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Kinesiology 2230A/B
Glen Belfry

Ventilation Notes Inspiration – external intercostal muscles move ribs and sternum, diaphragm contracts towards the abdomen - Boyle’s law PV=nRT, diaphragm pulls down, increasing volume of lungs resulting in decrease in intrapulmonic pressure and intrapleural pressure, Expiration – passive process, relaxation of inspiratory muscles + elastic recoil of lung tissue - Elastic recoil nature of lungs cause increased intrapulmonic and intrapleural pressure and a subsequent decrease in volume - Forced breathing – active process, internal intercostal muscles pull ribs down V E(pulmonary ventilation) – f x V ,Tfrequency of breathing and the depth of the breath, actual movement of air in and out of the lungs V A air entering perfused alveoli (alveolar volume), takes place in gas exchange V D dead space, non-perfuse alveoli + respiratory passages, no gas exchange V A(V TV )D = V EV D - Shallow breathing yields 0 alveolar volume b/c dead space equates to pulmonary ventilation Typical resting values: VT = 500 ml VD = 150/breath F = 12-15 breaths/min Static lung volumes – vital capacity (max amount of air exchanged in one breath), residual volume (amount of air left after maximal expiration), total lung volume = VC + RV\ Bird respiration: 1. Inspiration 1 – air moves to air posterior sacs, some passes through lungs 2. Expiration 1 – air moves from air sacs through respiration 3. Inspiration 2 – air moves into anterior sacs, fresh air moves into posterior sacs 4. Expiration 2 – air is expired from anterior sacs, fresh air moves through respiration This process allows for one time diffusion of air. This is more efficient than human lungs because once we inspire, the air in our lungs have a lower PO2 and upon expiration, there is less diffusion of oxygen simply because there is less oxygen in the intrapulmonary air. Pulmonary diffusion – 2 major functions (replenish oxygen supply + remove carbon dioxide) Dalton’s law – total pressure = sum of partial pressures (alveolar pressure = PO2 + PCO2 + PH2O + PN2) Oxygen exchange – PO2 inspired is 105 mmHg, PO2 in deoxygenated blood is 40 mmHg, by the time blood reaches venous end of pulmonary circulation, PO2 is 105 mmHg and fully oxygenated, blood returns to systemic circulation at 100 mmHg, losing 2% due to oxygen demands of lung tissue Factors affecting exchange – partial pressure gradient, surface area for diffusion and diffusion path length (Fick’s equation – rate of diffusion is proportional to surface area and inversely proportional to thickness of membrane) and hemoglobin/myoglobin conc. Gas transport by blood – most O2 carried by Hb (1.34 ml O2/g), 14-18 g Hb/100ml in males and 12-16 Hb/100 ml in females, 201 and 187 mlO2/L EPO – glycoprotein hormone regulates RBC production Oxygen/hemoglobin dissociation curve – buffering effect of Hb where any modest changes of altitude until about 60 mmHg will not result in significant change in saturation, same effect is seen in Mb, Mb has high oxygen binding below 40 mmHg b/c Hb is offloading most oxygen and muscle still requires a source of oxygen - Normal arterial blood is at 100 mHg, normal venous blood is at 40 mmHg, venous blood during exercise is at around 8 mmHg - Venous blood during exercise is devoid of saturated Hb, but there is still Mb Altitude + gas expansion – increases in altitude result in lower pressure and larger gas expansion, same percentage of oxygen, but air is not as packed O2 saturation at altitude – due to buffering capacity of Hb, altitude effects are blunted until it hits threshold and there is a sharp decrease in slope Respiratory changes at altitude – ventilation changes due to increases in gas volume causing decrease in pCO2 ▯ increase pH - Note: this is at threshold Oxygen-Hb dissociation curve and Bohr effect – if blood becomes more acidic, curve is shifted to the right (exercise ▯ increase CO2 ▯ increase blood acidity ▯ increased oxygen offload), this is called the Bohr effect, pH in lungs is high due to high CO2 levels, right shift of Hb curve makes it easier to load oxygen, increased blood temperature also shifts curve to the right Carbon dioxide transport – metabolic vs. non-metabolic (carbonic anhydrase), carbon dioxide and H2O combine to form carbonic acid which is highly unstable and is broken down by carbonic anhydrase, the H triggers the Bohr Effect in Hb, CO2 does bind with Hb, but not in heme group, thus it does not compete with oxygen, Hb binds CO2 much more readily when deoxygenated (Haldane effect) Buffer – ventilatory + kidneys (phosphate buffers) Ventilatory control – respiratory centres, peripheral input, cerebral (motor) cortex, originates in medulla of brainstem Respiratory centers – activity of inspiratory neurons in medial portion of the medulla which activate diaphragm and intercostal muscles and can inhibit expiratory neurons Neural Control – stretch receptors of lung can be overridden, as intensity of exercise increases, intercostal muscles are used in exhalation. Also cortex can override control when voluntary breathing is required. Chemical control – peripheral chemoreceptors in the aortic arch and carotid artery will detect PO2, PCO2, pH, central chemoreceptors only detect PO2 and pH, ventilation is mainly sensitive to PCO2, ventilatory responses are really only seen once PO2 drops below 60 At rest, when arterial PCO2 increases, there is an immediate increase in ventilation Respiratory control is also affected by lung stretch receptors and active muscles. Once active muscles are contracting, there is immediate increase in ventilation. Once lungs are stretched, there is immediate expiration, but this can be overridden. Estimating the lactate threshold – decrease in ratio is caused by increasing oxygen consumption while increase in ratio indicates that the need for oxygen is so great that ventilation increases. The lactate threshold is the point where VE/VO2 increases proportionally greater than the decrease of VE/VCO2. This means that the increase in ventilation to remove CO2 is disproportionate to the body’s need for O2. Ventilation increases due to increased levels of CO2. This increase in ventilation is shown as disproportionate increase in VE/VO2 when compared to VE/VCO2 because CO2 production is much higher than O2 consumption. The bends – increases in pressure results in an increase in PN2 which in high concentrations, impairs nerve conduction leading to hallucinations, when resurfacing, scuba divers need to ascend in stages in order for tissue to readjust and prevent nitrogen gas bubbling (the bends) As temperature decreases, vapor pressure decreases, hence why you can see your breath in cold temperatures, the air simply lacks the ability to hold moisture As work rate increases, there is an increase in production of CO2 and actively moving muscle leading to increased ventilation. Increased ventilation results in increased levels of O2 and increase clearance of CO2. At the same time, bicarbonate is broken down by carbonic anhydrase to release H2O and CO2. Lactic acid is being produced at high efforts, which is also buffered by bicarbonate, contributing to the decrease in HCO3. This coupled with increased levels of CO2 and breakdown of bicarbonate leads to decreased pH. Increased levels of H ion induce Bohr effect causing Hb to offload oxygen and subsequently bind H ions. This results in increased ratio of VE/VO2 which can be used to approximate the anaerobic threshold. Changes in ventilation are dependent on exercise level ▯ It is important to note that VE never approaches maximal voluntary ventilation and that VT never approaches VC As pulmonary ventilation increases, breathing frequency increases to the point where there
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