Adaptations to
Resistance Training
Resistance Training: Introduction
• Resistance training yields substantial
strength gains via neuromuscular changes
• Important for overall fitness and health
• Critical for athletic training programs
Resistance Training:
Gains in Muscular Fitness
• After 3 to 6 months of resistance training
– 25 to 100% strength gain
– Learn to more effectively produce force
– Learn to produce true maximal movement
• Strength gains similar as a percent of initial
strength
– Young men experience greatest absolute gains
versus young women, older men, children
– Due to incredible muscle plasticity
Mechanisms of Muscle Strength Gain
• Hypertrophy versus atrophy
–  Muscle size   muscle strength
–  Muscle size   muscle strength
– But association more complex than that
• Strength gains result from
–  Muscle size
– Altered neural control
Figure 10.1a
Figure 10.1b
Figure 10.1c
Mechanisms of Muscle Strength Gain:
Neural Control
• Strength gain cannot occur without neural
adaptations via plasticity
– Strength gain can occur without hypertrophy
– Property of motor system, not just muscle
• Motor unit recruitment, stimulation
frequency, other neural factors essential
Mechanisms of Muscle Strength Gain:
Motor Unit Recruitment
• Normally motor units recruited
asynchronously
• Synchronous recruitment  strength gains
– Facilitates contraction
– May produce more forceful contraction
– Improves rate of force development
–  Capability to exert steady forces
• Resistance training  synchronous
recruitment
Mechanisms of Muscle Strength Gain:
Motor Unit Recruitment
• Strength gains may also result from greater
motor unit recruitment
–  Neural drive during maximal contraction
–  Frequency of neural discharge (rate coding)
–  Inhibitory impulses
• Likely that some combination of improved
motor unit synchronization and motor unit
recruitment  strength gains
Mechanisms of Muscle Strength Gain:
Motor Unit Rate Coding
• Limited evidence suggests rate coding
increases with resistance training,
especially rapid movement, ballistic-type
training
Mechanisms of Muscle Strength Gain:
Autogenic Inhibition
• Normal intrinsic inhibitory mechanisms
– Golgi tendon organs
– Inhibit muscle contraction if tendon tension too high
– Prevent damage to bones and tendons
• Training can  inhibitory impulses
– Muscle can generate more force
– May also explain superhuman feats of strength
Mechanisms of Muscle Strength Gain:
Muscle Hypertrophy
• Hypertrophy: increase in muscle size
• Transient hypertrophy (after exercise bout)
– Due to edema formation from plasma fluid
– Disappears within hours
• Chronic hypertrophy (long term)
– Reflects actual structural change in muscle
– Fiber hypertrophy, fiber hyperplasia, or both
Mechanisms of Muscle Strength Gain:
Chronic Muscle Hypertrophy
• Maximized by
– High-velocity eccentric training
– Disrupts sarcomere Z-lines (protein remodeling)
• Concentric training may limit muscle
hypertrophy, strength gains
Mechanisms of Muscle Strength Gain:
Fiber Hypertrophy
• More myofibrils
• More actin, myosin filaments
• More sarcoplasm
• More connective tissue
Mechanisms of Muscle Strength Gain:
Fiber Hypertrophy
• Resistance training   protein synthesis
– Muscle protein content always changing
– During exercise: synthesis , degradation 
– After exercise: synthesis , degradation 
• Testosterone facilitates fiber hypertrophy
– Natural anabolic steroid hormone
– Synthetic anabolic steroids  large increases in
muscle mass
Mechanisms of Muscle Strength Gain:
Fiber Hyperplasia
• Humans
– Most hypertrophy due to fiber hypertrophy
– Fiber hyperplasia also contributes
– Fiber hypertrophy versus fiber hyperplasia may
depend on resistance training intensity/load
– Higher intensity  (type II) fiber hypertrophy
• Fiber hyperplasia may only occur in certain
individuals under certain conditions
Mechanisms of Muscle Strength Gain:
Fiber Hyperplasia
• Can occur through fiber splitting
• Also occurs through satellite cells
–
–
–
–
Myogenic stem cells
Involved in skeletal muscle regeneration
Activated by stretch, injury
After activation, cells proliferate, migrate, fuse
MODEL OF NEURAL AND
HYPERTROPHIC FACTORS
Mechanisms of Muscle Strength Gain:
Neural Activation + Hypertrophy
• Short-term  in muscle strength
– Substantial  in 1RM
– Due to  voluntary neural activation
– Neural factors critical in first 8 to 10 weeks
• Long-term  in muscle strength
– Associated with significant fiber hypertrophy
– Net  protein synthesis takes time to occur
– Hypertrophy major factor after first 10 weeks
Mechanisms of Muscle Strength Gain:
Atrophy and Inactivity
• Reduction or cessation of activity  major
change in muscle structure and function
• Limb immobilization studies
• Detraining studies
Mechanisms of Muscle Strength Gain:
Immobilization
• Major changes after 6 h
– Lack of muscle use  reduced rate of protein
synthesis
– Initiates process of muscle atrophy
• First week: strength loss of 3 to 4% per day
–  Size/atrophy
–  Neuromuscular activity
• (Reversible) effects on types I and II fibers
– Cross-sectional area  cell contents degenerate
– Type I affected more than type II
Mechanisms of Muscle Strength Gain:
Detraining
• Leads to  in 1RM
– Strength losses can be regained (~6 weeks)
– New 1RM matches or exceeds old 1RM
• Once training goal met, maintenance
resistance program prevents detraining
– Maintain strength and 1RM
– Reduce training frequency
Mechanisms of Muscle Strength Gain:
Fiber Type Alterations
• Training regimen may not outright change
fiber type, but
– Type II fibers become more oxidative with aerobic
training
– Type I fibers become more anaerobic with
anaerobic training
• Fiber type conversion possible under
certain conditions
– Cross-innervation
– Chronic low-frequency stimulation
– High-intensity treadmill or resistance training
Mechanisms of Muscle Strength Gain:
Fiber Type Alterations
• Type IIx  type IIa transition common
• 20 weeks of heavy resistance training
program showed
– Static strength, cross-sectional area 
– Percent type IIx , percent type IIa 
• Other studies show type I  type IIa with
high-intensity resistance work + shortinterval speed work
Muscle Soreness
• From exhaustive or high-intensity exercise,
especially the first time performing a new
exercise
• Can be felt anytime
– Acute soreness during, immediately after exercise
– Delayed-onset soreness one to two days later
Muscle Soreness:
Acute Muscle Soreness
• During, immediately after exercise bout
– Accumulation of metabolic by-products (H+)
– Tissue edema (plasma fluid into interstitial space)
– Edema  acute muscle swelling
• Disappears within minutes to hours
Muscle Soreness:
DOMS
• DOMS: delayed-onset muscle soreness
– 1 to 2 days after exercise bout
– Type 1 muscle strain
– Ranges from stiffness to severe, restrictive pain
• Major cause: eccentric contractions
– Example: Level run pain < downhill run pain
– Not caused by  blood lactate concentrations
Muscle Soreness:
DOMS Structural Damage
• Indicated by muscle enzymes in blood
– Suggests structural damage to muscle membrane
– Concentrations  2 to 10 times after heavy training
– Index of degree of muscle breakdown
• Onset of muscle soreness parallels onset of
 muscle enzymes in blood
Muscle Soreness:
DOMS and Performance
• DOMS   muscle force generation
• Loss of strength from three factors
– Physical disruption of muscle (see figures 10.8,
10.9)
– Failure in excitation-contraction coupling (appears to
be most important)
– Loss of contractile protein
Figure 10.10
Muscle Soreness:
DOMS and Performance
• Muscle damage   glycogen resynthesis
• Slows/stops as muscle repairs itself
• Limits fuel-storage capacity of muscle
• Other long-term effects of DOMS:
weakness, ultrastructural damage, 3-ME
excretion
Muscle Soreness:
Reducing DOMS
• Must reduce DOMS for effective training
• Three strategies to reduce DOMS
– Minimize eccentric work early in training
– Start with low intensity and gradually increase
– Or start with high-intensity, exhaustive training
(soreness bad at first, much less later on)
Muscle Soreness:
Exercise-Induced Muscle Cramps
• Frustrating to athletes
– Occur even in highly fit athletes
– Occur during competition, after, or at rest
• Frustrating to researchers
– Multiple unknown causes
– Little information on treatment and prevention
• EAMCs versus nocturnal cramps
Muscle Soreness:
Exercise-Induced Muscle Cramps
• EAMC type 1: muscle overload/fatigue
– Excite muscle spindle, inhibit Golgi tendon organ
 abnormal a-motor neuron control
– Localized to overworked muscle
– Risks: age, poor stretching, history, high intensity
• EAMC type 2: electrolyte deficits
– Excessive sweating  Na+, Cl- disturbances
– To account for ion loss, fluid shifts
– Neuromuscular junction becomes hyperexcitable
Muscle Soreness:
Exercise-Induced Muscle Cramps
• Treatment depends on type of cramp
• Fatigue-related cramps
– Rest
– Passive stretching
• Electrolyte-related (heat) cramps
– Prompt ingestion of high-salt solution, fluids
– Massage
– Ice