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Advanced Physiology Week 3

by: Heather Glovach

Advanced Physiology Week 3 EXSC 440

Marketplace > University of Scranton > exercise science > EXSC 440 > Advanced Physiology Week 3
Heather Glovach
U of S

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Advanced Physiology of Sport and Exercise
Dr. Venezia
Class Notes
Cardiorespiratory system
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This 9 page Class Notes was uploaded by Heather Glovach on Tuesday September 13, 2016. The Class Notes belongs to EXSC 440 at University of Scranton taught by Dr. Venezia in Fall 2016. Since its upload, it has received 2 views. For similar materials see Advanced Physiology of Sport and Exercise in exercise science at University of Scranton.

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Date Created: 09/13/16
Cardiorespiratory Responses to Acute Exercise  Chapter 8  Overview   Cardiovascular responses to acute exercise o Cardiac responses o Vascular responses o Integration of the exercise response  Respiratory responses to acute exercise o Ventilation (normal exercise, irregularities) o Ventilation and energy metabolism o Respiratory limitations o Respiratory regulation of acid–base balance Cardiovascular Responses to Acute Exercise   Increases blood flow to working muscle o Main goal   Involves altered heart function, peripheral circulatory adaptations o Heart rate o Stroke volume o Cardiac output o Blood pressure o Blood flow o Blood Resting Heart Rate (RPR)   Normal ranges o Untrained RHR: 60 to 80 beats/min o Trained RHR: as low as 30 to 40 beats/min o Affected by neural tone, temperature, altitude  Anticipatory response: HR above RHR increases just before start of exercise o Vagal tone decreases  o Norepinephrine, epinephrine increases  FIGURE 8.1   VO2 max­ maximal capacity of the cardiorespiratory system to take in or consume  oxygen, deliver oxygen to muscles, and consume that oxygen o Consume = to utilize and turn into energy   How do we estimate HRmax o 220 – age in years = HRmax Increase in Exercise HR   Increases rate of spontaneous depolarization in SAN cells   Repolarization to a less negative membrane potential that is closer to threshold  o How does this occur? Think ANS   Increase in sympathetic, increases the Na+ influx  o What happens to K+ and Na+ conductance?   Reduced out flux of K+ reduces hyperpolarization   Na+, increase of slope depolarization  Steady State Heart Rate – Optimal Heart Rate at Specific Work Rate   Steady­state HR: point of plateau, optimal HR for meeting circulatory demands at a given submaximal intensity o If intensity increases , so does steady­state HR o Adjustment to new intensity takes 2 to 3 min  Steady­state HR basis for simple exercise tests that estimate aerobic fitness and HRmax FIGURE 8.2 Factors that Increase Stroke Volume   Increase Preload: end­diastolic ventricular stretch o Volume of blood returning to the heart o Ventricular distensibility o Increase Stretch (i.e., increase EDV) will increase contraction strength  Frank­Starling mechanism  Increase Contractility: inherent ventricle property o Increase in Norepinephrine or epinephrine will increase contractility o Independent of EDV (increase ejection fraction instead)  Decrease Afterload: aortic resistance (R) FIGURE 8.4  FIGURE 8.5  Frank Starling Length­Tension  Ca++ Tension Relationship Leftward Shift of Ca++ Sensitivity   The more the heart stretches the more sensitive the heart contractility is to Ca++  You also get more Ca++ release at longer sarcomere lengths   Contractility is independent on stretch  o The length tension relationship and the force produced is not referred to  contractility  Rate­Dependent Regulation of Myocardial Contraction (contractility)   Staircase Phenomena  o When HR is increases the Ca++ influx is greater than Ca++ efflux  o The faster the heart beats the less able the heart is able to get rid of the Ca++  IMPORTANT  For the cardiac pump to cycle faster, both contraction and relaxation must occur faster  Must maintain filling time as best as possible Beta Adrenergic Modulation of Myocardial Contraction (contractility)   Norepinephrine released from sympathetic nerves  Increases peak contractile force generation  Accelerates myocardial relaxation o B­adrenergic stimulation influences Ca+2 release, storage, and removal. Review: Stroke Volume Changes During Exercise   Increase Preload at lower intensities will increase SV o Increase Venous return will increase EDV and increase preload o Muscle and respiratory pumps, venous reserves  Increase in HR will decrease filling time will lead to a slight decrease in EDV and  decrease SV  Increase Contractility at higher intensities will increase SV  Decrease Afterload via vasodilation will increase SV Cardiac Output Graph  FIGURE 8.7A FIGURE 8.7B  FIGURE 8.7C The Relationship between Work Intensity, Heart Rate, and Stroke Volume   Max cardiac output is the limiting factor in VO2 max Adolph Fick Principal   VO2 is determined by cardiac output   Calculation of tissue O2consumption depends on blood flow, O2 extraction  •V•O2= Q•x (a­v­)O2 difference  •V•O2= HR x SV x (a­v­)O2 difference FIGURE 7.11  FIGURE 8.10  Cardiovascular Responses: Blood Pressure   During endurance exercise, mean arterial pressure (MAP) increases o Systolic BP increases proportional to exercise intensity  >200 mmHg at high intensities  Due to increased CO o Diastolic BP slight decrease or slight increase (at max exercise)  MAP = Q•x total peripheral resistance (TPR) o Q• increase , TPR decreases slightly  Rate­pressure product = HR x SBP o Related to myocardial oxygen uptake and myocardial blood flow   Resistance exercise leads to periodic large increases in MAP o Up to 480/350 mmHg o More common when using Valsalva maneuver  Increase of pressure in the thoracic cavity from holding breath   Most common in weight lifting Redistribution of Blood Flow during Exercise  How is blood flow Redistribution Accomplished?  Flow Mediated Vasodilation is governed by Endothelial Cells   The flow of blood exerts shear stress on the endothelial cells lining the vessel lumen o Shear Stress: proportional to the product of blood flow velocity and blood  viscosity, related inversely to internal vessel diameter  The endothelium responds by releasing autacoids (e.g., nitric oxide and metabolites of  arachidonic acid) that induce relaxation of surrounding smooth muscle cells  Shear stress may also hyperpolarize endothelial cells by activating K+ channels in the  plasma membrane.  o this electrical signal can be transmitted directly to smooth muscle through  myoendothelial gap junction channels  o In hyperpolarization of smooth muscle cells will inhibit VOCC and the fall in  Cardiovascular Drift   Associated with increase of core temperature and  dehydration  SV drifts decreases  o Skin blood flow increases  o Plasma volume decreases (sweating) o Venous return/preload decreases  HR drifts increases to compensate (Q•maintained) Competition for Blood Supply an ultra­Endurance Dilemma?   Exercise + other demands for blood flow = competition for limited Q•. Examples:  o Exercise (muscles) + eating (splanchnic blood flow) o Exercise (muscles) + heat (skin)  Multiple demands may decrease muscle blood flow  Ultra­endurance athletes must consume substantial carbohydrates Plasma Volume   Capillary fluid movement into and out of tissue o Hydrostatic pressure o Oncotic, osmotic pressures  Upright exercise leads to a decrease in plasma volume of the blood to the interstitial  space o Compromises exercise performance o Increase in MAP leads to an increase in capillary hydrostatic pressure o Metabolite buildup leads to an increase in tissue osmotic pressure o Sweating further decreases plasma volume What goes up and what does down with exercise (that causes sweating)? Blood  Pressure Tissue  Pressure  Osmotic  Pressure  in Tissue Cardiovascular Responses: Hemoconcentration  Decrease in Plasma volume leads to hemoconcentration o Fluid percent of blood decreases, cell percent of blood increases o Hematocrit increases up to 50% or beyond   Net effects o Red blood cell concentration increases  o Hemoglobin concentration increases  o O2­carrying capacity increases  Mechanisms Mediating the Large Cardiovascular Responses to exercise   Cardiovascular Control during Exercise   Central Command (THEORY)  o The volition to exercise can elicit cardiovascular responses o Feedforward system o Most likely through inhibition of parasympathetic tone o Mainly responsible for the initial tachycardia observed at the onset of exercise  Baroreflexes o Carotid sinus and aortic arch o Increase in pressure = increase in baroreceptor activity o Increase in parasympathetic and decrease in sympathetic activity  ??? o Is the baroreflex turned off during exercise?? o Actually it is reset to a higher pressure o Can influence HR through both sympathetic and parasympathetic mechanisms  Skeletal muscle afferents o Muscle Mechanoreceptors  May increase HR and arterial pressure during dynamic exercise  Muscle metaboreceptors o Sensitive to metabolites of exercising muscle o Increases CO, HR, Ventricular performance, peripheral vasoconstriction, central  blood volume mobilization o Most likely not very active during low to moderate intensity activity Integration of Control Systems   Rest to mild dynamic exercise 1. Parasympathetic withdrawal –central command 2. Resetting of arterial baroreflexor activation of mechanoreceptors  Increased exercise intensity 3. Increased sympathetic activity –central command, or skeletal muscle afferents, or  resetting of arterial baroreflextor a higher set point  Maximal exercise 4. All are likely highly activated to increase the delivery of oxygen to the active  muscles and to maintain arterial pressure in the face of large peripheral  vasodilation   Importantly, these 3 systems are not independent and most likely interact Optimal Response Strategy of Ventilation during Exercise   Alveolar ventilation must increase in proportion to metabolic requirement  o Can’t be too much (wasteful: Figure 8.14  Want ventilation to match cardiac output  Respiratory Responses: Ventilation and Energy Metabolism   Ventilation matches metabolic rate  Ventilatory equivalent for O2 o V•E/V•O2 o Index of how well control of breathing matched to body’s demand for oxygen  Ventilatory threshold o Point where L air breathed > L O2consumed o Associated with lactate threshold and increases PCO2 Figure 8.15   Ventilatory threshold as surrogate measure? o Excess lactic acid + sodium bicarbonate o Result: excess sodium lactate, H2O, CO2 o Lactic acid, CO2 accumulate simultaneously Figure 8.16  Refined to better estimate lactate threshold  Anaerobic threshold  Monitor both V•E/V•O2, V•E/V•CO2 Is Lactate Necessary for Ventilatory Threshold?  Yes but it is not the sole contributor  Respiratory Responses: Limitations to Performance  Ventilation normally not limiting factor o Respiratory muscles account for 10% of V•O2, 15% of Q•during heavy exercise o Respiratory muscles very fatigue resistant  Airway resistance and gas diffusion normally not limiting factors at sea level  Restrictive or obstructive respiratory disorders can be limiting  Exception: elite endurance­trained athletes exercising at high intensities o Ventilation may be limiting o Ventilation­perfusion mismatch o Exercise­induced arterial hypoxemia (EIAH) Respiratory Responses: Acid­Base Balance   Metabolic processes produce H+ leads to a decrease in pH  H+ + buffer leads to H­buffer  At rest, body slightly alkaline  o 7.1 to 7.4 o Higher pH = alkalosis  During exercise, body slightly acidic o 6.6 to 6.9 o Lower pH = acidosis 


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