Lecture 3 (WEEK 4):

(Chapter 10)

Respiration
During Exercise
EXERCISE PHYSIOLOGY
Theory and Application to Fitness and Performance, 5th edition
Scott K. Powers & Edward T. Howley

Presentation revised and updated by

MOHD SANI MADON
ALI MD NADZALAN
UPSI 2015 (c) 2004 The McGraw-Hill Companies, Inc. All rights reserved.
O2 Transport in the Blood
Approximately 99% of O2 is
transported in the blood bound to
hemoglobin (Hb) (protein contained in RBC)
Oxyhemoglobin: O2 bound to Hb
Deoxyhemoglobin: O2 not bound to Hb
Each molecule of hemoglobin can
transport 4 O2 molecules

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O2 Transport in Blood
Amount of O2 that can be transported per unit
volume of blood is dependent on the
concentration of hemoglobin
Normal hemoglobin concentration:
healthy male: 150g per liter of blood
Healthy female: 130g per liter of blood
When completely saturated with O2, each gram
of hemoglobin can transport 1.34ml of O2.
Thus, if hemoglobin is 100% saturated with 02,
healthy male can transport ~200 ml (male) &
~174 (female) per liter of blood at sea level.

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Oxyhemoglobin
Dissociation Curve
Combination of O2 with hemoglobin in
the lung (alveolar capillaries) is
sometimes referred to as loading, &
release of O2 from hemoglobin at the
tissue is called unloading.
Loading & unloading is thus a
reversible action

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Oxyhemoglobin
Dissociation Curve

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Partial Pressure and
Gas Exchange

Fig 10.10
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Oxyhemoglobin
Dissociation Curve

Fig 10.14

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 O2-Hb Dissociation Curve:
Effect of pH
Blood pH declines
during heavy exercise
Decreased pH cause
decrease Hb-O2 affinity
Results in a rightward
shift of the curve
Bohr effect
Favors offloading
of O2 to the tissues

Fig 10.15
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Bohr Effect
The Bohr effect is a physiological
phenomenon first described in 1904
by the Danish physiologist Christian
Bohr, stating that hemoglobin's
oxygen binding affinity (see Oxygen
haemoglobin dissociation curve) is
inversely related both to acidity and
to the concentration of carbon
dioxide.

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O2-Hb Dissociation Curve:
Effect of Temperature
Increased blood
temperature
results in a
weaker Hb-O2
bond
Rightward shift of
curve
Easier
offloading of
O2 at tissues

Fig 10.16
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O2-Hb Dissociation Curve:
2-3 DPG
RBC must rely on anaerobic glycolysis to meet
the cells energy demands
A by-product is 2-3 DPG, which can combine
with hemoglobin and reduce hemoglobins
affinity of O2
2-3 DPG increase during exposure to altitude
At sea level, right shift of curve not to changes
in 2-3 DPG, but to degree of acidosis and
blood tempurature

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O2 Transport in Muscle
Myoglobin: O2 binding protein found in
skeletal muscle fibers & cardiac muscle

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O2 Transport in Muscle
Myoglobin: large quantity in
ST>FT I>FT II
Myoglobin has similar structure with
hemoglobin, but is about the
weight.

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Dissociation Curves for
Myoglobin and Hemoglobin

Fig 10.17
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 CO2 Transport in Blood
Dissolved in plasma (10%)
Bound to Hb (carbaminohemoglobin) (20%)
Bicarbonate (HCO3) (70%)
CO2 + H2O H2CO3 H+ + HCO3-

A high PCO2 causes CO2 to combine with water to

form carbonic acid. This reaction is catalyzed by
enzyme carbonic anhydrase, which is found in
RBC. After formation, carbonic acid dissociates
into a hydrogen & bicarbonate ion.

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CO2 Transport in Blood
At the tissue:
H+ binds to Hb
HCO3 diffuses out of RBC into plasma
Removal of ve charged ion cause
electrochemical imbalance in cell
membrane
Cl diffuses into RBC (chloride shift)
At the lung:
O2 binds to Hb (drives off H+)
Reaction reverses to release CO2
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CO2 Transport in Blood

Fig 10.18
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Release of CO2 From Blood

Fig 10.19
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Ventilation and Acid-Base
Balance

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 Rest-to-Work Transitions

Initially,
ventilation
increases
rapidly
Then, a
slower rise
toward
steady-state
PO2 and PCO2
are maintained
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 Exercise in a Hot Environment
During prolonged
submaximal exercise:
Ventilation tends to
drift upward
(Increased blood
temperature affects
respiratory control
center)
Little change in
PCO2 (Higher
ventilation not due
to increased PCO2)

Fig 10.21
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Incremental Exercise

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Ventilatory
Reponse to
Exercise:
Trained vs.
Untrained

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 Exercise-Induced Hypoxemia
1980s: 40-50% of elite male endurance
athletes were capable of developing
1990s: 25-51% of elite female endurance
athletes were also capable of developing
Causes:
Ventilation-perfusion mismatch
Diffusion limitations due to reduce time of
RBC in pulmonary capillaries due to high
cardiac outputs
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 Control of Ventilation
Precise regulation of pulmonary gas
exchange during rest & exercise is important
in maintaining homeostasis by providing
normal arterial O2 content & maintenance of
the acid base balance within the body

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 Respiratory Control Center
The initial drive to inspire or expire comes from
neurons located in the medulla oblongata.
Discharges from some of these neurons
produce inspiration, while discharges from other
neurons produce expiration.
At rest, the cycle of inspiration & a passive
expiration is built in the neural activity of the
medulla.
However the neural activity in the medulla can
be modified by neurons located outside the
respiratory rhythmicity center.
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 Respiratory Control Center
The caudal pons (apneustic area) directly communicates
with inspiratory neurons located in the rhythmicity area
to stop inspiratory neuronal activity.
Thus, it is believed that apneustic area functions as an
inspiratory cutoff switch that terminates inspiration.
Another group of respiratory neurons, the pneumotaxic
area fine-tunes the activity of the apneustic area.
The practical functions of the apneustic/pneumotaxic
areas is that they work in concert to regulate the depth of
breathing.

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 Peripheral Chemoreceptors

Peripheral chemoreceptors respond to

increases in arterial H+ concentration & PCO2.
Additionally, the carotid bodies are sensitive to
increases in blood potassium levels &
decreases in arterial PO2.
When comparing these 2 sets of peripheral
chemoreceptors, it appears that the carotid
bodies are more important.

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 Effects of Blood PCO2, PO2 &
Potassium on Ventilation
VE increase linearly to increase in arterial PCO2
Changes in PO2 have little effect on VE,
however, exposure to environment with lower
barometric pressure will increase VE.
Increase in blood potassium increase VE.

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Effect of Arterial PCO2
on Ventilation

Fig 10.24
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Effect of Arterial PO2
on Ventilation

Fig 10.25
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Neural input to the Respiratory
Control Center
Neural input from motor cortex & skeletal muscle
mechanoreceptors
Neural impulses originating in the motor cortex may
pass through the medulla & spill over, causing an
increase in VE that reflects the number of muscle motor
units being recruited
Afferent input during exercise may come from muscle
spindles, GTO or joint receptors
Additionally, it is possible that special chemoreceptors
located in muscle may respond to changes in potassium
& H+ concentrations & send afferent information to the
respiratory control center
Right ventricle of the heart contain mechanoreceptors
that sent afferent information back to respiratory control
center relative to increase in cardiac output.
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Ventilatory Control
During Exercise
Submaximal exercise
Linear increase due to:
Central command
Humoral chemoreceptors
Neural feedback
Heavy exercise
Exponential rise above Tvent
Increasing blood H+

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Ventilatory Control During
Submaximal Exercise

Fig 10.26
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Effect of Training on Ventilation
Ventilation is lower at same work rate
following training
May be due to lower blood lactic acid
levels
Results in less feedback to stimulate
breathing

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Effects of Endurance Training
on Ventilation During Exercise

Fig 10.27
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Do the Lungs Limit Exercise
Performance?

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