Download Neuromuscular Adaptations to Resistance Training

Physiological Aspects
of Human Performance

Adaptation refers to how the body adjusts to
repeated (chronic) stress.
 Disinhibition: reducing the inhibition of
muscle action by reflex protective
mechanisms.
 Size Principle: motor neurons with low
threshold, slow twitch velocity, and small
diameter are recruited first, with progressively
larger and higher threshold neuron
recruitment as more force is required.
 Synchronization: simultaneously recruiting
motor units.
Neural
On the
Neuromuscular
Systems
Muscular
Effects of
Resistance
Training
Skeletal
On Other Systems
Cardiovascular
•
•
•
•
•
Neural Control
Biochemical
Muscle Cells
Capillary Supply
Muscle
Hypertrophy
• Fiber
Hypertrophy
versus Fiber
Hyperplasia
• Muscle Atrophy
• Fiber Type
Alteration
• Initial increase in expression of strength due to
improved neural control of muscle contraction.
• Increased neural activation of the muscle
by recruiting more motor units and/or
activating higher threshold
motor units first to
enhance the rate of
force development
(alter the Size
Principle).
• More efficient recruitment pattern.
• Improved synchronization of motor units.
• Neural reflex facilitation and reduced
autogenic inhibition of motor neurons
(inhibit GTOs).
•
•
•
•
•
Equivocal increases in concentration of
muscle creatine, phosphocreatine, ATP, and
glycogen.
Enzyme activity of ATP-PC (creatine
phospho-kinase, myokinase) increased with
isokinetic training.
Little or no change in activity of ATP-PC
enzymes with resistance training.
Increase or no change in glycolytic enzyme
activities by resistance training.
Small but significant increases in aerobic
enzyme activities in high volume-short rest.
Myoglobin content in muscles
following strength training may
decrease.
 Mitochondrial density has been
shown to decrease with resistance
training because of dilution effects
of muscle fiber hypertrophy.

Increase number of capillaries in a muscle
helps support metabolism and contributes to
total muscle size.
 Improved capillarization has been observed
with resistance training by body builders but
decreased in power and weight lifters.
 Increase of capillaries linked to intensity and
volume of resistance training.
 Time course of changes in capillary density
slow (more than 12 weeks).

Transient hypertrophy: tissue edema
 Chronic hypertrophy: structural changes

Muscle enlargement is generally paralleled
by increased muscle strength.
 Increased muscle strength is NOT always
paralleled by gains in muscle size.
 Increase in fiber area of both ST and FT
muscle fibers.
 FT fiber area appears to increase to greater
extent than ST fiber area.

Increased size of
individual fibers due to:
 more myofibrils
 new actin & myosin
myofilaments added to
periphery of myofibrils
 more sarcoplasm
 more connective tissue
surrounding fiber
Increased number of
individual fibers
 muscle fibers split
longitudinally
 observed in animals
with intense training
 cross-sectional studies
in humans
•
•
•
Neither speed
(anaerobic) nor
endurance (aerobic)
training could alter
basic fiber type in
early studies
Only motor neuron
cross innervation
could alter fiber types
Specific training
improves specific (O
or G) metabolic
capacities
Supporting ligaments, tendons and
fascia strengthen as muscle strength
increases.
 Connective tissue proliferates around
individual muscle fibers, this thickens
and strengthens muscle’s connective
tissue harness.
 Bone mineral content increases more
slowly, over 6- to 12-month period.

Immobility causes decrease in muscle
size (use it or lose it)
 Atrophy primarily affects ST muscle fiber
types

Cardiovascular System
Heart Rate
Blood Pressure
Central Effects
Serum Lipids
Short-term resistive training studies show no
change or small insignificant changes of
about 5 to 12% in resting Heart Rate.
 Changes attributed to decreased sympathetic
and increased parasympathetic drive to heart.

•
•
•
Training effects of regular resistive training
on resting blood pressure are inconsistent.
Some short-term studies have shown
increases in SBP as a result of highintensity training.
Most studies of resistive training show
either no difference or decreases in
systolic or diastolic blood pressures.
•
Chronic resistance
training alters cardiac
dimensions:
concentric
hypertrophy.
•
•
Increased posterior
left ventricular and
intraventricular
septum wall
thickness.
Little or no change in
left ventricle chamber.
Left ventricular concentric hypertrophy
resulting from resistive training can be
accompanied by strengthened myocardium
and increased stroke volume at rest and
during exercise.
 Stroke volume is not significantly increased
when it is related to body surface area or lean
body mass.

The effect of resistance training on
the lipid profile are inconsistent.
 Short-term training studies are also
inconclusive.
 Both positive effects and no effect
have been shown in serum lipids as a
result of resistive training.
 Volume of training appears to be a
primary factor affecting serum lipids.

Acute muscular
soreness occurs
during and
immediately
following the exercise
period.
• Muscular contraction
causes ischemia.
• Because of ischemia,
metabolic waste
products accumulate
and stimulate pain.
Delayed onset muscular
soreness in days
following strenuous
unaccustomed physical
activity.
• Intensity of muscle
discomfort increases in
hours after activity,
reaching a peak 24-48
hours.
• Generally resolved
within a week.


Greater soreness
results from exercise
involving repeated
strain during active
lengthening than
concentric and
isometric actions.
Cell damage markers:
 Calcium leaks from SR
into cell
 Serum levels creatine
kinase and myoglobin.


Excessive mechanical forces disrupt
structural components in muscle
fibers, connective tissue,
extrasarcoplasmic cytoskeleton, and
sarcolemma.
Tissue injury initiates inflammatory
reaction in damaged muscle. Elements
of inflammatory process include
increased blood flow and tissue
permeability.



Physiological purpose of inflammatory
process is to rid cells of damaged tissue &
prepare the tissue for repair.
Edema and chemical substances (PGE2)
stimulate muscle afferents & increase
sensitivity of pain receptors.
Inflammatory reaction causes secondary
chemical reaction through formation of
oxygen radicals, proteases, and phospholipids
and nitric oxide. This is initiated early in the
injury process, but full manifestation is 1-3
days following stress begin DOMS.



Inflammation is followed by healing
phase and formation of protective
proteins.
There are increases in growth factors,
collagen, and fibronectin fragments,
enzyme inhibitors, oxygen scavengers,
and remodeling collagenase.
This process heals the tissue and
prevents further incidence of DOMS
during subsequent exercise sessions.


McArdle, William D., Frank I. Katch,
and Victor L. Katch. 2000. Essentials
of Exercise Physiology 2nd ed. Image
Collection. Lippincott Williams &
Wilkins.
Plowman, Sharon A. and Denise L.
Smith. 1998. Digital Image Archive
for Exercise Physiology. Allyn &
Bacon.