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Respiratory Regulation in Exercise

4 Separate Processes
1. Pulmonary Ventilation (VE)

2. Pulmonary Diffusion

3. O2 and CO2 Transport

4. Gas exchange at the tissues

1. Pulmonary Ventilation (VE)
Structure and Function
Nasal Cavity- warms, filters, humidifies air
Alveolus (alveoli)
Anatomical Dead Space

Lung Volumes
Inspiration (muscular) & Expiration (passive)
External respiration vs. internal respiration
Cellular Respiration ?
Average lung volume = 4-6 Liters
Dynamic lung volumeability to move air quickly
VE minute ventilation= tidal volume x breathing frequency
Alveolar ventilation=VE - Dead space
Lung Volumes (cony)
Tidal Volume TV
Inspiratory Reserve Volume IRV
Expiratory Reserve Volume ERV
Residual Volume RV
Total Lung Capacity TLC
2. Pulmonary Diffusion
Alveolar Gas Exchangeacross the respiratory membrane, the
aveolar-capillary membrane

Pressure drives gases across the respiratory membrane

Partial Pressure of Gas in Air

Partial Pressure Gradient (differences in PP)
Respiratory Membrane Solubility (gas dissolves in liquids in
proportion to their partial pressure)
Partial Pressures of Gas in Air
Atmospheric Pressure (sea level) = 760 mm Hg

Partial Pressure of Gas:

O2 = 159 mm Hg 21% of Total

CO2 = .2 mm Hg .03%
N = 600 mm Hg 79%

O2 Diffusion
CO2 Diffusionpartial pressure gradient is much smaller (.03
%), but membrane solubility is greater
PP changes with inspiration and gas delivery
Alveolar air: PO2 = 100 mmHg
PCO2 = 40 mmHg
Arterial blood: PO2 = 100 mmHg
PCO2 = 40 mmHg
Tissue Capillary: PO2 = 40 mmHg
PCO2 = 46 mmHg
Venous blood: PO2 = 40 mmHg
PCO2 = 46 mmHg
O2 and CO2 Transport and Exchange
O2 Transport
1. Attached to Hemoglobin: 98.5%
2. Dissolved in plasma: 1.5%
O2 and hemoglobin saturation: affected by PO2, temperature, and pH
Oxy-hemoglobin dissociation curve
Bohr Effect

O2 Transport and Hemoglobin (Hb)

Hb saturation of O2 = usually 98% saturated
Female: 12-16 gm Hb/100 ml blood
Male: 14-18 gm Hb/100 ml blood
Oxy-Hemoglobin Dissociation Curve
Partial Pressure changes of PO2 and PCO2
BOHR Effect effect of pH & temperature
Shifts curve down and to the right
1 gm of Hb can hold 1.34 ml O2
1.34 ml O2 x 15 gm= 20 ml O2/100 ml blood
Anemia means?
CO2 Transport
1. Dissolved in plasma: 7-10%
2. Bound to Hb: 20-30%
3. Bicarbonate ion: 60-70%
CO2 + H2OH2CO3 H+ HCO3
Carbonic Acid Bicarbonate
*Reverses in lungs CO2 + H2O
CO2 is Blown Off in the lungs
Cellular Gas Exchange
(at tissue & muscle)
Internal Respiration dependent upon partial pressure gradients
a-v O2 difference: arterial venous O2 content
Recall: arterial blood contains 20ml O2 / 100 ml blood
Rest a-v O2 diff = 5 ml O2 venous blood O2 content?
Exercise a-v O2 diff > 6-17 ml O2

Factors Influencing O2 Delivery and Use

1. O2 content of blood (Hb saturation)
2. Amount of blood flow (capillary density & dormancy)
3. Local changes ^ temperature
^ acidity (pH)
Differences in PP of O2 and CO2
^ CO2
Regulation of Ventilation
Regulation of VE respiratory center in medulla oblongata
CO2 and H+ levels= ^ rate and depth of breathing
PCO2 is the strongest stimulus (NOT absence of O 2)

Ventilation during exercise

VE= TV (tidal volume) x f (frequency)
TV= quiet breathing f= breaths per minute
BOTH ^ during exercise

Ventilatory Breakpoint
^ VE disproportionate to ^ VO2 (attempt to clear CO2)
Reflects respiratory response to ^ CO2 in the plasma
SOB (shortness of breath)
Decrease in ventilatory drive secondary to ^ CO2 unloading
Hyperventilation does NOT ^ O2 stores Why?
Valsalva Maneuver
VE and VO2 (reflects energy transfer)
Ventilatory breakpoint or Breakaway Breathing
Anaerobic Threshold ~ Lactate Threshold
AT represents ^ CO2 which reflects anaerobic metabolism
VE usually NOT the limiting factor for performance
(maybe in elite distance runners)

Respiratory Regulation of Acid/Base Balance

Plays crucial role in rapid adjustment of acid-base status during
and immediately following exercise
Lungs blow off H+ and CO2 from anaerobic energy transfer
^ H+ (means ^ acidity) = v ATP = v in Muscle contractility
Sprinters fast breathing post race? Blowing off excess H+ and
During recovery: ^ blood lactate removal facilitated by active


Physiology of Deep-Sea Diving
When human beings descend beneath the sea, the
pressure around them increases tremendously. To
keep the lungs from collapsing, air must be supplied
at very high pressure to keep them inflated. This
exposes the blood in the lungs also to extremely
high alveolar gas pressure, a condition called hyperbarism.
Beyond certain limits, these high pressures
can cause tremendous alterations in body physiology
and can be lethal.
Relationship of Pressure to Sea Depth.
A column of seawater 33 feet deep exerts the same pressure at
its bottom as the pressure of the atmosphere above the sea.
Therefore, a person 33 feet beneath the ocean surface is
exposed to 2 atmospheres pressure, 1 atmosphere of pressure
caused by the weight of the air abovethe water and the second
atmosphere by the weight of the water itself.
At 66 feet the pressure is 3 atmospheres, and so forth, in
accord with the table In table.

Being underwater means being under pressure, and that

pressure increases rapidly as you dive deeper. That means that the
various gas laws come into play, and those laws can impact the
"function of living organisms and their parts," i.e. YOU. So let's
quickly revisit those laws: Boyle's law says that as gas pressure
increases, gas volume decreases. Charles' law says that with
constant pressure, gas volume increases and decreases with its
temperature. Dalton adds that in a mix of gasses, the total gas
pressure is equal to the sum of their individual pressures. And Henry,
finally, figured that the amount of gas that will dissolve in a liquid is a
function of its partial pressure and how easily the liquid absorbs gas

The most important issue here is that, in accordance with

Henry's law, the increasing pressure correlates to increased
absorption of nitrogen. Once the pressure decreases as you ascend,
it takes that nitrogen time to get safely released from the body. If we
ascend too quickly, the nitrogen bubbles can get too large to safely
be eliminated through breathing, and that can have dire
Unfortunately, there's more. Other indirect effects of
underwater pressure include shallow water blackout,
oxygen toxicity, carbon monoxide toxicity, nitrogen
narcosis, and full blown decompressions sickness.
Shallow Water Blackout
This is an odd but dangerous syndrome based on the little-known fact that it is not the
lack of oxygen that creates in us the urge to breathe, but the build-up of carbon dioxide. Normally,
as the oxygen level in the blood falls, the carbon dioxide level rises and we feel a need to
breathe. When diving, things can be a different. For example, a breath-hold diver may rapidly
take a number of deep breaths before diving. That hyperventilation removes carbon dioxide and
thus increases the period of time before s/he'll be overcome with the urge to breathe again. Once
underwater, the diver may use up oxygen without feeling a need to breathe, and eventually s/he
may black out from insufficient oxygen in the blood, a state called hypoxia. A similar thing may
happen when a breathe-hold diver goes deeper. Upon ascent, the oxygen pressure drops below
the level to sustain consciousness. This is called deep water blackout.

Oxygen Toxicity
Oxygen toxicity means having too much oxygen in one's body. Too much?
Aren't we able to breathe even 100% oxygen? Yes, but only under certain
conditions. When diving, the rising water pressure increases, according to
Dalton's Law, the partial pressure of oxygen. Oxygen represents about 20% of air
at sea level. However, while that percentage stays the same at depth, we inhale
many more oxygen molecules. At the 130 feet dive limit for recreational divers,
the number of oxygen molecules we inhale would represent 100% oxygen at the
surface! Under pressure, oxygen atoms don't always combine with something
else, and roam as free radicals.

Symptoms of central nervous systems (CNS) oxygen toxicity, the kind

most often experienced by divers and also called the "Paul Bert" effect, include
tremors and seizures, ringing ears, nausea, tunnel vision and a dry cough.
This can lead to drowning or decompression damage when a diver ascends too
quickly in response to those symptoms. Beginning and recreational divers don't
generally have to worry about CNS as it is not much of an issue unless you go
below 200 feet. Another type, pulmonary, or whole-body, oxygen toxicity, also
called the Lorraine Smith effect, can cause irreversible lung damage, but
generally only occurs from very long exposure, much longer than what we
endure during recreational dives.

Oxygen toxicity may occur at much shallower depths if a diver uses Nitrox, a breathing
gas that contains a larger percentage of oxygen and a lower percentage of nitrogen than air.
Nitrox is increasingly popular as it decreases the risk of nitrogen narcosis and excessive nitrogen
absorption, thus reducing the risk of decompression sickness and allowing a diver to stay down
longer. Proponents of Nitrox report less fatigue after diving and a greater degree of
"clearheadeness" while diving with Nitrox in addition to its other benefits. Nitrox is available with
various levels of oxygen, and Nitrox air tanks usually have a bright green and yellow band. Nitrox
1 consists of 32% oxygen, Nitrox 2 36% oxygen, and some advanced divers go as high as 40%.
Hey, the motto of our very own Carol Cotton Walker is, "Air sucks, Nitrox rocks!"

Carbon Monoxide Toxicity

Carbon monoxide is an odorless, tasteless gas coming from the
combustion of organic matter. It combines with blood, hemoglobin
really, much more easily than oxygen, some 200 times more readily
in fact. It also won't easily let go of the hemoglobin and that means
the blood can carry less oxygen. Carbon monoxide poisoning can
happen if a faulty or poorly maintained air compressor adds carbon
monoxide into the tank or if it sucks in already contaminated air.

At depth, while the partial pressure of carbon monoxide remains the same,
the diver inhales many more carbon monoxide molecules, enough for poisoning
symptons such as headaches, confusion, tunnel vision and worse. Divers may
pass out because there is no longer enough oxygen. Signs of carbon monoxide
poisoning are flushed lips and cheeks. First aid treatment is pure oxygen and
fresh air. In serious cases recompression in a chamber with 100% oxygen may
bee necessary to reduce, or eliminate, longterm damage.
Smokers already inhale carbon monoxide and are therefore at greater risk
for hypoxicity (being low on oxygen).
Decompression Sickness (DCS)
It is vitally important to understand Decompression Sickness and what
causes it. We again have Henry's and Dalton's laws at work: More gas will
dissolve in body tissues under pressure (Henry), and there will be more of each
gas under pressure, though the percentages stay the same (Dalton). So as we
descend, nitrogen gets absorbed into our body tissues. Those tissues high in fat
absorb a lot, other tissues less. And tissues that have a large blood flow will
absorb and release gas more quickly than tissues with less blood flow, such as
tendons, cartilage, or fat.

So what happens is that we absorb a bunch of nitrogen that will then have
to be released again as we come back up. If the pressure is released slowly, the
nitrogen "out-gasses" slowly and will safely travel to the lungs where we breathe
it out. However, if the pressure drops too quickly, nitrogen bubbles form in the
blood and that can be very bad. While tiny little bubbles, generated by slow,
controlled acent, are harmless, large bubbles can get stuck and create
blockages. They may block circulation, and compress nerves because those are
surrounded by fatty tissue that absorbs a lot of nitrogen, or create dangerous
chemical reactions.

You will hear divers talk about the "bends" or having

been "bent." That's because nitrogen bubbles blocking
circulation in the small veins of joints (elbows, knees,
shoulders) cause pain that a diver may seek to relieve by
bending those joints. Even very experienced divers can get
bent, so do take this very, very seriously.

There is Type I DCS and Type II DCS. Type I - the non-neuralgic type - is
less severe and may manifest itself as rashes on the skin or joint pain, plus
sometimes fatigue and vertigo. The more serious Type II neuralgic DCS, caused
by larger bubbles that block blood flow can result in weakness, paralysis,
nausea, vomiting, tingling sensations, personality change and worse. First aid in
mild cases is 100% oxygen, drinking lots of fluid, aspirin as a blood thinner, and
plenty of rest. Type II DCS requires recompression in a hyperbaric chamber, and
the faster the better. That way, the bubbles dissolve again and are properly and
slowly eliminated through slow recompression