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Anaerobic Training Adaptations

KIN 416 - Berry College - Dept. of Kinesiology

David Elmer

on 17 March 2016

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Transcript of Anaerobic Training Adaptations

Anaerobic Training Adaptations
principle of specificity
principle of overload
heavy resistance
repeated sprints
short (< 3 sec)
long (~ 30 sec)
muscle growth
fiber type transition
fiber type growth
net increase in protein synthesis
actin and myosin (contractile)
titin and nebulin (structural)
may take a few weeks to be observed
- increase in the number of fibers - either doesn't occur or is very limited
From DNA to Protein...
tRNA brings amino acids coded for by mRNA
Protein Synthesis
Protein Balance
Ubiquitin-Proteasome Pathway
Lysosomal System
Calpain System
Protein Degradation
Ubiquitin binds to proteins and marks them for degradation
at least 4 ubiquitins bind
Requires 3 enzymes - E1, E2, E3 - as well as an ATP
exercise decreases the activity of this system
disuse increases the activity
break interior peptide bonds as well as breaking off individual amino acids

proteins must enter by endocytosis for this process to occur
Activated by calcium
partially responsible for the increase in protein degradation associated with exercise
Calpains act on structural proteins in the muscle as well
this is usually what is altered to determine the protein balance...
insulin receptors
amino acid pool
greater in young vs. old men (& women)
sarcopenia - age-related loss in muscle mass
aging: increased resistance to anabolism with feeding
aerobic energy
Protein degradation
increased when insulin is decreased and glucagon is increased
H = heavy/high intensity
M = Moderate
only AA shown to do this all by itself
high-intensity, dynamic exercise for a sufficient duration will use AA for Krebs cycle intermediates and fuel
increased in high-intensity, dynamic exercise due to increases in calcium and glucagon, and decreases in insulin
Protein Balance
Sensitive to different types of tension/stretch
high tension: hypertrophy without increasing resting length
passive stretch: increased resting length without hypertrophy
Can increase muscle protein synthesis for up to 48 hours
> 70% VO2max
Load must be at least 60% of 1RM to see net increase in muscle protein synthesis
Response is dampened in trained individuals

only breaks down non-contractile protein
trained vs. untrained people
Seynnes, de Boer, and Narici, 2007
Ahtiainen, et al., 2003
central adaptations
motor cortex - descending neural pathways
untrained people may only be able to recruit ~70% of available muscle fibers
this percentage can increase rapidly with training
Pensini et al., 2002
Adams et al., 1993
evidenced by increases in EMG output
increase in EMG = increase in electrical activity
neural drive
rate of force development
RFD can be increased
Aagaard et al., 2002
Aagaard et al., 2002
synchronization of neural firing
more synchronous firing in strength trained people
Semmler et al., 2004
may improve the timing of the force development
peripheral adaptations
Adkins et al., 2006
motor cortex - descending pathways
neuromuscular junction
increased area (surface and total)
more nerve-terminal branching
more ACh receptors
increased SR & t-tubule density
increased Na/K ATPase activity
increased calcium release
Ortenblad et al., 2000
side effects of hypertrophy:
decreased mitochondrial density
decreased capillary density
decreased neural activation requirement
reflex potentiation
increase in the strength/sensitivity of reflex contractions
increases the rate of force development
enhances transmission of neural signals
points of interest...
unilateral training results in slight strength increases in the contralateral, untrained limb
greater EMG in untrained limb indicates neural adaptation
~10% strength increase
bilateral deficit
when two limbs contract together, the force produced is less than the sum of the limbs contracting individually
decrease in corresponding EMG
deficit can be reduced with bilateral training
antagonist co-activation
normally used to stabilize joints, but it reduces net force production
can be reduced with training
timing of co-activation can be altered with training
"neuromuscular" adaptations
selective recruitment
under some circumstances, big, fast-twitch motor units may be recruited before small, slow-twitch motor units
lengthening contractions
sudden, corrective movements
sustained, low-force contractions
can this be increased with training?
not sure
fibers must be activated (used) in order to adapt
not all fiber types hypertrophy at the same rate
type II fibers hypertrophy more than type I fibers
amount of hypertrophy possible may be due to fiber type distribution
type I
type IIA
type IIX
evident after only 2-4 weeks of training
type IIX act as reserve fibers - when activated they change into type IIA fibers
increased stores of:
increased buffering capacity, so higher levels of lactate and acid-base disturbance can be tolerated
increases in muscular strength result in reduced neural input required to generate a particular force
principle of overload - principle of variation
connective tissue
bones, tendons, ligaments, etc.
mechanical loading during training induces remodeling
increased diameter and strength (BMD)
minimum essential strain
~ 1/10 of strain that would fracture bone
bone adapts so forces experienced regularly don't exceed MES
trabecular (spongy) bone adapts more quickly than cortical (compact) bone
may take a long time to observe (6 months), but the process begins quickly
mechanical forces stimulate collagen synthesis
amount of force is proportional to the degree of adaptation
areas of increase in strength:
tendon-bone junction
within body of tendon or ligament
in the network within skeletal muscle
how strength in increased:
increased collagen diameter
greater collagen-muscle links
more collagen fibrils
greater density of collagen fibrils
tendon stiffness may occur as a result of intense resistance training (>80% 1RM)
chronic changes of acute hormone response
may improve beneficial hormone response to acute exercise
e.g. greater growth hormone response
chronic changes in resting hormones
unclear, but probably little change
"chronic" changes may just be the most recent acute response
hormone receptor
increase in androgen receptors, which interact with testosterone
receptors are initially down-regulated after exercise and up-regulated later
resistance training increases the angle of pennation
muscle architecture
(in pennate muscles)
increases CSA and muscular strength
sprint training can increase the length of muscle fibers
increases the velocity of contraction
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