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8/3/2019 LSM3212_Lecture 13 Summary
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Human Physiology: LSM 3212Summary Lecture:
The application of Human Physiology in exerciseand sports performance
A/Prof Lim Chin Leong
BSc, MSc, MBA, PhDProgramme Director, Combat Protection and PerformanceHead, Military Physiology Lab
DMERI@DSO
Dept of Physiology,NUS NCAPSSC
Sport Med Trg ProgCOFMNUS
AUT,S’pore Sports School
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The Respiratory System
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Pulmonary Gas Exchange
Inhalation ofatmospheric
air
Trachea
. 0 3 %
C O 2 , 7
9 . 0 4 %
N 3
s E x c h a n g
e
d C O 2
g r a d
i e n t
e d b l o o d
h e m o g l o b i n
Left heart Heart pumps
oxygenated
blood to organs
Oxygenated blood
Exhalation
16% O2
4% CO2
O2
Bronchus
Bronchiole
s
Alveolar
A
t m o s p h e r i c a
i r 2 0 . 9 3 %
O 2 ,
P u l m o n a r y G
D r i v e n b y O 2 a
n
O x y g e n a
t r a n s p o r t e d
i
s ex rac e y e
organs
Deoxygenatedblood returns to
the lungsCO2
Right heart
Pulmonary System Pulmonary Capillary Cardiovascular system
80% N3
CO2
O2
O2
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Pressure Gradient in O2 – CO2 Exchange
Alveolus
PO2
100 mmHg
Trachea
PO2 149 mmHg
PCO2 0.3 mmHg
Inspired air
PO2 = 159 mmHg
PCO2 = 0.3 mmHg
PO2 = 40 mmHg
PO = 100 mmH
PCO2
40 mmHg
PCO2 = 46 mmHg
Venous Blood
PCO2 = 40 mmHg
Arterial Blood
Pulmonary capillary
PO2 = 100 mmHg
PCO2
= 40 mmHg
PO2 = 40 mmHg
PCO2
= 46 mmHg
O2 extraction
CO2 production
by tissue
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The Respiratory System and Sports Performance
Key Consideration
• Thickness of thealveolus wall
• Minute ventilation (>120L/min at maxexercise)
Application in Sports
•Exercise testing
•Lactate buffering
•
• Oxygen carryingcapacity in the blood
• CO2 removal rate
• Acid-Base balance
•EPO doping
•Blood doping
•Sodium biarbonatedoping
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VE of Subject 17 (Synbiotic Study)
100
120
140
160
180
t i o n ( L / m i n
)
Maximum
exercise
intensity
Maximum
exercise
intensity159.5 L/min
165.1 L/min
0
20
40
60
80
0:00:00 0:02:53 0:05:46 0:08:38 0:11:31 0:14:24 0:17:17 0:20:10 0:23:02 0:25:55 0:28:48
Time (min:sec)
M i n u t e V e n t
i l
Recovery
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Exercise Metabolism
PCr - ATPAnaerobic Alactate
Stored ATP
(3oz)
CO2
Mitochondria
Pyruvate
Acetyl
GlycolysisAnaerobic Lactate
Citric AcidCycle
H+
O2+
H2O
H+
Pyruvate
Lactic Acid
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Indirect CalorimetryDetermining VO2 measurement by the Fick equation:
VO2 = Cardiac Output x A-VO2 Difference
Stroke Volume x Heart Rate Peri heral O ExtractionX
• End diastolic volume• End systolic volume
• Ventricular compliance
• Contractility
• Ventricular volume
• Blood pressure
• Vascularization• Mitochondria volume
• Citric acid cycle enzymes
• Muscle type
• Pre-ETC events.
Delivery Extraction and utilisation
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Respiratory System in Indirect Calorimetry
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Indirect CalorimetryDetermining VO2 measurement by respiratory
equation:
=
Inspired O2 content
(20.93% at sea level)
InspiredVolume
(Measured)
Expired O2
(Measured)
Expired
air volume(Measured)
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Physiological Basis For Respiration
and Indirect Calorimetry
Inspiration O2 Delivery O2 Consumption
Ambient
Air
Respiratory
system
Cardiovascular
systemMuscle and metabolism
en a on rcu a onMetabolism
CO2 Production
Lactate Production
CO2 Delivery
Lactate Buffering
CO2 + Carbonic acid
Expiration
Expired
Air
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VO2 max: Maximum volume of oxygen consumption
METABOLIC MEASUREMENT
VO2
Intensity
VO2max
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VO2 max: Maximum volume of oxygen consumption
VO2peak: Highest volume of oxygen consumption
METABOLIC MEASUREMENT
VO2
Intensity
VO2max
VO2peak
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VO2: Volume of oxygen consumption
VO2 max: Maximum volume of oxygen consumption
VO2peak: Highest volume of oxygen consumption
METABOLIC MEASUREMENT
VO2
Intensity
VO2max
VO2peak
VO2
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RANGE OF VO2MAX VALUES
Data from Hermansen, L. & Anderson, K.L. (1965). Aerobic workcapacity in young Norwegian men and women,” Journal of Applied
Physiology 20: 425-431.
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ELITE vs UNTRAINED VO2MAX
Comparison of
elite distancerunners withaverage values
Data from Robinson, S. (1938). “Experimental studies of physicalfitness in relation to age,”
Arbeitsphysiologie 10: 251-323., andothers …….
women andmen.
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VO2max and Endurance Race Performance
60
65
70
75
i n / k g )
3:12:00
3:26:24
3:40:48
3:55:12
T r i a t h l on t
VO2max Race timing
R = 0.63
R2
= 0.4
35
40
45
50
55
0 5 10 15 20 25 30
Subjects
V O 2 m a x ( m
l /
2:00:00
2:14:24
2:28:48
2:43:12
2:57:36
i m
i n g ( h : mm: s s )
Lim et al, 2009
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Individual Differences in
Training Response
Variations in improvement inVO2 max following 20 weeks of
endurance training by family.
Average was 18% but therange was 0–53%.
The range was influenced bygenetics but was influencedvery little by age, sex and race.
Adapted from C. Bouchard et al., 1999, “Familiar aggregation of VO2 maxresponse to exercise training. Resultsfrom HERITAGE Family Study,” Journalof Applied Physiology 87: 1003–1008.
“ From a genetics point of view, the chance of having one individual in theworld endowed with the perfect genetic make-up for superior enduranceperformance is only 0.0005%, that is, provided he / she likes to run”
Lim CL The two-hour marathon debate, J Appl Physiol In print, Jan 2011
Williams et al, J Physiol 586.1: 113 – 121, 2008
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Exercise Metabolism
PCr - ATPAnaerobic Alactate
Stored ATP
(3oz)
CO2
Mitochondria
Pyruvate
Acetyl
GlycolysisAnaerobic Lactate Citric Acid
Cycle
H+
O2+
H2O
H+
Pyruvate
Lactic Acid
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Lactic Acid
• Buffers the accumulation ofpyruvate in cell duringexercise
• Prolonged intense exerciseperformance
• Alternative substrate for
Buffering of Blood Lactic Acid
• Neutralization by sodium
bicarbonate – Carbonic acid + CO2
– Increases PCO2
– Sharp increase in VE
major organs duringexercise (heart and kidney)
• Prevents competition forglycogen between musclesand major organs duringintense exercise
• Conservation of glycogen
• Utilized by heart and kidney asenergy fuel during exercise
• Returns to liver and stored asglycogen
• Returns to muscle to beconverted to pyruvate toparticipate in aerobicmetabolism
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Anaerobic Threshold
Inflection Point
s
Lactate clearance < Lactate production
L a c t i c A c i d
c o n c e n t r a t i o
Time / Intensity
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High Intensity Exercise
High CO2 production
from Kreb cycleL. Production > L. Clearance
Lactate Threshold Estimate
Sodium Bicarbonate Buffering
Lactate accumulation
CO2Carbonic Acid
Increased VE
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Early Studies
AV Hill, Lancet, 481 – 286, Sept 5, 1925
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Current Model of Endurance Performance
Performance Velocity or Power
Performance VO2Performance O2
deficit (> LT)
GrossMechanical
Efficiency
+ X
LT VO2 Total Buffering
VO2max
Musclecapillarydensity
Strokevolume
MHR HboConc
Aerobicenzymeactivity
Distributionof poweroutput
% STfibers
Anthropometryand elasticity
Joyner and Coyle J Physiol 586.1, 35 – 44, 2008
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Test of the classical model for predicting ERPMclaughlin JE et al, Med Sci Sports Exerc, 42: 991 – 997, 2010
Joyner model R2 = 0.954Noakes model R2 = 0.796Joyner + Noakes R2 = 0.978VO2max R2 = 0.902
VO2max + RE R2 = 0.973
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Altitude Training
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Exercise at Altitude
• Barometric pressure (Pb) is the sum of pressure exerted by all thegases comprising the atmosphere.
• Pb is 760 mmHg at sea level (normobaric), increases below sea
level (hyperbaric) and decreases above sea level (hypobaric)
• The composition of air is 20.93% O2, 0.03% CO2 and 79.4%nitrogen. Does not change even when Pb is decreased.
• Partial pressure of O2 (PO2) is the proportion of Pb exerted by O2
molecules in the air; 159 mmHg at sea level
• PO2 (mmHg) = 0.2093 X Pb i.e. decreases with increased altitude.
• It is the decrease in PO2 and not the O2 content in the air that affectsour physiology at altitude
– Decreased O2 delivery to the tissue
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CONDITIONS AT ALTITUDE*
• *At least 1,500 m (4,921 ft) above sea level
• Reduced barometric pressure (hypobaric)
• Reduced partial pressure of oxygen (PO2)
• Reduced air temperature (1 oC/150 m)
• Low humidity: Cold air holds little water.
• Consequences of exposure to altitude:
– Hypothermia
– Acute mountain sickness – High altitude pulmonary edema (HAPE)
– High altitude cerebral edema (HACE)
RESPIRATORY RESPONSES TO ALTITUDE
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RESPIRATORY RESPONSES TO ALTITUDE
• Pulmonary ventilation increases at rest and submaximal
exercise (immediate). – Driven by chemotactic, carotid and aortic PO2 receptors – Increased tidal volume. – Respiratory alkalosis – Ventilation at maximal exercise remains the same.
• Pulmonary diffusion between alveoli and arterial blood doesnot change.
• Oxygen transport is slightly impaired. – SaO2 of 97% at sea level PO2 104 mmHg – SaO2 of 80% at 4300 m PO2 46 mmHg
• Oxygen uptake is impaired due to decrease in PO2 gradientbetween arterial and body tissue – Sea level arterial PO2 is 100 mmHg, and tissue PO2 is 40 mmHg – At 4300 m, arterial PO2 is 47 mmHg and tissue PO2 is 27 mmHg
• Decreased VO2max.
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CHANGES IN VO2MAX WITH ALTITUDE
Due to:
• Decreased O2 delivery
• O2 uptake
• > m
• 8% - 11% / 1000 m
• Due to decreased arterial
PO2 up to about 5000 m
• Due to decreased Qmax at> 5000 m
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CARDIOVASCULAR RESPONSES TO ALTITUDE
• Decreased PV due to respiratorywater loss and increased urinevolume (up to 25%).
• Increased hemo-concentrationdue to the decrease in PV.
• Increased hemotocrit
• Increase in HR, SV, and Q duringsubmaximal exercise..
• Decrease in HR, SV, and Qmaxduring maximal exercise
• Increased erythropoietin fromkidneys leading to increased RBC
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ACCLIMATIZATION TO ALTITUDE
• Increased release of EPO (3 h)
• Increase in number of red blood cells
• Decrease in plasma volume
• Increase in hematocrit
• ecrease n musc e er areas an o a musc e area; may e ue
to under performance.
• Increase in capillary density – decreased diffusion distance.
• Increase in pulmonary ventilation (40 to 50% > sea level)
• Decrease in VO2max with initial exposure does not improve much
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Hemoglobin Concentrations and Altitude
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Sea-Level Performance Following Adaptation to Hypoxia
A Meta AnalysisBonetti DL and Hopkins WG; Sports Med 39: 107-127, 2009
• Types of AT – Live-high-train-high
(LHTH) – Live-high-train-low (LHTL)
– Artificial LHTL (8-18h/dcontinuous
– Artificial LHTL (1.5-5h/dcontinuous)
– Brief intermittent LHTL (<1.5h/d)
– Artificial Live-low-train-
high (LLTH)
• Reviewed 51 studies
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Sea-Level Performance Following Adaptation to Hypoxia
A Meta AnalysisBonetti DL and Hopkins WG; Sports Med 39: 107-127, 2009
• Aerobic Power: VO2max, sustainable VO2, performance economy
• Substantial improvement in maximal endurance power output insub-elite athletes
– Very likely in artificial intermittent LHTL (~2.6%)
– Likely with LHTL (~4.2%)
– Possible with artificial continuous LHTL (~1.4%)
– Unclear with LHTH (~0.9%)
– Unclear with artificial brief continuous LHTL (~0.7%)
– Unclear with LLTH (~0.9%)
• Substantial improvement in maximal endurance power output inelite athletes
– Possible with natural LHTL (~4%)
– Unclear with other altitude training protocols.
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Sea-Level Performance Following Adaptation to Hypoxia
A Meta AnalysisBonetti DL and Hopkins WG; Sports Med 39: 107-127, 2009
• Substantial improvement in VO2max in sub-elite
athletes – Possible with LHTH (4.3%)
– Unclear with other protocols
• Substantial improvement in VO2max in elite athletes
– Possible reduction with LHTH (-1.5%)
– Unclear with other protocols.