LSM3212_Lecture 13 Summary

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



The Respiratory System



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



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



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



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



Exercise Metabolism

PCr - ATPAnaerobic Alactate

Stored ATP

(3oz)

CO2

Mitochondria

Pyruvate

Acetyl

GlycolysisAnaerobic Lactate

Citric AcidCycle

H+

O2+

H2O

H+

Pyruvate

Lactic Acid



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





Respiratory System in Indirect Calorimetry



Indirect CalorimetryDetermining VO2 measurement by respiratory

equation:

=

Inspired O2 content

(20.93% at sea level)

InspiredVolume

(Measured)

Expired O2

(Measured)

Expired

air volume(Measured)



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



VO2 max: Maximum volume of oxygen consumption

METABOLIC MEASUREMENT

VO2

Intensity

VO2max




VO2peak: Highest volume of oxygen consumption


VO2

Intensity

VO2max

VO2peak



VO2: Volume of oxygen consumption


VO2peak: Highest volume of oxygen consumption


VO2

Intensity

VO2max

VO2peak

VO2



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.



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.





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



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



Exercise Metabolism

PCr - ATPAnaerobic Alactate

Stored ATP

(3oz)

CO2

Mitochondria

Pyruvate

Acetyl

GlycolysisAnaerobic Lactate Citric Acid

Cycle

H+

O2+

H2O

H+

Pyruvate

Lactic Acid



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



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



High Intensity Exercise

High CO2 production

from Kreb cycleL. Production > L. Clearance

Lactate Threshold Estimate

Sodium Bicarbonate Buffering

Lactate accumulation

CO2Carbonic Acid

Increased VE



Early Studies

AV Hill, Lancet, 481 – 286, Sept 5, 1925



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



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



Altitude Training



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





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



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.



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



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



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



Hemoglobin Concentrations and Altitude



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





• 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.





• 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.

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LSM3212_Lecture 13 Summary