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cardio final review.docx

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University of Toronto St. George
Human Biology

Functional capacity of the cardiovascular system Direct fick method  VO2= Q× avO2  Q=VO2mL × min a-VO2 difference Untrained characteristics of Q  HR=70 BPM  SV=70ml  Average women 25% lower due to smaller size Endurance athletes  Characteristics of Q o HR= 50 BPM o SV= 100mL  Mechanisms explaining increased Qmax: o Increased vagal tone with decreased sympathetic drive o Increased blood volume o Increased myocardial contractility and compliance of left ventricle Cardiac output during exercise  Q increases rapidly during transition from rest to exercise  Q at max exercise increases up to 4 times  Stroke volume is higher Acute response to CV exercise  HR increases as exercise intensity increases up to maximal heart rate  Stroke volume (SV) increases up to 40% to 60% VO2 max in untrained individuals and up to maximal levels in trained individuals  Increases in HR and SV during exercise cause cardiac output (Q) to increase  Blood flow and blood pressure change  All result in allowing the body to efficiently meet the increased demands placed on it. Maximum heart rate  The highest rate value one can achieve in all-out effort to the point of exhaustion  Remains constant day to day and changes slightly from year to year  Can be estimated: HRmax=220-age in years or HRmax=208 – (0.7×age) Steady-state heart rate  Heart rate plateau reached during constant rate of submaximal work  Optimal heart rate for meeting circulatory demands at the rate of work  The lower the steady-state heart rate ,the more efficient the heart Stroke volume and cardiac output  Stroke volume o Volume of blood pumped per contraction o End-diastolic volume—volume of blood in ventricle before contraction o End-systolic volume—volume of blood in ventricle after contraction o Sv=edv-esv  Cardiac output o Total volume of blood pumped by the ventricle per minute o Q=HR×SV Stroke Volume  Determinant of cardiorespiratory endurance capacity at maximal rates of work  Increases with increasing rates of work up to intensities of 40% to 60% of max or higher  May continue to increase up through maximal exercise intensity, generally in highly trained athletes  Magnitude of changes in SV depends on position of body during exercise Stroke volume during exercise  Frank starling mechanism-more blood in the ventricle causes it to stretch more and contract with more force  Increased ventricular contractility (without end-diastolic volume increases)  Decreased total peripheral resistance due to increased vasodilation of blood vessels to active muscles. Ventricular contractility  Increased contractility results in higher stroke volume o Circulating epinephrine and nor epinephrine o Direct sympathetic stimulation of heart Frank starling  Degree of stretching or lengthening of myocardial fibers during filling  Frank-starling law of the heart: increased filling leads to greater ejection  Result: increase in stroke volume and cardiac output Cardiovascular drift  Results from o Dehydration o Reduction in SV  HR drifts upward to maintain same cardiac output Cardiac output distribution  Blood flows to tissues in proportion to their metabolic activity  BUT: what if blood flow increases everywhere? What happens to BP? Cardiac output and oxygen transport  Rest cardiac output =5L  O2 transport= 1.34 ml/gm/Hb × 15gm/100ml o 20ml O2/100ml blood  1000ml O2 Exercise  Max Q averages 16L min (untrained)  O2 transport= 20ml/100ml blood  Result o 3200mL O2  Training enables Q to increase up to 40L min, increasing O2 transport up to 8000mL Close association between max Q and VO2 max  An almost proportionate in max Q accompanies increases in VO2 max with training  Slope is approximately 5-6L cardiac output/L of O2 consumption Av-O2 difference during exercise  20mL O2 dL arterial blood  5-15 ml O2 dL venous blood  Up to a threefold increase in O2 extraction (via increased BF) Factors that regulate cardiac output  Cardiac output= cardiac rate × stroke volume Thermal regulation in the heat and cold  Dissipate heat  Blood flow to skin  Sweating to cool  Cardiovascular function  Blood flow to muscle  Cardiac output and stroke volume Thermal balance  Core temperature: maintain at 37 or within narrow range  Heat transfer: mechanisms to LOSE heat, radiation, conduction, convection, evaporation  Heat absorption: gain heat, BMR, muscular activity, hormones, thermic effect of food, postural changes, environment  Heat loss/gain: net result Hypothalamic regulation of temperature  Hypothalamus—central coordinating center for temperature regulation  Activation of body’s heat-regulating mechanisms o Thermal receptors in the skin o Changes in blood temperature perfusing the hypothalamus Thermoregulation in cold stress: heat conservation and heat production  Vascular adjustments o Cutaneous cold receptors constrict peripheral blood vessels  Muscular activity o Shivering  Hormonal output o Epinephrine (short term) o Thyroxine (long term) Thermoregulation in heat stress: heat loss  Radiation o Electromagnetic heat waves  Conduction o Direct contact between molecules  Convection o Movement of adjacent air or water molecules  Evaporation o Vaporizing water  Evaporative heat loss at high ambient temperatures  Heat loss in high humidity Interaction of heat-dissipating mechanisms  Circulation o Blood redirected to skin to dissipate heat  Evaporation o Sweating begins with several seconds of the start of vigorous exercise o Cooled blood returns to core to absorb additional heat  Hormonal adjustments o Vasopressin and alderstone help maintain blood volume (controls reabsorption) Effects of clothing on thermoregulation  Clothing insulation (clo units) o Wind speed: does it block the wind? o Body movements: is it flexible? o Chimney effect-baggy clothes trap heat o Bellow effect-movement increases ventilation of air layers o Water vapor transfer: during activity o Permeation efficiency factor-clothes absorb sweat (e.g dryfit, wicking, etc Effects of clothing on thermoregulation  Cold-weather clothing o Layers trap air o Moisture properties  Warm-weather clothing o Light in colour o Moisture properties  Football uniforms-poor heat dissipation  Modern cycling helmet does not thwart heat dissipation Exercise in the heat  Circulatory adjustments o Vascular constriction and dilation o Maintenance or ‘DEFENDING’ of blood pressure  Core temperature during exercise o Temperature rises as intensity increases o More fit individuals generate more heat at the same percentage of VO2max but maintain a lower core temperature Summary of the effects of dehydration and concomitant hyperthermia, displaying the responses of endurance-trained cyclists during 120 min if exercise at 62-65%VO2 max in a 35 degree environment when they began exercise while euhydrated and become dehydrated by 4.9 % of body weight after 120 min if exercise. Data are not shown for another trial during which fluid was ingested to offset dehydration and all responses were remarkably stable. Metabolic consequences of exercise in the heat  Hot: HR higher, cardiac output lower, SV lower  Normal HR lower, CO higher, SV higher Water loss in the heat: dehydration  Magnitude of fluid loss o The more prolonged or intense the exercise, the greater the loss.  Significant consequences o Dehydration may threaten health o Physiologic and performance decrements occur o Decrease in total body water o Occurs at a faster rate during exercise in hot and/or humid environments o Sweat rates can to 2-3 L/Hr o Deleterious effects of dehydration on exercise occur with as little as fluid loss equal to 2% body weight.  For a 70kg male; 70×0.02=1.4kg~1.4L o This can occur with as little as 30 min of exercise. Maintaining Fluid Balance: Rehydration and Hyperhydration  A benefit from exogenous glycerol? o When consumed with 1 to 2 L of water, glycerol facilities water absorption and extracellular fluid retention.  Adequacy of rehydration o Thirst is a poor indicator o Use changes in body mass as guide Electrolyte replacement  Added sodium  Combining solid food with plain water  Drink 25-50% more fluid than that lost via sweating Maintaining hydration  400-600 ml of water 2h before exercise  Water losses due to sweating during exercise should ideally be replaced at a rate equal to the sweat rate but this is often not desired  Frequent (every 15-20 min) consumption of moderate (150ml) to large (350)ml volumes of fluid is advised.  Carbohydrates should be ingested throughout exercise at a rate of 30-60g/hr Whole-body precooling  Research shows mixed results o Cooling skin 5-6 degrees improving cycling performance for 30 minutes o Failed to improve triathalon or thermic responses to 90 minutes of soccer Factors that modify heat tolerance  Acclimatization o Physiologic changes that improve heat tolerance o Optimal acclimatization requires adequate rehydration  Training status o Increased sensitivity and capacity of sweating response o Plasma volume increases o Greater skin and GI blood flow o Larger volumes of more dilute sweat Advantage of acclimatization  HR and rectal temp stays lower Acclimatization to heat  Plasma volume expansion (10-12%) o Increased BV o Increased venous return o Increased CO o Decreased submaximal HR o Sustained sweat response o Increased capacity for evaporative cooling  Earlier onset of sweating o Improved evaporative cooling  Osmolarity of sweat o Electrolyte conservation (mainly Na)  Muscle glycogenolysis o Decreased likelihood for muscle fatigue Training status and sweat  Trained males and females have less Na (mmol/L) then untrained females have more  Trained males and females have less Cl (mmol/L) then untrained females have more  K is the same trained or untrained Factors that modify heat tolerance  Age o Age-related differences in heat tolerance o Some age-related factors affect thermoregulatory dynamics  Children o Lower sweating rate and higher core temp o Sweat is more concentrated Factors that modify heat tolerance  Gender o When studies control for fitness level and relative intensity, no gender differences are observed  Sweat-women o Sweat less prolifically then men despite having more heat-activated sweat glands o Sweat smaller volumes o Begin sweating at higher skin and core temp  Compared to men, women tend to cool faster.  Menstrual cycle alters skin blood flow and sweating response  Body fat insulates body, and adds to metabolic cost of weight-bearing activities. Complications from excessive heat stress  Heat cramps o Imbalances in fluids and electrolytes  Heat exhaustion o Blood pools in periphery o Core temp rises  Heat stroke o Exertional heat stroke  Heat from exercise  Hot, humid environment o Sign and symptoms o Stop sweating, core temp > 105 F, altered mental status o Requires immediate medical attention o Oral temperature unreliable Overall consequences of dehydration  Increases o Core temp o HR o Aterio-ventricular difference o Catecholamines o Blood lactate o VO2  Decreases o Plasma volume o Venous return o Stroke volume o Cardiac output o Skin blood flow o Exercise tolerance o Sweat rate o Evaporative cooling Exercise in the cold  Body fat, exercise, cold stress o Fat insulates o Higher body fat=greater cold tolerance  Children and cold stress o Large ratio of body surface area to mass o Don’t tolerate cold well o More effective peripheral vasoconstriction and increased energy metabolism How to conserve heat?  Shivering-rapid involuntary cycle of contraction and relaxation of muscles  Non-shivering thermogenesis- stimulation of metabolism  Peripheral vasoconstriction-reduces blood flow to skin Factors that affect body heat loss  Body size and composition  Air temperature  Wind chill  Water immersion Body weight, height, surface area, and surface area/mass ratios for an average sized adult and child  Adult 85 (kg), 103 (cm) 210 (cm2) 2.47 area/mass person ratio  Child 25, 100,79,3.16 Risk of cold exposure and the cold  Muscles weaken and fatigue occurs more rapidly: neural transmissions slow, vasoconstriction limits blood flow  Ability to regulate body temp is lost if T-body drops below 34.5 C (94.1 F)  FFA mobilization is impaired due to vasoconstriction of subcutaneous blood vessels  Hypothermia causes heart rate to drop, which further reduces cardiac output  Vasoconstriction in the skin reduces blood flow to skin, eventually causing frostbite  Approximate Thresholds: o Risk of frostbite in prolonged exposure (30 minutes) at -28 o Frostbite possible in 10 minutes at -40 (shorter time if sustained wind greater than 50 km/h o Frostbite possible in 5 minutes at -48 (shorter time if sustained wind greater than 50km/h) o Frostbite possible in 2 minutes or less at -55 Stages of hypothermia  Impending hypothermia: o Core temperature decreases to 36 C o The skin may become pale, numb and waxy o Minimal shivering/tenseness o Fatigue and signs of weakness begin to show  Mild hypothermia o Core temperature 35-34 o Uncontrolled, intense shivering begins o Alert and able to help self, however movements become less coordinated  Moderate hypothermia o Core temp- 33 o Shivering slows or stops, muscles begin to stiffen o Mental confusion and apathy sets in o Speech slows, slurs, breathing slows, and drowsiness and strange behavior may occur  Severe hypothermia o Core temp below 31 o Skin is cold, may be blue/gray color, eyes may be dilated o Victim is very weak, lack of coordination, slurred speech, exhausted, may appear to be drunk o Gradual loss of consciousness o There may me little or no apparent breathing, victim may be very rigid, unconscious, and may appear dead Cardiac and vascular adaptations to training the athlete’s heart  Historical perspectives o Large hearts in wold animals (early 1800’s) o 1892: observations in cross country skiers- first use of term ‘ athlete’s heart o Enhanced performance: risk of early death o Current use of echo, MRI for quantification of mass  The athletes heart o Long term training associated with incr4eased LV mass  Enlarged LV cavity size  Enlarged wall thickness (eccentric hypertrophy) o Typically modest in nature- ‘high-normal’ range o Largest dimensions seen in endurance athletes, smallest with static/ resistance work  Physiological vs. Pathological hypertrophy o Similarities  Similar loading stimuli  Myofibular arrangement (serial/parallel development) o Key differences  Modest remodelling vs. pronounced  Capillarization and mitochondrial volume  Systolic AND diastolic function  Regression  Exercise and cardiac remodeling o Growth factors from pressure and stretch-based stimuli o Increased mRNA for new myosin o Stretch channel o Tension-based growth factors  Ventricular hypertrophy o Pressure overload  weight lifting  hypertension  concentric growth (cells added in parallel)  Increased wall thickness  Pressure development with heavy resistance (weight-lifting) exercise o Peak blood pressures in excess of 300-400 o Highest: 480/350 o Resolution within 10s after  Ventricular hypertrophy o Volume overload  Endurance exercise  Eccentric growth (cells added in series)  Increased ventricular volume  Diagnostic dilemma: physiology vs. pathology o 27/145 (19%): marked repolarization abnormalities o 11/27 had t-wave inversion, with increased precordial R or S waves +/- deep Q waves…...HCM? o Only 1 basketball player had evidence of HCM  Coronary vascular adaptations o Epicardial arteries enlarged o Enhanced vasodilatory capacity (increased Nitric oxide bioavailability) o Increased capillarity but commensurate with myocardial growth  Vascular remodeling: Periphery o Hypothesized changes in artery function and structure (remodeling) in response to inactivity and exercise training in humans. Studies performed in both animals and humans suggest that rapid changes occur in artery function, including nitric oxide bioavailability, in response to exercise training and that the changed are superseded by arterial remodeling and normalization of function. Physical inactivity is associated with rapid changed in arterial diameter, with structural remodeling occurring within weeks of, for example, spinal cord injury. There is little function and structure occurs rapidly in response to activity and inactivity.  Inactivity and vascular remodeling o It works both ways:  Vascular remodeling responds to the stimulus or lack of  The vasculature is responsive is demanded of the circulatory system  So, what does exercise training do? o Increases luminal area (makes the vessels larger) o Reduces wall thickness o Increases the bioavailability of nitric oxide for vasodilation o Increases capillary growth o Reduces the vasoconstrictor tone Exercise and Altitude Learning Objectives o Why it’s hard to breath at high altitude: PO2, altitude and the O2 dissociation curve o How we adapt (and fail to adapt) at altitude o Effects of altitude on performance effects of ‘altitude training’ Altitude o Atmosphere pressure o Decreases at higher altitude o Partial pressure o Same percentages of O2, CO2, and N2 in the air o Lower partial pressure of O2, CO2 and N2 o Hypoxia: low PO2 (altitude) o Normexia: normal PO2 (sea level) o Hyeroxia high PO2 (below sea level) Highest human habitation o Aucanquilcha Volcano (North Chile) o Sulphur mine o Miners work in the sulphur mine @ 19,000 ft (5800) o Prefer to live at 14,000 (4300) o Travel daily to work o Upper limit for permanent residence is 19690 Calculating the PO2 Sea-level: PO2= .209×760 = 150mmHg 3280m: PO2= .209 × 520 = 108.6 mmHg PO2 will determine Hb saturation the specific altitude will greatly affect saturation % of oxygen .209 × ambient pressure mmHg Basis of Lowered Aerobic Performance o Challenge: lower partial pressure of O2 (PO2) How high is high? o Intermediate altitude: o 1500-2800m (5000-8000 ft) o Altitude-related problems/ illness rare (mild headaches if any) High altitude: o 2800-4500m (8000-14000ft) o Sickness relates to specific altitude and rate of ascent Very high altitude o 4500-5500m (14000-18000ft) o Numerous climbs in NA, Europe, Africa Extreme altitude o Short duration exposure by expedition climbers Immediate responses to altitude exposure: overview o Each adjustment to a higher elevation proceeds gradually , and full acclimatization need appropriate time o Elevations > 2300 initiates rapid physiologic adjustments to compensate for “ thinnier air” and accompanying reduction in alveolar PO2, including o Increase in the respiratory drive to produce hyperventilation o Increase in blood flow during rest an submaximal exercise Cardiovascular response: o Resting systemic blood pressure increases in the early stages of altitude adaptation o Submaximal exercise heart rate and cardiac output can rise to 50% above sea level values, while the heart’s stroke volume remains unchanged o The increased submaximal exercise blood flow at altitude largely compensates for arterial desaturation o Plasma volume loss (hyperventilation) Catecholamine Response  Sympathoadrenal activity progressively increases over time (rest and exercise)  Support the increased blood pressure and heart rate, plus vascular resistance and increased carbohydrate use Early adaptation to altitude  Early days of altitude: o Hyperventilation via hypoxic drive o Decreased saturation level of oxygen leads to stimulation of peripheral chemoreceptors o Enhanced oxygen loading in the lungs o Over hours and days…  Hyperventilation blows off CO2  Decreases CO2 and increases partial pressure of oxygen  Increased pH decreased H trend for o Alkalosis (excess base) decreased CO2: leftward shift of Hbo2 curve o Acid-base balance disturbed o Hypoxic ventilator drive is important for successful immediate adaptation altitude o Continuing- 3-10 days o Alkalotic state leads to: (high pH)  Increased HCO3 (bicarbonate) excretion (within 48 hrs) to normalize blood pH  Rightward shift of HbO2 curve  Normalized HbO3 curve  Hyperventilation continues as long as hypoxemia exists  HCO3 reserves challenged Longer-term adaptations (2-3 weeks+)  Continued hyperventilation (reduced)  Decreased plasma volume (fluid loss)  Increased RBC number & Hb within 2-days, notable after 5-10 days, effective after > 14-21 days) Polycythemia:  1% per day...can increase O2 carrying capacity up to 20%  Hypoxia  erythropoietin increased RBC from bone marrow increase hematocrit O2 carrying capacity ^ 2,3 DPG (via hypoxia).. a by-product of RBC glycolysis.. binds Hb, decreases O2 affinity..shifts O2 disssociation curve to right (helps unload O2) Blood Adaptations continued…  Increase in RBC’s via increased erythropoietin  Combined effects of blood volume expansion greatly increases O2 carrying capacity  Peruvian Residents @ 4500m: hematocrit (concentration of RBC’s in the blood- normally 40-w 45-m) = 65%  6 weeks exposure of similar altitude in sea-level dwellers: hematocrit increased 59%  Similar increases in hemoglobin observed Chronic Exposure to Altitude: Acclimatization  Cardiovascular Adaptations o No gains in VO2 max o Cardiac output reduces by 20-25%: reduced stroke volume o HR remains elevated Muscular Adaptations  Increased capillary, density and mitochondria, and lower fiber areas increase oxygen extraction  Reason for increased extraction with acclimatization is unclear- lack of chronic muscle biopsy data Effect of Altitude on VO2max  Decreases become noticeable (small) at about 560m  Decreases as altitude increases o Rate of decrease 7-9% per 1000m  Up to moderate altitudes (4000m) o Decreased VO2max due to decreased arterial PO2  At higher elevation o Rate of VO2 max reduction also due to fall in maximum cardiac output Percentage reduction in VO2max from sea-level value as a function of altitude  Male acclimatized endurance-trained athletes, with a mean > 60ml/kg/min o Reduction by 7.7% per 1000m altitude Effects of altitude on submaximal exercise  Elicits higher heart rate o Due to lower oxygen content of arterial blood  Requires higher ventilation o Due to reduction in number of O2 molecules per liter of air. Performance  Dependent on percentage contribution from aerobic energy (oxygen-dependent); little sprint effect but large endurance effect Cognition and related effects  Light sensitivity decreases  Visual acuity, postural stability, attention, cognition, pursuit tracking, reaction time, coding, recall Threshold for Acclimatization  2000-2300m (6500-7500 ft)  Acclimatization time: o About 2 weeks for 2300 o 1 week additional tine for each 610m (200ft) ruse (up to 4600)  Loss of acclimatization: 2-3 weeks after return to sea level Long-term adaptation natives of high altitude  Enlarged carotid chemoreceptors  Blunted chemoreceptor response to hypoxia (deprived of adequate oxygen supply)  Increase # and size of alveoli and capillary bed: why?  Increased skeletal muscle capillarity and myoglobin: why? Training at altitude  Minimum acclimatization process takes 4-6 weeks  Endurance performance at sea-level must occur within 48 hrs  Optimal elevation from traing 3000m (10000ft)- minimum is 1500m  Initial training intensity is lower: gradual increase over 14 days  End results: debated and not conclusive o Reduced training intensity o Psychological disruption o Timing o Delayed normalizing of cardiovascular function  Not effective for anaerobic events requiring high buffering capacity  Effectiveness of training at altitude on VO2 max varies o Due to degree of saturation of hemoglobin o May be due to training state before arriving at altitude  Some athletes have higher VO2 max upon return to low altitude, while others do not o Could be due to “de
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