Module: Muscle Contraction and Fatigue

Describe the conditions (e.g., metabolic fuels and breakdown products)

within a muscle fibre at the conclusion of a 30 second bout
of maximal exercise. (4 marks).
Include a discussion of how these conditions might contribute to skeletal
muscle fatigue during the 30 s maximal exercise bout. (6 marks)
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At the conclusion of a 30-second bout of maximal exercise, several key conditions exist within muscle fibres:

Metabolic Fuels
Glycogen: The primary fuel source for high-intensity exercise. Glycogen stores are rapidly depleted during maximal
efforts. This depletion can slow the flux through glycolysis and oxidative pathways, potentially interfering with calcium
release from the sarcoplasmic reticulum, which is crucial for muscle contraction.1
Creatine Phosphate (CP): Provides a quick source of energy through the phosphocreatine system, which is crucial for
short bursts of activity. CP levels rapidly decline within the first few seconds of exercise, and its depletion coincides
with fatigue.2
Breakdown Products
Lactic Acid: Produced from anaerobic glycolysis as glycogen is broken down to glucose and then to pyruvate, which is
converted to lactic acid when oxygen is limited. Lactic acid accumulation is associated with increased hydrogen ions,
which can impair muscle function.
Inorganic Phosphate (Pi): Released during ATP breakdown, contributing to muscle fatigue. Pi accumulation can impair
calcium handling in the sarcoplasmic reticulum and inhibit actin-myosin cross-bridging.
Hydrogen Ions (H+): Accumulate from lactic acid dissociation, leading to a decrease in pH (acidosis). This can decrease
cell membrane excitability and impair calcium release from the sarcoplasmic reticulum.
Contribution to Skeletal Muscle Fatigue
The conditions within the muscle fibres contribute to skeletal muscle fatigue in several ways:

Energy Depletion: As glycogen and CP stores are depleted, the muscle's ability to produce ATP diminishes, leading to
reduced contractile force. The depletion of glycogen can inhibit calcium release channels in the sarcoplasmic
reticulum, further reducing muscle contraction.3
Lactic Acid Accumulation: The increase in lactic acid and subsequent drop in pH can impair enzyme function and
disrupt the contractile proteins, leading to muscle fatigue. Although lactic acid is often blamed for fatigue, it is the
associated hydrogen ions that primarily contribute to the decrease in pH and muscle function.4
Inorganic Phosphate Accumulation: Elevated levels of Pi can interfere with the release of calcium ions from the
sarcoplasmic reticulum, which is essential for muscle contraction. This can also inhibit actin-myosin cross-bridging,
reducing muscle force production.
Hydrogen Ion Effects: The accumulation of H+ ions can lead to a sensation of burning in the muscles and can inhibit
muscle contraction by affecting the myofibrils' ability to interact with calcium. This can also decrease the rate of ATP
synthesis by inhibiting enzymes associated with glycolysis.
In summary, the combination of energy depletion, accumulation of metabolic byproducts, and changes in pH
significantly contribute to the onset of skeletal muscle fatigue during a 30-second maximal exercise bout.

Metabolism
An athlete performs an incremental exercise test on a cycle
ergometer under your supervision. As an exercise
physiologist, you measure the rate of carbohydrate and fat
use at low, moderate and high intensities of exercise. The
figure below shows the results from the test.
1. Describe the expected changes in fuel contributions from
muscle AND plasma sources, as exercise intensity transitions
from moderate to a high intensity of exercise. (4 marks).

2. Explain the physiological factors that result in the

increased use of carbohydrate sources at high exercise
intensities. In your answer include the important hormones,
key enzymes, and relevant tissues that contribute to the
increase in carbohydrate oxidation (6 marks).

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1. Changes in Fuel Contributions from Muscle and Plasma Sources
(4 marks)

As exercise intensity increases from moderate (65% VO₂ max) to high

intensity (85% VO₂ max):

 Carbohydrate use increases significantly, particularly from

muscle glycogen stores. This is evident in the graph, where the
white portion (carbohydrate contribution) rises sharply at 85% VO₂
max.

 Fat utilization decreases relatively as intensity increases.

Although total energy expenditure increases, the relative
contribution of fat (especially plasma free fatty acids)
decreases, shown by the relatively smaller black portion at higher
intensities.

 Muscle-derived fuels become dominant:

o At moderate intensity: there's a mix of plasma glucose,

plasma free fatty acids, muscle glycogen, and
intramuscular triglycerides.

o At high intensity: there is a shift toward intramuscular

fuels, particularly muscle glycogen and intramuscular
triglycerides, because they are more rapidly accessible.

 Plasma-derived fuels decline due to reduced blood flow to

adipose tissue and viscera, which limits the mobilization and
transport of free fatty acids.

2. Physiological Factors for Increased Carbohydrate Use at High

Intensities (6 marks)

At high exercise intensities, several physiological mechanisms promote a

greater reliance on carbohydrate oxidation:

1. Hormonal Regulation:

 Increased epinephrine and norepinephrine stimulate:

o Glycogen phosphorylase activation in muscle, enhancing

glycogenolysis (breakdown of glycogen to glucose).
 o Inhibition of insulin, which reduces glucose uptake in non-
exercising tissues and prioritizes glucose use in muscle.

 Glucagon levels increase, promoting hepatic glycogenolysis to

maintain blood glucose availability.

2. Enzyme Activation:

 Phosphofructokinase (PFK) and pyruvate dehydrogenase

(PDH) activities are upregulated, accelerating glycolysis and
carbohydrate oxidation.

 These enzymes are more pH-sensitive and oxygen-efficient,

making carbohydrate metabolism favorable during high-intensity
work when oxygen delivery may be limited.

3. Muscle Fiber Recruitment:

 Fast-twitch (Type II) muscle fibers, which are more glycolytic,

are recruited at higher intensities.

o These fibers rely heavily on muscle glycogen for ATP

production due to their high glycolytic enzyme content.

4. Oxygen Availability:

 At high intensities, the body shifts to anaerobic glycolysis due to

limited oxygen delivery to mitochondria.

o Carbohydrates can be metabolized anaerobically, unlike fats.

5. Lactate Production:

 High rates of glycolysis produce lactate, which regenerates NAD⁺,

sustaining glycolysis.

 The Cori cycle helps manage this lactate by transporting it to the

liver for conversion back into glucose.

Tissue Involvement:

 Skeletal muscle becomes the primary site of glucose uptake and

oxidation.

 Liver supports by releasing glucose via glycogenolysis and

gluconeogenesis.

 Adipose tissue contribution declines due to reduced lipolysis and

blood flow.
Module 3: O2 delivery
It is critical that oxygen delivery is adequate to match the metabolic
demand of the organs/tissues.
During exercise, an increase in oxygen delivery to the active tissues (i.e.
skeletal muscle) occurs through a combination of
increased cardiac output and a redistribution of blood flow.
i) As a proportion of total cardiac output, discuss the changes in blood
flow distribution to the major organs and tissues of the body that occur
during the transition from rest to moderate/high intensity exercise. Be
quantitative where possible (4 marks).
ii) Describe the local and central factors that regulate these changes in
cardiac output and blood flow during exercise. (6 marks).

i) Changes in Blood Flow Distribution from Rest to Moderate/High-Intensity

Exercise (4 marks)

During exercise, the total cardiac output (CO) increases significantly (from ~5 L/min at rest
to ~20–25 L/min during high-intensity exercise). This rise supports the increased oxygen and
nutrient demand, particularly by skeletal muscle, and occurs with a major redistribution of
blood flow:

At Rest (% of
Tissue/Organ During Exercise (% of CO)
CO)
~15–20% (~1
Skeletal Muscle ~80–85% (~20 L/min)
L/min)
~3–4% (absolute flow remains fairly
Brain ~13–15%
constant ~750 mL/min)
Heart
~4–5% ~4–5% (absolute flow ↑ 3–4x)
(Coronary)
Kidneys ~20–25% ~2–4%
GI Tract &
~20–25% ~3–5%
Liver
Variable (↑ during moderate exercise for
Skin ~5–10%
thermoregulation, ↓ during maximal exercise)

Key Takeaway:

 Skeletal muscle receives a dramatic increase in both absolute and relative blood
flow.
 Blood is shunted away from the splanchnic (GI), renal, and non-essential tissues to
support muscle function.
 Brain and coronary circulation are maintained to preserve vital function.
ii) Local and Central Factors Regulating Cardiac Output and Blood Flow
During Exercise (6 marks)

Central Factors (Neural and Hormonal Regulation):

1. Sympathetic Nervous System (SNS) Activation:

o Increased SNS outflow leads to:
 ↑ Heart Rate (HR)
 ↑ Stroke Volume (SV) via increased myocardial contractility
 Resulting in ↑ Cardiac Output (CO = HR × SV)
o Causes vasoconstriction in non-essential vascular beds (e.g., GI, renal)
through norepinephrine acting on α-adrenergic receptors.
2. Parasympathetic Withdrawal:
o Reduced vagal tone further increases heart rate at the onset of exercise.
3. Hormonal Control:
o Epinephrine from the adrenal medulla reinforces sympathetic effects:
 Increases HR, contractility, and glycogenolysis
 Causes vasoconstriction systemically, but vasodilation in skeletal
muscle via β2-adrenergic receptors

Local Factors (Metabolic and Myogenic Regulation):

1. Metabolic Vasodilation in Active Muscle:

o Accumulation of local metabolites causes vasodilation in working muscles:
 ↓ O₂, ↑ CO₂, ↑ H⁺ (↓ pH), ↑ K⁺, ↑ adenosine, and ↑ nitric oxide (NO)
o Overrides sympathetic vasoconstriction—a process called functional
sympatholysis
2. Endothelial-Derived Relaxing Factors (EDRFs):
o Especially nitric oxide (NO) promotes vasodilation in response to shear
stress and hypoxia.
3. Myogenic Response:
o Vessels constrict or dilate in response to changes in blood pressure, helping
to maintain perfusion pressure.
4. Muscle Pump Mechanism:
o Rhythmic skeletal muscle contractions aid venous return, increasing end-
diastolic volume and thus stroke volume via the Frank-Starling
mechanism.

Summary:

 Central regulation ensures systemic redistribution of blood.

 Local metabolic and endothelial factors fine-tune delivery to the most active tissues
(i.e., skeletal muscle), ensuring efficient oxygen delivery during varying exercise
intensities.
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Practical Lab Content

The figure below shows the VO2 response during an incremental exercise
test performed until exhaustion in two 25 year-old subjects that both
exhibit similar kinanthropometry. One subject is endurance trained, while
the other is untrained.

Considering the data presented in the graph above, answer the following
questions:

i. Identify which VO2 response (either A or B) likely represents that of the

trained and untrained subjects. (1 mark)

ii. Describe the similarities (2 mark) and differences (1 mark) between the
two subjects in their response to the exercise and the underlying
physiological basis (6 marks) for their responses.

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i. Identify VO₂ Response (1 mark)

 Curve A represents the untrained subject.

 Curve B represents the endurance-trained subject.

Justification: Curve B reaches a higher VO₂ max (~65 ml/kg/min vs. ~38 ml/kg/min) and
shows continued increases in oxygen uptake with increasing running velocity, which is
characteristic of a trained individual.

ii. Similarities and Differences in VO₂ Response and Underlying Physiology (9

marks total)

Similarities (2 marks)

1. Progressive VO₂ Increase with Running Speed:

Both subjects show a gradual rise in VO₂ as running velocity increases. This reflects
the body's increasing demand for oxygen with greater exercise intensity.
2. Linear VO₂ Kinetics Up to a Point:
Up to moderate intensities (~9–10 km/h), both exhibit a similar linear VO₂ response,
indicating that submaximal exercise elicits comparable metabolic demands
regardless of training status.
Difference (1 mark)

 The trained subject (B) demonstrates a higher maximal oxygen uptake (VO₂ max)
and continues to increase running velocity beyond the point where the untrained
subject (A) plateaus and fatigues.
 VO₂ max:
o A ≈ 38 ml/kg/min
o B ≈ 65 ml/kg/min
 This indicates a greater aerobic capacity and endurance performance in the
trained individual.

Physiological Basis of Differences (6 marks)

1. Higher Stroke Volume and Cardiac Output (1 mark):

o The trained subject has a larger stroke volume and therefore higher cardiac
output, enabling greater oxygen delivery to working muscles.
2. Increased Capillary Density (1 mark):
o Endurance training increases muscle capillarization, improving oxygen
diffusion from blood to muscle.
3. Greater Mitochondrial Density and Enzyme Activity (1 mark):
o The trained individual has more mitochondria and higher levels of oxidative
enzymes (e.g., citrate synthase, succinate dehydrogenase), enhancing aerobic
ATP production.
4. Improved Oxygen Extraction (1 mark):
o Due to better capillarization and mitochondrial function, the arteriovenous
oxygen difference (a-vO₂ diff) is greater in trained individuals.
5. Higher Lactate Threshold (1 mark):
o Trained subjects can sustain higher intensities without accumulating lactate
due to improved buffering capacity and aerobic metabolism, allowing them
to continue increasing intensity.
6. Improved Ventilatory Efficiency (1 mark):
o Trained individuals often have better respiratory muscle endurance and
more efficient gas exchange, supporting higher VO₂ values without premature
fatigue.

Summary:
The trained subject (Curve B) demonstrates superior cardiorespiratory and muscular
adaptations that allow for higher aerobic capacity, greater running speed, and delayed
fatigue compared to the untrained subject (Curve A), despite similar body types.
Muscle Contraction and Fatigue

 Describe the histochemical, biochemical, morphological

and physiological differences between fibre types in
skeletal muscle
 Explain how the muscle produces force that is sufficient
for the required task
 During exercise, identify the potential sites involved
with central and peripheral fatigue. Describe the
neural, contractile and metabolic factors that may be
linked to fatigue during exercise.

Metabolism

 What are the major fuels available to the muscle during

exercise?
 Discuss how exercise intensity and duration influence
carbohydrate and fat utilisation.
 What are the factors that regulate the mobilisation and
utilisation of carbohydrate and fat during exercise?

Oxygen Delivery

 Describe the changes in the cardiovascular system

during exercise that mediate oxygen delivery to
skeletal muscle, including cardiac output, blood flow
and oxygen extraction.
 Describe the changes in ventilation at the onset of
exercise and during exercise of increasing exercise
intensity and duration. What are the mechanisms that
regulate these changes?

Environmental Physiology
  Describe the hormonal, cardiovascular and metabolic
changes that occur during exercise in the heat.
 Describe some of the strategies to improve exercise
performance in the heat, including adaptations
occuring during heat acclimatisation.
 Describe the benefits of fluid replacement on
physiology, metabolism and exercise performance.

Here are some short answer questions on muscle

contraction and fatigue, relevant to exercise physiology:

Muscle Contraction

1. 1. What is the primary function of calcium ions in

muscle contraction?

 Answer: Calcium ions bind to troponin on actin,

which allows myosin to bind to actin and initiate
the sliding filament process.

2. 2. Describe the sliding filament theory in your

own words.

 Answer: Muscle contraction occurs when thin

(actin) filaments slide past thick (myosin)
filaments, shortening the sarcomere.

3. 3. Name the two main protein filaments involved

in muscle contraction.

 Answer: Actin and myosin.

4. 4. What is the role of ATP in muscle contraction?

 Answer: ATP provides the energy for myosin

heads to detach from actin and "re-cock" for
another cycle of cross-bridge formation.
 5. 5. What is the difference between concentric and
eccentric contractions?

 Answer: Concentric contractions shorten the

muscle, while eccentric contractions lengthen the
muscle.

6. 6. What is an isometric contraction?

 Answer: An isometric contraction is one where

muscle force is generated without a change in
muscle length.

7. 7. What is the neuromuscular junction, and what

role does it play in muscle contraction?

 Answer: The neuromuscular junction is the point

where a motor neuron communicates with a
muscle fiber. It's where the nerve impulse triggers
the release of acetylcholine, which then binds to
receptors on the muscle fiber membrane, initiating
an action potential and muscle contraction.

Muscle Fatigue

1. 1. Define muscle fatigue in simple terms.

 Answer: Muscle fatigue is a decline in the ability

of a muscle to generate force.

2. 2. What are some potential factors that can lead

to muscle fatigue?

 Answer: Depletion of energy stores (ATP,

glycogen, phosphocreatine), buildup of metabolic
byproducts (lactic acid, H+), changes in muscle
metabolism, and central nervous system
influences.

3. 3. What is the difference between peripheral and

central fatigue?
  Answer: Peripheral fatigue is due to factors within
the muscle itself (e.g., depletion of substrates),
while central fatigue is due to factors in the
nervous system (e.g., reduced neural drive).

4. 4. How does lactic acid accumulation contribute

to muscle fatigue?

 Answer: Lactic acid accumulation lowers pH in

the muscle, which can interfere with muscle
metabolism, reduce force production, and
potentially impact central nervous system
function.

5. 5. What role does the central nervous system

play in muscle fatigue?

 Answer: The central nervous system can

contribute to fatigue by reducing the neural drive
to muscles, potentially as a protective mechanism.

6. 6. Can muscle fatigue be overcome?

 Answer: Yes, muscle fatigue can be overcome

through rest, adequate nutrition, and potentially
strategies to manage metabolic byproducts.

7. 7. How can exercise training impact muscle

fatigue?

 Answer: Exercise training can improve the body's

ability to buffer lactic acid, increase glycogen
stores, and enhance the central nervous system's
drive to muscles, all of which can reduce fatigue.