3.0 and 3.1 Physiology of Exercise

Pulmonary gas exchange

Movement of gases in the blood between lungs and cells

Systemic gas exchange

Movement of gases from the blood into body tissues and cells

Alveoli

Final branching of respiratory tree with very thin walls, large surface area, and shared membranes with capillaries for gas diffusion

Pulmonary ventilation

Exchange of air from environment with air from lungs

Ve (Minute ventilation)

Volume of air breathed each minute

Fick’s Law of Diffusion

Movement of molecules from high to low concentration or high to low pressure

Breathing mechanics

Air movement due to pressure differences and accessory muscle use since lungs have no muscles

Diaphragm

Dome-shaped muscle under rib cage controlling thoracic cavity size

Inspiration

Diaphragm contracts, flattens, thoracic cavity increases, alveolar pressure lower than atmospheric

Expiration

Diaphragm relaxes, domes upward, thoracic cavity decreases, alveolar pressure higher than atmospheric

Breathing during exercise

Intercostals and scalene muscles assist to create larger pressure changes for more airflow

Bronchodilation

Bronchi get bigger to increase airflow during exercise

Pulmonary vasoconstriction

Slows blood flow in pulmonary circulation during exercise

Increase in Ve

During exercise ventilation rate rises to meet oxygen demands

Oxyhemoglobin

O2 bound to hemoglobin

Deoxyhemoglobin

O2 not bound to hemoglobin

Blood pH change during heavy exercise

pH decreases due to increased H+, weakening oxygen-hemoglobin bond

Tidal Volume (TV / VT)

Amount of air moved in and out of lungs during resting breath

Inspiratory Reserve Volume (IRV)

Amount of air that can be inhaled with maximum effort

Expiratory Reserve Volume (ERV)

Amount of air that can be exhaled with maximum effort

Residual Volume (RV)

Air remaining in lungs after complete exhalation

Vital Capacity (VC)

Max volume of air expired after a maximum inspiration (VC = IRV + TV + ERV)

FEV1

Volume of air exhaled in 1 second with maximal effort after a maximal inspiration

Inspiratory Capacity (IC)

Max volume that can be inspired after a normal inspiration (IC = IRV + TV)

Functional Residual Capacity (FRC)

Volume of air in lungs at end of normal expiration (FRC = RV + ERV)

Total Lung Capacity (TLC)

Max amount of air lungs can accommodate (TLC = VC + RV)

Heart rate

Number of heart beats per minute

Stroke volume (SV)

Amount of blood pumped by the heart per beat

Cardiac Output (Q)

Amount of blood pumped per minute (Q = HR x SV)

Resting cardiac output

~5 L/min

Systole

Heart contraction

Diastole

Heart relaxation

Venous return

Blood coming back to heart

Skeletal muscle pump

Helps venous return by muscle contractions squeezing veins

Respiratory pump

Pressure changes during breathing move blood toward heart

End Diastolic Volume (EDV)

Blood in ventricles at end of diastole (preload)

Frank-Starling Law

Increased EDV stretches myocardial fibers → stronger contraction → increased SV → higher Q

Normal resting heart rate

60–100 bpm

Bradycardia

Heart rate less than 60 bpm

Tachycardia

Heart rate greater than 100 bpm

Blood pressure

Pressure of blood on arterial walls measured in mmHg

Systolic BP

Pressure during ventricular contraction

Diastolic BP

Pressure between contractions

Mean Arterial Pressure (MAP)

MAP = Q x TPR OR DBP + 1/3(SBP − DBP)

Total Peripheral Resistance (TPR)

Resistance to blood flow in vessels

Vasoconstriction

Blood vessels get smaller, increasing TPR, decreasing blood flow

Vasodilation

Blood vessels widen, decreasing TPR, increasing blood flow

Korotkoff sounds

Sounds heard while measuring blood pressure

Central Command Theory

Cardiovascular activation begins in the brain

Parasympathetic nervous system

Active at rest, lowers HR

Sympathetic nervous system

Activated during exercise, increases HR, SV, Q, breathing rate, sweating, and blood flow to muscles

Fick Equation

VO2 = Q x a-vO2 diff

a-vO2 difference

Oxygen unloaded from arteries to tissues

VO2 max

Maximum oxygen consumption during exercise

Endurance training effects

Increases SV and a-vO2 diff; HRmax does not change

Increasing SV during training

Increased blood volume, increased filling time, increased EDV

Increasing a-vO2 diff

More capillary density and mitochondria

Autorythmic fibers

Cardiac fibers that generate their own action potentials

SA Node

Heart’s pacemaker, spontaneously depolarizes

AV Node

Receives signal from SA node and delays 0.1 sec before ventricles contract

Bundle of His

Conducts AP into ventricles

Right and left bundle branches

Pathways down ventricles

Purkinje fibers

Spread AP across ventricular walls for contraction

Electrocardiogram (EKG)

Records electrical signals of the heart

Depolarization

Contraction

Repolarization

Relaxation

P Wave

Atrial depolarization (atrial systole)

QRS Complex

Ventricular depolarization (ventricular systole), also hides atrial repolarization

T Wave

Ventricular repolarization (ventricular diastole)

P-Q Interval

Time for AP to travel from atria to ventricles

S-T Segment

Ventricles contracting and pumping

Q-T Interval

Beginning of ventricular depolarization → end of ventricular repolarization