{"id":792,"date":"2017-11-20T10:33:52","date_gmt":"2017-11-20T10:33:52","guid":{"rendered":"http:\/\/physicality.info\/?p=792"},"modified":"2017-11-20T10:40:08","modified_gmt":"2017-11-20T10:40:08","slug":"physiology-of-exercise-1-aerobic-capacity-monthly-talk-61117","status":"publish","type":"post","link":"http:\/\/physicality.info\/?p=792","title":{"rendered":"Physiology of Exercise 1 &#8211; Aerobic capacity monthly talk 6\/11\/17"},"content":{"rendered":"<p><img loading=\"lazy\" class=\"aligncenter wp-image-359 size-large\" src=\"http:\/\/physicality.info\/wp-content\/uploads\/IMG_3262-600x400.jpg\" alt=\"\" width=\"600\" height=\"400\" srcset=\"http:\/\/physicality.info\/wp-content\/uploads\/IMG_3262-600x400.jpg 600w, http:\/\/physicality.info\/wp-content\/uploads\/IMG_3262-150x100.jpg 150w, http:\/\/physicality.info\/wp-content\/uploads\/IMG_3262-300x200.jpg 300w\" sizes=\"(max-width: 600px) 100vw, 600px\" \/><\/p>\n<p>Aerobic capacity is the ability to take in, transport and utilize oxygen and is a major factor in endurance performance. So when we train,\u00a0 increasing our aerobic capacity is always a goal.<\/p>\n<p>But how does this happen?\u00a0How does the body handle oxygen?\u00a0 How do we measure aerobic capacity and what are the physiological effects of training on the way we handle oxygen?<\/p>\n<p>Here are the notes from the talk which attempted to address a massive subject and summarise the main points.<\/p>\n<p>&nbsp;<\/p>\n<p>PHYSIOLOGY OF EXERCISE 1 \u2013 AEROBIC CAPACITY<\/p>\n<p><img loading=\"lazy\" class=\"aligncenter wp-image-108 size-large\" src=\"http:\/\/physicality.info\/wp-content\/uploads\/image-3-338x600.jpeg\" alt=\"\" width=\"338\" height=\"600\" srcset=\"http:\/\/physicality.info\/wp-content\/uploads\/image-3-338x600.jpeg 338w, http:\/\/physicality.info\/wp-content\/uploads\/image-3-84x150.jpeg 84w, http:\/\/physicality.info\/wp-content\/uploads\/image-3-169x300.jpeg 169w, http:\/\/physicality.info\/wp-content\/uploads\/image-3.jpeg 540w\" sizes=\"(max-width: 338px) 100vw, 338px\" \/><\/p>\n<p>WHAT (physiological parameters) are we training and why, not HOW to train them. That comes later!<\/p>\n<p><strong>Aerobic Capacity is the ability to consume O2<\/strong>.<\/p>\n<p>(See pdf file <a href=\"http:\/\/physicality.info\/wp-content\/uploads\/Doc_752043.pdf\">Doc_752043<\/a>\u00a0also at the foot of the page for supporting diagrams Figure 2 \u2013 Carl\u2019s blood lactate curve.)<\/p>\n<p>Endurance athletes have superior aerobic energy transfer and so aerobic capacity is a major factor in endurance performance.<\/p>\n<p><strong>Maximum O2 consumption is referred to as VO2max<\/strong>.(See Figure 3 \u2013 VO2max\/lactate\/running speed treadmill test)<\/p>\n<p>It represents the maximum amount of O2 that can be removed from the circulating blood and used by the working muscles. Elite athletes have around twice the VO2max of sedentary people. A high VO2max requires integration of pulmonary, cardiovascular and neural systems and is a good indicator of endurance performance.<\/p>\n<p>However, VO2max is NOT the sole determinant of endurance performance. Other factors, mainly at the local tissue level strongly influence a muscle\u2019s ability to utilize oxygen and hence the ability to sustain a high level of aerobic activity.<\/p>\n<p><strong>VO2max<\/strong><\/p>\n<p><strong>Absolute <\/strong>VO2max is measured in L\/min. <strong>Relative<\/strong> VO2max is measured in ml\/kg\/min and takes in to account the body mass of the subject. For example:<\/p>\n<p>-a huge rower 120kgs may have an absolute VO2max of 7L\/min which is a relative VO2max of 7000\/120=58mls\/kg\/min.<\/p>\n<p>-a petite cyclist 50kgs may have an absolute VO2max of 4L\/min which is a relative VO2 max of<\/p>\n<p>4000\/50=80mls\/kg\/min<\/p>\n<p>So the cyclist can consume more O2 for their size.<\/p>\n<p>Average relative VO2max for 35yo men in the general population is around 35mls\/kg\/min.<\/p>\n<p>It declines with age and is lower for women.<\/p>\n<p>Table of relative VO2 max scores for elite sports (mls\/kg\/min)<\/p>\n<table>\n<tbody>\n<tr>\n<td width=\"140\">&gt;75<\/td>\n<td width=\"340\">Elite runners, cross country skiers, cyclists<\/td>\n<\/tr>\n<tr>\n<td width=\"140\">65<\/td>\n<td width=\"340\">Squash players<\/td>\n<\/tr>\n<tr>\n<td width=\"140\">60-65<\/td>\n<td width=\"340\">Premiership football players<\/td>\n<\/tr>\n<tr>\n<td width=\"140\">55<\/td>\n<td width=\"340\">Rugby<\/td>\n<\/tr>\n<tr>\n<td width=\"140\">50<\/td>\n<td width=\"340\">Volleyball<\/td>\n<\/tr>\n<tr>\n<td width=\"140\">50<\/td>\n<td width=\"340\">Baseball<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>&nbsp;<\/p>\n<p>VO2 max is a good indicator of endurance performance. It will differ between sports in the same person as the exercise requirements are not the same eg running involves more all body activity than cycling, so running VO2max will be higher .<\/p>\n<p>For interest<\/p>\n<p>Carl:\u00a0\u00a0 Cycling VO2max = 68mls\/kg\/min\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 Carole:\u00a0 Cycling VO2max 58 mls\/kg\/min<\/p>\n<p>Running VO2max= 77mls\/kg\/min<\/p>\n<p>What are the physiological steps in the consumption of oxygen? See Figure 1<\/p>\n<ol>\n<li>Ventilation &#8211; LUNGS<\/li>\n<li>Circulation \u2013CARDIOVASCULAR SYSTEM (heart, blood vessels, blood)<\/li>\n<li>Oxygen utilisation &#8211; MUSCLES<\/li>\n<\/ol>\n<p><strong>VENTILATION \u2013 LUNGS<\/strong><\/p>\n<p>O2 =21% of inspired air<\/p>\n<p>Airways \u2013 mouth\/nose\/trachea\/lungs\/bronchi\/bronchioles\/alveoli<\/p>\n<p>Chest cavity (thorax) \u2013 negative pressure from diaphragm contraction\/other respiratory muscles causes inspiration, relaxation of diaphragm \u2013 expiration (passive at rest). Rises in CO2\/H+\u00a0 levels are the stimulus to breathe, not lack of O2.<\/p>\n<p>FVC = Functional Vital Capacity = max inspiration \u2013 max expiration over 1 second<\/p>\n<p>FVC is 4-5L in men and 3-4L in women, is mainly genetic and is NOT altered by training<\/p>\n<p>FVC is NO indication of aerobic fitness or performance as long as it is within a normal range and untrained people the same size as a trained athlete may have similar FVCs.<\/p>\n<p>Alveolar gaseous exchange \u2013 diffusion of O2 to the red blood cells (rbcs) and return of CO2<\/p>\n<p>Gaseous exchange is NOT a limiting factor in O2 uptake except in disease<\/p>\n<p>Blood flow velocity is NOT a limiting factor either (except in EIH=Exercise Induced Hypoxia in elite athletes, thought to be a ventilation\/perfusion mismatch)<\/p>\n<p>Women have smaller lungs, reduced lung function measures, reduced airway diameter and reduced alveolar surface area even after allowing for their smaller stature and so have reduced aerobic capacity than men.<\/p>\n<p>Exercise Hyperpnoea = desperate gasping\/heavy breathing at intense levels of exercise is NOT due to inability to breathe in enough O2 as alveolar O2 levels rise and CO2 levels fall in this state of hyperventilation. Stimulus for this is thought to be neural.<\/p>\n<p>Summary<\/p>\n<ul>\n<li>Pulmonary ventilation does NOT limit maximal aerobic performance (normal FVC, no disease)<\/li>\n<li>Larger FVCs are genetic<\/li>\n<li>Untrained individuals are breathless due to a failure to regulate blood CO2\/H+ levels<\/li>\n<li>Exercise Hyperpnoea (hyperventilation) at intense levels is NOT due to lack of O2<\/li>\n<li>Women have lower ventilatory capacity than men<\/li>\n<\/ul>\n<ol>\n<li><strong>CIRCULATION \u2013 CARDIOVASCULAR SYSTEM<\/strong> (heart, blood vessels, blood)<\/li>\n<\/ol>\n<ul>\n<li>Heart \u2013 a pump, 4 chambers, receives deoxygenated blood from the organs and muscles, pumps it to the lungs from which oxygenated blood returns to be pumped back out to the organs and muscles again<\/li>\n<li>Arteries &#8211;\u00a0 a high pressure delivery system, muscular walls, pulse, systolic and diastolic pressure<\/li>\n<li>Capillaries \u2013 exchange of gases, very small, dense network, site of gaseous exchange<\/li>\n<li>Veins \u2013 low pressure return system, thin walled, no muscles, rely on muscle pump (death by crucifixion\/post race collapse), flow direction controlled by valves<\/li>\n<li>Blood \u2013 cells suspended in plasma. Red blood cells carry O2 from the lungs to the muscles by binding it with haemoglobin Hb<\/li>\n<\/ul>\n<p><strong>Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)<\/strong><\/p>\n<p>What happens to the CV system on exercise?<\/p>\n<p><strong>Stroke Volume SV<\/strong><\/p>\n<p>SV is higher at rest to start with in trained athletes.<\/p>\n<p>On exercise SV increases with intensity\u00a0 up to an exercise intensity of about 50%VO2max then plateaus. Further increases in CO are due to an increase in HR only, until max HR (and max CO) is reached.<\/p>\n<p><strong>Heart rate HR<\/strong><\/p>\n<p>Increases with intensity rapidly within 30 seconds to 2 minutes of a run then gradually increases further to a maximum, roughly (10% variation) 220-age<\/p>\n<p>Why is HR lower in fit people? SV increases with training.<\/p>\n<p>At rest, 75kg male has a CO of 5L\/min.<\/p>\n<p>Untrained:\u00a0 HR is ~70bpm, SV = 5000ml\/70 = 71mls<\/p>\n<p>Trained:\u00a0\u00a0\u00a0\u00a0\u00a0 HR is 50bpm,\u00a0\u00a0 SV= 5000ml\/50 = 100mls<\/p>\n<p><strong>Cardiac Output CO<\/strong><\/p>\n<p>College students increase their CO 4x to 20L\/min on maximum exertion (max HR 195)<\/p>\n<p>Elite athletes increase their CO 7-8x to 35-40L\/min (SV = 180-200mls) (max HR 195)<\/p>\n<p>Racehorse max CO = 600L\/min!<\/p>\n<p>The changes in SV (and hence CO) are due to increases in:<\/p>\n<ul>\n<li>Blood volume (increased plasma volume \u2013 increased \u201cpreload\u201d)<\/li>\n<li>Mycocardial (heart muscle) contractility (Frank-Starling mechanism i.e. force of contraction is proportional to the initial length of the muscle fibre))<\/li>\n<li>Compliance (elasticity) of the left ventricle<\/li>\n<\/ul>\n<p>and are a result of training.<\/p>\n<p>Larger SV ~ larger CO ~larger VO2max ~ enhanced endurance performance<\/p>\n<p><strong>Myocardium (heart muscle)<\/strong><\/p>\n<p>Relies on aerobic metabolism and has 3x the oxidative capacity of skeletal muscle.<\/p>\n<p>At low exercise intensities it oxidises mainly fat. At moderate intensities it oxidises both fat and glycogen. Trained heart muscles uses more fat and spares glycogen, as does skeletal muscle.At high exercise intensities it oxidises lactate as fuel (produced anaerobically by the skeletal muscle).<\/p>\n<p><strong>Blood Pressure<\/strong><\/p>\n<p>Normal BP 120\/80mmHg, high &gt;140\/90, low 90\/60 or less<\/p>\n<p>Systolic BP increases rapidly with exercise at first then in proportion to intensity, reaches about 200mmHg. Increase in mean arterial pressure combined with reduced peripheral resistance as blood vessels dilate (resistance to flow is inversely proportional to radius to the power of 4 (eg if the radius doubles the resistance to flow falls by a factor of 16, so a small dilation massively reduces resistance to blood flow)<\/p>\n<p>Diastolic BP remains stable or falls slightly due to blood vessel dilation.<\/p>\n<p><strong>Blood (= rbcs suspended in plasma)<\/strong><\/p>\n<ul>\n<li><strong>Rbcs<\/strong><\/li>\n<\/ul>\n<p>Rbcs carry O2 from the lungs to the working muscles,bound to Hb<\/p>\n<p>At the muscle cell, myoglobin Mb has a greater affinity (250x) for O2 than Hb and so the O2 moves from the rbc to the muscle cell. CO2 moves out from the muscle cell to the blood and is carried away \u00a0dissolved in plasma (as H+ and HCO3-) to the lungs where it is breathed out (as CO2 and H2O).<\/p>\n<p>Number of rbcs (haematocrit) increases with training. Normal range is 39-50% (men) 35-44% (women).<\/p>\n<p>Concentration of Hb in rbcs increases with training.<\/p>\n<p>Dietary Fe important \u2013 main sources of haem iron are red meat, fish seafood, poultry and other animal products, also in leafy green veg. Non haem iron is found in plants and is more difficult to absorb, hindered by phytates in some vegetables and pulses and by dairy products.<\/p>\n<p>Iron deficient anaemia is common in female endurance athletes, reducing their aerobic capacity.<\/p>\n<p>Women have 5-10% less Hb per L than men.<\/p>\n<p>Rbc production is stimulated by lack of oxygen ( hypoxia) in the working muscles, causing release of Hypoxic Factor which stimulates release of EPO (erythropoietin) from kidneys which stimulates bone marrow to produce more rbcs.<\/p>\n<p>Note \u2013 training must be of sufficient intensity ( i.e.around LT) for adequate time and repeated bouts of training for Hypoxic Factor to be released.<\/p>\n<p>Blood doping \u2013 autologous blood transfusions or injecting with EPO, dangerous increases in blood viscosity result.<\/p>\n<ul>\n<li><strong>Plasma<\/strong><\/li>\n<\/ul>\n<p>Plasma volume increases with training.<\/p>\n<p>Untrained haematocrit 45%, plasma 55%<\/p>\n<p>Trained haematocrit 38%, plasma 62%<\/p>\n<p>So a trained athlete is borderline anaemic on standard blood tests with a haematocrit of 38% (normal range 38-50% for men), due to increased plasma volume. However, total rbc mass increases as well. The increased blood volume increases both SV and total rbc mass, thus increasing CO and aerobic capacity.<\/p>\n<p><strong>Capillary network<\/strong><\/p>\n<p>Only one cell thick wall (i.e. very thin), rolled up, with a diameter of 1\/100<sup>th<\/sup> mm=one rbc wide. At rest only 1\/40<sup>th<\/sup> of the capillaries are open.<\/p>\n<p>Muscle and heart capillaries dilate massively on exercise to increase the blood flow and O2 supply (reduced \u201cafterload\u201d).<\/p>\n<p>Controlled by autonomic nervous system (sympathetic\/parasympathetic). HR and blood flow to muscles increase in anticipation of exercise as a result of training the neuromuscular pathways (148bpm before 100m sprint, 122bpm before 800m, 118bpm before 1m, 108bpm before 2m races)<\/p>\n<p>\u201cShunting\u201d of blood away from non-vital organs and the skin (5% blood to skin at rest, 20% during exercise in warm conditions but shunting away from the skin still occurs on maximal exercise).<\/p>\n<p><strong>Cardiac drift<\/strong><\/p>\n<p>In prolonged periods (&gt;15 minutes) of submaximal exercise, SV falls and HR rises as intensity remains constant. Due to sweating and an increase in core body temperature causing a fluid shift from the plasma to the tissues, so plasma volume falls and SV falls, reducing VO2max. A trained person has reduced cardiac drift.<\/p>\n<ol>\n<li><strong>OXYGEN UTILISATION \u2013 MUSCLES<\/strong><\/li>\n<\/ol>\n<p>Finally the oxygen laden blood arrives at the muscles. O2 uptake and utilisation at the muscle depends upon the following factors:<\/p>\n<p>Density of the capillary bed \u2013 a network of tiny blood vessels throughout the muscle.<\/p>\n<p>Blood flow<\/p>\n<p>Muscle myoglobin concentration (Hb4O8 releases O2 to 4MbO2)<\/p>\n<p>Oxygen exchange rate<\/p>\n<p>Size of mitochondria<\/p>\n<p>Number of mitochondria<\/p>\n<p>Oxidative enzymes<\/p>\n<p>Aerobic ATP production in mitochondria<\/p>\n<p>ALL of these increase with training, thus increasing aerobic capacity.<\/p>\n<p><strong>SUMMARY<\/strong><\/p>\n<p>Important factors which influence endurance performance are:<\/p>\n<ol>\n<li>Aerobic capacity \u2013 the ability to consume oxygen<\/li>\n<li>VO2max \u2013 maximum capacity to consume oxygen<\/li>\n<li>Lactate Threshold \u2013 maximum level for steady state exercise<\/li>\n<\/ol>\n<p>The main variables affecting aerobic capacity, VO2max and LT are:<\/p>\n<ul>\n<li>CO (cardiac output) , which depends on heart rate and stroke volume<\/li>\n<li>Haemoglobin concentration<\/li>\n<li>Erythrocyte (red blood cell) production<\/li>\n<li>Capillary density in the muscles<\/li>\n<li>Oxidative enzymes in the mitochondria of muscle cells<\/li>\n<li>Running economy<\/li>\n<\/ul>\n<p><strong>Take home message:<\/strong><\/p>\n<p>Endurance training at different levels of intensity enhances aerobic capacity.<\/p>\n<p>Training must include intensities at or around LT, for an adequate length of time per workout and workouts at this level must be repeated.<\/p>\n<p>VO2max may not increase following training whilst endurance performance does improve.<\/p>\n<p>As endurance is performed at LT (race pace) not at VO2max (a higher level of intensity than LT), training induced improvements in performance correlate more with training an increase in LT than with changes in VO2max.<\/p>\n<p>LT increases with training due to improved aerobic capacity at lower intensity of exercise<\/p>\n<p>(see figure 4 \u2013 Effect of training on LT).<\/p>\n<p>Think of it a bit like HR. Training doesn\u2019t change your max HR, but resting HR is lower if you are fit because you are physiologically more efficient. Similarly training doesn\u2019t necessarily increase your VO2max, but your ability to consume oxygen (aerobic capacity) at submaximal exercise intensities (up to LT) does. Your LT increases, as you can utilize oxygen better and delay going anaerobic.<\/p>\n<p>So you can run faster at your race pace (LT).<\/p>\n<p>The diagrams to support this text can be found below:<\/p>\n<p><a href=\"http:\/\/physicality.info\/wp-content\/uploads\/Doc_752043.pdf\">Doc_752043<\/a><\/p>\n<p>&nbsp;<\/p>\n<p>&nbsp;<\/p>\n<p>References<\/p>\n<ol>\n<li>The Science of Running Steve Magness 2014<\/li>\n<li>Exercise Physiology \u2013 Nutrition, Energy and Human Performance MacArdle, Katch and Katch 8<sup>th<\/sup> edition 2015<\/li>\n<li>Daniels Running Formula\u00a0 Jack Daniels PhD 3<sup>rd<\/sup> edition 2014<\/li>\n<li>The Cyclist\u2019s Training Bible Joe Friel 4<sup>th<\/sup> edition 2009<\/li>\n<li>Triathlon Science Joe Friel Jim Vance 2013<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"<p>Aerobic capacity is the ability to take in, transport and utilize oxygen and is a major factor in endurance performance. So when we train,\u00a0 increasing our aerobic capacity is always a goal. But how does this happen?\u00a0How does the body handle oxygen?\u00a0 How do we measure aerobic capacity and what are the physiological effects of &hellip; <a href=\"http:\/\/physicality.info\/?p=792\" class=\"more-link\">Continue reading <span class=\"screen-reader-text\">Physiology of Exercise 1 &#8211; Aerobic capacity monthly talk 6\/11\/17<\/span><\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":[],"categories":[1],"tags":[],"_links":{"self":[{"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/posts\/792"}],"collection":[{"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"http:\/\/physicality.info\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=792"}],"version-history":[{"count":4,"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/posts\/792\/revisions"}],"predecessor-version":[{"id":797,"href":"http:\/\/physicality.info\/index.php?rest_route=\/wp\/v2\/posts\/792\/revisions\/797"}],"wp:attachment":[{"href":"http:\/\/physicality.info\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=792"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/physicality.info\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=792"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/physicality.info\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=792"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}