Exercise Physiology Notes PDF

**Lecture 1:** Cardiovascular system - Blood - Heart - Blood vessels Blood properties - Approx 8% of body weight - Sodium concentration 140mM (135-145 mM) - pH range 7.35-7.45 Blood functions - Transport of O2, CO2, nutrients, waste, enzymes, heat energy - Regulation of PH...

**Lecture 1:** Cardiovascular system - Blood - Heart - Blood vessels Blood properties - Approx 8% of body weight - Sodium concentration 140mM (135-145 mM) - pH range 7.35-7.45 Blood functions - Transport of O2, CO2, nutrients, waste, enzymes, heat energy - Regulation of PH and water content of cells - Protection against fluid loss via clotting and toxins and foreign microbes - Transport, regulation and protection Physical characteristics of blood - Made up of plasma and blood cells - Haematocrit % of blood that is composed of cells - Males 42%, females: 38% Plasma - 55% of blood volume - 91% water - 9% plasma proteins: serum albumin 60%, serum globulin 36%, fibrinogen 4% - Minerals, ions, hormones Blood cells - 45% of blood volume - Formed elements - Red blood cells: erythrocytes - White blood cells: leucocytes - Platelets: thrombocytes Red blood cells - 99% of blood cells are RBC - Contains haemoglobin which is an important buffer and contains carbonic anhydrase - Carry O2 from the lungs to tissues - Biconcave discs - Pliable and can change shape to squeeze through capillaries Haemoglobin - A protein centre, globin, four iron containing groups called heme to which oxygen bind - Carbon dioxide is carried by globin - Males: 16g/dL - Female: 14/dL - At birth: 17/dL - 1 Hb combines with 1.34mL of O2 Erythropoiesis - Production of red blood cells - 0-5 years all bones but especially long bones - 5-20 years long bones - Marrow becomes less productive as age increases - Stress can stimulate marrow to produce large quantities of red blood cells if required 102 DELIVERY TO KIDNEYS t ERYTHROPOIETIN SECRETION t PLASMA ERYTHROPOIETIN Bone marrow t PRODUCTION OF ERYTHROCYTES t BLOOD Hb CONCENTRATION t BLOOD 02 CARRYING CAPACITY RESTORATION OF 02 DELIVERY  Regulation of Red blood cells production - Tissue hypoxia results due to high altitude, cardiac failure, haemorrhage, anaemia - Increases in response to decrease in O2 tension and quantity of O2 transported to tissues Polycythaemia - An increase in proportion of red blood cells - Absolute or relative - Secondary: due to hypoxic conditions - Physiologic: altitude - Vera: due to tumour Hct can rise to 60-70% Layers of the Pericardium and of the Heart Wall Pulmonary trunk Pericardium Myocardium Fibrous pericardium (dense CT) Parietal layer of pericardium Pericardial cavity (Tilled w/ serws nud) Epicardium (Visceral layer) Heart wall Myocardium Endocardium Heart chamber Myocardium - The heart muscle - Responsible for contraction - Receives its blood supple via the right and left coronary arteries that branch off the aorta - Similar to slow twitch muscle fibres - Highly aerobic - Extensive capillary network - Striated like skeletal muscle Control of heart rate - 3 ways: neural, hormonal and intrinsic - Neural control: most dominant control mechanism, CV regulatory centre in the medulla, signals delivered via autonomic nervous system - SNS and PNS - Central command: signals pass through medulla Electrical conductivity - Sympathetic nervous system: cardiac accelerator nerves secrete norepinephrine and some epinephrine to increase HR - Parasympathetic nervous system: vagus nerve endings secrete acetylcholine to slow the heart, most increase in HR during exercise Central command- voluntary movement - Motor cortex -\> impulse to cardiac regulatory centre in medulla - Vagus nerve inhibited PNS - Cardiac accelerator nerve is excited SNS - HR increases - Feedback to medulla is regulated by higher brain centres and receptors  Voluntary movement - Motor Cortex of the brain is activated, impulses sent to muscles and cardiac regulatory centre of the medulla - Cardiac accelerator nerve is excited and vagus inhibited thus ↑HR - Medullary activity continually modulated by the brains somatomotor central command centre - Neural coordination between the centres allows for rapid adjustment of heart and blood vessels to optimise tissue perfusion and maintain blood pressure. - This neural control operates both in the pre-exercise anticipatory period as well as during exercise. - Motor cortex stimulation of the medulla increases with the size of the muscle mass activated in exercise. Cardiac accelerator erves (sympathetic) Cardiovascular (CV) center O John Wiley & Sons. Ire. INPUT TO CARDIOVASCULAR CENTER (nerve impulses) From higher brain centers: cerebral cortex, limbic system, and hypothalamus From sensory receptors: Proprioceptors---monitor movements Chemoreceptors---monitor blood chemistry Baroreceptors---monitor blood pressure OUTPUT TO HEART (increased frequency of nerve impulses) Increased rate of spontaneous depolarization in SA node (and AV node) increases heart rate Increased contractility of atria and ventricles increases stroke volume Decreased rate of spontaneous depolar- ization in SA node (and AV node) decreases heart rate Pre exercise anticipatory rise in HR - Thought be caused by an emotional stimulation of the cardiac accelerator centre and increase in circulating catecholamines  Intrinsic regulation - Regulated by 2 nodes named according to their location - Sinoatrial: Pacemaker of the heart - Atrioventricular: l - Specialised myocardial cells capable of initiating electrical activity Electrical conduction - SA node initiated contraction - Impulse then spreads out the atria causing contraction O SINOATRIAL (SA) NODE O ATRIOVENTRICULAR (AV) NODE Right atrium Right ventricle Arch Of aorta Left atrium O ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) O RIGHT AND LEFT BUNDLE BRANCHES Left ventricle CONDUCTION MYOFIBERS (PURKINJE FIBERS) Electrical conduction - Depolarisation spreads to the AV node which then continues to propagate the signal through a series of highly conductive fibres - Depolarisation then spreads down the AV bundle (Bundle of His) to the left and right BB towards the apex of the heart - Continues to spread through the Purkinje fibres and up and around the ventricles causing contraction - Contraction begins at the apex and flows upwards forcing blood out of the ventricles from the apex to the top - SA node tends to increase rate d/t (due to) being stretched as more blood returns to the heart during rhythmic exercise Cardiac cycle - Systole: ejection of blood, contraction phase of the cardiac cycle - Diastole: filing of blood, relaxation phase of the cardiac cycle - At rest diastole longer than systole, during exercise both systole and diastole are shorter Pressure changes during the cardiac cycle - Diastole: pressure in ventricles is low, filling with blood from atria - Systole: pressure in ventricles rises, blood ejected in pulmonary and systemic circulation - Heart sounds: first- closing of AV valves, second- closing of aortic and pulmonary valves  Arterial blood pressure - Expressed as systolic/diastolic 120/80 mmHg - Systolic pressure: pressure generated during ventricular contraction - Diastolic pressure: pressure in the arteries during cardiac relaxation - Pulse pressure: difference between systolic and diastolic - Mean arterial pressure: average pressure in the arteries throughout the cardiac cycle Arteries maintain pressure - The LV ejects blood into the aorta the artery distends acting as a pressure reservoir - After systole, the pressure within the aorta begins to drop, allowing the arterial walls to reassume their normal state - This reversal squeezes blood through the systemic circulation acting like a secondary pump. No sound is heard because there is no blood flow when the cuff pressure is high enough to keep the brachial artery closed. 2. Systolic pressure is the pressure at which a Korotkoff sound is first heard. When cuff pressure decreases and is no longer able to keep the brachial artery closed during systole, blood is pushed through the partially opened brachial artery to produce turbulent blood flow and a sound. The brachial artery remains closed during diastole. 3. As cuff pressure continues to decrease, the brachial artery opens even more during systole. At first, the artery is closed during diastole, but, as cuff pressure continues to decrease, the brachial artery partially opens during diastole. Turbulent blood flow during systole produces Korotkoff sounds, although the pitch of the sounds changes as the artery becomes more open. 4. Diastolic pressure is the pressure at which the sound disappears. Eventually, cuff pressure decreases below the pressure in the brachial artery and it remains open during systole and diastole. Nonturbulent flow is reestablished and no sounds are heard. 300 250 Starting with a high pressure 200 No sound Sound 150 Degree to which brachial artery is open during: Systole Diastole o Systolic pressure (120 mm Hg) Diastolic pressure (80 mm Hg) Arm Pressure cuff 100 Elbow 50 first heard Korotkoff sounds Sound disappears No sound O O Blocked Blocked or partially open Open In summary The purposes of the cardiovascular system are: - the transport of O~2~ to tissues and removal of wastes, - the transport of nutrients to tissues, and - the regulation of body temperature. - Protection - The heart is two pumps in one. The right side of the heart pumps blood through the pulmonary circulation, while the left side of the heart delivers blood to the systemic circulation. - The contraction phase of the cardiac cycle is called *systole* and the relaxation period is called *diastole*. - The pacemaker of the heart is the SA node. - The average blood pressure during a cardiac cycle is called *mean arterial pressure*. **Lecture 2:** Humoral control of HR - Relating to body fluids - Circulating hormones in the blood can influence HR - Epinephrine and norepinephrine increases HR - Thyroid hormone increases HR - Increase body temp also causes the SA node to discharge more quickly increasing HR Peripheral input - Modification of HR as a result of input received from - Muscle chemoreceptors - Arterial chemoreceptors - Specific mechanoreceptors - Provide feedback to the CNS to regulate blood flow and pressure Heart rate - Is high at birth 140 bmp - Is lower at adolescence 70-80 bpm - Resting HR rises again as you get older - Maximal HR decreases with age Stroke volume - Volume ejected per beat - Cardiac output Q= HR X SV -  Fick equation - VO2 = Q(a-vO2) - VO2 = HR x SV (a-vO2) - The VO2 (volume of oxygen consumed by the cells) is equal to the cardiac output multiplied by the amount of oxygen extracted from the blood VO2 - The volume of oxygen consumed by the cells - Consumed or used but not inhaled - Units are usually in L/min or ml/kg/min - RestingVO2 is 1 met = 3.5 ml/kg/min Nomenclature is important Dot indicates that it is a rate i.e. /min = Q(a-v02 Subscript 2 Uppercase V for volume. Lowercase v for venous.  Cardiac output and exercise - Muscles and organ require increase blood flow for increases O2 delivery - Increased BF result from redistribution from non working muscles and organs and or increase cardiac output - SV= EDV - ESV - -EDV= end diastolic volume - -ESV= end systolic volume - Increase in diastolic volume increases stroke volume= starlings law Starlings law of the heart - Intrinsic control of SV mechanism - The SV increases in response to an increase in EDV- the volume of blood prior to contraction - Cardiac muscle increases its strength when stretched - Cardiac muscle is similar to skeletal muscles in that in its resting state its length is less than that which yields maximal tension Stretch tension relationship Sarcomeres excessively stretched 170% o 100 o 50 Sarcomeres greatly shortened 75% 60 Sarcomeres at resting length Optimal sarcomere operating length of resting length) 80 100 120 140 160 180 Percent of resting sarcomere length Factors that increase EDV - Any factor that increases venous return or slows HR - Produce greater ventricular filling - Increase in EDV = greater stretch = greater force of contraction = increase SV - Note effect of decrease HR with training Regulation of cardiac output  Extrinsic control of SV - Increase in SNS activity and norepinephrine release increases HR and increases contractibility - Increased contractibility is important because diastolic filling time is significantly reduced at very high rates - Changes in the Cardiac cycle during exercise Systole 0.3 second Systole Diastole Rest Heart rate = 75 beats/min 0.5 second Diastole 0.2 second 0.13 second % Time spent in Diastole At rest 0.5/0.8 = 62.5% During Exercise 0.13/0.33 - Heavy exercise Heart rate = 180 beats/min Why is this relevant? - 39% Think Exercise & filling time Factors assisting the rate of venous return 3 principles mechanisms - venoconstriction - Muscle pump - Respiratory pump Venoconstriction - Increases venous return by reducing the volume capacity of veins to store blood - Occurs via a reflex sympathetic constriction of smooth muscle in veins draining muscle  Muscle pump - The result of the mechanical action of rhythmic skeletal muscle contractions. As muscles contract they compress veins and push blood back towards the heart to heart blood squeezed forward to heart open relaxed skeletal muscle contracted Skeletal musCle 6 valve closed Respiratory pump - The rhythmic pattern of breathing also provides a mechanical pump by which venous return is promoted -  Extrinsic control of SV - Varies with body position - Due to pressure gradient, the largest SV when body is in horizontal position - In untrained individuals stroke volume is max at 40-60% VO2 max Major factors determining cardiac output Begin t END-DIASTOLIC VENTRICULAR VOLUME t ACTIVITY OF SYMPATHETIC t PLASMA EPINEPHRINE Cardiac muscle STROKE VOLUME NERVES TO HEART ACTIVITY OF PARASYMPATHETIC NERVES TO HEART SA node 5 CARDIAC OUTPUT t CARDIAC OUTPUT STROKEVOLUME x HEART RATE Defining aerobic exercise intensity - VO2 max = maximal amount of O2 that the body can utilise - Gold standard for aerobics CV changes with incremental exercise - HR and Q increases in direct proportion to VO2 - Blood flow to working muscles increases as a function of V)2 requirements Circulatory adjustments to exercise - Blood flow, working muscles may use 10-20x more O2 than at rest - Therefore Q and BF to the muscles must increase - Increase BF due to increase in Q and redirection of BF - Dilation of BV in the working muscles - Constriction of vessels in non working muscles and organs Circulatory adjustments to exercise - Exercise in a hot humid climate at same relative VO2 results in higher HR due to - Loss to plasma volume from sweating and redistribution of blood to skin for cooling -  Prolonged steady state exercise - Steady state = stable/unchanged VO2 Remember i/02 (ml.min-l) a-v02 (ml.dL-1) Q is maintained SV decreases Therefore, HR increases to maintain Q Skin blood flow - The hypothalamus is stimulated by increase of temperature of the blood and skin and control skin bf - At the start of exercise: there is a small decline in BF - During prolonged submaximal exercise: skin blood flow may increase 4-7 times that of resting levels to facilitate cooling - Short term maximal work: vessels are constricted to reduced skin BF and to make more blood available to working muscles. After cessation of maximal short term work skin blood flow increases during recovery to facilitate heat loss -  - FIGURE 14-68 Surnmary Of cardiovascular changes during mild exercise. Skeletal muscle blood flow Mean arterial pressure Systolic arterial pressure Diastolic arterial pressure Total peripheral resistance Cardiac output Heart rate Stroke volume End-diastolic ventricular volume EXERCISE t 175% 50% 50% t 100% t 20% Time Maximal aerobic exercise - Q and HR plateau at VO2max although HR can often continue to rise marginally above HR at VO2 max - This point represents the maximal ceiling for O2 transport Blood pressure response to exercise - Blood pressure during changes due to increase in Q, blood viscosity - Geometry of the vessel: the length and radius of a vessel affects its resistance, resistance to flow increases markedly as the radius decreases  Influences of metabolites - The metabolites generally thought responsible in promoting and maintaining vasodilation are: - --- 02 (V tension in muscle) --- Adenosine (\'TN) - c02 (t) ---pH (V) --- Phosphate (\'TN) All increase with muscle activity -  In summary - Q = HR x SV - The pacemaker of the heart is the SA node. - PNS activity slow the HR, SNS speeds it up Heart rate increases at the beginning of exercise due to a withdrawal of parasympathetic tone. At higher work rates, the increase in heart rate is achieved via an increased sympathetic outflow to the SA node - Stroke volume is regulated by: - EDV, - aortic blood pressure, and - the strength of ventricular contraction - Venous return increases during exercise due to: - Venoconstriction, - Muscle pump, and - Respiratory pump. - Heart - Adjustments to HR at commencement of exercise are immediate - Anticipatory rise in HR - Response to exercise 1. Increased neural activity 2. Muscle and joint mechanoreceptor reflexes 3. Muscle chemoreceptor reflexes 4. Circulating Hormones 1. Ep and Norep 5. Intrinsic Factors 1. Frank Starling Law - Factors affecting EDV\... - Increased temp during exercise - Blood is composed of two principle components, plasma and cells. - Blood flow through the vascular system is directly proportional to the pressure at the two ends of the system, and inversely proportional to resistance. - The most important factor determining resistance to blood flow is the radius of the blood vessel. - The greatest vascular resistance to blood flow is offered in the arterioles. - The changes in heart rate and blood pressure that occur during exercise are a function of the duration, type and intensity of exercise performed, and the environmental conditions. - At the same level of oxygen consumption, heart rate and blood pressure are greater during arm exercise than during leg exercise. - Cardiovascular drift is the increase in heart rate that occurs during prolonged exercise - The central command theory of cardiovascular control during exercise proposes that the initial signal to "drive" the cardiovascular system at the beginning of exercise comes from high brain centers. - Once initiated the cardiovascular response to exercise is fine-tuned by feedback from muscle chemoreceptors, muscle mechanoreceptors, and arterial baroreceptors to the cardiovascular control center. **Lecture 3:** Structure of the respiratory system - Includes the nose, nasal cavity, pharynx, larynx, trachea, bronchial tree and lungs - 2 main zones - Conducting zone - Respiratory zone     O Name Of branches Trachea Bronchi Bronchioles Terminal bronchioles Respiratory bronchioles Alveolar ducts Alveolar sacs Number Of tubes in branch 2 4 8 16 32 6x104 5x105 8x106    Conducting zone - Consists of everything from the trachea to the terminal bronchioles - To transfer air from the outside environment to the alveoli for gas exchange - Warms and humidifies air - Filters air: mucus, cilia and macrophages in alveoli   Respiratory zone - Major function is Gas exchange - Occurs in the alveoli - 300 million alveoli - Provides a large SA for diffusion total area 60-80 m2 - Very thin allowing for rapid diffusion - Secrete surfactant to prevent collapsing   The lungs and respiration - Pulmonary respiration: refers to ventilation and exchange of gases in the lungs- external respiration - Cellular respiration: relates to O2 utilisation and CO2 production by the cellular tissues- internal respiration     Pulmonary ventilation - Occurs by a process known as bulk flow - Movement of molecules along a passage way due to pressure differences between the two ends of the passageway At Rest Inspiration Thorax is expanded from inspiration. Expiration Ribs and sternum return downward, diaphragm relaxes and is pushed upward, and lung tissue recoils. Stemum Ribs Diaphragm Pressure at rest: Lung pressure = atmospheric pressure. Muscles contract, lungs expand: Lung pressure \< atmospheric pressure. Inspiration: Air rushes into lungs to balance pressure. After inspiration, thorax is expanded. Lung pressure = atmospheric pressure Thorax returns to resting dimensions: Lung pressure \> atmospheric pressure. Expiration: Air rushes out Of lungs to balance pressure.     The respiratory cycle - Inspiration: occurs due to the pressure in the lungs being reduce below atmospheric pressure, boyles law - At rest the diaphragm performs most of the work 75% for inspiration - External intercostals elevate the ribs during inhalation 25% of air movement at rest   The respiratory cycle- inspiration - During exercise accessory muscles aid with breathing, pec minor, scalene, sternomastoid     The respiratory cycle- expiration - Boyles law - During rest or normal quiet breathing, elastic properties of the lungs and chest wall return the lungs to an equilibrium position without necessity for the diaphragm to receive stimulus for relaxation   Factors affecting pulmonary ventilation - Compliance of the lungs: how much effort is required to stretch the lungs and chest wall, high compliance= easy, due to elastic fibres in lung tissue and surfactant - Airway resistance: diameter of the airway, smooth muscle regulates airway diameter, walls of bronchioles expand and contract like the lungs - Surface tension of alveolar fluid: surface tension must be overcome to expand the lungs during inhalation, surfactant reduces the surface tension so the lungs don't stick together at the end of exhalation   Measures of pulmonary ventilation - V = volume - V (with the dot) = volume per unit time (one minute) -  Adding subscripts to V, ~T~ (tidal), ~D~ (dead space), ~A~ (alveolar), ~I~ (inspired), ~E~ (expired) - e.g. V~I~ - Defn = Movement of gas into and out of the lungs - V = V~T~ x f       Anatomical dead space - Space occupied by the volume of air not participating in gaseous exchange - Dead space = Vd   Alveolar ventilation - Air that reaches the respiratory zone - Va - Va= Vi-Vd     Vt= Va=Vd      Breathing patterns and Va TABLE 15-5 Subject c EFFECT OF BREATHING PATTERNS ON ALVEOLAR VENTILATION Tidal volume, ml/breath 150 500 1000 x Frequency, breaths/min 40 12 6 Minute ventilation, ml/min 6000 6000 6000 Anatomic dead-space ventilation, ml/min 150 6000 150 x 12 1800 150 x 6 900 Alveolar ventilation, ml/min 4200 5100       Breathing patterns and Vi        Tension/partial pressure and diffusion - Tension= partial pressure ( the pressure of a specific gas in mixture of gasses) - pO2 in the lung is greater than the blood so O2 moves from the lungs into the blood - PCO2 in the blood is greater that pCO2 in the lungs so CO2 moves from blood to the lungs for exhalation     Diffusion - Random movement of molecules from a low to high area of concentration - The diffusion of gases is dependant upon: - The partial pressure gradient - Inversely proportional to the membrane thickness - The solubility of gases - Occurs rapidly in the lungs due to: - Large surface area - Short diffusion distance - O2 and CO2 tensions in blood leaving the lungs is almost in complete equilibrium with O2 and CO2 tension in the lung     Partial pressure of gases - Important in the understanding of diffusion capacity - The partial pressure of each gas in a mixture is called the partial pressure of the gas - Daltons law: the total pressure of a gas mixture is equal to the sum of the partial pressures Ptotal = P1+P2+P3+ - The pressure that each gas exterts can be calculated by multiplying the percentage by the absolute pressure     P total = 2.4 atm He = 6.0 atm 1.25 mol He 0.50 mol H 2 (a) 5.0 L at 20 oc 2.4 atm (b) 5.0 L at 20 oc PHe= 6.0 atm total p = 8.4 atm 1.25 mol He 0.50 mol H2 I.75 mol gas (c) 5.0Lat200C = 2.4 + 6.0 8.4 atm        Gas Oxygen Nitrogen Percentage 20.93 79.04 Carbon Dioxide 0.03 Fraction 0.2093 0.7904 0.0003 Barometric pressure at sea level is 760 mmHg Partial pressure of Oxygen (p02) at sea level PO? = 760 x 0.2093 po = 159 mmHg Partial Pressure of Nitrogen (pN2) at sea level 760 x 0.7904 pN2 = 600.7 mmHg     Fick\'s law of diffusion - The rate of gas transfer is proportional to the tissue area, the diffusion coefficient of the gas and the difference in the partial pressure of the gas on the two sides of the tissue and inversely proportional to the thickness     Henry\'s law - The quantity of a gas that will dissolve in a liquid is proportional to the partial pressure of the gas when temperature remains constant   Gas laws - Blood temperature and solubility of the gas remains fairly constant so the major factors that determines the amount of dissolved gas is partial pressure -      Atmospheric air PO \_ 159 po = 05 co = 40 To lungs To right heart 40 p = 0.3 p EXTERNAL RESPIRATION (a) INTERNAL RESPIRATION (b) Interstitial fluid Alveoli Pulmonary capillary To left heart To tissue cells Systemic capillary Gas Concentrations Blood entering the lung: --- pC02 N46 mmHg. --- p02 N40 mmHg Alveolar gas is: --- pC02 N40 mmHg --- p02 N 105 mmHg Blood leaving the lung is: --- p02 N 100 mmHg --- pC02 N40mmHg.---a-v02 diff? coz Systemic tissue cells     Internal respiration - Exchange of gases between the bloodstream and tissues - Involves aerobic and anaerobic metabolism and the provision of O2 for energy production in the muscle cell and the removal of CO2, hydrogen and water   Gas transport        Gas transport Hb - Oxyhemoglobin= oxygen bound to haemoglobin - Deoxyhemoglobin= haemoglobin not bound to O2   Blood O2 capacity 02 carrying capacity of blood = \[Hb (g/\ H2CO Muscle Lung + HC03-   Blood buffering - The H+ ion formed when H2CO3 dissociated will increase the acidity of venous blood - The free H+ ions are buffered by Hb -  - As O2 is released from Hb and diffuses into the tissues buffering of H+ ions facilitated - In turn more HCO3- can be formed and more CO2 transported without change in blood acidity     Pulmonary blood flow: ventilation perfusion ratio - Normal gas exchange requires a matching of ventilation to blood flow (perfusion) - An alveolus can be well ventilated but if blood flow to the alveolus does not match ventilation, normal gas exchange does not occur - At rest V/Q= 0.82 - During exercise it may exceed 5   Percent oxyhemoglobin saturation Oxygen content (ml 02/100 ml blood)     Exercise and oxyhemoglobin dissociation curve - Temperature increase and decrease pH result in a downward and rightward shift - The effect of acidity, CO2 and increased temperature on the oxyhemoglobin dissociated curve are referred to as the bohr effect   Oxyhemoglobin dissociation curve - Loading= combination of O2 with Hb - Unloading= release of O2 from Hb - Deoxyhemoglobin + O2 \-\--\> oxyhemoglobin - Factors affecting the direction of this reaction are: - Blood pO2 - Bond strength between Hb and O2 - At the lung: high pO2=formation and oxyhemoglobin - At the tissue: low pO2= release of O2 to tissues= deoxyhemoglobin - Flat portion Provides protection against low atmospheric pO2, a large decrease in pO2 only results in a small desaturation of the Hb - Steep portion Provides protection at tissue level for unloading of O2, small decrease in tissue O2 results in large unloading of O2 from Hb -        Effects of pH on the oxygen haemoglobin dissociation curve o o Percent oxyhemoglobin saturation 0 0 0 0 00 0 O o    Increase of H+ = decrease in pH       Effects of temperature on the oxygen haemoglobin dissociation curve 등 그 100 90 80 70 60 20 0 10 320 20 30 370 40 50 60 P02 (mm Hg) 420 70 80 90 100 O2 affinity to Hb is the same as the predicted by Henry\'s law Same as O2 dissolved in the plasma       Exercise and oxyhemoglobin dissociation curve - 2-3 DPG - Byproduct of RBC metabolism - Results in a rightward shift of the curve - Assists with the unloading of O2 - Not a major cause of rightward shift during exercise     Dissociation curve of myoglobin and haemoglobin  - The higher affinity of myoglobin for O2 compared with haemoglobin assists in the exchange of O2 bound to haemoglobin and transported to muscle tissue     Summary - Most of the O~2~ transported in blood is chemically bonded with hemoglobin. The effect of the partial pressure of O~2~ on the combination of O~2~ with hemoglobin is illustrated by the S-shaped O~2~-hemoglobin dissociation curve. - An increase in body temperature and a reduction in blood pH results in a right shift in the O~2~-hemoglobin dissociation curve and a reduced affinity of hemoglobin for O~2~.     Respiratory centre - Are located in the brain stem - Medulla oblongata and pons - Midbrain Brain stem respiratory pons Pneumotaxic center Caudal pons Retrotrapezoid nucleus PreBötzinger cornplex Wdulla oblongata - Controls rhythm of ventilation - Inspiratory area nerves innervate diaphragm and external intercostals via the phrenic nerves - Impulses last 2 sec=contraction - During exercise- expiratory area becomes active - Active contraction of internal intercostals and abs     Input to the respiratory control centre - Neural input - High brain centres: voluntary regulation of breathing, emotional response via hypothalamus and limbic system - Sensory information: skeletal muscle and right ventricle mechanoreceptors, chemoreceptors in muscle - Humoral input: central chemoreceptors, located in the medulla, respond to the changes in pCO2 and H+     The location of the peripheral chemoreceptors - Aortic and carotid bodies - Respond to increase pCO2, increase in H+, decrease in pO2 and increase in K+ -  - Effect of arterial pCO2 on ventilation - 20 15 10 40 41 42 43 44 45 Arterial PC02 (mm Hg)   Effect of arterial pO2 on ventilation   -    - Sa02 160 140 p 102 120 100 80 Pa02 40 20 760 2000 590 6000 Altitude (m) 306 8000 277 100 70 50 10000 215 Barometric pressure (mm Hg)        Rest to work transitions - At the onset of constant load submaximal exercise - Initially ventilation increase rapidly, then a slower rise towards steady state - pO2 and pCO2 are relatively unchanged, slight decrease on pO2 and increase in pCO2   Transition from rest to exercise 100 р 02 (mm Нд) 90 F\>C02 40 (mm Нд) 39 30 Е 20 (C/min) 10 о Exercise time (min)       Prolonged exercise - Ventilation may drift due to: - increase in body temperture - The effects of fluid loss - Decrease in PV= increase in H+ = chemoreceptors   Incremental exercise in an untrained subject - Ventilation: linear increase up to 50-75% VO2 max - Exponential increase beyond this point - Ventilatory threshold: inflection point where Ve increases exponentially - pO2: maintained within 10-12 mmHg of resting value        Ventilatory thresholds - There\'s actually 2 - Shown here is 62 and 77% VO2 mac - Rises are due to increased arterial pCO2 - 응€8     Incremental exercise in an elite athlete - Ventilation: VT1 occurs at higher % of VO2 max - pO2: decreases of 30-40mmHg at near maximal work, hypoxemia - Due to: ventilation/perfusion mismatch: short RBC transit time in pulmonary capillary due to high cardiac output    \"Untrained Student\" 100 90 80 70 7.4 7.3 7.2 110 90 60 30 25 50 75 100 Work rate (% \\702 max) \"Elite, Trained Runner\" 100 90 80 70 7.4 7.3 7.2 140 110 80 50 25 50 75 100 Work rate (% V02 max)     In summary - At the onset of constant-load submaximal exercise, ventilation increases rapidly, followed by a slower rise toward a steady-state value. Arterial pO~2~ and pCO~2~ are maintained relatively constant during this type of exercise. - During prolonged exercise in a hot/humid environment, ventilation "drifts" upward due to the influence of rising body temperature on the respiratory control centre. - Incremental exercise results in a linear increase in V~E~ up to approximately 50% to 70% of O~2~ max; at higher work rates, ventilation begins to rise exponentially. This ventilatory inflection point has been called the *ventilatory threshold*.     Ventilatory control during exercise - Submaximal exercise: primary drive, higher brain centres, fine tuned by humoral chemoreceptors, neural feedback from muscle - Heavy exercise: a non linear rise in Ve, increasing blood H+ stimulates carotid bodies, also K+, body temp, and blood catecholamines may contribute      **Lecture 5:** Introduction - Metabolism - Sum of all chemical reactions that occur in the body - Anabolic reactions: synthesis of molecules - Catabolic reactions: breakdown of molecules - Bioenergetics: converting foodstuffs (fats, protein, carbohydrates) into energy     Revision of cell structure - Cell membrane- sarcolemma: semipermeable membrane that separates the cell from the extracellular environment - Nucleus: contains genes that regulate protein synthesis - Cytoplasm: fluid portion of cell, contains organelles, mitochondria   Energy to perform work - Energy is stored in chemical bonds within molecules - Energy is released when the bonds are broken   ATP - Adenosine triphosphate - Energy currency of the cell - Energy rich phosphate bonds   Structure of ATP - Adenosine diphosphate (ADP) Inorganic phosphate (Pi) Adenosine triphosphate (ATP) NH2 (1) Adenine CH (3) Three phosphates - ---P---O 2 H OH H (2) Ribose OH     Enzymes - Complex protein structure - Catalysts that regulates the speed of reactions - Lower the energy of activation   Enzymes catalyse reactions      Enzyme action - Substance ENZY\>E Product AB ENZYPE      Enzymes - Substrate react with reactants, to generate a product - The enzyme decrease the amount of energy required to allow the reaction to proceed - Substrate= the starting material, but not an enzyme or coenzyme   Enzyme types - Kinases: add phosphate groups to the substrates- creatine kinase - Dehydrogenases: remove hydrogen from their substrate- lactate dehydrogenase   Factors that alter enzyme activity - temperature - Small rise in body temperature increases enzyme activity - Exercise results in increases body temperature - Large increases in temp can result in decreased activity - pH - Change in pH reduces enzyme activity - Acid produced during exercise   Control of bioenergetics - Rate limiting enzymes - An enzyme that regulates the rate of a metabolic pathway - Sometimes demand is greater that what the body can supply - Increase opportunity for the reaction to progress - Increase the number of enzymes   Rate limiting enzyme Substance 1 Enzyme A (rate-limiting) Substance 2 Enzyme B Substance 3 Enzyme C Substance 4 Enzyme D Product o       Control of bioenergetics - Modulators of rate limiting enzymes - High Levels of ATP inhibit ATP production - Low levels of ATP and high levels of ADP+P stimulate ATP production   The energy systems - All energy systems function to restore ATP or similar high energy phosphate - Energy for muscular contraction can be provides by ATP, Pcr, glycolysis, oxidative phosphorylation, beta oxidation -    The Three Energy Systems ATP-CP system Glycogen to lactate system 50 o Muscle ATP 30 60 90 120 02 system 150 180 Duration (s) Muscle ATP + ATP-CP system Muscle ATP + ATP-CP + Anaerobic glycolysis Muscle ATP + ATP-CP system + Anaerobic glycolysis + Q system Power + Strength Predominantly anaerobic Predominantly aerobic F I G U RE 13.1 Time course of the contribu- tion of the various systems of ATP replenishment during maximal exercise lasting from a few seconds to about 3 minutes. Reprinted, by permission, from C. Bouchard et al., 1989,Testing anaerobic power and capacity. In Physiological testing of the elite athlete, 2nd ed., edited by J.D. MacDougall et al. (Cham- paign, IL Human Kinetics), 1989.   No one energy system provide all of the energy for ATP regeneration, involves varying contribution for each system          ATP Hydrolysis (breakdown) ATP ---.\>ADP + Pi + Free energy for biological work The enzyme ATPase breaks the chemical bond of ATP ATPase ATP ADP + Pi + free energy hergy     ATP - There is enough for 1 sec maximal contraction contained within the cell - Repletion occurs very rapidly via ATP-PC, lactic acid system, aerobic system     Phosphocreatine system - Abbreviated to PCr/PC/CP/CrP - Energy rich phosphate bond - Most readily available fuel source for muscle contraction - Stored within the muscle fibre, 5-10 sec worth -    Phosohocreatine system ATP-PC system --- Immediate source of ATP PC + ADP ATP + C Creatine kinase --- Rapid d/t Short uncomplicated rxn that doesn\'t require 02 Easily accessible Used in throwing, jumping, sprinting, power lifting, events lasting \< IOS And up to \'\"30s   Regulation of creatine phosphate - Creatine Kinase CK - Activated by increase - Inhibited by an increase in ATP - Increase of ADP instantly trigger the breakdown of CP to replenish ATP        Glucose and glycogen - Glycogenesis= formation of glycogen from glucose - Gluconeogenesis= formation of glycogen from substrate other than glucose - Glycogenolysis= breakdown of glycogen: occurs one glucose at a time - 2 possible endpoints: anaerobic pathway (glycolysis), aerobic pathway ( oxidative phosphorylation)   Glycolysis - The breakdown of glucose or glycogen to form pyruvate - Occurs with the sarcoplasm   Phase of glycolysis Glucose Energy investment phase 2 ATP required 2 4 ATP produced Energy generation phase 2 NADH produced 2 pyruvate or 2 lactate et production: Output nput glucose 2 pyruvate or 2 lactate ADP 2 ATP     Interaction between blood glucose and muscle glycogen in glycolysis      Glycolysis: energy investment phase - Glycolysls Steps glucose 1. Phosphorylation 0t glucose by ATP produces an activated molecule. (Ce---P) Energy-investment Steps glucose.6-phosphate tructose-6-pmspt-,ate 2. Rearrangement, tollowed by a second phosphorylation by ATP. gives fructose-I , 6-bisphosphate. fructose-I , 6-bisphosphate 3. The 6-carbon molecule is split into two a-carbon G3P molecules. ADP ADP (P     Glycolysis: energy generation phase        Hydrogen and Electron Carrier Molecules Transport hydrogens and associated electrons -To for ATP generation (aerobic) --- To convert pyruvate to lactate (anaerobic) Nicotinamide adenine dinucleotide (NAD) NAD\* + H NADH Flavin adenine dinucleotide (FAD) FAD + 2H FADH2     NADH is shuttled into mitochondria - NADH produced in glycolysis must be converted back to NAD+ - By converting pyruvate to lactate - By shuttling H+ into the mitochondria - A specific transport system shuttles H+ across the mitochondrial membrane - Located in the mitochondrial membrane     Conversion of pyruvic acid to lactic acid  The addition of two H to pyruvic acid forms NAD and lactic acid       Lactic acid - Lactic acid is not actually formed within the cell, however lactate the salt is - Lactate is produced in quantities equivalent to the amount of H+ so remains a good indirect marker - The pyruvate lactate reaction - Consumes 2 H+ therefore actually increase pH - Converts NADH and NAD+ allowing glycolysis and ATP generation to continue - Lactate is a valuable fuel source     In summary   - The immediate source of energy for muscular contraction is the high-energy phosphate ATP. ATP is degraded via the enzyme ATPase as follows: - ATP ADP + Pi + Energy ATPase - Formation of ATP without the use of O~2~ is termed *anaerobic metabolism*. In contrast, the production of ATP using O~2~ as the final electron acceptor is referred to as *aerobic metabolism*. - Muscle cells can produce ATP by any one or a combination of three metabolic pathways: (1) ATP-PC system, (2) glycolysis, (3) oxidative formation of ATP. - The ATP-PC system and glycolysis are two anaerobic metabolic pathways that are capable of producing ATP without O~2~. **Lecture 6:** Regulation of glycolysis - During sprint activity glycolysis must occur several hundred times faster than at rest - Glycolysis is regulated by: concentration of glycogen phosphorylase, hexokinase, Phosphofructokinase and pyruvate kinase - Levels of fructose 1,6 diphosphate - Levels of O2        Key glycolytic enzymes - Glycogen phosphorylase - Hexokinase - Phosphofructokinase - Pyruvate kinase - Lactate dehydrogenase   Glycogen phosphorylase - Glycogen \--\> glucose -1- phosphate - Activated by increase in ADP, ca2+, epinephrine - Inhibited by an increase in ATP and fatty acids   Hexokinase - Blood glucose \--\> glucose-6-phosphate - Has a high affinity for glucose - Inhibited by its product, glucose-6-phosphate, important because ATP is used in this step, prefer to use glycogen to produce glucose-6-phosphate - Increase in fatty acid   Phosphofructokinase PFK - Fructose-6-phosphate \-\--\> fructose 1,6 bisphosphate - Key rating limiting step - Activated by increase in fructose-6-phosphate, ADP, decrease in CP - Inhibited by: increase in H+, citrate, ATP, fatty acid   Pyruvate kinase - Final glycolytic step - Activated by: increase fructose 1-6 biphosphate - Inhibited by: ATP and alanine   Lactate dehydrogenase LDH - Catalyses the conversion of pyruvate to lactate in both directions - Activated by presence of the substrate - Two different isoforms found in different muscle fibres - Type 1 fibres favours lactate to pyruvate - Type 11 fibres favours pyruvate to lactate   Lactate system and performance - Supplements ATP-PC system when O2 supply rate is inadequate for the energy demand - Primary energy system for max efforts lasting 20-50s - In 50-200m events lactate may rise from 1mmol/kg \>25mmol/kg in muscle   **Gender** **Distance** **Time** **Aerobic** **Anaerobic** ------------ -------------- ---------- ------------- --------------- Male 400m 52s 41% 59%   800m 126s 60% 40% Female 400m 60s 44% 56%   800m 151s 70% 30%     Lactate system and performance   - Phosphofructokinase PFK - Extended reliance on glycolysis for energy production results in fatigue - Anaerobic enzyme concentrations increase with anaerobic training     Removal of lactate and H+ following exercise - Following severe exercise - 70% re-oxidised to pyruvate then enters the krebs cycle - Often occurs in the non working muscles and the heart - 20% gluconeogenesis in the liver - Small amounts lost in sweat, urine - Light to moderate exercise during recovery improves recovery by maintaining high blood flow and oxidative functioning of working musculature - Intense exercise may result in further lactate production     Electron transport chain   First ритр ГЧАOН 0uter mitochondrjal Second NAD+ lnnet mit0ChondriaI membrane hird итр Н2О 2Н+У20а АОР АТР Synthase ДТ р Matrix     Aerobic energy system - Oxidative energy system - Only occurs within the mitochondria - Interaction of 2 separate pathways - Krebs cycle - Electron transport system - Responsible for majority of energy production for bouts lasting 60sec+ - Requires O2   Krebs cycle - Citric acid cycle or tricarboxylic acid cycle TCA - Complete oxidation of CHO, fats and sometimes protein - Uses NAD+ and FAD+ as hydrogen carriers   Regulation of krebs cycle - Key regulatory enzyme - Isocitrate dehydrogenase - Activated by - High ADP - High NADH - Inhibited by: 2-oxoglutarate, high citrate   Oxidation and reduction - Oxidation: the removal of H+ from a compound or the addition of O to it - Reduction: addition of H+ or removal of O - NAD+ and FAD+ are then reduced to NADH and FADH2 while the fuel is oxidised - The H+ are the high energy molecules - H+ is carried by the NADH and FADH2 to the ETC   Pre krebs cycle - Pyruvate broken down to Acetyl CoA - 1x CO2 produced in the process -  Lactate not pyruvate enters the mitochondria.avN HCJVN emuaw au ul aaeds XJemuou\_uołu1 (xeuJE04%) Havw.ovN          For each pyruvate - 1x FADH2 - 3x NADH are produced - 1x ATP   Aerobic ATP production - Electron transport chain - Oxidative phosphorylation occurs in the mitochondria - NADH and FADH releases H+ and electrons to ETC - Electrons passed along a series of carriers cytochromes   The chemiosmotic hypothesis of ATP formation - Electron transport causes cytochromes to pump H+ across inner mitochondrial membrane - Results in H+ gradient across membrane - As H+ transported back across membrane \--\> energy released to form ATP - H+ and electrons are accepted by O2 to form water      Figure 3.14 Simple representation of the formation of ATP at three sites in the electron transport chain. This process is known as oxidative phosphorylation. S NADH NAD C ATP FADH Reduced COQ Oxidized Cytochrome b c ATP ADP + Pi Cytochrome and C Cytochrome ADP + PI Cytochrome a3 1/ H20 02       Glycolysis + aerobic metabolism control      Summary energy production       ATP yield      A diagram of a cycle Description automatically generated     Krebs cycle and ventilation - Metabolic and non metabolic CO2    A chemical formula with arrows Description automatically generated       Fat metabolism - Triglyceride: glycerol + fatty acid FA - Many different FA: different bonding and different length -    -   Fat metabolism - ATP production varies with the length of the fatty acid chain - Steric acid 18 carbon chain= 147 x ATP - Palmitic acid 16 carbon chain= 130 x ATP     Fat metabolism - B- oxidation: broken down to acetyl coA 2 carbons at a time - 1 ATP used - 1 x FADH2 and 1x NADH generated - Then enters into krebs cycle -    Fat metabolism - Fat metabolism less Efficient than glucose - 3.96 L of O2 required per mole of ATP resynthesised from palmitic acid - Therefore 15% more O2 required for FA oxidation   Regulation of ß Oxidation \' FA utilised for energy by muscle come from 1. Triglyceride stored in the muscle 2. Triglyceride stored in the body fat 3. Triglyceride or FA circulating in the blood stream \' Lipases split FA from Glycerol portion of TG --- Activated by hormones \'frEp, NorEp cortisol and Glucagon and insulin --- \'T in SNS activity release of FA and TG stores Insulin conc decreases during prolonged exercise During exercise lasting \>1 hour blood FA conc may increase by x5     In summary - Metabolism is regulated by enzymatic activity. An enzyme that regulates a metabolic pathway is termed the *rate-limiting* enzyme. - The rate-limiting enzyme for glycolysis is phosphofructokinase - In general, cellular levels of ATP and ADP+P~i~ regulate the rate of metabolic pathways involved in the production of ATP. High levels of ATP inhibit further ATP production, while low levels of ATP and high levels of ADP+P~i~ stimulate ATP production. Evidence also exists that calcium may stimulate aerobic energy metabolism. - The rate-limiting enzymes for the Krebs cycle and electron transport chain are isocitrate dehydrogenase and cytochrome oxidase, respectively. - Oxidative phosphorylation or aerobic ATP production occurs in the mitochondria as a result of a complex interaction between the Krebs cycle and the electron transport chain. The primary role of the Krebs cycle is to complete the oxidation of substrates and form NADH and FADH to enter the electron transport chain. The end result of the electron transport chain is the formation of ATP and water. Water is formed by oxygen-accepting electrons; hence, the reason we breathe oxygen is to use it as the final acceptor of electrons in aerobic metabolism   **Lecture 7:** - Most energy supplied via aerobic system - 2/3 from fats - 1/3 from carbohydrates - VO2 = 0.3 L/min - Blood lactate = 1mmol/l - Relative contributions depend on - Intensity of exercise performed - Training state - Diet of the athlete -  - Peak power 6s sprint - Anaerobic capacity 30s wingate - Blood lactate concentration - \% critical power - \%VO2 max - \%HR max - Rating of perceived exertion (RPE) - VO2 max values - Sedentary 2.2 -3.2 L/min for F and M - Trained 3.0 -5.0 L/min for F and M - Endurance 4.0 -6.0 L/min for F and M - Relative values are important for weight bearing activities - Varying definitions - Characterised by a stable VO2 - HR + Ve may drift by will appear stable over consecutive minutes - It takes for O2 consumption to stabilise to new, higher level exercise demands - Lab definition: \ - Performance is limited by oxygen delivery and utilisation - VO2 = SV x HR x a-vO2 - A marathoners blood lactate at the conclusion if the may only be 3-4 mmol/L but they\'re exhausted, due to - Depleted muscle and liver glycogen stores - Muscle fatigue due to trauma - Dehydration and electrolyte loss and increase in body temperature - Marker of glycolytic energy production - Allows glycolysis to continue - - good marker of the internal cell environment - Accumulates due to - Hypoxia - Rapid rate of NADH production - Recruitment of fast twitch muscle fibres - Decreased removal - Maintained at relatively low levels even during intense exercise bout lasting 15 mins - Closely corresponds to the highest metabolic power output for which constant blood lactate, PCr, and VO2 are possible - The CP represents a power output that could theoretically be maintained indefinitely on the basis of principally aerobic metabolism - The CP is unlimited in capacity but limited in rate - It is an important predictor of endurance - Asymptote: the distance between the curve and the asymptote tends to zero as they head to infinity - Cp is the power asymptote - Power that can be maintained indefinitely -  - The W represents a finite work capacity available to the athlete once he or she attempts a power output above CP - The W remains constant regardless of rate of discharge - Acts like the anerobic work capacity - But it changes with oxygen availability - Steady state is unable to be attained - PCr decreases - VO2 increases - Muscle Ph decreases - Increased anerobic contribution to energy production - - - Dependant on intensity - Aerobic systems are used first - If intensity is too high than anaerobic production is increased -  - Source for short duration, incremental or high intensity exercise - Is the major substrate used at the onset of low to moderate intensity exercise - During prolonged work \20 min there is a gradual shift from carbohydrate metabolisms towards an increasing reliance on fat as a fuel substrate - Increased ADP and Pi stimulate glycolysis - Availability of NAD+ - O2 availability - H+ concentration - Epinephrine is released during periods of high stress or heavy exercise, stimulates glycogenolysis and promotes carbohydrate metabolism - Glycogen phosphorylase activated by Ca2+ release and Ep release - - Plasma glycose maintained through four processes - Mobilisation of glucose from liver glycogen - Mobilisation of FFA from adipose tissue, spares blood glucose - Gluconeogenesis from amino acids, lactic acid, and glycerol - Blocking the entry of glucose into cells, forces use of FFA as a fuel - Controlled by hormones, - fast acting, glucagon, epinephrine, norepinephrine, - Slow acting, cortisol, growth hormone - Insulin increases cellular uptake of glucose - Declines during exercise of increasing intensity and duration - Glucagon increased blood glucose - Increased mobilisation of liver glycogen - Increased liver glucose output - Increased sensitivity of the liver to epinephrine - At rest the process is facilitated by insulin - During exercise additional transporters are activated - First fat triglyceride must be broken down via lipase into FFA - Then metabolised via B oxidation into 2 carbon chains and oxidised in the krebs cycle -  - Epinephrine, norepinephrine and glucagon increase lipase activity promoting lipolysis - During prolonged exercise insulin levels decline and epinephrine increases promoting higher levels of fat metabolism - Lipolysis is a slow process, occurs only after several minutes of exercise - Mobilisation of FFA is inhibited by - Insulin: inhibits lipase activity, decline in insulin during longer duration exercise results in increased FFA and glycogen sparing - Lactate: high levels promote recombination of FFA and glycerol to form fats thereby decreasing the available FFA as fuel - FFA mobilisation dependant on hormone sensitive lipase - FFA mobilisations decreases during heavy exercise above critical power - This occurs in spite of persisting hormonal stimulation for FFA mobilisation - May be due to: high levels of lactic acid, elevated inhibits HSL, inadequate blood flow to adipose tissue - Contribution to fuel supply 4-15% depending on duration 2+ hours and diet - Skeletal muscle can directly metabolise some amino acids with the help of protease - Liver can convert alanin into glucose - Protease may become active in prolonged exercise - Plasma glucose is maintained during exercise by increasing liver glycogen mobilisation, using more plasma FFA, increasing gluconeogenesis, and decreasing glucose uptake by tissues. The decrease in plasma insulin and the increase in plasma glucagon, E, NE, GH, and cortisol during exercise control these mechanisms to maintain the glucose concentration. - Energy to perform exercise comes from an interaction of anaerobic and aerobic pathways. - In general, the shorter the activity (high intensity), the greater the contribution of anaerobic energy production. In contrast, long-term activities (low to moderate intensity) utilise ATP produced from aerobic systems. **Lecture 8** Sarcolemma (muscle cell plasma membrane) c. Acetylcholine reticulum (muscle cell endoplasmic reticulum) Axon terminal Synaptic vesicles (9 Acetylcholine receptor Synaptic cleft T tubule (ego 9) Acetylcholine Acetylcholinesterase 1. Acetylcholine released from the axon terminal binds to receptors on the sarcolemma. 2. An action potential is generated and travels down the T tubule. 3. Ca2 is released from the sarcoplasmic reticulum in response to the change in 4. Ca2+ binds troponin; Cross-bridges form between actin and myosin. ADP 5. Acetylcholinesterase removes acetylcholine from the synaptic cleft. 6. Ca2 is transported back into the sarcoplasmic reticulum. 7. Tropomyosin binds active sites on actin causing the cross-bridge to detach. ** ** ** ** **Contractile proteins** - **Myosin: thick filaments with globular heads** - **Actin: thin filaments: actin, tropomyosin, troponin** ** ** **Mechanisms of muscle contraction** - **Myosin head binds to an active site on actin** - **Myosin head moves pulling actin filaments towards the centre of the sarcomere** - **Sarcomere shortens, muscle shortens, force is generated** - **Cross bridges detach** - **Dependant upon sufficient Ca2+ and ATP** ** **  ** ** ** ** **Sliding filament theory** - **Calcium binds to troponin moving the tropomyosin exposing the binding site** - **ATP is hydrolysed on the myosin head** - **Myosin head binds to actin filament forming the cross bridge** - **ADP + Pi released from the myosin head causing it change position** - **Binding of ATP to myosin head it from the active site** ** ** ** ** **The role of Ca2+** - **At rest, myosin and actin are unable to bind due to tropomyosin and troponin** - **Tropomyosin covers the binding site on actin** - **Troponin holds tropomyosin in place** - **Ca2+ binds to troponin \--\> moves tropomyosin away to expose myosin binding site** ** ** **The role of ATP** - **myosin head contains a binding site for ATP** - **ATP \--\> ADP + P = cross bridge + power stroke** - **A new ATP binds to myosin to release it from actin** ** ** **Excitation contraction coupling** - **Sequence of events that begin with a neural impulse and end with contraction** - **Excitation of a motor nerve** - **Propagation of an action potential** - **Events at the neuromuscular junction** - **Calcium release from sarcoplasmic reticulum** - **Sliding filament theory** - **Relaxation (action potential is reversed leading to reversal of step 2-4)** ** ** **Muscle fibre types** - **Type 1 fibres (slow twitch)** - **Type 11 fibres (fast twitch) - type 11a and type 11x** - **Differences in speed of contraction, maximum force production, oxidative capacity, fatigability** - **Power production requirement is the ley determinant of recruitment** ** ** **Type 1 muscle fibres** - **Relatively small in diameter** - **Slow contractile speed** - **Low force production** - **High oxidative capacity** - **Many mitochondria** - **Many capiliaries** - **Lots od myoglobin** - **Great aerobic enzyme activity** - **Highly resistant to fatigue** - **LDH converts lactate to pyruvate** - **Dominant muscle fibre during exercise below CP** ** ** ** ** E 90 80 70 60 50 40 40 20 Athletes Nonathletes 60 80 100 % Slow-Twitch Fibers (ST) Figure 5.17. Relationship between maximal aerobic power (max V02) Of male athletes and male nonathletes and their percentage of distribution Of slow-twitch (ST) muscle fibers. The max V02 is higher with higher percentages of ST fibers in both groups; for a given percentage of ST fibers above 40%, the max V 02 is higher in athletes. (Based on data from Bergh et al.7) ** ** ** ** ** ** **Type 11 muscle fibres** - **Relatively large in diameter** - **Fast contractile speed** - **High force production** - **High glycolytic capacity** - **Lots of glycolytic enzymes** - **Greater glycogen and PCr stores** - **Highly fatigable** - **LDH converts pyruvate to lactate** - **Recruited during high intensity exercise** ** ** ** **  ** ** ** ** ** ** Type Il muscle fibresubtypes Type Largely anaerobic Large fibces High contractile speed, force, power Great glycolytic capacity High concentration of CP Few mitochondria Highly fatigable Recruited during short (\ lack of improvement** -  - **If the stimulus is excessive or overly varied the athlete will be unable to adapt: excessive stimulus \--\> maladaptation \--\> decrease in performance** - 8 Training stimulus.2 Excessive training stimulus s Excessive training stimulus Excessive training stimulus Figure 1.5 Training stimulus and adaptation. (a) Increasing stimulus (load) adaptation performance improvement. (b) Lack Of stimulus plateau = of improvement. (c) Excessive stimulus --- maladaptation decrease in performance. = increased performance = decreased performance. ** ** ** ** **Overload and fatigue** - **A properly designed program will allow for adequate recovery while imposing sufficient stress** - ![Fatigue C\] Workload microcycle Restitution microcycle 1 2 3 4 Microcycle ](media/image131.png) ** ** **Reversibility** - **Training adaptations is not permanent** - **Training adaptations will decay once the stimulus has been removed** - **Detraining** ** ** **Monitoring training loads** - **The FITT principle** - **Training loads can be monitored and modified by assessing:** - **Frequency** - **Intensity** - **Time** - **Type** ** ** **Training intensity** - **Energy expenditure or work per unit time- the effort invested into a training session** - **Often regarded as the most significant component of the training stimulus for applying overload** - **Important to monitor** - 0.6 0.5 0.4 \> 0.3 0.2 1.0 1.2 Women 1.4 1.6 1.8 Men 2.0 Relative Training Intensity 5 days/week O 7 weeks 4 days/week 2 days/week 4 days/week 13 weeks 2 days/week - **More training = better performance** ** ** ** ** **Determining training intensity** - **% if VO2 max** - **% of CP or LT** - **RPE** - **HR** - **Most common and accessible** - **Monitoring HR is an indirect estimate of O2 consumption during exercise** - **Used to indicate the overload placed on the body** - **The maximal HR method** - **Anchor training to a power/pace** - **Critical power** - **Minimum power or pace for intervals** - **Can also used HR to determine intensity** - **Power/ pace at VO2 max** ** ** ** ** ** ** **Summary** ** ** - **Exercise training is guided by the principles of specificity, overload and reversibility** - **The purpose of applying these principles is to promote improvement through adaptation** - **Monitoring training loads (intensity in particular) is important for optimising training benefits and avoiding overtraining** ** ** **Lecture 9:** **Acute response to aerobic exercise** - **Ventilation: increases due to neural input and feedback from central and peripheral receptors** - **Heart rate: increases due to reduced PNS influence and increased sympathetic drive and hormonal effects** - **Stroke volume: increases due to increased SNS drive (increased contractility), increased temperature and increased EDV** - **Blood pressure: SBP increases due to increase in cardiac output, DBP remains unchanged or may increase/ decrease slightly due to vasodilation, redistribution of blood flow** - **Oxygen consumption** -  ** ** ** ** **Oxygen deficit and debt** - **O2 deficit is the difference between the oxygen requirement and the oxygen utilisation at the commencement of exercise** - **EPOC: excess post exercise oxygen consumption- increased oxygen consumption due to increased metabolic demand post exercise** ** ** **Aerobic training** - **Improves the ability to sustain a particular level of physical effort** - **Occurs via improvements in functional capacities related to oxygen transport and utilisation** - **Fick equation: VO2 = Q x a-vO2** - **Central adaptations- increase Q** - **Peripheral adaptations- increase a-vO2 difference** - (ол-е ** ** **Central adaptations** - **How do we increase Q** - **Heart rate** - **Reduced at rest and during** - **Submaximal exercise** - **Training increases vagal tone** - **Lower cardiac O2 cost** - **Permits greater filling time** -  - **Stroke volume: increases with training due to increased left ventricular volume and mass** +-----------------------+-----------------------+-----------------------+ | **Cardiac** | **World Class** | **Controls** | | | | | | **Dimensions** | **Runners** | | +=======================+=======================+=======================+ | **LV volume** | **154 ml** | **101 ml** | +-----------------------+-----------------------+-----------------------+ | **LV wall** | **10.8 mm** | **10.3 mm** | +-----------------------+-----------------------+-----------------------+ | **LV mass** | **283 g** | **211 g** | +-----------------------+-----------------------+-----------------------+ ** ** - 180 160 140 120 100 Athlete Untrained ---o---After Training Oxygen Consu mption (L/min) ** ** **Increase in stroke volume** - **Load placed on the heart during contraction** - **EDV (preloaded)** - **Afterload = pressure in the wall of the left ventricle during ejection** ** ** ** **  ** ** ** ** **Central adaptations** - **Plasma volume** - **Increase of 10-20% following 3-6 aerobic training sessions** - **Increased EDV** - **Increased SV** - **Improved temperature regulation** - **Subsequent increase in Hb** - **Blood flow** - **Distribution of blood flow to more oxidative muscle fibres** - **Reduced splanchnic and renal blood flow** - **Increase in skeletal muscle blood flow** - **Due to increase in cardiac output and increase in cross sectional area of capillaries** ** ** VR Size Contractility o a-v02 HR EDV sv Ejection fraction Increased Mitochondria Enzymes Capillaries ** ** ** ** ** ** **Peripheral adaptations** - **Mitochondria** - **Increase size and number** - **Increased oxidative enzymes in the mitochondria** - **Due to tissue hypoxia** - **Capillaries** - **Increased number of capillaries- dt increased shear stress in capillaries** - **Results in increased O2 delivery** - **Increased transit time** - **Fibre type** - **Type 11x- type 11a- type 11ac** - **Myoglobin** - **Possibly small increase in intramuscular myoglobin content** -  ** ** ** ** **Adaptations to aerobic training** - **Magnitude of response is determined by: genetics, previous training status, training load** ** ** **Aerobic performance** - **Determined by VO2 max, critical power, economy** - **VO2 max is an important determinant** - **The highest rate that oxygen can be taken up and used by the body during exercise** - **A result of both central and peripheral adaptations to training** - **Critical power: power speed/pace/power at critical power is perhaps the most important determinant of endurance performance** - **Closely linked terms- lactate threshold, anerobic threshold, ventilatory threshold, MLSS** ** ** ** ** **Critical power** - **Maximum intensity at which work can be sustained indefinitely** - CRITICAL POWER PROFILE PEAK POWER Anaerobic Work Capacity (W\') e.g. 11.5 Kilojoules o 2 Wattsßg TIME (min) Critical Power max work rate sustainable without drawing on W\' e.g. 270W Predictive of TT 20m in performance ** ** ** ** **Lactate threshold** - **Intensity of exercise where lactate begins to accumulate in the blood** - **Lactate production outstrips utilisation** - **Associated with increase H+ and increase fatigue** -  ** ** **Ventilatory threshold** - **Intensity of exercise where a non linear increase in Ve is observed** - **Increase in CO2 and H+** - The \"Thresholds\" CP, LT, VT MLSS are all slightly different When do they occur? N40-60% VO in untrained individuals 2m ax N 70-75% VO in trained individuals 2m ax Up to 80-90% V02max in elite marathon runners Up to 85-90% V02max in elite distance swimmers V02max in sprint athletes ** ** ** ** **The effects of training** - **Threshold occurs at a higher work rate** -  ** ** ** ** ** ** **Economy** - **Energy cost of movement** - **0.9 kcal to run 1km vs 1.1kcal** - **Determines how efficiently the fuel can be used to perform movement** ** ** ** ** **Implications for performance** - **VO2 is greater importance for shorter events than CP** - **CP very important for events 1-2 hours in duration** - CRITICAL POWER PROFILE Anaerobic Work Capacity (W) e.g. 11.5 Kilojoules o 2 Watts/kg TIME (min) + Critical Power max work rate sustainable without drawing on W\' e.g. 270W Predictive of TT 20min performance ** ** ** ** **Training to improve critical power** - **High volumes principally produced central adaptations** - **Should comprise the majority of training** - **Peripheral adaptations in type 11 fibres** - **Resilience of musculoskeletal structures to training** - **Interval training principally results in peripheral adaptations** - **Increases capillary density** - **Increased mitochondria** - **Changes in LDH and PDH enzymes** - **Increased myoglobin content** - **Increased fat utilisation** - **Increased injury risk** - **High intensity interval training- intervals above CP 90% VO2 max, aim is to accumulate time at or close to VO2 max** ** ** **Threshold training** - **Tempo, sweet spot** - **Be careful with volume** - **Limited research basis** -  ** ** ** ** **Aerobic training alterations to fuel metabolism** - **What is the effect of repetitive prolonged training on fuel metabolism** - \(a) 0 Hormonal responses to graded exercise Epinephrine Norepinephrine Growth hormone Cortisol Glucagon (b) o O Hormonal responses to prolonged exercise Epinephrine Norepinephrine Growth hormone Cortisol Glucagon 0 o Insulin 20 40 60 80 100 o Insulin 10 20 30 40 50 Percent V02 max Time (min) ** ** -  ** ** - 1000 200 30 \...Trained Untrained 120 90 Duration (min) ** ** ** ** **Summary** - **Aerobic training produces central (Q) and peripheral (a-vO~2~ difference) adaptations** - **Central adaptations include:** ** ** - **Reduced HR at rest and during exercise** ** ** - **Increased SV** ** ** - **Increased plasma volume** ** ** - **Increased blood flow to skeletal muscles** - **Peripheral adaptations include:** ** ** - **Increased mitochondria** ** ** - **Increased capillary density** ** ** - **Increased oxidative capacity of muscle fibres** ** ** - **Increased myoglobin content** - **These adaptations improve oxygen transport and utilisation our ability to sustain a given work output over time** - **VO2max, CP and economy are the key determinants of aerobic performance** - **Critical Power (CP) (or LT, VT, etc) is the highest intensity of exercise that can be sustained without accumulating H^+^, CO~2~ and lactate in arterial blood. The LT is an important determinant of endurance performance.** - **Endurance training should be undertaken to improve both oxygen delivery (central changes) and oxygen utilization (peripheral changes).** - **Endurance training may improve the b-oxidation pathway** ** ** **Lecture 10:** **Anaerobic training** - **Improves the ability to perform exercise powerfully** - **adaptations dependant on the primary energy system** - **Glycolytic vs PCr** - **Higher neural component than aerobic training** ** ** **Limitations to anerobic performance** - **Rate of energy production** - **Fuel availability** - **Enzyme activity** - **Muscle buffer capacity** - **Power of movement** - **Function of force and speed** - **CSA** - **Neuromuscular coordination** ** ** **Adaptations to anaerobic training** - **Muscle fibre type changes** - **Increased levels of anaerobic substrate** - **Changes in concentration and activity of enzymes** - **Increased capacity to generate high levels of lactate** - ** ** **Pre-Training** **Post-Training** **%Change** ------------------------------ ------------------ ------------------- ------------- **Muscle Fibre Type II (%)** **54.2** **63.8** **17.7** **Free Cr** **10.7** **14.5** **35.5** **PCr** **17.07** **17.94** **5.1** **PFK** **22** **43** **95.5** **LDH** **175** **260** **48.6** **Blood Lactate** **11.1** **13.0** **17.1** **Muscle Lactate** **16.9** **22.5** **33.1** ** **  ** ** Table 4 Changes (X SE) in percentage and area of type I and type Il muscle fibres before and after training (n 7) % Type 1 % Type 11 Diameter type I (gm) Diameter type Il (gm) % Area type I % Area type Il Pre-training 45.8 (6.9) 54.2 (6.9) 50.7 (0.8) 57.9 (2.0) 43.0 (6.6) 57.0 (6.6) Post-training 36.2 63.8 52.7 (l.0) 57.8 (3.8) 34.4 65.6 ** ** ![Table 2 Performance test scores \[mean (SE)\] measured before and after training (n --- 9 except for repeated sprint test where n (RST repeated sprint test, maximal oxygen consumption) 10 m Time (s) 40 m Time (s) Supramaximal run (s) RST total time (s) RST % decrement V. 02max (I min-Ip Pre-training 1.87 (0.02) 5.50 (0.05) 49.9 (3.5) 35.66 (0.65) 7.1 (2.6) 4.40 (0.18) Post-training 1.81 (0.03) 5.37 (0.08)\*\*\* 55.5 34.88 (O.49) \* 5.9 (1.2) 4.67 V02max (ml kg- min-I) 57.0 (2.4) \* p \< 0.05 \*\*\* P \< 0.01, significantly different from pre-training scores ](media/image151.png) ** ** ** ** **Training for increased alactic power** - **Energy system** - **Aim: to maximally recruit type 11x muscle fibres** - **Consider: when are they recruited, time to resynthesise PCr** - **Use sprint training methods: strength, speed, coordination, force transfer** ** ** ** ** **Factors affecting fatigue \