Unit 3 KINE 326 Notes PDF
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California State University, San Marcos
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These are lecture notes on the mechanics of ventilation, including discussions on inspiration, expiration, and pulmonary ventilation. The notes cover lung volumes, lung capacities, and gas exchange.
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Unit 3 KINE 326 Notes Lecture 15 Muscles of Ventilation Inspiration ➔ Rest (diaphragm) ➔ Exercise (sternocleidomastoid, scalenes, external intercostals Expiration ➔ Rest (passive relaxation of diaphragm) ➔ Exercise (internal intercostals, external abdominal obliques, internal abdominal...
Unit 3 KINE 326 Notes Lecture 15 Muscles of Ventilation Inspiration ➔ Rest (diaphragm) ➔ Exercise (sternocleidomastoid, scalenes, external intercostals Expiration ➔ Rest (passive relaxation of diaphragm) ➔ Exercise (internal intercostals, external abdominal obliques, internal abdominal obliques, transverse abdominis, rectus abdominis) Mechanics of Ventilation ➔ Changes in pressure during inspiration and expiration create gradient for air flow in and out of lung Pulmonary Ventilation ➔ The amount of air moved in or out of the lungs per minute ➔ Product of tidal volume (Vt), rest 500 ml; breathing frequency (f) rest 15 breaths per minute ➔ Dead Space ventilation (Vd): unused ventilation, does not participate in gas exchange, anatomical dead space, conducting zone ➔ : volume of inspired gas that reaches respiratory zone Measuring Lung Volume ➔ Spirometry is the measurement technique used to measure lung volumes Lung Volumes ➔ Tidal Volume (TV): vol used inspired and expired per breath (men 600 ml women 500 ml) ➔ Inspiratory Reserve Volume (IRV): max inspiration at end of tidal inspiration (men 3000 ml women 1900 ml) ➔ Expiratory Reserve Volume (ERV): max expiration at end of tidal expiration (men 1200 ml women 800 ml) ➔ Residual Lung Volume (RLV): volume in lungs after maximal expiration (men 1200 ml women 1000 ml) Lung Capacities ➔ Total Lung Capacity (TLC): volume in lung after max inspiration (men 600 ml women 4200 ml) ➔ Forced Vital Capacity: max volume expired after max inspiration (men 4800 ml, 3200 ml) Effects of acute exercise on breathing frequency ➔ Breathing frequency increases with exercise Effects of acute exercise on lung volumes ➔ Tidal volume increases with exercise ➔ Decrease in both inspiratory and expiratory reserve volumes ➔ Inspiratory > expiratory Effects of exercise on ventilation ➔ Rest: 12 breaths/min, 0.5 tidal volume L/breath, pulmonary ventilation 6 L/min ➔ Moderate Exercise: 30 breaths/min, 2.5 tidal volume, 75 pulmonary ventilation ➔ Vigorous exercise: 50 breaths/min, 3.0 tidal volume, 150 pulmonary ventilation Lungs are over built Cross sectional and longitudinal studies ➔ Clanton et al. 1987 ➔ Cross sectional data (swimmers have larger lung volumes than control subjects) ➔ Longitudinal (swim training in “trained” subjects increases resting lung volumes) O2 and CO2 Diffusion ➔ Partial Pressure ◆ Fractional composition of gas x absolute pressure Absolute Pressure Barometric pressure) at sea level is 760 mmHg Air is made up of oxygen, nitrogen, and carbon dioxide O2 = 760 mmHg x.2093 =159 mmHg CO2= 760 mmHg x.0003 = 0.228 mmHg Fick’s Law of Diffusion ➔ O2 and CO2 will diffuse across tissue if a pressure gradient is achieved across the tissue according to Fick’s law of diffusion Lecture 16 ➔ Approximately 99% of the O2 is transported in the blood bound to hemoglobin (Hb) ➔ Oxyhemoglobin is O2 bound to Hb ➔ Deoxyhemoglobin is O2 not bound to Hb ➔ 280 million Hb molecules ➔ At rest Hb remains 75% saturated after perfusing skeletal muscle ➔ Every Hb will have oxygen bound to it ➔ PO2 decreases during exercise and more oxygen is released from Hb ➔ Resting Ph is about 7.4 ➔ Blood pH declines during heavy exercise, which results is a “rightward” shift on the curve (Bohr effect, favors “Offloading” of O2 to the tissues) ➔ Myoglobin O2 binding protein found in skeletal muscle; acts as site of O2 storage; Mb+O2 arrow MbO2 CO2 transport in Blood Dissolved in plasma (10%) Bound to Hb - carbaminohemoglobin (20%) Bicarbonate (70%): ○ CO2+H2O=H2CO3=H++HCO3- ○ Carbon dioxide and water being turned into bicarbonate and hydrogen ○ Catalyzed carbonic anhydrase ○ High PCO2 drives equation to right ○ Low PCO2 drives equation to left ○ Also important for buffering H+ Transport of CO2 into blood Carbonic anhydrase (catalyzes CO2 and H2o reaction to carbonic acid Carbonic acid dissociates to hydrogen ion and bicarbonate ion Hydrogen ion binds to hemoglobin Chloride Shift (Bicarbonate moves out of RBC and chloride moves in to RBC to maintain electrochemical balance electrochemical balance) Oxygen binds to hemoglobin and releases hydrogen ion Chloride leaves RBC and bicarbonate enters RBC Bicarbonate and hydrogen form and carbonic acid Carbonic acid dissociates to water and carbon dioxide Rest to work Transitions Initially, ventilation increases rapidly ○ Then a slower rise toward study state ○ Po2 and Pco2 are maintained Exercise in a hot environment During prolonged submaximal exercise: ○ Ventilation tends to drift upward ○ Little change in PCo2 ○ Higher ventilation not due to increased PCO2 Incremental Exercise Linear increase in ventilation ○ Up to 50-75% VO2 max Exponential increase beyond this point Ventilatory threshold (Tvent) ○ Inflection point where Ve increases exponentially ○ Thought to correspond to OBLA or lactic acid threshold Trained vs Untrained In trained runner ○ Decrease in arterial PO2 near exhaustion (exercise induced hypoxia) Elite male endurance athletes (40-50%) Elite female athletes (25-51%) Due to increased CO and decreased RBC transit time Ph maintained at a higher work rate Tvent occurs at a higher work rate Neural Input to the Respiratory Control Centers Efferent Input ○ Motor cortex ○ “Spill over” ○ Most important in the regulation of ventilation during exercise Afferent input ○ Skeletal muscle Muscle spindles, golgi tendon organ, joint pressure receptors H+ and potassium ○ Heart Right ventricle Pressure receptors Humoral Input to the respiratory control centers H ○ Located in medulla ○ PCO2 and H+ in cerebrospinal fluid H ○ Aortic bodies Arterial PCO2 and H+ Carotid bodies ○ Arterial PCO2, H+, potassium, and PO2 ○ More important than aortic bodies Facilitating Oxygen during exercise Lowers PO2 Lowers pH Increases temperature Rightward shift in graph Change in partial pressure from rest goes down from 40 to 5 mmHg Untrained ppl have lower ventilatory threshold versus trained individuals Lecture 17- Altitude Increased altitude leads to decrease in PO2 Mechanism ○ Reduction in barometric pressure with increased altitude ○ Relative percentage of O2 in air not affected by altitude Initial studied on the effects of altitude on human physiology were performed by early balloonists James Glaischer and Henry Coxwell 1862 8850 meters Coxwell brought balloon down by pulling rope with teeth to vent helium Symptoms ○ Blurred vision ○ Paralysis of limbs ○ Unable to speak ○ Loss of consciousness Sivel, Tissandier, Croce-Sinelli 8600 meters Only Tissander survived and regained consciousness at 6000 meters Symptoms ○ Loss of consciousness Aircraft Commercial ○ 10000 meters ○ BP 179 mmHg, PO2 38 mmHg ○ 30 seconds before unconscious Concorde ○ 18000 meters ○ BP 54 mmHg, PO2 11 mmHg ○ Unconscious immediately Payne Stweart 14000 meters BP 110 mmHg, PO2 23 mmHg Historical evidence that altitude may impact performance 37-32 BC: merchants describe the physical challenge of going over mountain passes in Afghanistan Greeks observe standing at top of Mount Olympus made them breathless Spanish conquistadors are unable to follow fleeing Inca’s into the mountains Pioneering work on the effects of altitude on performance 1966 sponsored by US olympic committee and NIH Buskirk and Faulkner set out to answer question of performance and altitude Determined VO2 max in elite endurance athletes at different altitude ○ Mexico City (2400 m) ○ Leadville (3100 m) ○ Nonoa (4000 m) Effects of altitude on VO2 max VO2 max decreases 11% every 1000m at altitudes greater than 1500 meters (5000 ft) Mexico City (VO2 max 12% decrease) Leadville (Vo2 max 20%) Nunoa (VO2 max 27%) Effects of Altitude on Performance Short term anaerobic performance ○ Lower PO2 at altitude should not have effect on performance O2 transport to skeletal muscle does not limit performance Lower air resistance may improve performance Long term aerobic performance Lower PO2 results in poorer aerobic performance since this type of exercise is dependent on O2 transport to skeletal muscle ○ Exception in 1968 olympics (Kip Keno born and lived at similar altitude to Mexico CIty) Up to moderate altitudes (4000m); rate of VO2 max reduction also due to fall in maximum cardiac output ○ Myocardial hypoxia = not enough O2 to heart Maximal oxygen consumption of high altitude natives Sea level natives ○ VO2 max at sea level 46-50 ml/kg/min High altitude natives ○ Vo2 max at altitude 46-50 ml/kg/min Similar VO2 maxes suggest that adaptations occur as a result of living at altitude Physiological Adaptations of living at altitude Barrel shaped chest Larger lungs Smaller in stature Ratio of lung volume to body size is high Larger hearts Increased capillary density Increased mitochondrial density Greater red blood cell content Increased hemoglobin ○ Erythropoietin (EPO) Influence of developmental adaptations on aerobic capacity at high altitude Frisancho et al 1973 Highland control had highest VO2 max Lowland migrants had high VO2 max as well but not as high Other groups had the lowest Results suggest ○ Complete physiological adaptations to high altitude occur only in individuals that spend developmental years at altitude ○ Age and time at altitude during developmental influence the completeness of physiological adaptations ○ In those recently arriving at altitude adaptations are less complete How was Mount Everest Climbed 1953 Tenzing Norgay and Edmund Hillary Success was due to: ○ Base camps at several different altitudes helped them acclimatize (increase RBC) ○ Use of supplemental O2 Climbed without oxygen in 1978 (Messener and Habeler) ○ Previously thought this would be impossible (Pugh) due to low PO2 ○ Actually PO2 at summit was higher High Vo2 maxes are not a critical component too summiting everest Average VO2 max =60 ml/kg/min Messengers VO2 max = 48 ml/kg/min Successful climbers have a great capacity for hyperventilation Drives down PCO2 and H+ in blood Allows more O2 to bind with hemoglobin at same PO2 Increase in altitude Leads to decrease in PO2 ○ Affects skeletal and cardiac muscle Myocardial hypoxia leading to decrease in CO Lecture 18-Thermoregulation (Heat) Temperature Homeostasis Resting core temperature 37 degrees celsius (98.6) Above 45 degrees celsius ○ May destroy proteins and enzymes and lead to death Below 34 degrees celsius ○ May cause slowed metabolism and arrhythmias Temperature homeostasis maintained by ○ Heat Production Voluntary ○ Exercise 70-80% energy expenditure appears as heat ATP Hydrolysis Involuntary ○ Shivering Increases heat production by -5x Non shivering thermogenesis (Increased metabolism via hormones ○ Thyroxine ○ Catecholamines Heat Loss Radiation ○ Transfer of heat via infrared rays Conduction ○ Heat loss due to contact with another surface Convection ○ Heat transferred to air or water Evaporation ○ Heat from skin converts water (sweat) to water vapor Requires vapor pressure gradient between skin and air Regulation of Body Temperature Anterior hypothalamus ○ Responds to increased core temperature by Sweating Increased skin blood flow Posterior hypothalamus ○ Responds to decreased core temperature by Shivering Decreased skin blood flow Nonshivering thermogenesis Heat production during incremental exercise As exercise increases: ○ Heat production increases Linear increase in body temperature ○ Core temperature proportional to active muscle mass Higher net heat loss ○ Lower convective and radiant heat loss (small role during exercise) ○ Higher evaporative heat loss (most important during exercise) Effects of ambient air temperature on heart production during exercise As ambient temperature increases during steady state exercise: ○ Heat production remains constant ○ Lower convective and radiant heat loss ○ Higher evaporative heat loss Exercise and relative humidity Heat index ○ Measure of body’s perception of how hot it feels Accounts for relative humidity and air temperature High relative humidity reduces evaporative heat loss due to less vapor pressure gradient between sweat and pressure ○ Lowers heat loss ○ Increases body temperature Exercise in a hot/humid environment Inability to lose heat due to less evaporative heat loss ○ Higher core temperature ○ Risk of hyperthermia and heat injury Higher sweat rate ○ May be as high as 4-5 L/hour ○ Risk of dehydration Impact of heat stress during exercise on submaximal VO2 No impact of heat stress on submaximal VO2 during exercise Impact of heat stress during exercise on cardiac output Heat stress and exercise ○ Decreased cardiac output ○ Increased Prevention of exercise related heat injuries Exercise during the coolest part of the day Minimize exercise intensity duration on hot/humid days Expose a maximal surface area of skin for evaporation Provide frequent rests/cool-down breaks with equipment removal Rest/cool-down breaks should be in the shade and offer circulating, cool air Avoid dehydration with frequent water breaks Prevention of dehydration during exercise Dehydration of 1-2% body weight can impair performance Guidelines ○ Hydrate prior to performance 400-800 ml fluid within three hours prior to exercise ○ Consume 150-300 ml fluid every 15-20 min ○ Ensure adequate rehydration Consume equivalent of 150% weight loss 1 kg body weight = 1.5 L fluid replacement ○ Monitor urine color Heat Acclimation: Requires exercise in hot environment Adaptations occur in 7-14 days ○ Increased plasma volume ○ Earlier onset of sweating ○ Higher sweat rate ○ Reduced sodium chloride loss in sweat ○ Reduced skin blood flow ○ Increased cellular heat shock proteins Lecture 19: Thermoregulation (Cold) Exercise in a cold environment Enhanced heat loss ○ Reduces chance of heat injury Hypothermia occurs when heat loss is greater than heat production ○ Loss of judgment and risk of further cold injury Less research than exercise in the heat ○ Majority of research done during cold water immersion Weller et al. 1997 Aim of the study was to establish the effects of a cold, wet, windy environment on the physiological responses to prolonged intermittent walking, when exercise periods were maintained at a low or high intensity Why were they interested in this? ○ Pugh’s hypothesized “cutoff” point Study Protocol 14 active men 360 minutes of intermittent walking ○ Low intensity (30% VO2 max) 5km/hr, 0% grade ○ High intensity (60% vo2 max) 6km/hr, 10% grade ○ Neutral environment 15 degrees celsius ○ Cold environment 5 degrees celsius, air=5 m/s, wet clothing Multiple subjects dropped out of study Environmental chambers Measurements Body fat Temperatures ○ Skin ○ Rectal Gas exchange ○ VO2 ○ VCO2 ○ RER Blood samples ○ Glucose, lactate, glycerol, plasma free fatty acids, Norepinephrine, Epinephrine, hematocrit Results (Skin temperature) Low Intensity ○ coldneutral (240-360 min) High Intensity ○ Norepinephrine Cold>neutral (final measurement) ○ Epinephrine cold=neutral Conclusion When intermittent higher intensity exercise is prolonged, several physiological response to exercise were influenced by the cold, wet, windy environment, although to a lesser degree than the lower intensity conditions During 60% VO2 max if clothing is inadequate, a cold, wet, and windy environment will influence physiological responses to exercise and potentially impair performance Limitations to Interpretation Activity level Gender Body composition Acclimation/location Lecture 20: Ergogenic Aids A substance or phenomenon that can improve athletic performance ○ Mechanical ○ Pharmacological ○ Physiological ○ Nutritional ○ Psychological Lecture will focus on legal ergogenic aids ○ Steroids ○ Blood doping Illegal Ergogenic Aids Steroids ○ Increase skeletal muscle hypertrophy Increase strength Blood doping ○ Increase RBC content Increase O2 delivery Both steroids and blood doping increase performance significantly Health risks are very high Creatine Monohydrate Supplementation #1 supplement purchased by college athletic programs Claims ○ Skeletal muscle hypertrophy ○ Strength ○ Anabolic performance Physiology of Creatine Monohydrate Rapid formation of ATP ○ PC (phosphocreatine) + ADP =ATP + creatine Impacts exercise of short duration ○ Less than 5 seconds in duration Results of Creatine Monohydrate 20g/day over 5 days increases intramuscular stores of PC ○ Improves performance in short duration (