Chapter 1 Structure and Function of Exercising Muscle

Muscle Fiber Types

Type I fibers/ slow-twitch
Take about 110 ms to reach peak tension
Compose 50% of most muscles
Type II fibers/ fast-twitch
Take about 50 ms to reach peack tension
Type IIa
o 25% of fibers in muscle
Type IIx
o 25% of fibers in muscle
Type IIc
o Limited info and knowledge
*These numbers are only averages and varied not only based on the
muscles, but on the individual
Type I VS. Type II Fibers Differentiation (Characteristics)

Speed of myosin ATPase varies

o Type I = slow form of ATPase slower contraction cycle
o Type II= fast form of ATPase faster contraction cycle
Sarcoplasm Reticulum
o Type II fibers have a more highly developed SR
o Faster Ca2+ release. 5 to 6 times faster Vo than type I
o Power is 3 to 5 times greater bcs of faster shortening velocity
Motor Units
o Type I has a smaller cell body, innervates <300 muscle fibers
o Type II has a larger cell body, innervates >300 muscle fibers

Peak power: type IIx> type IIa > type I

o Effects of different SR, motor units, etc
o Single fiber recording
Regardless of fiber type, all muscle fibers reach peak power at 20%
peak force.

Fiber Type and Exercise

Type I High aerobic endurance
Can maintain exercise for prolonged periods
Require ATP for oxygen production
Recruited most during low-intensity endurance and daily activities
Efficiently produce ATP from fat and carbohydrate
Type II

 General
Poor aerobic endurance, fatigue quickly
Produce ATP anaerobically
Type IIa
Generate more force, faster fatigue than type I
Short, high-intensity such as mile run or 400m swim
Type IIx
Seldom used for everyday activities
Used in highly explosive sprints such as 100 m dash or 50m swim
Fiber Type Compositioning and Endurance Training
Type I fibers: greater oxidative capacity
o More mitochondria
o High oxidative enzyme concentrations
o Type II better for glycolytic energy production
Type II fibers: greater glycolytic energy production Endurance
Training
o Enhances oxidative capacity of type II fibers
o Develops more (and larger) mitochondria
o More oxidative enzymes per mitochondrion
Distribution of Fiber Types: Type I: Type II Ratios

Each person has different ratios

Determined within first few years of life
Changes very little from childhood to middle age
Arm and leg ratios are similar in one person
Endurace athletes: Type I predominates
Power athletes: Type II predominates
Soleus: type I in everyone due to walking

Determination of Fiber Type

Genetic Factors
o Determine which alpha motor neurons innervate muscle fibers
o Fibers differentiate based on alpha motor neuron
Training Factors
o Endurance versus strength training, muscular inactivity
o Can induce small (10%) change in fiber type
Aging: muscle loses type II motor units and type I increases

Fiber Type and Athletic Success

Endurance athletes- type I

Sprinters- Type II

Fiber
o
o
o
o

type not sole predictor of success

Cardiovascular function
Motivation
Training habits
Muscle size

Concentric contraction (shortening) = dynamic contraction

Isometric (unchanged)
Eccentric (lengthening)
Chapter 2 Fuel for Exercise: Bioenergetics and Muscle Metabolism
Carbohydrate

All carbohydrate converted to gluocose

o 4.1 kcal /g; -2500 kcal stored in the body
o Primary ATP substrate for muscles/ brain
o Extra glucose stored as glycogen in liver, muscles
Glycogen converted back to glucose when needed to make more ATP
Glycogen stores limited (2500 kcal), must rely on dietary carbohydrate to
replenish

Fat

Efficient substrate , efficient storage

o 9.4 kcal/g
o +75,000 kcal stored in the body
Energy substrate for prolonged, less intense exercise
o High net ATP yield but slow ATP production
o Must be broken down into free fatty acids (FFA) and glycerol
o Only FFAs are used to make ATP

Protein

Minor source of energy

o Can supply about 5% or 10% of the energy needed to sustain
prolonged exercise
o 4.1 kcal
In severe depletion, protein can be used to generate FFAs for energy
o Only amino acids can be used for energy

The Three Basic Energy Systems

1. The ATP-PCr system
Anaerobic-does not require oxygen
ATP yield: 1 mol ATP/ 1 mol PCr
Duration: 3 to 15 s
Because ATP stores a very limited, this pathway is used to reassemble ATP
Phosphocreatine(PCr): ATP recycling

o PCr amd creatine kinase Cr + Pi + energy

o PCr energy cannot be used for cellular work
o PCr energy used to reassemble
Replenishes ATP stores during rest
Recycles ATP during exercise until used up (3-15 s of maximal exercise)

Creatine Kinase (CK)

PCr breakdown catalyzed by CK

CK controls rate of ATP production
o Negative feedback system
o When ATP levels decrease, CK activity increases
o When ATP levels increase, CK activity decreases
2. The Glycolytic
Anaerobic
ATP yield: 2 to 3 mol ATP/ 1 mol of substrate
o Due to different energy costs for glucose versus glycogen
Rate Limiting Enzyme: Phosphofructokinase (PFK)
o Low ATP, High PFK
o High ATP, Low PFK
Exercise Duration Time: 15 s to 2 mins maximal exercise
Cons

Low ATP yield

Insufficient use of substrate
Lack of O2 converts pyruvic acid to lactic acid
o Lactic acid impairs glycolysis, muscle contraction

Pros

Allow muscles to contract when O2 limited

Predominates during shorter-term, higher intensity exercise

3. The Oxidative System

Aerobic
ATP yield: depends on the substrate
o 32-33 ATP/ 1 glucose/ glycogen or 100+ ATP/ 1 FFA
Duration: steady supply for hours
Most complex of the three bioenergetics systems
Occurs in the mitochondria, not cytoplasm
Rate Limiting Enzyme: Isocitrate dehydrogenase
o Similar to PFK for glycolysis
o Regulates electron transport chain
o Inhibited by ATP, activated by ADP
o Negative Feedback regulates Krebs cycle
Interaction Among Energy Systems

All three systems interact for all activities

o No one system contributes 100%
o One single system dominates for a given task
More cooperation during transition periods

Chapter 4 Hormonal Control During Exercise

Hormonal Regulation of Metabolism During Exercise
Hormones released by these glands affect metabolism of carbohydrate and
fat during exercise
Anterior Pituitary
o Exercise is a strong stimulus to the hypothalamus because exercise
increases the release of most anterior pituitary hormones
o 6 hormones (four tropic hormones + GH and prolactin)
Thyroid Gland
o T3 and T4 regulate metabolism (Increase the metabolic rate of almost
all tissues and can increase the bodys basal metabolic rate by 60 to
100%)
o Increase protein synthesis
o Increase size and number of mitochondria in most cells
o Promote rapid cellular uptake of glucose
o Enhance glycolysis and gluconeogenesis; and
o Enhance lipid mobilization, increasing FFA availability for oxidation
Adrenal Glands
o 80% epinephrine and 20% norepinephrine
Increased heart rate and force of contraction
Increased metabolic rate
Increased glycogenolysis in the liver and the muscle
Increased release of glucose and FFAs into the blood
Redistribution of blood to the skeletal muscles
Increased blood pressure and increased respiration
Cortisol
the body
Stimulates gluconeogenesis to ensure an adequate fuel supply
Increases mobilization of FFAs, more available as an energy
source
Decreases glucose utilization, sparing it for the brain
Stimulates protein catabolism to release amino acids for use in
repair
Acts as an anti-inflammatory agent
Depresses immune reactions
Increased the vasoconstriction by epinephrine
Pancreas
o Insulin
Facilitates glucose transport into the cells, especially muscle
fibers
o

Promotes glycogenesis
Inhibits gluconeogenesis
Growth Hormone released proportional to exercise intensity

Regulation of Carbohydrates During Exercise

Adequate glucose during exercise requires

o Glucose release by the liver
o Glucose uptake by the muscles
o Glycogenolysis is promoted in the liver
o Cortisol, Glucagon, GH, Epi, and Norepinephrine

Regulation of Fat Metabolism During Exercise

FFA mobilization and fat metabolism critical to endurance exercise

performance
Triglycerides FFAs + glycerol
o Rate of triglyceride breakdown into FFAs may determine rate of cellular
fat metabolism
Lipolysis using lipase is stimulated by
o Decreased insulin
o Epinephrine
o Norepinephrine
o Cortisol
o Growth Hormone
o Thyroid Hormone

Hormonal Regulation of Fluid and Electrolytes During Exercise

During exercise, plasma volume decreases, causing

o Increase hydrostatic pressure, tissue osmotic pressure
o Increase plasma water content via sweating
o Increase heart strain, decrease blood pressure

ADH (Antidiuretic Hormone)

1. Muscular activity promotes sweating
2. Sweating causes loss of blood plasma resulting in hemo-concentration and
increased blood osmolality
3. Increased blood osmolality stimulates osmoreceptors in the hypothalamus
4. The hypothalamus sends a neural signal to the posterior pituitary gland
5. The posterior pituitary gland secretes ADH
6. ADH acts on the kidneys increasing water permeability of the renal tubules
and collecting ducts, leading to increased reabsorption of water
7. Decreased urine output aids in minimizing body fluid loss
Renin Angiotensin Aldosterone System
1. Prolonged exercised without adequate fluid replacement can lead to
dehydration

2. Dehydration can, in turn, cause a decrease in blood pressure, which is sensed

by the kidneys
3. Renin is secreted by the kidneys
4. Renin converts angiotensin into angiotensin I
5. ACE in the lungs converts angiotensin I into II
6. Angiotensin II stimulates the adrenal cortex to secrete aldosterone and
vasoconstricts blood vessels, increasing blood pressure
7. Aldosterone acts on the kidneys to increase Na+ reabsorption
8. Urine volume decreases
Hormonal Regulation of Caloric Intake

Hypothalamus is appetite control center of the brain

o Satiety center in the ventromedial nucleus
o Hunger center in lateral hypothalamus
CKK-decreases appetite
Leptin- decreases appetite
Peptide YY- decreases appetite
GLP-1-decreases appetite
Insulin- decreases appetite
Ghrelin- increases appetite
Exercise affects hunger and satiety hormones
Acute, vigorous exercise increases PPY and GLP-1, reducing hunger
Exercise training does not affect ghrelin except in energy deficit

Chapter 5 Energy Expenditure and Fatigue

Submaximal Aerobic Exercise

Slow component of O2 uptake kinetics

o At high power outputs, VO2 continues to increase
o More type II (less efficient) fiber recruitment
VO2 drift
o Upward drift observed even at low power outputs
o Possibly due to increased ventilation and catecholamines

Maximal Aerobic Exercise

VO2 max point at which O2 consumption does not increase with further
increase in intensity
VO2 peak O2 consumption at time of volitional fatigue (I cant continue, Im
tired)
o Best single measurement of aerobic fitness but not best predictor of
endurance performance
o Plateaus after 8-12 weeks of training
o Performance continues to improve
o More training allows athlete to compete at higher percentage of VO2
max

Maximal Oxygen Uptake

VO2 max expressed in L/min

o Easy standard units and non-weight bearing activities
VO2 max normalized for body weight
o mL O2 x kg-1x min-1
o More accurate comparison for different body sizes
o Used for weight baring activities

Energy Expenditure: Aerobic vs Anaerobic

No activity 100% aerobic or anaerobic

Estimates of anaerobic effort involve
o Excess postexercise O2 consumption
o Lactate threshold

Excess Post Exercise Consumption (EPOC)

O2 demand > O2 consumed in early exercise

O2 consumed > O2 demand in early recovery
o The shorter amount of exercise and the lower the intensity, the less
EPOC will be until person comes back to resting values

Anaerobic Energy Expenditure: Lactate Treshold

Lactate threshold: point at which blood lactate accumulation increases markedly

Lactate production rate > lactate clearance rate

Interaction of aerobic and anaerobic systems
Good indicator of potential for endurance exercise (expressed as percentage
of VO2max)
Lactate accumulation increases fatigue
o Ability to exercise hard without accumulating lactate beneficial to
athletic performance
o Higher lactate threshold = higher sustained exercise intensity = better
endurance performance
For two athletes with same VO2 max, higher lactate threshold predicts better
performance

Energy Expenditure During Exercise: Economy of Effort

As athletes become more skilled, use of less energy for given pace
o Independent of VO2 max
o Body learns energy economy with practice
Multifactorial phenomenon
o Economy increases with distance of race
o Practice better economy of movement (form)
o Varies with type of exercise (running vs. swimming)

FATIGUE AND ITS CAUSES

Causes of fatigue
1. A decreased rate of energy delivery (ATP-PCr, anaerobic glycolysis, and
oxidative metabolism)
2. Accumulation of metabolic by-products (lactate and H+)
3. Failure of the muscle fibers contractile mechanism
4. Alterations in neural control of muscle contraction
PCr Depletion

PCr depletion coincides with fatigue

o PCr used for shorter term, high intensity effort
o PCr depletes more quickly than total ATP
Pi accumulation may be potential cause
Pacing helps defer PCr depletion

Glycogen Depletion

Glycogen reserves are limited and deplete quickly

Depletion correlated with fatigue
o Related to total glycogen depletion
o Unrelated to rate of glycogen depletion
Depletes more quickly with high intensity
Depletes more quickly during the first few minutes of exercise
versus later stages

Glycogen Depletion in Different Fiber Types

Fiber type and recruitment patterns

o Fibers recruited first or most frequently deplete fastest
o Type I fibers depleted after moderate endurance exercise
Recruitment depends on exercise intensity
o Type I fibers recruit first light/ moderate intensity
o Type IIa next moderate/ high intensity
o Type IIx fibers recruit last maximal intensity

Glycogen Depletion in Different Muscle Groups

Activity-specific muscles deplete fastest

Recruited earliest and longest for given task

Glycogen Depletion and Blood Glucose

Muscle glycogen insufficient for prolonged exercise

Liver glycogen broken down to provide constant supply of blood glucose
As muscle glycogen decreases, liver glycogenolysis increases
Muscle glycogen depletion = hypoglycemia = fatigue

Certain rate of muscle glycogenolysis required to maintain

o NADH production in Krebs cycle
o Electron transport chain activity
o No glycogen = inhibited substrate oxidation
With glycogen depletion, Free Fatty Acids metabolism Increases
o But FFA oxidation too slow, may be unable to supply enough ATP for
given intensity

Metabolic Waste Products and Fatigue

Inorganic Phosphate
o Accumulation of Pi during intense short term exercise is the largest
contributor to fatigue
Excess Pi impairs contractile function of myofibrils and can
reduce Ca2+ release from the sarcoplasmic reticulum
Increases in Pi and ADP also inhibit ATP breakdown
Heat and Muscle Temperature
o Heat alters metabolic rate
Increases rate of carbohydrate utilization
Hastens glycogen depletion
Impair both skeletal muscle function and metabolism
High temperature and humidity causes early fatigue
Lactic Acid
o Lactic acid accumulates during brief, high intensity exercise
If not cleared immediately, converts to lactate and causes an
accumulation of H+ ions
H+ accumulation cause muscle acidosis = decrease in pH
o Buffers help muscle pH but not enough
Buffers minimize drop in pH (7.1 to 6.5, not to 1.5)
pH<6.9 inhibits the action of phosphofructokinase, a glycolytic
enzyme, slowing the rate of glycolysis and ATP production
pH = 6.4 prevents further glycogen breakdown
o May be beneficial during exercise
Accumulation can bring on fatigue
But if production = clearance, it is not fatiguing
o Serves as a fuel source
Lactate is directly oxidized by type I fiber mitochondria
Shuttled from type II fibers to type I for oxidation
Converted to glucose via gluconeogenesis (liver)

NEUROMUSCULAR FATIGUE
Neural Transmission

Failure may occur at the neuromuscular junction, preventing muscle

activation
Possible causes are due to the following processes
o Decrease Ach synthesis and released

AchE may be hyperactive/ upregulated preventing sufficient Ach

concentration from initiating an action potential
o Increase in muscle fiber stimulus threshold
o Altered muscle resting membrane potential
Fatigue may inhibit Ca2+ release from Sarcoplasmic Reticulum
o

Central Nervous System

CNS undoubtedly plays a role in fatigue but not fully understood yet
Fiber recruitment has conscious aspect
o Stress of exhaustive exercise may be too much
o Subconscious or conscious unwillingness to endure more pain
o Discomfort of fatigue = warning sign
o Elite athletes learn proper pacing, tolerate fatigue

MUSCLE SORENESS

Acute muscle soreness- pain and soreness usually disappear within a few
minutes to several hours after the exercise.
Delayed-onset muscle soreness (DOMS)- muscle soreness felt a day
of two after a heavy bout of exercise
1. Pathway begins with structural damage (microtrauma) to muscle
fibers and to the surrounding connective tissues.
Eccentric muscle action is the primary initiator of DOMS
2. Membrane damage disturbs Ca2+ homeostasis in injured fiber
Inhibits cellular respiration
Activates enzymes that degrade z-discs
3. Within a few hours, circulating neutrophils increase (inflammatory
response)
4. Products of macrophage activity, intracellular contents accumulate
Histamine, kinins, and K+
Stimulate pain in the free nerve endings
Worse with eccentric exercise
5. Fluid and electrolytes shift into the area, creating edema. Muscle
spasms may also be present.
DOMS = reduction in the force-generating capacity of the affected muscles.
Loss of strength is the result of
o Physical disruption of the muscle
o Failure within the excitation-contraction coupling process
o Loss of contractile protein

MUSCLE CRAMPS

Exercise associated muscle cramps (EAMCs)

o Painful, spasmodic, involuntary contractions of skeletal muscles that
occur during or immediately after exercise
1. Neuromuscular control becomes altered

a. Excitation of the muscle spindle and inhibition of the Golgi

tendon organ
b. Abnormal alpha-motor neuron activity and reduced inhibitory
feedback
c. Localized to the overworked muscle
2. Heat cramps
a. Occurs due to extensive sweating and significant electrolyte
disturbances (sodium and chloride).

Basal metabolic rate

Calorie (cal)
Central governor theory

Direct calorimetry
Excess postexercise oxygen consumption (EPOC)
Haldane Transformation
Indirect calorimetry
Lactate threshold
Maximal oxygen uptake (Vo2max)
Oxygen deficit
Peak oxygen uptake (Vo2peak)
Respiratory exchange ratio (RER)
Resting metabolic rate (RMR)
VO2 drift