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ENERGY TRANSFER IN THE BODY AND METABOLISM DURING EXERCISE a. What is Energy? - Energy in biological reactions produce heat. Hence energy intake and output measured in either kilocalories (kcals) or joules (1 kcal = 4.184 (4.2) kjoules) - 1 kcal (or 4.2 joules) represents the amount of energy necessary to raise the temperature of 1kg of water 1C at 15C. - 60-70% of energy used in our bodies is released as heat. Why so inefficient? b. Where do we get energy? FOOD + O2 --- CO2 + H2O + ENERGY 40 % CAPTURED & 60 % RELEASED AS HEAT Nutritional Sources FAT CARBOHYDRATE PROTEIN All composed of carbon, hydrogen and oxygen with nitrogen in the case of PROTEIN kcals per litre O2 FAT (LIPID) 4.7 CARBOHYDRATE (CHO) 5.05 If CHO is the most efficient and readily available fuel, why don't we store more? c. Factors affecting energy production. - the primary factor affecting energy production is the total energy demand coupled with the rate of demand. 1. Anaerobic - two systems - produces energy in the absence of oxygen 2. Aerobic - - one system - oxygen is present these systems are arranged in metabolic pathways which allow for the release of energy from food in sequential steps or reactions. Hence, more usable energy may be obtained. These pathways also allow control to be exerted over the process of metabolism. - chemical reactions move towards equilibrium as reactions move towards equilibrium they release energy SOME USEFUL TERMS FREE ENERGY CHANGE (G) - that part of the total energy change in a reaction that is capable of doing work - when energy is released G is considered negative and the reaction is exergonic and the reaction may occur spontaneously - when energy is added G is considered positive and the reaction is endergonic. It can only occur when coupled to an exergonic reaction. Assume reactants A+B produce products C+D and that in the process energy may be released. ie: A+B ----- C+D If we have a lot of A+B and little C+D (large -G) then the reaction will proceed rapidly to the right. As the level of C+D builds up however the reaction will proceed more and more slowly until it is proceeding equally rapidly in both directions. At this point the reaction is in equilibrium (G=0). How may we control? Two prime examples are substrate concentration and enzyme activity. A -- B -- C -- D+cofactor -- P ENERGY ENZYMES protein catalysts which help regulate the rate of a reaction which would normally occur anyhow. The activity of some enzymes are under complex control. The point in a metabolic pathway were ultimate control is exerted is termed rate-limiting. Anaerobic Systems i. ATP-PCr system (immediate, phosphagen) this system provides energy at a high rate but has a low capacity ie. total of 3 - 15 sec in an all out sprint. following exercise the CP must be replaced by ATP ultimately this ATP is aerobically produced. ii. Blood g l- u c o s e The glycolytic system Cell insulin & glut 4 ATP ADP phosphorylase - glucose -- glucose-6-phosphate -- glycogen hexokinase glycogen synthase ATP phosphofructokinase ADP one 6 C unit changed to 2 3 C units NAD ---- if O2 NADH + H+ - 4 ADP + Pi mito 4 ATP if O2 2 pyruvate --- lactate dehydrogenase 2 lactate - lactate still has 80% of the original energy of glucose - with anaerobic glycolysis get a net of 2-3 ATP depending upon starting point - some lactate is always produced even when adequate oxygen in present simply because substrate for the LDH reaction is present - anaerobic glycolysis has an intermediate rate & capacity - glycolysis may only employ carbohydrate as a fuel MORE USEFUL TERMS GLYCOLYSIS - the breakdown of glucose to pyruvic acid GLYCOGENOLYSIS - the breakdown of glycogen to glucose GLUCONEOGENESIS- the formation of glucose from protein or fat Aerobic Metabolism (Oxidative Phosphorylation) - both fat and CHO may be used aerobically, fat cannot be used anaerobically. - energy production occurs in the mitochondria - if the exercise intensity is low enough and oxygen is available then pyruvate produced in glycolysis may move into the mitochondria to changed to acetyl CoA via the pyruvate dehydrogenase complex - the acetyl CoA is broken down in the Kreb's cycle (also known as the tricarboxylic acid or TCA or the citric acid cycle). The Kreb's cycle produces carbon dioxide (CO2) and hydrogen (H2). The hydrogen is coupled with coenzymes (NAD & FAD) which enter the Electron Transport Chain (ETC) where ATP is produced and oxygen is used to make H2O. - in the ETC 3 ATP are produced per NADH + H+ and 2 ATP per FADH2. - it is also in the Kreb's cycle where the decision to employ lipids or CHO is made. How is this decision made? Oxidation of Lipids f. Significance of Various Energy Sources g. Oxygen Uptake - oxygen uptake represents the ability to: 1. take up; 2. transport and 3. utilize oxygen. - at maximal capacity this is termed maximal oxygen uptake, maximal aerobic power, mVO2, VO2max, maxVO2 - VO2max is probably the best single measure of cardiorespiratory capacity - VO2max may be reported in as either absolute or relative values eg. Dick Jane Weight (kg) 90 49 VO2max (l/min) 4.0 2.5 VO2max (ml/kg/min) 44.4 51.0 - the relative VO2max is a better indicator of cardiorespiratory fitness than the absolute value - VO2 = O2inspired - O2expired - to arrive at this number we must know (i) the volume of air inspired (ii) the volume of air expired (iii) the percentage of O2 in each What factors might affect this measurement? 1. Volume 1/Pressure (Boyle's Law) 2. Volume Temperature (Charles' Law) - to correct for these effects we use two types of standardization (i) (ii) STPD - standard temperature and pressure, dry BTPS - body temperature and pressure, saturated - the conditions under which air is collected are know as ATPS - ambient temperature and pressure, saturated - in a like manner, we can determine the amount of CO2 expired - under steady state conditions these values can be used to estimate the pattern of fuel use - RER = Respiratory Exchange Ratio = VCO2/VO2 - eg. glucose 6O2 + C6H12O6 --- 6CO2 + 6H2O + ENERGY RER = 6CO2/6O2 = 1.0 - eg. palmitate 23O2 + C16H32O2 --- 16CO2 + 16H2O + ENERGY RER = 16CO2/23O2 = 0.7 - resting RER is typically around 0.8 - 67% fat and 33% CHO (Table 5.4) - RER increases with exercise and in non-steady state exercise many increase above 1.0 - estimating energy expenditure like this is termed indirect calorimetry - basal metabolic rate (BMR) - the minimal energy needed to maintain body function - represented by a metabolic equivalent (MET) = 3.5 ml/kg/min O2 - typical VO2max values: female male - 38 - 42 ml/kg/min - 44 - 50 ml/kg/min Why are there gender differences? 1. Cardiovascular - have smaller hearts/body mass - have less hemoglobin - lower blood volume 2. Body Composition - have less fat-free mass (muscle) - when compared on a per kg muscle basis much of the difference disappears - endurance training may VO2max by 10-25% - training may also affect efficiency of O2 use - Efficiency = - output based on weight, activity etc. - input = VO2 l/min) x 5.0 kcal/lO2 work output x 100 25% work input h. Lactic Acid Production - as exercise intensity increases, LA production > LA use and muscle and blood LA - point at which begins is called LA threshold - another common measure of LA production is called onset of blood lactate (OBLA) = 4 mM blood levels - the %age of VO2max at which this threshold occurs may affect endurance performance i. Oxygen debt or EPOC - components contributing to EPOC - 2 phases - Fast (alactic) - 30 sec half-life - Slow (lactic) - 20-30 min half-life - several reasons for EPOC other than ATP-PCr restoration and LA removal 1. myoglobin recovery (fast) 2. temp & metabolic rate 3. hormonal stimulation 4. tissue repair 5. extra cardiorespiratory work What happens to the LA remaining after exercise? j. Metabolic causes of Fatigue - 3 exercise types: 1. short duration, high intensity 2. moderate duration, moderate intensity 3. long duration, low intensity 3. PULMONARY VENTILATION - for VO2 this system involved in uptake - also involved in removal of CO2 - important in acid-base status a. Lung structure and function - lungs are suspended in pleural sacs and intrapleural pressure is always negative. - lungs just improve on simple diffusion b. Mechanics of Ventilation - action of diaphragm and costal muscles affects intrapleural and intrapulmonary pressures leading to inspiration and expiration - VE = pulmonary or minute ventilation - VE represents the actual movement of air in and out of the lungs - VE is a function of the frequency of breathing (f) and the depth of the breath or tidal volume (VT). VE = f x VT - only air entering perfused alveoli or the alveolar volume (VA) takes part in gas exchange. non-perfused alveoli & respiratory passages where no gas exchange occurs termed dead space (VD) - VA = (VT - VD)f = VE - VD - at rest, typical: - VT = 500 ml VD = 150/breath (doesn't change much with exercise) f = 15 breaths per minute VE = 500 ml/breath x 15 breaths/min = 7.5 l/min VA = (500 ml/breath x 150 ml/breath) 15 breaths/min = 5.25 l/min What if f and VT so that VE same? c. Static lung volumes - passive measures taken at rest which represent lung capacity - vital capacity (VC) - the maximum amount of air that can be exchanged in 1 breath - residual volume (RV) - the amount of air left in the lungs at the end of a maximal expiration - total lung volume = VC + RV - these measures largely based on body size and can't be changed with training d. Gas pressures and exchange - gas diffuses from high pressure to low pressure - total pressure = sum of partial pressures If barometric pressure = 760 mm Hg PO2 = 760 mm Hg x 20.93% = 159 mm Hg PCO2 = 760 mm Hg x 0.03% = 0.23 mm Hg Factors affecting exchange: * 1. Partial pressure gradient 2. Surface area for diffusion 3. Diffusion path length 4. Hemoglobin (Hb) and myoglobin (Mb) concentration e. Gas transport by the blood Oxygen Transport - most O2 carried by Hb - 1 Hb can combine 4O2 - oxyhemoglobin - saturated Hb can carry 1.34 ml O2/g - average 14-18 g Hb/100 ml blood - average 12-16 g Hb/100 ml blood - 12 g Hb/ 100 ml blood x 1.34 ml O2/g = 16 ml O2/ 100 ml blood - typical values range are 201 & 187 ml O2/ 100 ml blood for & respectively - about 3 ml of O2 are dissolved per l of plasma Carbon Dioxide Transport 1. dissolved in plasma 2. carbamino compounds 3. CO2 + H2O - H2CO3 - H+ + HCO3 60-70% What happens if we add lactic acid? - non-metabolic production of CO2 7-10% 20-33% - raises RER above 1.0 f. Ventilatory control a. Neural - respiratory centres - peripheral input - cerebral (motor) cortex b. Chemical - H+ (pH), PCO2, PO2, K+ c. Temp g. Ventilation during exercise - ventilation increases linearly early in exercise - later an exponential increase - breakpoint called ventilatory threshold (breakpoint) - anaerobic threshold is the when VE/VO2 without in VE/VCO2 - ventilatory, anaerobic & LA thresholds all occur at about the same point How are these exercise changes controlled? h. Ventilation as a limiting factor 1. VE never approaches maximal capacity (MVV) and VT never approaches VC 2. gas pressures are maintained 3. VE/VO2 with heavy exercise 4. VE > cardiac output (Q) 4. THE CARDIOVASCULAR SYSTEM VO2 = HR x SV x (a-vO2diff) this is known as the FICK equation a. Cardiac structure and function b. The circulatory system c. Cardiac output Q = HR x SV i. Heart rate: - bradycardia - slow heartrate (clinically less than 60) - tachycardia - fast heartrate (clinically over 100) - sinus rhythm - normal rate (SA node) - heart rate increases linearly as exercise intensity increases ii Stroke volume: - volume of blood pumped per heart beat SV = EDV - ESV - End Diastolic Volume = amount of blood in the ventricle after diastole (rest between contractions) - End Systolic Volume = amount of blood in ventricle after contraction (systole) - ejection fraction - proportion of blood in ventricle ejected SV/EDV X 100 - stroke volume increases linearly with exercise but levels off at 40-60% VO2max Factors affecting stroke volume: 1. Contractility - the force with which the heart contracts - increased by sympathetic stimulation and circulating catecholamines - with contractility, more of the EDV is pumped out ( EF) REST EXERCISE EDV 85 ml 120 ml ESV 30 ml 20 ml SV 55 ml 100 ml EF 65 % 83 % - well trained endurance athletes may reach a SV of 200 ml 2. Frank-Starling Mechanism - ventricle ejects whatever blood it receives - EDV is a measure of the blood received - often called preload - several factors affect the EDV: i. venous tone ii. muscle pump iii. respiratory pump iv. ventricular size and distensibility v. prolonged exercise and heat - both lead to cardiovascular drift - in each case insufficient venous return and hence EDV vi. supine or prone exercise - decreased hydrostatic load - lower heart rate, larger stroke volume vii. resistance to blood flow (afterload -the load the heart has to work against) Flow = Pressure Resistance 1/Total Peripheral Resistance = radius4 length x viscosity or Flow (Q) = Pressure x radius4 length x viscosity - during exercise TPR drops dramatically - radius is most important factor and control is exerted in arterioles (resistance vessels) d. Relationship between cardiac performance and oxygen uptake VO2 = HR x SV x (a-vO2diff) - at rest only a small portion (25%) of available VO2 in blood is used - with exercise amount dropped off - with exercise HR x SV VO2 HR x SV Rest 0.225 l/min 5 l/min 45 ml/l Ex 2.38 l/min 17 l/min Rest 0.225 l/min 5 l/min 45 ml/l Ex 3.89 l/min 25 l/min a-vO2diff UTr 140 ml/l Tr 155 ml/l e. Blood pressure and exercise - the driving force which keeps blood flowing around the circulatory system - at rest fluctuates between 80 and 120 mmHg in the systemic circulation and 10 and 25 mmHg in the pulmonary circulation - Mean Arterial Pressure (MAP) is a measure of the driving force MAP = dias BP + [.33(sys BP - dias BP)] = 80 + [.33(120 - 80)] = 93.3 mmHg or MAP = (systolic) + (2 X diastolic) 3 = 120 mmHg + 160 mmHg = 93.3 mmHg 3 - rate-pressure product (RPP) = estimate of cardiac work RPP = SBP X HR * - MAP doesn't change much with exercise - muscle contraction or Valsalva f. Distribution of blood flow * - at least part of a-vO2diff due to better blood flow distribution - blood distribution is set up as a series of parallel vascular beds - arterioles control flow to these beds - arterioles influenced by extrinsic neural control and autoregulation 1. Extrinsic neural control - both vasoconstriction (adrenergic) & vasodilation (cholinergic) - NET EFFECT = VASOCONSTRICTION - some areas more sensitive than others 2. Autoregulation - vasoconstriction overcome in working tissue ie. O2, CO2, temp, H+, K+ - direct on blood flow in working tissue 3. Long-term - vascularization - blood volume g. Cardiac Control 1. Intrinsic - Frank-Starling mechanism - EDV get contractility and HR 2. Extrinsic i. Autonomic N.S. - sympathetic - catecholamines HR & contractility - parasympathetic (vagus) - cholinergic - HR - parasympathetic predominates at rest and with exercise sympathetic takes over - well-trained have resting HR due sympathetic & parasympathetic ii. Baroreceptors & Chemoreceptors - in aortic arch and carotid sinus - feedback to pressure changes - chemoreceptors alter Q in response to O2, CO2 & pH Overall - general vasoconstriction overcome by local factors with flow to muscles - sympathetic (including adrenal release) & decreased sympathetic causes HR and contractility and Q - baroreceptors, chemoreceptors & muscle receptors all alter cardiac output - MAP very little while Flow 4-5 X because of resistance (largely due to r) 4. MUSCLE AND MOVEMENT (Chpts. 2-4) a. Muscle structure and function 1. types of muscle cardiac smooth skeletal 2. components of skeletal muscle 3. connective tissue - the connective tissue all coalesces in the tendon which transmits force to bone 4. an individual muscle fibre 5. an individual sarcomere 6. contractile proteins 7. nervous input - action potential - rapid and sustained depolarization of the nerve membrane - membrane must first reach threshold before action potential occurs - propagation of action potential - large neurons conduct faster as less resistance to current flow - a synapse carries information from one nerve to another - the information may be inhibitory or excitatory - summed effect of inputs determines whether or not an action potential occurs - summation - neuromuscular junction (NMJ) acts like synapse for motor nerve to muscle fibre 8. conduction along and into fibre b. Mechanism of muscular contraction - sliding filament hypothesis c. Some important contractile properties 1. length-tension relationship - there is an optimum length for maximum force production 2. force-velocity relationship - highest force is generated at slowest velocity d. Neuromuscular control of movement 1. - motor units - motor nerve and all the muscle fibres innervated by it may be spread throughout the muscle - all fibres within a given motor unit share the same characteristics - motor units are of different sizes and allow graded contraction - sizes differ due to fibre size & number 2. recruitment pattern i multiple motor unit summation - size principle - small motor units recruited first - results in principle of orderly recruitment ii wave summation - increased rate of stimulation leads to tetany 3. muscle fibre types - 2 broad categories - fast-twitch (FT) - slow-twitch (ST) - FT can easily be subdivided into several subgroups - remember fibres represent are influenced by the properties of the nerve innervating them - all fibres within a given motor unit are the same in their properties - recently another type of FT unit (Type IIx or IId) has been discovered. It is somewhat like the FOG type unit - different muscles have different fibre compositions probably related to function - typically successful athletes have fibre type profiles that may vary with event - these profiles are probably a result of genetic endowment - exercise training may influence the fibre composition, but it is unclear how much MUSCLE FIBRE CHARACTERISTICS Name Contraction Speed Relaxation Speed Aerobic Capacity Mitochondrial Content Fatigue Resistance Anaerobic Capacity Fat Content Glycogen Content Capillary Supply Tetanic Tension Recruitment Pattern * - in humans only Type I SO S S slow slow high high high low high high great low frequent Type IIa FOG FTa FR fast fast int - high int - high int - high int - high high high great int frequent Type IIb FG FTb FF fast fast low low low high low high * small high seldom 4. Feedback loops - afferent information to control muscle contraction and movement - several levels of information i muscle spindles * important in the stretch reflex - indicate change in length of muscle fibres - indicate both absolute amount and rate of change - spindles are activated by gamma motor neurons and can assist in rapid movement ii golgi tendon organs - located in tendons at muscle interface - sensitive to tension - probably perform a protective function by inhibiting agonists and contracting antagonists e. Muscle soreness and recovery - acute muscle soreness - may be pain due to ischemia, accumulation of end products (H+ & H2O) - delayed onset muscle soreness (DOMS) - not directly related to lactate build up - observed most with eccentric (lengthening) vs concentric (shortening) contractions - DOMS peaks at 24-48 hours after the exercise bout - symptoms include; increased muscle enzymes (CPK) & myoglobin in blood, histological evidence of damage, local muscle pain, soreness & swelling - may be due to increased intracellular Ca++ & inflammatory response subsequent to muscle damage - may result in decreased muscle force which persists for several weeks - muscle repair follows the induction of a complex inflammatory response and activation of satellite cells - once muscle soreness has occurred, protection against subsequent soreness may last 3-4 weeks 5. SUMMARY OF PHYSIOLOGICAL EFFECTS OF TRAINING (Chpts. 4,7,10) a. Muscle adaptations 1. Strength - several factors may influence strength, eg. synchronous motor unit/muscle activation and coordination, reduced autogenic inhibition - maximal increases in muscle strength dependant upon muscle size (force/area) - two theories for increased muscle size are hypertrophy and hyperplasia - usually muscle increases in size due to hypertrophy of existing fibres as muscle fibre # is normally set at birth - strength-training induced changes are movement, speed and load specific - unlikely that fibre type changes 2. Metabolism - muscle adapts to become a more effective energy provider - adaptions are specific to muscle (fibres) utilized - intensity and duration influence adaptation a. aerobic exercise - key points: 1. capacity 2. fuel storage 3. sparing of CHO - in mitochondrial size and number - with mito's get enzyme activity - this results in an increased respiratory capacity of the muscle - this increase occurs over time and gradually levels off - both duration and intensity of exercise are important influence on these adaptations Why is intensity important? - in ability to use oxygen is accompanied by fuel supply & better control of metabolism - CHO levels may double, ß-oxidation & fat globules in muscle - with resistance training leading to muscle mass, aerobic capacity of muscles actually b. anaerobic exercise - probably need a minimal duration (30 sec) to be effective - in creatine phosphokinase (CPK) & myokinase (MK) (10 - 15%) - in ATP and PCr (25 - 40%) - minor in glycolytic enzymes after sprint training but muscle buffering capacity may (12 50%) allowing LA 3. Cardiorespiratory adaptations a. Cardiac system - changes in heart size & weight occur as a result of training - heart walls get thicker effect of resistance training - stroke volume is greater in aerobic trained at all levels of activity - this is a result of EDV and EF - heart rate is reduced with aerobic training at rest and during submaximal exercise - maximal HR is about the same or slightly reduced - at rest and at an absolute submaximal WL cardiac ouput is - maximal cardiac output is following training CARDIORESPIRATORY CHANGES WITH TRAINING (absolute load) CONDITION REST Oxygen Uptake Heart Rate Stroke Volume Cardiac Output Heart Size Blood Volume Capillary Density a-vO2diff Muscle Blood Flow VE frequency Tidal Volume Diffusing Capacity Work Capacity - - SUBMAX - - - - - - - - - MAX - - - - - - 4. Factors influencing training 1. Specificity and Overload - must be energy source, movement and sport specific eg. if train individuals by swimming and measure VO2max while running may get 2% but if measure by swimming may get 12% 2. Frequency - 3X per week is sufficient for a training effect but may get slight improvement with 5-7X per week. 6. TEMPERATURE REGULATION (Chapt. 11) a. Heat Balance: - ability to rid the body of heat is a major problem for exercising individuals - although changes have occurred, heat stroke - loss of ability to control one's own temperature - still occurs. HOMEOTHERMS: - animals capable of maintaining body temperature within narrow limits. ADVANTAGE: chemical reactions run at relatively higher rates as temperature increases 2X increase in rate for a 10C increase in temperature this means more energy and faster use of energy DISADVANTAGE: temperature must be precisely regulated increase to 41C can cause convulsions increase to 43C is incompatible with life temperature can decrease with little tissue damage When our heat content is constant, ie. our core temperature is constant, we are in THERMAL BALANCE. THERMAL BALANCE = HEAT GENERATED - HEAT TRANSFERRED 1. HEAT GENERATED - measured in kcals, ie. 1 kcal will raise the temperature of 1 kg water 1 C - body tissue (which is mostly water) may also be heated - its SPECIFIC HEAT is 0.83 kcal/kg/C. eg. a 77 kg man must "store" 64 kcals of heat (0.83 x 77) to increase body temperature 1C. QUESTION: If no thermoregulatory mechanisms existed, how much would the temperature increase in this 77 kg person "running" at a pace of 9 minutes per mile for 30 minutes, if the energy cost was 14.3 kcal/min? ANSWER: Man is about 25% efficient hence 75% or 10.7 kcal/min is liberated as heat. Hence per minute, the core temperature would increase: 10.7 kcal/min divided by 64 kcal/deg = 0.17C/min. By 10 minutes at this pace, the body temperature would increase 1.7C and by 30 minutes, the temperature would increase by 5.1C, or well above the danger level. - 2. one can readily exercise for 30 minutes and maintain a temperature well below 41C, therefore adequate HEAT TRANSFER must take place. HEAT TRANSFER - body temperature is ultimately regulated through the hypothalamus - neural outflow can change both HEAT PRODUCTION (shivering) and HEAT LOSS capacity - temperature regulation is based on a REFERENCE TEMPERATURE - this "set point" may change ie. fever - the hypothalamus regulates the setpoint, but to be efficient, we require a means to determine if the setpoint is achieved. - we have: 1. CENTRAL - hypothalamus receptors 2. PERIPHERAL - skin receptors - central receptors are the most important but peripheral receptors can modify the action Core temperature is what's closely regulated eg. blood flow to the SKIN is an important temperature regulator and if skin flow is increased then body temperature is decreased - with exercise as one gets warm, then skin blood flow is increased - if the skin is suddenly cooled, the initial reaction is to decrease heat loss and therefore decrease blood flow to the skin. - this response is soon overridden by increases in core temperature and blood flow to the skin resumes. 2.a MECHANISMS OF HEAT TRANSFER: 1. Conduction - transfer of heat between 2 objects at different temperatures 2. Radiation - heat is radiated in the form of electromagnetic waves - 60% of all heat lost at rest occurs by this means 3. Convection - once the air next to the body is warmed, then heat loss decreases unless warm air is taken away - the body cools by the removal of this air. 4. Evaporation - this method is especially important during exercise - to be effective, water must be changed to vapour - even under sedentary conditions, evaporation may account for 150-200 mls water loss per day All mechanisms, except evaporation, rely somewhat on PASSIVE heat loss from the body surface to the environment - in this regard, the body may be considered as two layers; 1. a core and 2. a shell of changing thickness - this allows us to effectively increase or decrease the temperature gradient and therefore control passive heat loss - under cold conditions we are willing to sacrifice the periphery in order to maintain the core temperature Note: - under hot conditions, evaporation is about the only manner in which heat may be lost - if conditions are both hot and humid then evaporation is greatly retarded and exercise is potentially dangerous - for every litre of water evaporated, 580 kcal of heat energy is lost - so if we return to our earlier example: When an individual of 77 kg jogged at a 9min/mile pace, for 30 min then the total excess heat generated was 321 kcal (10.7 kcal/min x 30 min) hence the person must lose 321 kcal/580 kcal/l = 0.55 l of water if they lose the excess heat by evaporation only - unacclimatized persons can sweat up to 1.5 l/hr - acclimatized individuals may sweat up to 3-4 l/hr b. - Exercise in the Heat during exercise in the heat, the body is faced with 2 competitive demands: 1. sustain O2 to the muscles 2. transport heat to the surface - Hence, at any given workload in the heat, cardiac output must be increased - the increased cardiac output is associated with an increased heart rate and a decreased stroke volume - the decreased stroke volume results from decreased venous return - all of the blood is in the periphery this gradual exercise associated increase in heart rate is known as CARDIOVASCULAR DRIFT - the net effect is that at max, not as much blood can be pumped and therefore MVO2 may be decreased 6-8% in hot, humid conditions at the same time that we are trying to transport extra fluid to the surface to decrease core temperature, we are continuing a high rate of evaporation ie. a marathoner may lose up to 5 l. of water or 5-10% of body weight during a run d. Training and Acclimatization 1. CORE TEMPERATURE: - with exercise core temperature increases as a function of the relative workload (ie. % of MVO2) - after training the same situation exists except that at a given % of MVO2 one can perform more work 2. SWEAT RATE: - sweat rate, important in evaporative heat loss may be enhanced by both exercise training and acclimatization to increased environmental temperatures the adaptive mechanism is different for the two conditions a. acclimatization causes one to begin sweating at a lower temperature b. training does not affect the temperature at which sweating starts, but increases the responsiveness to changes in temperature - with training the composition of sweat is altered so that it is more dilute - this means that not as much salt is lost during exercise following training 3. BLOOD VOLUME: - with exercise training, blood volume is increased (often by about 20%) - this increase enables the body to counteract the fluid lost through sweating and helps to maintain stroke volume when exercising in the heat - the increased fluid volume adjustment is very rapid and probably results from the actions of antidiuretic hormone (ADH) which increases fluid resorption in the kidney - aldosterone also acts to increase sodium resorption in the kidneys d. The Importance of Water - water may be the most important of the nutrients we receive - a water loss of 9-12% may be fatal - fluid loss may inhibit performance of longer duration exercise - fluid replacement will help maintain performance 1. Practical tips to avoid dehydration - for training, initiate slowly and gradually increase the workload - even individuals accustomed to exercise may experience problems with a sudden increase in repetitive work especially in the heat - fluid composition - for maximum benefit the fluid ingested should contain some salt and some carbohydrate (6-8% glucose, fructose or glucose polymers) - the salt will depress excretion and enhance thirst - do not consume drinks with caffiene or alcohol - prehydrate - take in as much fluid as comfortable 45 min - 2 hr prior to exercise - hydrate - drink at least 1 cup of fluid every 15 min prior to the activity - rehydrate - drink 2 cups of fluid for every pound of body weight lost during exercise - cold fluid not only helps maintain body temperature, it is absorbed faster - do not count on thirst to guide your fluid replacement 7. NUTRITION FOR EXERCISE (Chpts. 14,15) a. Nutritional Sources 1 Energy Nutrients a. Carbohydrates - essential for action of CNS - stored in muscle and liver - stored in limited quantities - muscle glycogen most important during exercise but blood glucose may supply 10-30% of CHO needs - type of carbohydrate consumed may affect CHO use - simple sugars such as sucrose or fructose are readily absorbed and rapidly increase the blood sugar/insulin levels - complex sugars such as starch are consumed more slowly and cause a lesser rise in insulin b. Lipids - essential for cell membrane formation, steroid hormone production, protection, insulation and fuel - hyperlipidemia due to overconsumption of lipids is a major cause of cardiovascular disease - saturated fats (most animal fats and those that are solid at room temperature) are most associated with CHD risk - unsaturated fats carry less risk cholesterol is an essential fat which we both consume and produce - high levels of cholesterol are associated with CHD - lipids are carried in the blood in association with proteins - the more protein in the complex, the more dense it is, hence lipoproteins may be described on the basis of their density - low density lipoproteins (LDL's) are likely to cause atherosclerosis whereas high density lipoproteins (HDL's) may protect against CHD - the critical factor is the HDL/LDL ratio, the higher the better - lipid stores may also be viewed as essential or storage - essential fat - 3-4% in 's - 12-15% in 's c. Proteins - differs from previous nutrients in that they contain nitrogen as well as C, O, H formed from 20 amino acids - 8 (9) of the amino acids must be derived in the diet - perform structural and catalytic function and used little as a fuel - dietary requirements (RDA) = 0.8 g/day - this would be about 80 g for a 100 kg person - several studies have demonstrated that some athletes require 1.5 - 2X the RDA - the typical protein consumption is at least 2X the RDA, hence protein supplementation is not generally recommended - excess protein may be dangerous - high quality protein has all the essential amino acids i.e. red meat - low quality proteins do not contain all the essential amino acids d. Ideal Diet Composition Protein - 10 - 15% Lipid - 25 - 30% (less than 10% saturated) Carbohydrates - 55-60% 2 Vitamins and Minerals a. Vitamins - generally act as catalysts in rx's - fat soluble (A, D, E, and K) are longer lived in body - water soluble (B-complex and C) are flushed out if taken in excess - vitamins are essential to proper growth and performance, but deficiency is unusual - vitamins C and E may act as antioxidants - about 4% of all oxygen consumed becomes free radicals and can lead to cell damage - exercise increases oxygen consumption and hence potential for tissue damage - vitamin E and C supplementation may protect against oxidative damage and improve healing - best results with 200 - 400 mg of vitamin E and 500 - 1000 mg of vitamin C b. Minerals 1 Calcium - most abundant in body - reduced calcium leads to loss of bone density & ultimately osteoporosis 2 Phosphorus - stored in bone in conjunction with calcium - attached to lipids, ATP etc. 3 Iron - mineral important in oxygen transport and energy production - this is the mineral most likely to be deficient - many females have some degree of deficiency which may with exercise - many male aerobic athletes also have deficiency although Hb content OK - initial signs are reduced iron stores i.e. ferritin - vegetarians are at particular risk - iron absorption best from foods as opposed to ferrous sulphate tablets, with Vitamin C reduced with caffeine c. Nutrition for exercise 1. Importance of carbohydrates - for long-term (and possibly short-term) exercise CHO's are very important and should be: 1. manipulated 2. spared 2. Pregame meal
