Exercise Physiology Flashcards
Dynamic Exercise
Rhythmical movement of joint and contraction and relaxation of muscles
Swimming, running + cycling
Static Exercise
Maintained contraction for a length of time
Weight-lifting
Immediate Energy system
Fastest supply of ATP (creatine phosphate/phosphocreatine)
Rapid mobilisation of high energy phosphates
No oxygen
Anaerobic glycolysis
Can supply ATP when requirements high
Less efficient at ATP generation
No oxygen
Aerobic (oxidative metabolism)
Sustained supply of ATP
Uses O2
Immediate Energy MOA
Phosphocreatine in muscles at high conc.
Creatine phosphate provides store of high-potential phosphate to maintain contraction
Catalysed by creatine kinase
Non-oxidative Energy MOA
ATP generated from glucose via glycolytic pathway Less efficient Excess pyruvate --> lactate Lactic acid build up Drop in pH --> muscle fatigue
Oxidative Energy MOA
Require molecular O2 (oxidative phosphorylation)
VO2
Vol of oxygen consumed
Determined by Fick equation
Fick equation
VO2= Q x (CaO2-CvO2) Q= CO CaO2= arterial oxygen content CvO2= venous oxygen content
CaO2-CvO2
Arteriovenous oxygen difference
Vol of O2 consumed at ret
VO2= 250ml/min (70kg person)
3.6ml O2 consumed/min for each kg of body mass
VO2 max
Highest peak O2 uptake that an individual can obtain during dynamic exercise using large muscle groups during a few minutes performed under normal conditions at sea level
When is VO2 max reached
When O2 consumption remains at steady state despite an increase in workload
COPD/advanced heart disease VO2 max
10-20 ml O2/(min x kg)
Mildly active middle aged adults VO2 max
30-40ml O2/(min x kg)
Elite endurance athletes VO2 max
80-90ml O2/(min x kg)
Anaerobic threshold
Point where lactate begins to accumulate in bloodstream
Lactic acid metabolism
Produced faster than it can be metabolised –> metabolic acidosis –> exercise endurance reduced
2 Major consequences of increased exercise
Rise in CO
Redistribution of CO to active muscles
Exercise Begins…
Reduced parasympathetic activity
Increased sympathetic nerve activity
Increased HR + mobilisation of blood from great veins (vasoconstriction)
Exercise change in parameters
Increased venous return
Increased End-Diastolic Volume
Increased SV according to Starling’s Law
Positive inotropic response on heart
Change in end-diastolic vol. in exercise
Increase
Change in venous return during exercise
Increase
Positive inotropic response
Increase in rate + force of contraction
SV + HR changes with Increased O2 uptake
SV increases –> reaches maximum levels + plateaus at moderate exercise intensity
Heavy exercise- CO sustained by increasing HR
Heart remodelling
Heart adapts to sustained increases in BP by increasing muscle mass mostly by hypertrophy
Heart remodelling MOA
Physiologically (pregnancy/athletes)
Pathologically (hypertension)
Athlete’s heart
Increase muscle mass
Thickening LV wall + LV dilation
Normal cardiac function
Reversible
Failing heart
Increased muscle mass
Reduced cardiac function
Irreversible
Cell death + fibrosis
Endurance athlete
Runner, swimmer
Thickening LV wall
LV dilation
Strength athlete
Weightlifter
Thickening LV wall
Mild LV dilation
Combination athlete
Gross thickening LV wall
LV dilation
Hypertension on heart
LV wall thickening
No dilation early stages of disease
Dilated cardiomyopathy, HF
Thinning LV walls
Significant LV dilation
Hypertrophic cardiomyopathy
Gross thickening LV wall
No dilation/decrease in LV chamber size
Bradycardia in Athletes
Vol-induced cardiac hypertrophy increases resting end diastolic vol. and SC
Slower resting HR than untrained individuals
Distribution of CO at rest
20-25% resting CO to muscles (1L/min)
Distribution CO at max exercise
80-90% increased CO goes to muscle (22L/min)
Systemic regulation redistribution blood flow
Adrenergic receptors
Alpha, beta 1 and beta 2
Alpha adrenoreceptors
Constrict vessels in gut + cause vasoconstriction of veins
Beta 1 adrenoreceptors
Found in heart
Increase rate and force of myocardial contraction
Beta 2 adrenoreceptors
Relax smooth muscle (i.e. in bronchi) and increase ventilation and O2 uptake
Cause vasodilation of blood vessels (specifically ones supplying skeletal muscle)
Blood vessels themselves response to exercise
Endothelial factors + myogenic mechanisms
NO acts to relax smooth muscle cells –> dilation of blood vessels
Surrounding tissues (tissue factors)
Tissue factors Adenosine + inorganic phosphates CO2 H+ K+ Released from contracting muscles
Total Peripheral Resistance during exercise
Drops dramatically
Approx. 1/3rd of resting resistance
Decrease in TPR
Offset by increases in CO
Can lead to decrease in diastolic pressure
Systolic BP change in exercise
Increased force of ventricular contraction causes increase in systolic BP
Diastolic BP change in exercise
Diastolic BP remains relatively stable or even decreases
Resp system in exercise
Increased pulmonary minute ventilation + oxygen extraction in tissues
Pulmonary ventilation at rest
8l/min
Pulmonary ventilation heavy exercise
100l/min
Increased ventilation
Rise in resp. rate and tidal volume
Moderate work rates
Steady state ventilation is directly proportional to the work done as measured by O2 consumption
Severe exercise
Increase in ventilation is disproportionately large in relation to O2 uptake (limiting factor)
Uptake of O2 in lungs
pulmonary ventilation
Delivery of O2 to muscle
blood flow and O2 content
Extraction of O2 from vlood
delivery + PO2 gradient between blood/cell/mitochondria
O2 blood gases high exercise
Partial pressure O2 in arterial blood declines slightly
As O2 consumption rises, partial pressure of O2 in mixed venou blood also declines
CO2 blood gases high exercise
Partial pressure CO2 rises
Arteriovenous difference in oxygen content in exercise
Rises
As exercise increases, arteriovenous difference also increases
Increase gradient –> drives O2 uptake into cells
O2 delivery to tissues in exercise
Facilitated by decrease in Hb-O2 binding affinity
During exercise, Increased CO2, H+ and temp
Cause right shift in Hb binding curve
Reduced affinity of Hb for O2–> increases delivery in tissues
Post-exercise O2 consumption
Measurable increase in rate of O2 intake/uptake following strenuous activity
Oxygen debt
At beginning of exercise body builds up O2 debt
Measurable increase in rate of O2 intake following strenuous activity to eliminate O2 debt
Oxygen decline initial phases
ATP + creatine phosphate are resynthesized (via oxidative pathways)
Excess lactate is resynthesized into glucose + glycogen
Central command
Modulate baroreceptor reflex sensitivity
Receives feedback from increased activity in afferent nerves from exercising limbs
Metaboreceptors
Respond to changes in metabolite concentrations (mainly pH and K+)
Factors involved in Resp. response to exercise
Neural mechanisms activate resp. muscles
Initiation of motor activity from premotor area of cerebra cortex –> increase ventilation
Chemoreception
Contributes to Resp Response to exercise
CO2 Major driver for ventilation
Denervated carotid bodies
Slower ventilatory response compared to normal subjects
Plasma K+ concentrations
Elevated during exercise
Extra stimulus to peripheral chemoreceptors
