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As training proceeds into the
competitive phase some athletes place a higher proportion of their
loading on intensity whilst reducing the total volume of training.
Cycles such as this one may be biannual or biennial. Importantly,
periodisation and cyclic loading is not restricted to any particular
time frame. Although, it does place emphasis on incremental
loading moreover it places emphasis on optimal regeneration and recovery.
Additionally, such a methodology provides a 'base' for the next cycle
of training activities. Each macrocycle may be made up from microcycles
which can last days, weeks, months or years. Remember, each time you
train to change your bodies abilities you are stressing the system
and therefore recuperation is important.


Motor learning theory devised by Bernstein
suggests that the body will use the momentum of the limbs to optimize
the degrees of freedom in the system. Similar to a mass-spring
analogy where the perturbations of the mass will be dependent on the
damping characteristics of the spring, the brain will introduce
muscle tone to dampen the angular velocity and hence acceleration
of the system. Therefore, instead of the muscles of the leg
lifting the limb, the antagonistic muscles are decelerating the limb
towards the end of trajectory. Moreover, by using eccentric
(muscle lengthening and contracting) muscle contractions the system
becomes efficient through these decelerating movements through enhanced
visco-elastic rebound as well as the conservation of momentum.
Changing speed of training, not only
allows the use of various metabolic energy systems, but it also trains
mechanical efficiency and therefore should reduce the rate of energy
expenditure. The more efficient the system the greater the time
to fatigue may be. Importantly, acceleration places an emphases
on the changing velocity. Sprint training, Fartlek training
(progressive increases and decreases in speed), counterjumps (plyometrics),
eccentric-concentric leg pressing, eccentric-concentric lunging, undulating
hills, running-jumping are all exercises which may improve angular
momentum and therefore efficiency.
Besides training implications, there
are also clinical considerations when for example a component of the
kinetic chain isn't functioning in it's stretch-shortening cycle and
energy dissipation function as it is supposed.
Cooling muscles will also profoundly
affect the rate of contractile responses to neural input

Finally, recent investigations into
the immune system of endurance athletes suggests that inflammation
and immune sensitivity may be inversely proportional. For example,
upper respiratory tract infections are common amongst runners.
This may be due to irritation of the airways by air. Alternatively,
it may be due to the irritation set up by the mechanical loading of
the musculoskeletal system during training. Periodisation of
training allows the body to recuperate, it provides a learning experience
for the athlete of what they can tolerate and how to peak at the required
time (see below). Some of the recent investigations have highlighted
the lack of salivary immunoglobulins in the period up to 2 hours after
the cessation of training. These investigators have suggested
the use of carbohydrate nutritional supplementation immediately after
exercise. During my time in Switzerland, leading up to the Barcelona
Olympic Games, there was an emphasis placed on carbohydrate supplementation
(multodextrene), as well as magnesium for tired muscles in addition
to regular blood checks of ferratin levels for women. The supermarket
and gym shelves are full of nutritional supplements. With such
a wide variety of choices available, it would seem appropriate to
seek a consultation with a sports nutritionist. Some information
regarding carbohydrate
supplementation can be found elsewhere on this website. Additionally,
aging and vitality have been related to the capacity to enhance the
immune system through exercise elsewhere
on this website
Link
to Training and Rehabilitation

Plyometrics and eccentric muscle adaptation
(Martin Krause 2003)
The eccentric component to this exercise
cause more profound changes to the connective tissue of the muscle
(broadening and streaming of Z bands). Investigations into eccentric
exercise revealed pain 8 hours after initial exercise which was maximal
48 hours later (Newham, Mills, Quigley, Edwards 1983).
These investigators found low frequency fatigue 10 minutes after a
20 minute period of stepping (Newham et al 1983). Additionally,
they demonstrated progressive increases in IEMG during the exercise
in the rectus femoris (160% increase) and vastus medialis (140% increase)
in the eccentric contracting leg (Newham et al 1983). Mechanical
damage to the sarcoplasmic reticulum resulting in less calcium release
for each excitatory action potential was suggested as the cause of
the low frequency fatigue (Newham et al 1983).

However, a number of sites in the
myofibrillar complex such as reduce binding sensitivity and capacity
of Troponin C for calcium, altered troponin-tropomysosin interaction
to impaired binding and force generation by actin and myosin have
been implicated in impaired force generation (Green 1990). Indeed,
in the absence of any association between relaxation rates and Calcium
kinetics raises support for the notion of a rate-limiting process
controlling the relaxation of fatigued muscles being located in the
contractile proteins (Hill et al 2001). During fatigue the relaxation
times can be prolonged as much as 50% (Bigland-Ritchie et al 1986)
thus resulting in increased force generation during submaximal stimulation
due to tetanic fusion despite a substantial fall in the maximum tetanic
force (Bigland-Ritchie et al 1986).
The initial overall loss of force
production seen may be due to Desmin and Titan damage (Lieber &
Friden 2002). Desmin acts as an extra-sarcomeric mechanical
stabilizer between adjacent Z discs and the attachment to the costomere
at the sarcolemma (Lieber, Shah & Fridén 2002). The
costomere complex contains Talin, Vinculin & Dystrophin which
attach to the trans-sarcolemmal proteins Integrin and Dystrophin associated
proteins. These proteins allow the lateral transmission of force
from actin to the basal lamina containing type IV collagen which is
contiguous with the endomysium (Kovanen 2002). Desmin loss after
eccentric exercise can occur within 5 minutes, possibly as a result
of increased intracellular Calcium leading to Calpain activation and
selective hydrolysis of intermediate filament network (Lieber &
Fridén 2002). This may result in the ‘popping of sarcomeres'
of different length thereby potentially loosing their myofilament
overlap of actin and myosin (Lieber & Fridén 2002).
Hence, reduced force production would be expected. Additionally,
the release of matrix metalloproteinase (MMP) which may degrade the
extramyocellular type IV collagen (Korskinen, Kovanen, Komulainen
et al 1996). However, this effect occurs many days after exercise
(Korskinen et al 1996) and could even effect torque production 28
days after exercise (Lieber & Fridén 2002). This
has significant implications in exercise training prescription.
flash file created by
Martin Krause 2003
Titan molecules span the
gap between the ends of the thick filaments and Z-bands. At the 2007
MPA conference in Cairns, Rob Herbert, provided the AJP oration whereby
he explained the significance of Titan as a major determinant of extensibility
in muscle fibres. Additionally, he stated that Titan is differentially
expressed in human skeletal muscle as short stiff fibres and long
compliant fibres
-
Costomeres are 15 different proteins
- Low oxidative muscles have a tendency to tear
during eccentric exercise
- Loss of desmin proceeds loss of fibronectin membrane
- Fibre strain results in increased intracellular
and extracellular calcium which ?may lead to desmin hydrolysis
through calpaine?
- Sarcomere shortening occurs to the detriment
of tendon lengthening
- Excitation-contractile coupling may be the area
disrupted rather than pure sarcomere disruption
- Structural changes of the disruption of the cytoskeleton
include dystrophin (sublaminal membrane protein), sometimes desmin
and titin, whereas alpha actin is always OK ?suggesting that calpaine
is not the enzyme responsible for protein dysruption?
- Creatine Kinase has no correlation with these
cytoskeletal changes
- Inflammatory process important for tissue cleaning
and remodelling
- Mechanism for muscle adaptation may be myosin
gene regulation - heavy chain myosin isoform upregulation
- Oxygen into the Mitochondria and through the
electron transfer chain (ETC) results in ATP use of 20% for power
and 80% for heat, therefore people producing less heat may be
producing more power?
- Slow twitch muscle fibre concentration varies
with the years of training
- Cycling cadence velocity at peak efficiency for
slow twitch muscle fibres is 80rpm
Vibration fatigue is probably reduced through enhanced
transverse forces by wearing pressure garments such as SKINS
(non-sponsored link). Additionally, venous return is probably also
improved through the pressure gradient which these garments provide.
Also check out the 'tensegrity model' as it applies
to microbiomechanical and macrobiomechanical structure, flexibility
and integrity - the new way of the future
http://fig.cox.miami.edu/~cmallery/255/255chem/tensegritymodel.htm
http://reality.sculptors.com/~salsbury/Synergy/largest-synergy-ball.html

An example from cycling
REFERENCES:
Bigland-Ritchie B, Bellemare F, Woods JJ (1986) Excitation frequencies
and sites of fatigue. In : Jones NL, McCartney N, McComas AJ
(Eds) Human Muscle Power . Human Kinetics Publisher, Champaign Ill
, pp197-213.
Green HJ (1990) Manifestations and sites of neuromuscular fatigue.
In: Taylor AW, Green HJ, Ianuzzo D, Sutton J (Eds). Biochemistry
of Exercise Human Kinetics Publisher, Champaign, Ill.,
pp 13-25
Hill CA, Thompson MW, Ruell PA, Thom JM, White MJ (2001).
Sarcoplasmic reticulum function and muscle contractile character following
fatiguing exercise in humans. Journal of Physiology , 531.3
, 871-878.
Koskinen S, Kovanen V, Komulainen J, Hesselink H, Kuipers H,
Vihko V, Takala T (1996). Type IV collagen, MMP-2, and TIMP-2
mRNA levels in skeletal muscle subjected to forced eccentric contractions.
Medicine & Science in Sports & Exercise , 28 , 153
Kovanen V (2002). Intramuscular Extracellular matrix: complex
environment of muscle cells. Exercise Sports Science Reviews
, 30 , 20-25
Krishnathasan D, Vandervoort, AA (2000). Eccentric strength
training prescription in older adults. Topics in Geriatric Rehabilitation
, 15 , 3, 29-40.
Lieber RL, Fridén J (2002). Mechanisms of muscle
injury gleaned from animal models. American Journal of Physical
Medicine and Rehabilitation , 81 , 11, S70-S79
Lieber RL, Shah S, Fridén J (2002). Cytoskeletal
disruption after eccentric contraction-induced muscle injury.
Clinical orthopaedics and related research , 403S , S90-S99.
Newham DJ, Mills KR, Quigley BM, Edwards RHT (1983). Pain
and fatigue after concentric and eccentric muscle contractions. Clinical
Science , 64 , 55-62
Immune System and training
Title
Overtraining effects on immunity
and performance in athletes.[Article]
Author MACKINNON,
LAUREL T
Institution School of Human Movement Studies, The
University of Queensland, Brisbane, Queensland, Australia
Source Immunology & Cell Biology. 78(5):502-509,
October 2000.
Abstract Summary: Over-training is a process of excessive
exercise training in high-performance athletes that may lead to over-training
syndrome. Over-training syndrome is a neuroendocrine disorder characterized
by poor performance in competition, inability to maintain training
loads, persistent fatigue, reduced catecholamine excretion, frequent
illness, disturbed sleep and alterations in mood state. Although high-performance
athletes are generally not clinically immune deficient, there is evidence
that several immune parameters are suppressed during prolonged periods
of intense exercise training. These include decreases in neutrophil
function, serum and salivary immunoglobulin concentrations and natural
killer cell number and possibly cytotoxic activity in peripheral blood.
Moreover, the incidence of symptoms of upper respiratory tract infection
increases during periods of endurance training. However, all of these
changes appear to result from prolonged periods of intense exercise
training, rather than from the effects of over-training syndrome itself.
At present, there is no single objective marker to identify over-training
syndrome. It is best identified by a combination of markers, such
as decreases in urinary norepinephrine output, maximal heart rate
and blood lactate levels, impaired sport performance and work output
at 110% of individual anaerobic threshold, and daily self-analysis
by the athlete (e.g. high fatigue and stress ratings). The mechanisms
underlying over-training syndrome have not been clearly identified,
but are likely to involve autonomic dysfunction and possibly increased
cytokine production resulting from the physical stress of intense
daily training with inadequate recovery.
Exercise,
Immune System, Cytokines, Heat Shock Proteins, Glutamine and muscle
mass

Exercise
and fine-tuning the immune system through the development of sympathetic
nervous system control over allostasis - implications for over-training,
stress, pain management and cognitive behavioral therapy
Sun Tzu : The Art of War
mastery of energy, mastery of the heart, mastery of strength,
and mastery of adaptation
they who know themselves and know their adversary will always
win
Last update : 26 January 2009
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