9/30b Acute and Chronic Responses to Aerobic Activity (Examination, Evaluation, Intervention) Flashcards
determinants of VO2
VO2 = CO x a-vO2diff = CO x (CaO2-CvO2)
Cardiac Output determinants
CO = HR x SV = L/min
when does HR increase?
Initially: (<100bpm) because of parasympathetic withdrawal
Later: Increased beta1 receptor activation by SNS stimulation and circulating catecholamines
with SCI vs HTx, what accounts for the differences in resting HR and the initial HR response? what accounts for increase in HR response?
Higher resting HR in HTx b/c no parasympathetic innervation. Early withdrawal of PNS innervation explains the early rise in SCI
with SCI vs HTx, what accounts for the similar values of max HR
max HR is blunted in SCI and HTx due to lack of direct SNS stimulation, only circulating catecholamines
with HTx vs sedentary, what accounts for the differences in HR response?
lack of innervation in HTx causes:
- higher resting HR
- slowed initial response
- blunted max hr response
what is the difference in HR for sedentary vs athlete
Lower resting and submax HR in athlete due
to ↑ parasympathetic activity/↓ sympathetic activity at all
submaximal workloads. Max HR is similar
what is stroke volume affected by?
Preload - initial stretching of cardiac myocytes, related to ventricular filling
Afterload - force or load against which the heart has to contract to eject blood
Contractility - innate ability of heart muscle to contract
-Sympathetic Stim
-Circulating Catecholamines
SV of SCI vs. HTx
SCI has no venous muscle pump to
augment venous return with exercise. This blunts the SV
response compared to HTx
SV of sedentary vs. HTx
Initial similar increase due to intact venous muscle pump/↑ preload/Frank-Starling mechanism. Later increase in sedentary due to sympathetic innervation, which increases contractility. HTx has no direct innervation
SV of sedentary vs. athlete
Athlete has larger ventricular volume and slower HR at all submaximal workloads, allowing longer filling time and a greater SV.
what impacts cardiac output
increased due to both HR and SV
- SV contributes to up to 45% of VO2max
- Further increase due solely to HR
CO of SCI vs HTx
Lack of muscle pump blunts SV increase in SCI, and therefore CO. Also, VO2 max limited due to less activated muscle mass
CO of Sedentary vs HTx
Initially similar due to similar SV response. But blunted HR response in HTx due to lack of sympathetic innervation of heart limits later increases
CO of Sedentary vs Athlete
Similar at low workloads. However, athlete can achieve
higher CO because SV is much higher than sedentary at all workloads
a-vO2 difference significance
increases in VO2 due to increases in CO and Oxygen Extraction by Muscle
- Oxygen extraction increases because of:
1. increased oxygen consumption in active muscle due to aerobic metabolsm
2. restribution of blood to working muscle
athlete vs sedentary a-vO2 difference
Maximal oxygen extraction is similar. Higher CO in
athlete allows him to achieve same VO2 with less
oxygen extraction.
Mean Arterial and Pulse Pressure
Pulse Pressure = Psystolic - Pdiastolic
MAP = Pdiastolic + 1/3(Pulse Pressure)
Pulse Pressure
- directly proportional to SV
- decrease SV due to ischemia -> decrease pulse pressure
- increase SV during exercise -> increase pulse pressure - Inversely proportional to vessel compliance
- arterial stiffening with aging and arteriosclerosis -> increase pulse pressure
Systolic Blood Pressure
Affected by:
• Stroke volume
• Arterial compliance
• Diastolic pressure
SBP of SCI vs HTx
Lack of a muscle pump in SCI blunts the SV response, and therefore the SBP response.
SBP of HTx vs sedentary
SV, and therefore SBP, doesn’t increase as much in HTx
because of lack of sympathetic innervation
SBP of athlete vs sedentary
Athlete has greater increase in SV, so greater SBP
response
Diastolic Blood Pressure
Primarily related to:
- CO, primarily HR
- TPR
DBP of athlete vs HTx
- DBP falls in the athlete because the fall in TPR is greater than the increase in CO. TPR falls due to vasodilation in skeletal muscle via vasodilator metabolites produced
-In HTx, DPB is elevated at rest because resting HR is
higher than the athlete. During exercise, DBP stays
the same or increases slightly. This indicates that
the fall in TPR is balanced by the increase in CO.
by muscle.
Effects of Training
- increase VO2 max
- increase maximal CO
> decrease HR at rest and submaximal workloads due to increased PNS and Decreased SNS
>SV due to ventricular filling (large chamber) and slower HR = longer filling time for diastolic filling
-no change or slight increase in max a-v02 diff
-Decrease myocardial oxygen demand during exercise decrease Rate pressure product
-decrease resting BP