecule found in fats and oils. In each triacylglyceride, there is a glycerol molecule
with three fatty acids attached by ester bonds. Fatty acids are long chain
hydrocarbons with polar ends. When the carbon chain is completely hydrogenated,
the fatty acid is referred to be a Saturated Fatty Acid. An Unsaturated Fatty Acid
contains double bonds along the carbon chain.
The compositions of fatty acids in different fat vary and can affect the physical
properties of the fat. In general, fats containing more saturated fatty acids have
higher melting points; fats containing a higher percentage of unsaturated fatty acids
have lower melting points and are liquid at room temperatures.
COMMON FATTY ACIDS IN FOODS AND SOURCE CLASSIFICATION:
Common
Common Fatty
Chemical
Melting
Systematic Name
o
Acid Name
Abbreviation
Point ( C) Source
Lauric
Dodecanoic
C12:0
43.6
Coconut
Myristic
Tetradecanoic
C14:0
53.8
Coconut and
Milk Fat
Palmitic
Hexadecanoic
C16:0
62.9
Animal and
Vegetable
Stearic
Octadecanoic
C18:0
69.9
Animal and
Vegetable
Arachidic
Eicosanoic
C20:0
75.2
Peanut Oil
Palmitoleic
9-Hexadecenoic
C16:19
-1.5
Milk Fat
Oleic
9-Octadecenoic
C18:1w9
14.0
Animal and
Vegetable
Linoleic
9,12-Octadecenoic C18:2w6
-11.0
Animal and
Vegetable
Linolenic
9,12,15Octadecatrienoic
C18:3w3
-30.0
Linseed and
Rubberseed
Arachidonic
5,8,11,14Eicosatetraenoic
C20:4w6
n/a
Lecithin and
Lard
As used in the above table, three nomenclature systems are commonly used to
describe fatty acids. They are common name, systematic names, and chemical
abbreviation.
Chemical Abbreviation:
•
•
•
•
The first letter C represents
Carbon
The number after C and before
the colon indicates the Number of Carbon
The letter after the colon shows the Number of Double Bond
The letter n (or w) and the last number indicate the Position of the Double
Bonds
Positional Distribution of Fatty Acids in Fats
Distribution patterns of fatty acids in triacylglycerol vary among animals and
plants. In general, long polyunsaturated fatty acids are preferentially located at the
center position, while the short chain acids in milk fat are located at the sn-3
position.
Essential Fatty Acids
Although our bodies are capable to synthesize a number of fat compounds from
sugars and proteins, linoleic (C18:2n6) and linolenic (C18:3n3) acids must be come
from foods; n-6 and n-3 fatty acids are essential.
Subsequent elongation and desaturation of these fatty acids will lead to the
production of a number polyunsaturated fatty acids (PUFAs).
ESSENTIAL N-6
n-6
†
& N-3 FATTY ACIDS PATHWAYS
n-3
†
TRANS-FATTY ACIDS COMPROMISE OPTIMAL HEALTH
Trans-unsaturated fatty acids are commonly found in hydrogenated vegetable oils.
Oils are hydrogenated to eliminate the double bonds in the carbon chain in order to
improve oxidation stability and to increase melting point. Liquid vegetable oil
becomes hardened and remains solid at room temperature. However, during
hydrogenation, some unsaturated fatty acids that are normally in the cis
configuration are converted to the trans isomers. The resulting trans-fatty acids
have long straight carbon chains with properties similar to those of saturated fatty
acids.
Sources of Trans-Fatty Acids
In the past, margarines made with hydrogenated vegetable oil are the major source
of trans-fatty acids in Westen diet. However, new processing techniques allow the
production of margarines with reduced trans-fatty acids. Currently, commercially
baked goods, fast foods and other prepared foods are the dominant sources of transfatty acids in our diets. Current estimates of trans-fatty acid intake in developed
countries range from 0.5 to 2.6% of energy.
FOOD
TRANS-FATTY ACID %
Hard Margarine
12.4
Soft Margarine, Low in PUFA
9.1
Chocolate Cake with Icing
7.1
Soft Margarine, High in PUFA
5.2
Butter
3.6
Beefburger, Fried or Grilled
0.8
Safflower, Sunflower, Soy Oils
0.0
TRANS-FATTY ACIDS INCREASE THE RISK OF CORONARY DISEASES
A number of studies have been conducted to evaluate the effects of trans-fatty acids
on plasma lipids. Results from the various studies are similar. In general, it is
agreed that the consumption of trans-fatty acids or hydrogenated fats instead of cisfatty acids or natural oils led to increases in total blood cholesterol levels but not as
much as the consumption of saturated fatty acids. However, unlike saturated fat,
trans-fatty acids also led to an increase in LDL cholesterol and a decrease in HDL
cholesterol when used. As a result, the net effect of trans-fatty acids on the
LDL/HDL cholesterol ratio is approximately double that of saturated fat.
Furthermore, the consumption of trans-fatty acids also led to increased plasma
triglyceride levels. These changes may increase the risk of coronary diseases.
Apparently, replacing butter with margarine high in trans-fatty acids may obtain no
benefit; instead, the consumption of trans-fatty acids may even increase the risk of
having coronary hear diseases. Though soft margarine is slightly better than hard
margarine, or reducing the overall consumption of fat will maintain heart health.
Avoid the use of processed solid at room temperature fats, your heart health and
performance will benefit immediately.
LIPID OXIDATION IN IRRADIATED FOOD
Lipid oxidation is a three-steps process including initiation, propagation, and
termination.
1. Initiation: Hydroperoxide (LOOH) in the presence of metal ions undergoes
initiation to give peroxyl radical (LOO o).
LOOH ¼LOO o
2. Propagation: The peroxyl radical (LOO o) attracts the weak C-H bonds on
fat (LH) and generates a fatty acid radical (L o). The L o reacts with oxygen
(O2) to form another peroxyl radical (LOO o). The newly formed LOO o
will enter the reaction cycle again to form more LOOH and L o.
LOO o + LH ¼LOOH + L o
L o + O2 ¼ LOO o
It is found that the rate constants for reactions with oxygen are lower for
unsaturated and polyunsaturated fatty acids that those of saturated fatty
acids. THUS, FOODS CONTAINING A HIGH LEVEL OF UNSATURATED FATS ARE PRONE TO
LIPID OXIDATION.
3. Termination: Two free radicals can undergo termination reaction to
produce a stable and inactive product.
L o + L o -- > stable end product
LOO o + LOO o ¼ stable end product
LOO o + LOO o ¼ stable end product
In general, foods that contain a high level of unsaturated fats are prone to
oxidation. In addition, rates of lipid oxidation can be accelerated by the presence of
UV light, infrared rays, metals, and prooxidants. As lipids oxidize, hydroperoxides
are formed and lead to further oxidation. Eventually, secondary reaction products
such as aldehydes, ketones, acids, and alcohols are formed and adversely affect
flavor, aroma, color, nutritional values, and the overall quality of the food.
How can lipid oxidation be prevented?
• Antioxidants
• Low Temperature Storage
• Oxygen Resistant Packaging
• Minimize UV Exposure
Food irradiation is a processing method applied to foods in order to inactivate food
borne bacteria and to extend the shelf-life of target foods. During irradiation,
gamma ray or radioactive particles are being bombarded to the food materials.
Consequently, electrons from water molecules are removed and FREE RADICALS ARE
FORMED. Although these free radicals are responsible for the inactivation of microorganisms, they also PROMOTE LIPID OXIDATION in high fat food products such as
ground beef and poultry. Irradiation at 1.5 to 10 kGy doses has been reported to cause
an increase in lipid oxidation in turkey meat and fish muscles. At higher irradiation
dosage, more lipid oxidation occurs and eventually leads to the production of rancid
flavor and odor in irradiated meats.
Fortunately, the addition of antioxidants such as vitamins C and E to food prior to
irradiation has been found to be an effective method to minimize lipid oxidation and
the production of off flavor as discussed above. Extensive studies are being
conducted to reduce the effects of irradiation dosages, packaging materials, and
storage methods on lipid oxidiation of various meat and meat products. At present I
am convinced that heating, microwaving foods is not better than consuming those
nutrients in their native uncooked state. COMMENT: Am I a total raw foodist? Not
totally, I still cook meats from fish or poultry in order to control a variety of active
microbes in meat.
FAT SUBSTITUTES
Fat is an important component in determining the sensory attributes of foods. It
contributes to mouthfeel, aromatic, and textural properties in the foods we
consumed. Ironically, over consumption of fat is associated with a number of
diseases; namely, hypertension, atherosclerosis, breast and colon cancer, and the
development of obesity. Only 25-30% of our energy should from fat and no more
than 10% from saturated fat in our diet.
QUESTIONABLE FAT REPLACERS OLESTRA & SIMPLESSE
OLESTRA
Olestra is a trade name for sucrose polyester manufactured by Proctor & Gamble.
This substance is composed of SUCROSE (table sugar) with six to eight fatty acids
bound to it. These fatty acids are from vegetable oils such as soybean or corn oil.
Since the Olestra molecule is large in comparison to a triacylglyeride, it is not
hydrolyzed by the digestive enzymes and therefore is not absorbed. As a result, it
passes through the digestive system unchanged and provides zero calories to the
human body. One drawback of the consumption of Olestra is that it causes a
DECREASED ADSORPTION OF FAT-SOLUBLE VITAMINS. It has also been
reported that the consumption of olestra may lead to DIARRHEA.
Physical and chemical properties of olestra are very similar to fat and are
determined by the chain length and saturation of the fatty acids. The color, taste,
heat stability, and shelf-life of oil made with Olestra is comparable to those of
conventional fats. In addition, Olestra is heat stable and can be used for cooking,
baking, and deep-fat frying. A Food Additive Petition filed in April 1987 is currently
being reviewed by the FDA for the approval of the use of Olestra as shortening.
SIMPLESSE
Simplesse was first introduced by The NutraSweet Company in 1988. It is made
with egg white and/or milk or whey proteins through a process called
microparticulation. During microparticulation, proteins in solution are deaerated
and hearted to a temperature just below the coagulation point of the proteins. The
solution will then be homogenized and sheared at elevated temperatures. As a
result, the proteins aggregate into small, round particles range in size from 0.1 to 2.0
um. The protein aggregates are so small that the mouth cannot perceive them
individually. Instead, they roll over one another, creating a creamy taste and texture
just like fat. Once ingested, Simplesse is digested and absorbed by the body as
protein. However, due to its high water content, each gram of Simplesse yields only
1 to 2 kcal. Simplesse is used in a variety of food applications. It is added to dairy
products such as ice cream, yogurt, cheese sour cream, dips, and oil-based foods
such as salad dressings and mayonnaise. However, the compound cannot be used to
cook foods because heat causes the protein to gel and lose its creamy quality. The
FDA approved the use of Simplesse in frozen desserts in February of 1990. The
resulting product is nutritionally improved compared to a 16 percent butterfat ice
cream, yet it has the taste and texture of high-fat ice cream.
DHA PREVENTS ALZHEIMERS
Learning and memory depend on dendritic spine actin assembly and
docosahexaenoic acid (DHA), an essential n-3 (omega-3) polyunsaturated fatty acid
(PFA). High DHA consumption is associated with reduced Alzheimer's disease (AD)
risk, yet mechanisms and therapeutic potential remain elusive. Here (1), researchers
report that reduction of dietary n-3 PFA in an AD mouse model resulted in 80%90% losses of the p85alpha subunit of phosphatidylinositol 3-kinase and the
postsynaptic actin-regulating protein drebrin, as in AD brain. The loss of
postsynaptic proteins was associated with increased oxidation, without concomitant
neuron or presynaptic protein loss. n-3 PFA depletion increased caspase-cleaved
actin, which was localized in dendrites ultrastructurally. Treatment of n-3 PFArestricted mice with DHA protected against these effects and behavioral deficits and
increased antiapoptotic BAD phosphorylation. Since n-3 PFAs are essential for p85mediated CNS insulin signaling and selective protection of postsynaptic proteins,
these findings have implications for neurodegenerative diseases where synaptic loss
is critical, especially AD.2
COMMENT: While improving or reducing butterfat content is a healthy choice, the
long term side effects of either Simplesse or Olestra remains undetermined in spite
of the fact their nutrient density reduces some of the harmful fats in processed
2
Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model.
Calon, F., Lim, G. P., Yang, F., Morihara, T., Teter, B., Ubeda, O., Rostaing, P., Triller, A., Salem, N.
Jr., Ashe, K. H., Frautschy, S. A., Cole, G. M., Neuron 2004 Sept 2;43(5):633-645.
foods. I advise against modified dietary fatty acids in favor of using only 2 essential
fatty acids from plant foods or fish oils. The conversion of desaturase and elongase
enzymes, linoleic (C18:2n6) and linolenic (C18:3n3) acids are converted to
arachidonic acid (AA; C20: 4n6) and decosahexaenoic acid (DHA; C22:6n3),
respectively. These PUFAs are thought to play important roles in supporting
normal growth and in developing cell structures in the brain, peripheral nerve
growth, and are precursors of bioactive metabolites such as prostaglandins,
thromboxanes, and leukotrienes. Since the desaturation and elongation of n-6 and
n-3 as well as the n-9 series utilize the SAME ENZYMES, the proportion of dietary n-6
and n-3 fatty acids will affect the amount and the type of metabolites produced. Try
to consume N-3 separate from N-6 and N-9. Two to four grams of Carlson’s
Norwegian Salmon Oil rich in DHA & EPA is my (biased) personal favorite daily
fatty acid supplement. Not only is Omega-3 DHA a cardiovascular protective
macronutrient, it is also a remarkable preventative for cognition in later years. In
over 70 dietary analysis performed on athletes and non-athletes, none were
consuming the required amount of the essential fatty Omega-3 fatty acids for
minimal health outcome. It is from the Omega-3 fatty acid that docosahexaenoic
acid is metabolized. Our present-tense need for DocosaHexaenoicAcid is blood
sugar, HDL, LDL, and triglycerides control, without which cardiovascular
pathology and cognitive deterioration may result.
______________________________________________________________________
#2 What is the rationale behind the performance enhancing report of the “COMPEX
SPORT” from top pro cyclists, Olympic Time Trial Champion Tyler Hamilton, 6time Tour de France top sprinter, Erik Zabel, and 3-time female winner of the Tour
de France, Joane Somarriba?
WHY ELECTROTHERAPY (FORM VS FUNCTION)
Physical therapists, athletic trainers and doctors have often wondered why Compex
was better tolerated when all the settings were the same; Same Frequency; Same
Pulse Width; Same Amplitude. The difference is in the quality of the signal. This
makes sense since the objective of the Compex is to take healthy muscle to greater
gains in strength, power, endurance and recovery. People manage pain in many
ways. Electrotherapy, also called electromuscle stimulation (EMS) is commonly
used for pain relief or increasing circulation.
There are several different methods of administering electrotherapy3:
TENS
The most commonly used is TENS. (transcutaneous electrical nerve
stimulation). TENS is a specific modality used for pain management. TENS
stimulates sensory nerves to block pain signals, and stimulate endorphin
production. Interferential therapy is characterized by the crossing of two
3
See full text article compex_endurance list @:
http://health.groups.yahoo.com/group/compex_endurance/files/
medium, independent frequencies that work together to effectively stimulate
large nerve fibers. These fibers interfere with the transmission of pain
messages at the skin easily penetrating underlying tissue.
IF
IF (interferential) differs from TENS by providing deeper penetration with
more comfort and increased circulation.
PDC
High volt PDC (pulsed direct current) is used primarily for local blood flow
stimulation through muscle pumping and through the “polarity effect”, by
placing positive or negative polarity into a damaged muscle. Negative
polarity applied over the injury site helps to help disperse negatively charged
proteins away from the site, helping to move the excess fluid thus acting
EXACTLY like ice … constriction. Positive polarity applied over the injury
site 48+ hours after an injury will dilate EXACTLY like heat. Many athletes
will use PDC before (dilate or heat) and after (constriction or ice) training or
events.
NMES
NMES (neuromuscular electrical stimulation) is used by doctors and
therapists for muscle reeducation and post-surgical rehabilitation. It is
characterized by a low volt stimulation targeted at motor nerves to cause a
muscle contraction. Common uses are to prevent disuse atrophy, re-educate
muscles, postop orthopedic surgery, gait training and reduction of muscle
spasms. NMES is different from the other therapeutic EMS modalities in
that it stimulates motor nerves to contract muscles, while TENS and
interferential (IF) and high volt PDC stimulates sensory nerves to help block
pain and assist with decreasing inflammation.
COMPEX
Compex is a neuromuscular stimulation device that is available over the
counter without a prescription. The Compex is a 4 channel neuromuscular
stimulator that is used for sports training to increase the strength and
recovery of healthy muscle. It uses a symmetrical biphasic waveform (similar
to most neuromuscular stimulators) producing safe, consistent muscle
contractions without muscular, cardiovascular or psychological fatigue,
thereby optimizing and enhancing muscle performance. The different
training programs allow for the stimulation of slow to fast and very fast
twitch fibers. Each program is designed to have dramatically different effects
on the muscle.
WHAT MAKES COMPEX DIFFERENT THAN REHAB NMES DEVICES?
Typically, the medical community uses NMES devices to treat damaged or injured
muscle tissue. The key parameters in any NMES device are the following:
Frequency – 1 to 300 Hertz (or # of pulses per second) 1 Hz will cause the muscle to
relax while 100 Hz will cause the muscle to increase explosive strength.
Rehab professionals typically begin treatment at 25 to 40 Hz and
Compex does not have that rehab frequency but does have a range of 1
Hz to 120 Hz.
Pulse Width – when a muscle is treated the muscle is subjected to a relatively
narrow pulse width of 50 to 100 microseconds. Compex imposes 200 to
400 microsecond pulse widths because it is being applied to healthy
tissue.
Amplitude – measure in mAmps, think of this as the volume on a stereo system. A
pacemaker can go as high as 4 mAmps whereas a heart defibrillator
begins around 150 mAmps. Compex has a range of 1 to 100 mAmps.
Wave Form – modern day NMES devices use a square wave or bi-phasic electrical
wave which translates to comfort. Older devices used triangular or
sinus waves which is why the things I used in the late 1980’s did not feel
comfortable. Compex uses a bi-phasic rectangular or square wave so
there is plenty of comfort.
Signal Quality – Like the comparison of a good versus a bad stereo system, Compex
has taken NMES to new heights by eliminating “noise” and interference
that typically is present in the medical devices. This allows Compex to
use higher levels of power/energy without a noisy signal that can cause
discomfort.
ELECTROMUSCULAR PHYSIOLOGY 101
Small motor units are responsible for generating small forces over long periods of
time and are predominantly Type 1, slow-twitch i.e. aerobic in their energy
metabolism. Large muscle units are responsible for generating massive amounts of
force over a short period of time. They are classified as Type 2 fast-twitch i.e.
anaerobic in their metabolic properties. Most muscles like our thigh muscles
(quadriceps or quads) are comprised of a mixture of fast and slow twitch fibers.
When a muscle is contracted voluntarily, and against increasing resistance, the first
motor units to be activated are the small, slow twitch Type 1 motor units. With
increasing force, the larger, more powerful, fast twitch Type 2 units come into play.
The process of bringing more motor units online with increasing resistance or
muscular force is called recruitment. The order of recruitment (small to large) is
governed by the Size Principle – i.e. small units go first. What this means to athletic
training is that it requires very high effort to recruit the very largest and most
powerful motor units in any mixed population of motor units encountered in a
skeletal muscle. This is one reason that people can generate “superhuman” strength
is emergency situations. This is also a reason that it is hard to do strength training
unless you are really focused and highly motivated. In contrast to the size principle,
which is as elementary to neuromuscular physiology as gravity is to life on earth,
electrical myoneural stimulation (EMS) recruits motor units based on the frequency
of stimulation. At low frequency stimulation – 20 hertz for example – the motor
units that are stimulated are small and slow twitch. At high frequencies – more than
80 hertz – increasing proportions of powerful fast twitch units are worked. Training
effects can be tailored by the frequency selected, to the desired population of motor
units and fiber types. Fast twitch units can be trained without the risk of injury
inherent in lifting super heavy weights and independent of motivation. In addition,
potential negative effects of strength training on cardiovascular performance can be
avoided. There is a good amount of data regarding the effects of Compex on the
biochemical characteristics of muscle. With training, fast twitch, Type 2 fibers
become more fatigue resistant and increase their capacity to utilize glucose and
oxygen. Microscopic studies show microscopic tears that are believed to be
necessary to induce increased muscular size and strength once repaired. State- ofthe-art histochemical characterization of the muscle contractile proteins called
myosin isoforms indicate a change in the transcription of the DNA of the muscle cell
nucleus that is fundamental to developing better muscles. Muscles become denser,
somewhat larger, and more richly vascularized.
The “Compex Advantage” graphic explanation of the electromuscular patterns the
Compex Sport implodes when applied to human muscle fiber groups…
COM PEX CYCLING
ADVANTAGE
The Compex rationale is:
• Compex Sport stimulates Fiber Type I Slow twitch zenith 30 ms to nadir 100
ms
•
Compex Sport stimulates Fiber Type II Fast Twitch Zenith 15 ms to nadir 30
ms
• Compex Sport stimulates Fiber Type I @ 10-33 HZ
• Compex Sport stimulates Fiber Type II @ 33-66 HZ
• Compex Sport stimulates high frequency continually 20% higher than
normal muscle contractile peaking to failure (See: Figure 1. HIGH
FREQUENCY FIRING EFFECT)
• Compex Sport increases dynamic strength gains by 2 effects (Muscle
Consequences) stimulating both potentate and unpotentiate fibers equally to
enhanced eccentric, concentric, and isometric strength (See Muscle
Consequences: 1st & 2nd Effects)
• Compex Sport training “types” are organized into categories such as “active
recovery”, “endurance” or “strength”. Recovery programs stimulate the
nerve at a low frequency that results in a muscle twitch and increased blood
flow, improving recovery from strenuous efforts. Training programs such as
strength or resistance employ higher frequency stimulation to induce
sustained (tetanic) contraction. The user controls the strength of stimulation,
but the frequency is determined by the type of program and level that the is
selected. Russian Stim stimulates at about 33 hertz (stimulate 33 times a
second) however, the Compex Sport stimulates from 1 to 130 hertz4.
Note the differences between fiber types: How Type I peaks slowly and is
sustained longer while Type II peaks higher faster but lasts only a 1/3rd of
contractile time as a Type I contraction.
FFA
ASSTT TTW
WIITTC
CH
H FFIIBBEER
R IIII
Æ
Æ
SLOW TWITCH FIBER I
Æ
F IB E R I
F IB E R II
W H IT E
RED
S
S
S
s
t
E
30m s
100m s
A E R O B IC
e
15m s
A N A E R O B IC
SLO W
4
30m s
See full text article compex_endurance list @:
http://health.groups.yahoo.com/group/compex_endurance/files/
FAST
t
Type I’s require less hertz to peak contraction:
SLOW TWITCH FIBER TYPE I 10-33 HZ
†
S
SLO W
TW ITC H
FIB E R S
T IM E R E C R U IT M E N T
SLOW
TW ITCH
FIBERS
TIM E RECRUITM ENT
S
33 H ertz
10 Hertz
t
t
0
100
200
300
400
500
600
700
800
900
1000
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
0
30
60
90
120
150
180
210
240
270
300
330
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
SLOW TWITCH TYPE I @ 10 HZ
SLOW TWITCH TYPE I @ 33 HZ
Type II’s require higher hertz levels above that required by Type I:
FAST TWITCH FIBER TYPE II 33-66 HZ
†
TIME RECRUITMENT
S
FAST
TWITCH
FIBERS
FAST
TWITCH
FIBERS
TIME RECRUITMENT
S
33 Hertz
66 Hertz
t
0
30
60
90
120
150
180
210
240
270
300
ms ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
FAST TWITCH @ 33 HZ
t
0
15
30
45
60
75
90
105
120
135
150
165
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
ms
FAST TWITCH @ 66 HZ
COMPEX FREQUENCY SUSTAINS FIRING EFFECT5
VOLUNTARY
VS
COMPEX EMS
Æ
Æ
E H IG H
VOLEVOLUT
E L C O P E X E M S E C T R IC A L
F (H z)
F (H z )
100
100
80
50
0
t (s)
0
t (s)
4
0 ,5
4
Figure 2. HIGH FREQUENCY FIRING EFFECT
TW ITCH AM PLITUDE
M aximum Strength Twitch ¼
S1
t
Strength Zenith Peak Rapid Duration Short
5
Note: TheCompex Sport EMS sustains firing effect well beyond what a voluntary muscle
contraction can achieve. Creating this firing effect pattern within the muscle advances contractile
adaptation resulting in performance gain.
TWO MUSCLE EFFECTS RESULT FROM COMPEX SPORT APPLICATION
M USCLE CO NSEQ UENCES
1 st e ffe c t
M A X IM A L
STR EN G TH
S tr e n g th
at 50 H z
S tr e n g th
at
`
50 H z
U n p o te n tia te d
T w itc h
P o te n tia te d
T w itc h
µ
ECONOMY OF CNS See above
1 st EFFECT
,-
FOR SUB-MAXIMAL FREQUENCY
FIBERS WILL DEVELOP MORE STRENGTH.
Strength
„
Start
tetanisa
To
50H z
70Hz
potentiated fiber
unpotentiated fiber
100 Hz
tio n
DEVELOP IDENTICAL = STRENGTH, THE CNS HAS TO FIRE ´ WITH A LOWER
FREQUENCY
2nd EFFECT:
SPEED TO REACH MAXIMAL STRENGTH
strength
Potentiated fibers
Max strength
Unpotentiated fibers
70ms
40ms
time
Explosivity gain
PRACTICALITY
Strength
Potentate fibers
Unpotentiate fibers
Eccentric strength gain
Identical Maximal Isometric Strength!!
Concentric strength gain
Eccentric
Isometric
Concentric
Motion speed
Dynamic Strength gain ( Eccentric+ + +)
COMMENT: Dynamic strength gains result when potentate and unpotentiate fibers
equally increase eccentric, concentric, and isometric strength gain. These are
reported by applying Compex Endurance, Strength, Potentiation, and Recovery
modes during progressive training resulting in improved performance.
I confess that electrostimulation is difficult to explain, understand and that the more
I learn about such recorded objective effects the less I actually understand. I began
a complete sceptic from having been exposed to 14 years seeing limits of several
forms of clinical therapeutic electrostimulation. However, it is difficult to argue with
personal observations namely that some of my best performances (me against me)
were recorded were in association with modest applications of Compex Sport
recovery or endurance modes. These comments are credible –3D, pronounced via
incredible performances of Erik Zabel, Tyler Hamilton, and Joane Somarriba.
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#3 Is there a genetic relationship between endurance sports, cognitive health, and
longevity?
Shimokata summarized (2001) "Genetic background is an important factor for
longevity. Life-style and environmental factors, such as nutrition, physical activity,
smoking and alcohol, are also important. For example, obesity is negatively
associated with health and longevity. It is known that dietary restriction is the most
consistent method of extending life span in rats. In human, however, under nutrition
as well as over nutrition is a risk factor for a short life. Losing weight is often
dangerous in the elderly, in whom reserved physiological functions are limited.
Smoking, diabetes mellitus and hypertension accelerate human aging, while physical
activity and a moderate amount of alcohol is good to live long."
EXERCISE GENETIC INFLUENCE ON LIFE SPAN
Niemi & Majamaa (2005) presented the first quantitative gene expression analysis
of cardiac aging under conditions of sedentary and active lifestyles using highdensity oligonucleotide arrays representing 11,904 cDNAs and expressed sequence
tags (ESTs). With these data, they tested the hypothesis that exercise attenuates the
gene expression changes that normally occur in the aging heart. Male mice (Mus
domesticus) were sampled from the 16th generation of selective breeding for high
voluntary exercise. For the selective breeding protocol, breeders were chosen based
on the maximum number of wheel revolutions run on days 5 and 6 of a test at 8 wk
of age. For the colony sampled herein, mice were housed individually over their
entire lifetimes (from weaning) either with or without access to running wheels. The
hearts of these two treatment groups (active and sedentary) were assayed at middle
age (20 mo) and old age (33 mo). Genes significantly affected by age in the hearts of
the sedentary population by at least a 50% expression change (n = 137) were
distributed across several major categories, including inflammatory response, stress
response, signal transduction, and energy metabolism. Genes significantly affected
by age in the active population were fewer (n = 62). Of the 42 changes in gene
expression that were common to both treatment groups, 32 (72%) displayed smaller
fold changes as a result of exercise. They concluded that exercise offset many agerelated gene expression changes observed in the hearts of the sedentary animals.
These are results that suggest adaptive physiological mechanisms are induced by
exercise can retard many effects of aging on heart muscle at the transcriptional level
(Niemi & Majamaa 2005).
IF A LITTLE EXERCISE IS GOOD, IS MORE BETTER?
Perhaps only a little is good, period. Tomporowski (2003) reviewed studies that
assessed the effects of acute bouts of physical activity on adults' cognitive
performance. Three groups of studies were constituted on the basis of the type of
exercise protocol employed. Each group was then evaluated in terms of informationprocessing theory. It was concluded that submaximal aerobic exercise performed
for periods up to 60 minutes facilitate specific aspects of information processing;
however, extended exercise that leads to dehydration compromises both information
processing and memory functions. Interestingly, researchers examined possibility
that plasma levels of malonaldehyde (MDA) were excessively altered by exercise.
The presence of MDA has been recognized to reflect peroxidation of lipids resulting
from reactions with free radicals. Maximal exercise, eliciting 100% of maximal
oxygen consumption (VO2max) resulted in a 26% increase in plasma MDA (P less
than 0.005). Short periods of intermittent exercise, the intensity of which was varied,
indicated a correlation between lactate and MDA (r2 = 0.51) (p less than 0.001).
Blood lactate concentrations increased throughout this exercise regimen. A
significant decrease (10.3%) in plasma MDA occurred at 40% VO2max. At 70%
VO2max plasma MDA was still below resting values, however the trend to an
increase in MDA with exercise intensity was evident. At exhaustion, plasma MDA
and lactate were significantly greater than at rest. These results suggest, that
exhaustive maximal exercise induces free radical generation while short periods of
submaximal exercise (i.e. less than 70% VO2max) may inhibit it and lipid
peroxidation (Lovlin et al. 2003). This indicates a preference for easy exercise over
both aerobic race pace or worse yet the high demand speed workout in terms of
what is best for our health. Furthermore it has been shown from C-reactive protein
levels, observed indicators of tissue death, begin rise in runners who race beyond 21
kilometers of roughly 13 miles distance, and becomes progressively worse as
distance raced is increased.(Strachan 1984, Kuipers 1989) There is a
correlation(somewhat) of time, 90 minutes and the distance (21 k)or a 13-mile halfmarathon distance when systemic markers of tissue damage appear. Blood serum
markers of aging, and increased predisposition to degenerative disease are similar to
those found in an overtrained athlete, yet the athlete rebounds during periods of rest
because the exercise-induced free radical accumulates are mostly neutralized, but
not all, by his or her conditioned antioxidant defense system. Over time and years
however, free radical damage accumulates resulting in an increased rate of fatigue,
decreased recovery rate, deteriorated cellular immune response, increased
predisposition to degenerative disease, and eventual death.
Dekkers (1996) reported, "Increased oxidative stress induced by exercise is
compromised by increased antioxidant activity, preventing lipid perioxidation after
exercise." Human studies have shown that dietary supplementation with
antioxidant vitamins has favorable effects on lipid perioxidation after exercise.
(Olin 1996) has shown that intake of antioxidants with food can reduce exerciseinduced oxidative stress.
"Exercise in its own right improves thinking. Most of us seem to believe this
anecdotally; however, an enterprising scientist from the US has just published a
critical review in this field demonstrating that concentration, information
processing, decision making and reaction times were all improved by aerobic
exercise. The longer the bout of exercise, the better the response. So keep moving is
the message—in fact don’t stop and you may be as clever as Albert Einstein. In a
recent paper from Science, researchers reportedly extended the lifespan of
transgenic roundworms to the human equivalent of 500 years without
compromising their health. It turns out that in most life forms, insulin like growth
factor 1 (IGF-1), plays a central role in both growth and longevity. An excess of
IGF-1 shortens your life span. This is a point that many elite athletes may want to
ponder as they inject either IGF-1 or its precursor, growth hormone, into their
bodies. Tweaking the roundworm’s genes was one aspect of this line of study but
excising the germ line cells (i.e. neutering the critter) was the critical step extending
the lifespan by approximately 60% (McCrory 2003)."
In the nematode Caenorhabditis elegans, mutations that inhibit insulin/IGF-1
(insulin-like growth factor 1) signaling, such as daf-2 insulin/IGF-1 receptor
mutations, can double the life-span of the animal (Tatar et al. 2003). Removing the
germ-line precursor cells also extends life-span by approximately 60% (Hsin &
Kenyon 1999). This life-span extension is not a result of sterility; it appears to be
due to altered endocrine signaling (Tatar et al. 2003; Hsin & Kenyon 1999).
Removal of the germ line or the entire reproductive system of daf-2 mutants can
further extend life-span: these animals can live four times as long as normal (Hsin &
Kenyon 1999).
Strong reduction of daf-2 activity causes juvenile animals to enter a quiescent state
of diapause called dauer. In contrast, partial loss-of-function daf-2 mutants grow to
adulthood and have long life-spans. We found that reducing daf-2 activity further
by subjecting weak daf-2 mutants, such as daf-2(e1368), as young larvae to dal-2
RNA interference (RNAi) produced larger increases in life-span without triggering
dauer formation (Fig. 1 below). Moreover, when we removed the reproductive
systems of these RNAi-treated animals, they lived six times as long as normal.
Whereas the mean life-span of wild type was 20 days, these animals had mean lifespans of 124 days (Fig. 1 below). In fact, only 15% of the animals died in the first 3
months (Arantes-Oliveira et al Science Magazine 2003).
Longevity’s suggested price tag is 1-hour aerobic exercise a day, a vegetarian diet,
brain application, halitosis, flatulence, no friends, and no sex. The soon attainable
500-year lifespan may be like an eternity (according to McCrory 2003).
FIGURE 1. LIFE-SPANS OF EXPERIMENTAL ANIMALS
Fig. 1. Life-spans of experimental animals. N2 (wild type) on control bacteria
(black), m = 20.7 ± 0.9 days, n = 56/49 [observed/uncensored events (10)]; daf2(e1368) on control bacteria (blue), m = 32.4 ± 1.2, n = 80/48, P < 0.0001; daf2(e1368) on bacteria expressing daf-2 dsRNA (green), m = 51.0 ± 1.9, n = 80/68, P <
0.0001; gonad-ablated daf-2(e1368) on bacteria expressing daf-2 dsRNA (red), m =
124.1 ± 5.9, n = 46/39, P < 0.0001. Like gonad-ablated daf-2(e1368,RNAi) animals,
N2, e1368, e1368(RNAi) and gonad-ablated e1368 animals were healthy and active.
We repeated this experiment once, initiating RNAi at the L2 stage. Again, the
gonad-ablated daf-2(e1368,RNAi) mutants were very healthy and long-lived (m =
113 days). As observed previously (2), gonad ablation did not further extend the lifespan of daf-2(e1368) mutants. [In wild type and daf-2 mutants, ablation of the
germline extends life-span. In wild type but not daf-2(e1370) animals, ablation of the
somatic gonad as well prevents this life-span extension. Thus, somatic gonad
ablation may shorten life-span by increasing daf-2 activity. It seems likely that e1370
and e1368 mutants differ in their response to somatic gonad ablation because of
having different levels of residual daf-2 activity (only e1368 mutants have sufficient
daf-2 activity to shorten life-span after somatic gonad ablation). This would explain
why whole gonad (germline plus somatic gonad) ablation can extend the life-span of
daf-2(e1368,RNAi) but not daf-2(e1368) animals
REFERENCES
Arantes-Oliveira N, Berman JR, Kenyon C. Healthy Animals with Extreme
Longevity. Science, Vol 302, Issue 5645, 611, 24 October 2003.
Bronikowski AM, Carter PA, Morgan TJ, Garland T Jr, Ung N, Pugh TD,
Weindruch R, Prolla TA. Lifelong voluntary exercise in the mouse prevents agerelated alterations in gene expression in the heart. Physiol Genomics. 2003 Jan
15;12(2):129-38. PMID: 12429864 [PubMed - indexed for MEDLINE]
Corrigan B. DHEA and sport. Clin J Sport Med. 2002 Jul;12(4):236-41. Review.
PMID: 12131057 [PubMed - indexed for MEDLINE]
Dekkers JC., et al. The role of antioxidant vitamins and enzymes in the prevention
of exercise-induced muscle damage. SPORTS MED, 1996, 21:3, 213-218.
Kuipers H., et al. Structural and ultrastructural changes in skeletal muscle
associated with long distance training and running, INT J SORTS MED 10:S156S159.
M. Tatar, A. Bartke, A. Antebi, Science 299, 1346 (2003). [Abstract/Free Full Text]
McCrory P. Mens corpora e mens sano. Br J Sports Med. 2003 Dec;37(6):471.
PMID: 14665578 [PubMed - indexed for MEDLINE] @:
http://bjsm.bmjjournals.com/cgi/content/full/37/6/471
Niemi AK, Majamaa K. Mitochondrial DNA and ACTN3 genotypes in Finnish elite
endurance and sprint athletes. Eur J Hum Genet. 2005 May 11; [Epub ahead of
print] PMID: 15886711 [PubMed - as supplied by publisher]
Olin HH., et al., "An antioxidant-fortified energy bar can reduce exercise-induced
oxidative stress," FASEB JOURNAL, 1996, Volume 10:2752.
Science Magazine, by permission; for free-full text, [DOI: 10.1126/science.1089169]
See @: H. Hsin, C. Kenyon, Nature 399, 362 (1999). [CrossRef][ISI][Medline]
http://www.sciencemag.org/cgi/content/full/302/5645/611?ijkey=503c20a87511e8cbe
59f45d16376d9165eb0fb85&keytype2=tf_ipsecsha
Shimokata H. [Physiological requirements for longevity] Nippon Ronen Igakkai
Zasshi. 2001 Mar;38(2):174-6.
Strachan AF., et al., C-reactive protein levels during long-distance running.
BRITISH MEDICAL JOURNAL. 289:1249-1251.
Tomporowski PD. Effects of acute bouts of exercise on cognition. Acta Psychol
(Amst) 2003;112 (3):297–324.[CrossRef][Medline]
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#4 What foods chronically consumed are shown to enhance life span?
Introduction
Nutrition plays an important role in the maintenance and
improvement of human life expectancy. The 'Food Habits in Later Life'
(FHILL) is a cross-cultural study conducted under the auspices of the
International Union of Nutritional Sciences (IUNS) and the World Health
Organization (WHO). Baseline data on food habits, health status and social
variables were collected from five cohorts aged 70 and over (Japanese in
Japan, Swedes in Sweden, Anglo-Celtic in Australia, Greeks in Australia and
Greece). Objective: To identify protective dietary predictors amongst
long-lived elderly people (n=785) from the FHILL population after
controlling for ethnicity.
Methods: The validated FFQ were used to collect data on food intakes in all cohorts
except Japanese where the 3d weighed food record method was employed. Intakes
in gram/week were calculated by multiplying the serving size by the weekly
frequency of intake. These values were further translated into gram/day and were
adjusted to 2500 kcal (10,460 kJ) for men and 2000 kcal (8,368 kJ) for women.
Food items were grouped into nine food groups based on key features of the
Traditional Mediterranean Diet:
• Vegetables
•• LLEEEG
G
U
M
E
GU
UM
ME
ESSS
• Fruits and nuts
• Cereals (including starchy roots),
• Dairy products
• Meat
• Fish
• Monounsaturated:saturated ratio
• Ethanol
All-cause mortality data were obtained from up to seven years follow-up.
Alternative Cox Proportional Hazard model adjusted to age at enrolment (in 5-year
interval), gender, and smoking was developed to analyse the survival data. Each
Cox model was tested against controlling for cohorts' location and ethnicity.
Results: Only for legumes intake was the result plausible, consistent and statistically
significant across collective FHILL cohort's data. There is a 7%-8% reduction in
mortality hazard ratio for every 20g increase in daily legume intake with
adjustment for location/ethnicity (RR 0.92; 95% CI 0.85 - 0.99) and without
adjustment for location/ethnicity (RR 0.93; 95% CI 0.87 - 0.99).
CONCLUSIONS: This longitudinal study shows that a HIGHER LEGUME INTAKE is
the most protective dietary predictor of survival amongst the elderly, regardless of
their ethnicity. The significance of legumes persisted even after controlling for age
at enrolment (in 5-year interval), gender, and smoking.
Legumes have been associated with long-lived food cultures:
• Japanese (SOY, TOFU, NATTO, MISO)
• Swedes (BROWN BEANS, PEAS)
• Mediterranean People (LENTILS, CHICKPEAS, WHITE BEANS).
COMMENT: For every (20 grams = 0.7 ounce+ potion of legumes 8% loss in
mortality occurs (1 ounce = 28.3 grams). I recommend, " SOY, TOFU, NATTO, MISO,
BROWN BEANS, PEAS, LENTILS, CHICKPEAS, AND WHITE BEANS."
Reference
(1) Legumes: the most important dietary predictor of survival in older
people of different ethnicities. Darmadi-Blackberry, I., Wahlqvist, M. L.,
Kouris-Blazos, A., Steen, B., Lukito, W., Horie, Y., Horie, K., Asia
Pacific Journal of Clinical Nutrition 2004 June 13(2):217-220.
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#5 What foods increase serum triglyceride levels?
Fructose increases serum triglyceride levels (especially in diabetes mellitus
patients): fructose is incorporated into triglycerides more readily than glucose (i.e.
Fructose has a greater propensity to increase serum triglycerides compared to
glucose).
Excessive consumption of SIMPLE SUGARS6 (like table sugar, sucrose) increases the
body's production of triglycerides (due to the body converting excessive sucrose into
triglycerides in order to protect itself from the toxic effects of excessive sucrose).
Excessive circulating glucose (blood sugar) is converted to glycerol and stored
within the body as triglycerides. Insulin stimulates the conversion of glucose (blood
sugar) to triglycerides for storage within adipose tissue. SIMPLE SUGAR significantly
increases the uptake of supplemental creatine (and creatine from creatine
monohydrate) into muscles (when simple sugars are consumed at the same time as
supplemental creatine or creatine monohydrate, muscle creatine concentration
increases far greater than when creatine or creatine monohydrate supplements are
consumed alone (without concurrent simple sugars).
EXCESS SIMPLE SUGAR:
1. Increases the body's production of adrenaline by up to 400%.
2. Accelerates the aging process by causing cross-linking (glycosylation) of
the body's proteins.
3. Increases the risk of atherosclerosis (due to simple sugars causing crosslinking of the collagen that is a constituent of blood vessels).
4. Damages the blood vessels (due to simple sugars causing cross- linking
of the collagen within blood vessels).
5. Increases the risk of hypertension (due to simple sugars causing crosslinking of the collagen in the blood vessels).
6. Exacerbates irritable bowel syndrome (by reducing the buffering effect
of polysaccharides).
7. Damages the kidneys (due to simple sugars causing cross-linking of the
collagen that is a component of the tiny filters within the kidneys).
8. Increases the risk of cataracts (due to simple sugars causing crosslinking of the collagen that is a component of the eyes).
6
Glutamine, Vegetables, Fennel reduce the craving for simple sugars.
9. Accelerates the development of food allergies.
10. Feed cancer cells and cancer patients are therefore advised to reduce
their consumption of dietary simple sugars.
11. Feed the detrimental candida albicans yeast and people with overproliferation of candida albicans should minimize their consumption of
simple sugars.
12. Excessive consumption of simple sugars suppresses the immune system
by impairing the ability of neutrophils to function as phagocytes.
13. Causes production of excessive quantities of acetic acid and contributes
to excessive production of endogenous cholesterol:
14. Lowers HDL (good) cholesterol production.
15. Cause the cross-linking (glycosylation) of the body’s endogenous
proteins.
16. Causes premature fatigue.
17. Stimulate the production of free radicals.
18. Direct cause of obesity by converting to triglycerides and are then
stored within the body as adipose tissue.
19. Causes the body's joints to become brittle and stiffer (due to simple
sugars causing cross-linking of the collagen that is a component of the
joints).
20. Interact with detrimental bacteria that reside on the teeth
(streptococcus mutans and streptococcus sobrinus) and result in the
production of lactic acid that causes tooth decay.
21. Increases the risk of pre-menstrual syndrome (pms) and exacerbates
the symptoms of PMS.
22. Increases the formation of wrinkles (due to simple sugars causing crosslinking of the collagen component of the skin).
23. Contribute to Linoleic Acid (LA) deficiency by preventing its release
from the body's adipose tissue.
24. Increase the body’s excretion of magnesium.
25. Increase loss of potassium from the body.
26. Depletes vitamin B6 reserves (this occurs because vitamin B6 is
required for the utilization/metabolism of simple sugars).
27. Interfere with the transport of vitamin C through the body - as simple
sugars use the same transport system as vitamin C.
THE LONG CHAIN CARBOHYDRATE DIFFERENCE
Polysaccharides are a group of carbohydrates that contain up to 10,000 SIMPLE
SUGARS (i.e. monosaccharides or disaccharides) or uronic acid molecules linked
together. The monosaccharide or disaccharide constituents of polysaccharides are
linked together either in straight or branched chains; they may be either all the
same or two or more different simple sugars.
When simple sugars are linked together in long chains each individual type of
polysaccharide possesses specific potential health benefits.
POLYSACCHARIDES ARE THE BEST SOURCE OF CARBOHYDRATEDERIVED ENERGY:
•
•
Polysaccharides are slowly reverted back to monosaccharides within the
body, eventually forming glucose which is then oxidized (burned for energy)
at the same rate at which it is produced.
Polysaccharides are also involved in the production of energy through the
production of volatile saturated fatty acids (including acetic acid, butyric
acid and propionic acid) from fermenting polysaccharides within the large
intestine.
Excessive consumption of dietary fats can increase serum triglyceride levels - 95%
of dietary fatty acids are consumed in the form of triglycerides.
Trans-fatty acids increase triglyceride levels by up to +47%.
Cafestol (a diterpene lipid found in (unfiltered) coffee increases serum triglycerides
levels.
Alcohol (ethanol) increases the endogenous production of triglycerides - liver cells
eliminate the excess hydrogen formed from the breakdown of alcohol by utilizing it
to form alphaglycerophosphates and fatty acids which are precursors for
triglycerides).
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