Chapter 6 Shit Flashcards
What is cardiac output (Q)?
-amount of blood pumped by the heart in liters per minute.
-stroke volume x heart rate
-Increases rapidly during initial aerobic activity
-Followed by a gradual increase and plateau
-Resting level = 5L/min
-Can increase to a maximum of 20-22L/minute
How does stroke volume change during aerobic exercise or exercise in general?
-Rises during the onset of exercise
-Plateaus once oxygen uptake reaches 40-50% maximum
-Untrained stroke volume of college men - 100-120ml blood/beat
-Trained men = up to 150-160ml per beat
-Women = 25% less than men
-End=diastolic volume and catecholamine action determine stroke volume
How is venous return increased during exercise?
-Vasoconstriction (from sympathetic activation)
-Increased skeletal muscle pump
-Increased respiratory frequency and tidal volume
-Increased venous return results in more forceful heart contractions via the Frank-starling mechanism
What is Frank-starling mechanism?
-Increased end-diastolic volume stretches myocardial fibers resulting in more forceful contraction and increased systolic ejection
-Increased cardiac ejection characterized by increased ejection fraction - the fraction of the end-diastolic volume that is ejected during heart contraction
How is heart rate effected by aerobic exercise?
-Increased immediately before and at the beginning of exercise
-HR increases linearly with exercise intensity
-Increases during acute bout of aerobic exercise
-Proportional to the mass of muscle used
What is maximal oxygen uptake?
- greatest amount of O2 usable at the cellular level
-Correlates with degree of physical conditioning
-Related to heart and circulatory system’s ability to transport O2 and body tissue’s ability to use it
-Resting O2 uptake estimated - 3.5mL O2/kg bodyweight per minute - defined as one metabolic equivalent (MET)
-Normal VO2 max = 25-80ml/kg/minute
-Fick equation is used to determine oxygen uptake/beat
What is the fick equation?
- VO2=Qxa-VO2 difference
- a-VO2 = Arteriovenous difference - the difference in O2 content of arterial and venous blood
EXAMPLE- I.E. HR=72bpm, stroke volume = 65ml blood, a-VO2=6, weight = 80kg
VO2= 281mlO2/min/80KG
VO2=3.5 mlkg
What happens to blood pressure with aerobic exercise?
-Systolic blood pressure = pressure during contraction
-Combined with HR to estimate oxygen consumption of the heart
-Rate-pressure product = heart rate x systolic blood pressure
-Diastolic blood pressure = BP exerted on arterial walls when no blood being ejected
-Typical resting BP = 120 mmHg/80mmHg
-Maximal exercise can raise BP to 220-260mmHg/90mmHgdiastolic
-Mean arterial pressure - average pressure throughout cardiac cycle
-Typically, lower than average of systolic and diastolic
-MAP = ((systolic - diastolic)/3) + diastolic
What happens to the control of local circulation for aerobic exercise?
-Vasoconstriction and vasodilation are the primary mechanisms regulating blood flow
-Blood flow to active muscles increased via local dilation of arteries
-Restricted in other areas by constriction of arterioles
-At rest 15-20% of cardiac output to muscles
-During work up to 90% of cardiac output to muscles
What happens to the ventilation of your body during aerobic exercise?
-During exercise breathing increases from 12-15 breaths to 35-45 breaths per minute
-Tidal volume (volume of air inhaled and exhaled with each breath) increases from between .4 and 1.0 L to upwards of 3L or greater
-Low-moderate exercise increases O2 uptake and CO2 removal in proportion to increased ventilation
What is the ventilatory equivalent?
-ration of minute ventilation to oxygen uptake
-Ranges from 20-25 L of air/liter of O2 consumed
-Intense exercise increases the role of breathing frequency
-Minute ventilation rises disproportionately to oxygen uptake
-Parallels the rise in blood lactate
-Upwards of 35-40 L of air per liter of O2 during intense exercise
What is the alveoli?
- functional unit of pulmonary system where gas exchange occurs
What is anatomical dead space in the lungs?
- the area not functional for gas exchange (trachea, nose, mouth)
-150 mL in young adults
-Increases with age
-Area increases during deep breathing due to stretching of passages
-Increases similar to tidal volume during deep breathing
-Tidal volume increases more than anatomical dead space
What is physiological dead space in the lungs?
-Alveoli with poor blood flow, ventilation, or other problems
-Lung diseases can increase physiological dead space
What are the overall effects of aerobic exercise on the lungs?
-Larger amounts of O2 diffusion from capillaries to tissues
-Increased CO2 from blood to alveoli
-Increased minute ventilation to maintain gas concentrations
What are the gas responses to aerobic exercise?
Increased diffusion of O2 and CO2 due to decrease in partial pressure of O2 (40mmHg - 3,,Jg) in interstitial fluid and increase in CO2 (46mmHg - 90mmHg) partial pressure
What are the mechanisms of blood transport of gasses and metabolic by-product?
Oxygen and Carbon dioxide
How is oxygen involved in blood transport of gasses and metabolic by-product?
-Either dissolved in plasma or carried by hemoglobin
-Low fluid solubility of oxygen - less than 3ml oxygen per liter of plasma
Most oxygen is carried in hemoglobin
-15-16g hemoglobin per 100mL blood in men
-14g hemoglobin/100mL blood in women
-One gram of hemoglobin can carry 1.34mL of oxygen
-Oxygen capacity of 100mL blood around 20mL in men and slightly less in women
How is Carbon dioxide involved in blood transport of gasses and metabolic by-product?
-Removal more complex than oxygen delivery
-Diffuses across cell and then transported to lungs
-Around 5% of metabolic CO2 in plasma
-Some CO2 via hemoglobin (small amount)
-Some CO2 removed via bicarbonate (HCO3+)
-Reversible reaction
+Formation of carbonic acid with the water in red blood cells
+Sped up by carbonic anhydrase
+Acid broken into H+ and bicarbonate
+H+ combines with hemoglobin due to its buffering properties
+Maintains blood ph
+Bicarbonate diffuses to plasma while chloride diffuses into red blood cells
-Lactic acid begins to accumulate when O2 availability cannot meet exercise demands
What are the chronic cardiovascular adaptations to aerobic exercise?
-Increased maximal cardiac output
-Increased stroke volume
-Reduced resting and submaximal exercise heart rate
-Increase capillary density in muscle fibers
+Function of volume and intensity of training
+Decreases diffusion distance for oxygen and metabolic substrates
Why is increased maximal oxygen uptake crucial for aerobic performance?
-Enhanced cardiac output results in lowering discharge rate due to increased stroke volume
-Slow resting heart rate (bradycardia) seen in highly conditioned athletes (40-60bpm)
-Slow HR rise in response to standardized submaximal efforts a hallmark of aerobic endurance training
-Over 6-12 months of aerobic training results in large increase in cardiac output
-Increased left ventricle chamber volume and wall thickness increases stroke volume
What are Respiratory adaptations to aerobic training?
-Increased tidal volume with maximal exercise
-Increased breathing frequency with maximal exercise
-Reduced tidal volume and breath frequency at submaximal exercise
-Adaptations largely occur in the specific muscles being trained
What are neural adaptations to aerobic training?
-Increased efficiency
-Delayed fatigue in contractile mechanisms
-Rotations of neural activity between synergists and motor units within the muscle
-More efficient locomotion and lower energy expenditure
What are muscular adaptations to aerobic training?
-Increase in glycogen-sparing (decreased glycogen use)
-Increased fat-utilization within the muscle
+Raises the intensity at which OBLA occurs - up to 80-90% aerobic capacity
-Increased oxidative capacity of type 2a fibers
+Reduced glycolytic enzymes and some size reduction will occur
+Conversion of type 2x to type 2a fibers
+No evidence of type 2 to type 1 transitions
-Some limited hypertrophy of type 1 muscle fibers
-Increased mitochondrial density
+Mitochondria produce ATP from oxidation of glycogen and free fatty acids
+In combination with increased O2 availability more mitochondria increase the oxidative capacity of muscle tissue
-Increased myoglobin content - a protein that transports oxygen within the muscle cell
-Increased activity of the enzymes involved in aerobic metabolism
-Increase in glycogen and triglyceride stores
What are bone and connective tissue adaptations?
-Intense aerobic activities stimulate bone growth most successfully
-Must exceed the minimum threshold intensity and strain frequency for bone growth
-Must systematically increase to continually overload the bone
-Eventually bone growth may be limited due to the inability to continually overload via aerobic exercise
-High-intensity intervals provide greater osteogenic stimulus along with the benefits of aerobic exercise
-Ligaments, tendons, and cartilage grow stronger in proportion to the intensity
-Weight-bearing surfaces in joints show increased thickness in response
-Requires full range of motion for optimal results
What are endocrine adaptations to aerobic exercise?
-Increases circulating hormones
-Increased number of receptors
-Increased hormone turnover rate
-Increased cortisol secretion - increases catabolic activity
-Offset by increased IGF and testosterone
-Net protein synthesis does occur in endurance-trained athletes
-Likely associated with increased mitochondrial proteins, not contractile proteins
How does altitude influence adaptations to acute and chronic aerobic exercise?
-Elevations above 3900 ft (1200m) cause acute physiological adjustments to compensate for reduced partial pressure of oxygen
-Immediate adjustments:
+Increased pulmonary ventilation at rest and during exercise (hyperventilation)
+Caused by increasing breathing frequency
+Over time, tidal volume will increase
-Increased resting and submaximal cardiac output
+Up to 30-50% increase over sea level value
+Reflects increased need for blood flow
-Longer term adjustments (3-6 weeks)
+HR and cardiac output return to normal values (10-14 days after altitude exposure)
+Increased red blood cell concentration - 30-50% increase
+Increased hemoglobin formation - 5-15% increase
+Increased diffusing capacity of O2 through pulmonary membranes
+Increased renal excretion of HCO3+ to maintain acid-base balance
+Improved performance relative to initial altitude
++Generally still less aerobic performance than at sea level
How does hyperoxic breathing influence chronic and acute adaptations to aerobic exercise?
-Breathing oxygen-enriched gas mixtures
-Performed during rest periods or following exercise
-May positively affect some performance measures
-Effects not fully elucidated
-Sea level blood O2 saturation already near 98%
How does Smoking influence chronic and acute adaptations to aerobic exercise?
How does Blood doping influence chronic and acute adaptations to aerobic exercise?
-Process of artificially increasing the red blood cell mass
-Accomplished through
+Infusion of blood cells from the individual or another person
+Administration of erythropoietin (EPO) - stimulates red blood cell production
-Increases blood’s ability to carry oxygen
+More oxygen available for working muscles
-Up to 11% increased oxygen uptake from blood doping and/or EPO administration
-Decreases HR, blood lactate levels
-Increases pH levels
-Increases resistance to environmental impacts on performance
+Decreases acute effects of altitude
+Increases submaximal exercise tolerance in hot conditions
++Mostly applies to acclimatized athletes
How does Genetic potential influence chronic and acute adaptations to aerobic exercise?
-Limit of physical adaptations to exercise largely determined by genetic potential
-Gains harder to achieve as athletes get closer to genetic potential
-Small performance differences in elite athletes determine huge variations in victory
+Careful program design crucial to elite athletes
How does age and sex influence chronic and acute adaptations to aerobic exercise?
-Maximal aerobic power decreases with age
-Women typically have 73-85% of the values men
-Physical responses to endurance training similar in men and women
-Max aerobic power difference in men and women may be caused by
+Higher body fat
+Lower blood hemoglobin
+Larger heart size in men
What are health risks to blood doping?
-Increased hematocrit increases the risk of:
+Stroke
+Myocardial infarction
+Deep vein thrombosis
+Pulmonary embolism
-EPO use may also result in
+Increased arterial pressure
+Flu-like symptoms
+Increased plasma potassium levels
What is overtraining?
Continuum of responses to intensified training without proper recovery (3 stages)
What are the three stages of overtraining?
Functional overreaching
Nonfunctional overreaching
Overtraining syndrome
What is functional overreaching?
-Short period of intensified training
-Can be used strategically before competition for a performance boost
-Intense training followed by days or weeks of recovery and volume reduction is called tapering
-Leads to supercompensative improvement
What is nonfunctional overreaching?
-An extended period of excessive training beyond FOR
-Leads to significant drop in performance
-Requires weeks to months to return to baseline
-Leads to OTS when not managed
What is overtraining syndrome?
-Causes significant drop in performance
-Altered nervous system and immune function
-Requires months to return to baseline
What is the cardiovascular response to overtraining?
-Decreased heart rate variability with onset of OTS
+Indicates reduced parasympathetic input or excessive sympathetic input
-Lowered maximum heartrate from exercise
-Resting blood pressure generally unaffected
+Potential for increased diastolic pressure, no change in systolic pressure
What is the biochemical response to OTS?
-High level of creatine kinase
-Decreases or no change in lactate concentrations increase
-Blood lipids and lipoproteins unaffected
-Decreased muscle glycogen content
+Often diet-related
+May result in lowered lactate response
What is the endocrine response to overtraining?
-Lowered total testosterone levels in men
-Decreased testosterone-cortisol levels
+Associated with catabolic state
+30% decrease in ratio from baseline may indicate OTS
-Decreased growth hormone secretion from the pituitary gland
-Decreased nocturnal epinephrine - represent basal levels
-Increased epinephrine and norepinephrine responses to a given workload
+Maximum levels do not change
-Decrease basal dopamine levels
-Decreased dopamine response to relative workloads
What are some good general strategies to prevent overtraining?
-Follow proper nutritional guidelines
-Ensure sufficient sleep and recovery
-Provide variety in intensity and volume
-Keep accurate performance records to catch OTS early
-Ensure athlete has access to multidisciplinary health team
+Coach
+Physician
+Nutritionist
+Psychologist
What is detraining?
-The partial or complete loss of training-induced adaptations in response to insufficient training stimulus
-Aerobic adaptations most susceptible due to their enzymatic basis
-Exact cellular mechanisms unknown
-In highly trained athletes
+Short term - decrease in VO2 max between 4 and 14%
+Long term - decrease in VO2 max between 6 and 20%
++Result of
+++Decreased blood volume
+++Decreased stroke volume
+++Decreased maximal cardiac output
