Kin 465

Lecture 8
Adaptations to Resistance Training

Heather Flebbe, M.S.

Winter 2015
 Overview
A. Morphological Adaptations
B. Neural Adaptations
C. Biochemical Adaptations
D. Body Composition Adaptations
 A. Morphological Adaptations
1. Myocardial hypertrophy
2. Skeletal muscle hypertrophy
3. Improvements in Connective Tissue
4. Increased Bone Density
1. Cardiac Hypertrophy
 Cardiac Hypertrophy
Normally in the left ventricle
Cause
Aortic pressure increases during RT
Ventricle must pump harder
Get hypertrophic response just like in skeletal muscle
Similar to
Hypertension response or aortic stenosis
Result
Heart can overcome higher TPR
Normal = 110/70 mmHg
During RT = 300/180 mmHg
 2. Skeletal Muscle Hypertrophy
Strength training causes protein catabolism (degradation)
Muscle fibers are damaged during resistance training
Muscle cells undergo hypertrophic growth (anabolism) in
response to the damage
 Satellite Cells
Adult skeletal muscle cells cannot divide, so in order to undergo
hypertrophic growth, they need satellite cells
Satellite cells are committed stem cells responsible for muscle growth
in adults
When muscle becomes damaged,
satellite cells activate

Satellite cells are

found between the
sarcolemma and
basal lamina

Hawke T J , Garry D J J Appl Physiol 2001;91:534-551

2001 by American Physiological Society
 Muscle Damage Activates Satellite Cells
A. Damaged muscle cells attract
inflammatory cells

B. Inflammatory cells recruit

satellite cells to the site of
the injury

C. Satellite cells differentiate

and fuse to muscle fibers

D. New muscle protein strands

(myofibrils) are formed from
the fused satellite cells

E. The regenerated muscle fiber

has increased in myofibril
thickness and number
 Hypertrophy vs. Hyperplasia
Hypertrophy
The supercompensation of muscle protein in response to
degradation
Occurs through increases in the cross-sectional area of
each muscle fiber
Happens in humans
Hyperplasia
Increase in number of muscle fibers
Happens in animals but not yet proven in humans
Soleus muscle in rat
G has greater CSA than H

Disruption of either the Nfkb1 or the Bcl3 gene inhibits skeletal

muscle atrophy
R. Bridge Hunter, Susan C. Kandarian
Published in Volume 114, Issue 10
J Clin Invest. 2004; 114(10):15041511
 Hypertrophy Through Cross-sectional Area
Get an increase in cross-sectional area by increasing the
number and size of myofibrils and myofilaments

Through resistance
training, myofibril or
myofilament size
increases
The larger fibers
eventually split off,
increasing cross-sectional
area
 3. Connective Tissue Improvements
Resistance training affects
the properties of ligaments
and tendons, primarily
through changes in
collagen
Collagen
The most abundant protein
in the human body
Has high tensile strength, so
is abundant in tissue that
must resist high pulling
forces
 Ligaments
Connect bone to bone
Formed from collagenous
fibers that run mostly in the
same direction
Resistance training increases
collagen concentration and
crosslinking of fibers
Results in increased stiffness
and load-bearing capability http://www.upei.ca/~morph/webct/Modules/Connective_Tiss
ue/irregct.html

of ligaments
 Tendon
Connects muscle to bone
Parallel, longitudinal
arrangement of collagen and
elastin fibers
Resistance training increases
collagen synthesis and
number of collagen fibrils
Results in increased stiffness
and tendon hypertrophy
 4. Increase in Bone
Resistance training leads to
increases in bone cross-sectional
area through bone remodeling
Bone remodeling is stimulated by
mechanical stress
Adaptations are specific to the
angle of stress placed on the bone
Thus, forces from exercise get
distributed over a greater area of
bone, leading to a reduction in
stress per unit area
New trabeculae of
spongy bone are aligned
parallel to stress
 B. Neural Adaptations
1. Lower AP Threshold
2. Increased rate coding
3. Increased synchronicity
4. Decreased inhibition of fast twitch motor
units
5. Decreased cocontraction of antagonists
 1. Lower AP Threshold
As a result of resistance training, motor neuron excitability
A lower action potential threshold is required for motor unit
activation and recruitment

Before training : Stimulus only causes a

graded potential

After training: Same stimulus causes an

action potential
 2. Rate Coding
Increased rate coding or frequency of stimulation
results in greater muscular force production
More Ca2+ is released
More Ca2+ is then available to bind to troponin,
leaving more sites available for cross bridge
binding
More crossbridging = more force production
 Increased Rate Coding

Untrained = relaxation between stimuli no tetanic fusion

Trained = no relaxation between stimuli tetanic fusion

Celichowski J et al. Exp Physiol 2006;91:887-895

 3. Synchronicity
With increased
synchronicity,
more of the
muscle fiber in
one motor unit
contracts at the
same time
Results in
greater force
production
 4. Inhibition of Fast Motor Units
In a series of experiments on motor unit recruitment,
Henneman et al. (1965) found:
Slow motor units were small and generated low force
Fast motor units were large and generated large
forces
Slow motor units were recruited before fast motor
units
Larger motor units were subject to greater neural
inhibition than smaller motor units
Resistance training decreases neural inhibition of
large motor units, resulting in more fast twitch
neurons firing during maximal contractions
 5. Antagonist Contraction
Decreased
contraction of
antagonist (i.e.
triceps) during
agonist (i.e. biceps)
contraction
Roles of Neural and Muscular Adaptations

8-20 wks
 C. Biochemical Adaptations
1. Hormonal adaptations
2. ATP/CP adaptations
3. Increased lactate removal
 1. Hormonal Adaptations
Anabolic hormones such as testosterone and growth
hormone increase acutely in response to heavy resistance
exercise

The magnitude of release appears to be related to the size

of muscle groups used, exercise intensity and rest period
High intensity, short rest periods and large muscle groups
produce the highest concentrations (Kraemer et al., 1999)

Testosterone appears to be the principal muscle-building

hormone in men (Deschenes & Kraemer, 2002)
Growth hormone appears to be the principle muscle-
building hormone in women (Deschenes & Kraemer, 2002)
 2. ATP/CP
Resistance training may increase ATP and
creatine phosphate (CP) stores, but changes
are not large enough to have practical
significance (MacDougall et al., 1979)

Heavy, explosive resistance exercises result in

decreased activity for oxidative enzymes (i.e.
citrate synthase) (Tesch, 1988)
 3. Lactate Removal
Mitochondrial density decreases following
chronic resistance training (RT) due to
increased muscle CSA

However, capillary density increases due to RT,

which enhances lactate removal during
moderate-intensity, high-volume RT
 D. Body Composition Adaptations
Increased fat-free mass (inclusive of bone mineral)
Decreased fat mass
Increased resting metabolic rate
Adipose tissue uses very little energy
Each additional pound of muscle tissue increases
resting metabolism by 30 50 kcal/day
30 50 kcal/day = 10,950 18,250 kcal/year
1 lb = 3500 kcal, so 3 5 lbs of fat/year
 References
Deschenes, M.R. & Kraemer, W. J. (2002). Performance
and physiologic adaptations to resistance training.
American Journal of Physical Medicine and
Rehabilitation, 8, S3-S16.
MacDougall, J.D., Sale, D. G., Moroz, J.R., Elder, G.C.,
Sutton, J.R. & Howalk, H. (1979). Mitochondrial volume
density in human skeletal muscle following heavy
resistanc etraining. Medicine and Science in Sports, 11,
164-166.
Tesch, P.A. (1988). Skeletal muscle adaptations
consequent to long-term heavy resistance exercise.
Medicine & Science in Sports & Exercise, 20, S132-S134.