Chapter 6 Flashcards
What are the acute cardiovascular responses to aerobic exercise?
The cardiovascular system delivers oxygen and nutrients while removing metabolites and waste
products during aerobic exercise.
Cardiac Output (Q)
• The amount of blood pumped by the heart in liters per minute.
• Q = 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
Stroke Volume
• 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
• Venous return increased via:
➢ 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
▪ 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
Heart Rate
• Increased immediately before and at the beginning of exercise
• HR increases linearly with exercise intensity
What are the acute oxygen uptake responses to aerobic exercise?
Oxygen uptake is the amount of oxygen consumed by body tissues.
• Increases during acute bout of aerobic exercise
• Proportional to the mass of muscle used
• 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- used to calculate oxygen uptake
▪ VO2 = Q x a-vO2 difference
▪ a-vO2 =Arteriovenous difference - the difference in O2 content of
arterial and venous blood
▪ I.E. hr = 72BPM, Stroke volume = 65ml blood/beat, a-vO2 = 6, weight =
80kg
▪ VO2 = 281 mLO2/min / 80kg
▪ VO2 =3.5 mlkg
What are the acute blood pressure responses to aerobic exercise?
Blood Pressure
• 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 = 120mmHg/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
Control of Local Circulation
• 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 are the respiratory responses to aerobic exercise?
Significant increases in O2 to tissues, CO2 production, and minute ventilation (volume of air
breathed per minute) occur following the beginning of 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 0.4 and 1.0 L to upwards of 3 L or greater
• Low-moderate exercise increases O2 uptake and CO2 removal in proportion to
increased ventilation
• Ventilatory equivalent (ratio of minute ventilation to oxygen uptake)
➢ Ranges from 20-25 L 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
• Alveoli - functional unit of pulmonary system where gas exchange occurs
• Anatomical dead space - 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
➢ Decreases proportionally to tidal volume during deep breathing
▪ Tidal volume increases more than anatomical dead space
• Physiological dead space
➢ Alveoli with poor blood flow, ventilation, or other problems
➢ Lung diseases can increase physiological dead space
• Overall effects
➢ Larger amounts of O2 diffusion from capillaries to tissues
➢ Increased CO2 from blood to alveoli
➢ Increased minute ventilation to maintain gas concentrations
• Gas Responses
➢ Increased diffusion of O2 and CO2 due to a decrease in partial pressure of O2
(40mmHg - 3mmHg) in interstitial fluid and increase in CO2 (46mmHg -
90mmHg) partial pressure
What are the mechanisms of blood transport of gases and metabolic byproducts?
Oxygen
• 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
• The oxygen capacity of 100mL blood around 20mL in men and slightly less in women
Carbon dioxide
• 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)
• Most CO2 removed via bicarbonate (HCO3-)
• Reversible reaction:
1. Formation of carbonic acid with the water in red blood cells
➢ Sped up by carbonic anhydrase
2. Acid broken into H+ and bicarbonate
3. H
+
combines with hemoglobin due to its buffering properties
➢ Maintains blood pH
4. Bicarbonate diffuses to plasma while chloride diffuses into red
blood cells
• Lactic acid begins to accumulate when O2 availability cannot meet exercise demands
What chronic adaptations occur from aerobic exercise?
Cardiovascular Adaptations
• 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
Increasing maximal oxygen uptake is 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
Respiratory Adaptations
• 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
Neural Adaptations
• 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
Muscular Adaptations
• 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 IIa muscle fibers
➢ Reduced glycolytic enzymes and some size reduction will occur
➢ Conversion of Type IIx to Type IIa fibers
➢ No evidence of type II to type I transitions
• Some limited hypertrophy of Type I 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
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 optimum results
Endocrine Adaptations
• Increases in 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
List the external and individual factors that influence aerobic adaptations.
Describe the main considerations for each.
Altitude
• Elevations above 3,900 ft (1,200 m) 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 increased 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
Hyperoxic Breathing
• 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% capacity
Smoking
• Decreases performance via:
➢ Increased airway resistance from nicotine related bronchiole constriction
➢ Paralysis of cilia on the respiratory surfaces
➢ Carbon monoxide impairs the oxygen transport capacity of hemoglobin
▪ CO has a higher affinity for hemoglobin the O2
Blood Doping
• Process of artificially increasing red blood cell mass
• Accomplished through:
➢ the infusion of blood cells from the individual or another person
➢ The 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
• Health Risks
➢ Increased hematocrit increases the risks 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
Genetic Potential
• Limit of physical adaptations to exercise largely determined by genetic potential
➢ Gains harder to achieve as athletes get closer to the genetic potential
➢ Small performance differences in elite athletes determine huge variations in
victory
▪ Careful program design crucial to elite athletes
Age and Sex
• Maximal aerobic power decreases with age
• Women typically have 73%-85% of the values of 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
List the main phases and characteristics of each phase of overtraining. What is
the general cause of overtraining?
Overtraining (OT)
• A continuum of responses to intensified training without proper recovery
1. Functional overreaching (FOR)
• 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
2. Nonfunctional overreaching (NFOR)
• 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
3. Overtraining Syndrome (OTS)
• Causes significant drop in performance
• Altered nervous system and immune function
• Requires months to return to baseline
What are the biological responses that occur during aerobic overtraining?
Cardiovascular Responses 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
Biochemical Responses to Overtraining
• High level of creatine kinase
• Decrease or no change in lactate concentrations increase
• Blood lipids and lipoproteins unaffected
• Decreased muscle glycogen content
➢ Often diet-related
➢ May result in the lowered lactate response
Endocrine Responses to Overtraining
• Lowered total testosterone levels in men
• Decreased testosterone-cortisol levels
➢ Associated with a 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
• Decreased basal dopamine levels
• Decreased dopamine response to relative workloads
What are some strategies for preventing OTS?
Strategies for Preventing OTS
• 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
Discuss the process of aerobic detraining. What can coaches do to prevent
detraining?
Detraining • The partial or complete loss of training-induced adaptations in response to an 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 6% - 20% ▪ Result of: • Decreased blood volume • Decreased stroke volume • Decreased maximal cardiac output Preventing Detraining: • Proper exercise variation • Proper intensity • Maintenance programs • Active recovery
