cardiovascular response to exercise long Flashcards
PO 1.48 cardiovascular response to exercise
what is the point of the response and a summary of it overall
Increases oxidative metabolic activity so need to increase blood flow and O2 delivary to heart and skeletal muscles – O2 consumption increases 60 fold, increased O2 extraction and increased muscle blood flow (1-20L/min)
Summary of changes
o systemic vascular resistance – decreases
• but not as much as CO increases so get increase in MAP
• metabolic vasodilation to muscles and heart
• cutaneous vasodilation (from decreased sympathetic)
• sympathetic vasoconstriction of splanchnic, non active muscle and renal – limits fall in SVR and moves blood to active muscle
o venous return - increases
• prevents fall in preload you would get from increased HR and increases CO by frank starling
• sympathetic venous constriction
• skeletal muscle and abdominothoracic pumps
o cardiac output increases (3-5 fold)
• sympathetic increase in HR (3 fold)
• sympathetic increased inotropy/lusitropy/CVP increases SV (10-30%)
o Systolic and pulse pressure increase, MAP slightly increase
• CO increases more than SVR decreases from increased HR and SV
• Increased SV increases pulse pressure
• Increased pressure means greater drive to flow (Flow = change in p/R) and stretch open vessel walls
PO 1.48 cardiovascular response to exercise
4 mechansims (plus 2)
o mechanical
• muscle and thoracic pump, happens first →increased VR and preload →CO
o metabolic
• ph, pCO2, K+, adenosine, O2 - cause dilation of resistance vessels in seconds and recruitment of extra vessels→increased flow and O2 extraction (increased AV difference)
• this means increased VR and CO
• drop in SVR means increased hydrostatic pressure leading to net movement of neutrients and water into tisue
o autonomic
• hypothalamus increases sympathetic and decreases vagal outflow due to
• central command from cortex (anticipation)
• mechano/chemoreceptors in muscles which pick up change in activity and increased lactic acid
• CNS resets baroreceptors so don’t get bradycardia
• increases HR, inotropy, lusitropy → CO (cardiac output curve moves left and up image 51)
• constricts resistance and capacitance (everywhere but coronary and cerebral and muscular) →MAP and CVP (venous return curve up and to the right)
o hormonal
• adrenaline/noradrenaline
- sympathetic to adrenal medulla →adrenalin >noradrenaline
- sympathetic nerves release noradrenaline and some diffuses, this spillover is higher with high sympathetic activity
- these act on A and B to improve cardiac function and constrict or dilate vessels
- low levels adrenaline bind B2 in skeletal – dilate
- high levels adrenaline A1 and A2 – constrict (all but heart, skeletal muscle and brain as metabolic mechanisms dilate)
- noradrenaline a1>A2 – constrict (all but heart and skeletal muscle and brain as metabolic mechanisms dilate)
• renin
- from sympathetic on kidney
- form angiotensin II, forms aldosterone - increased Na and water reabsorption
- angiotensin II augments sympathetic
vasopressin release
- also holds onto water (counteracts loss in sweat and resp)
o Right shift in oxyhaemoglobin curve – bohr effect
• From increase in H+, temp and 2,3,DPG
• Improves O2 unloading at muscle and O2 loading at lung
o Respiration
• Stimulated by medullary resp centre – increased MV
PO 1.48 cardiovascular response to exercise
summary of changes in graph and flow to organs graph
o as workload increases
• HR, CO, MAP increase proportionally
• SVR falls
• SV (and pulse pressure) increases initially (from increased VR and inotropy) then plateaus as HR limits filling time. This point changes with ppl and exercise type and environment
o As increase exercise, more flow to muscle, heart and skin (to expel heat), same flow to brain (metabolic and pressure autoregulation) and less to other organs
• If work too hard and need more blood, skin stops getting flow - heat stroke (dangerous elevation in core temp, organ damage and loss of autonomic control)
PO 1.48 cardiovascular response to exercise
isotonic vs isometric
o isometric/static muscle contraction
• initial centrally mediated increase HR same as isotonic (anticipation)
• No muscle or abdominal thoracic pump so little increase in VR
• Large SVR increase, espec if large muscle, because of mechanical compression of vessels by muscle contraction, minimal change in SV
• Can cause hypertension and haemorrhagic stroke
PO 1.48 cardiovascular response to exercise
o Body posture
• If supine (swim) higher resting VR and SV and lower HR so when start can’t increase SV by much more (increses by inotropy) but compensated for by bigger increase in HR – overall CO increase is the same
• higher CVP while swimming
o physical conditioning
• if conditioned, max CO higher as atria and ventricle more responsive to sympathetic nerves
• hypertrophied hearts and muscles – more VR via pump, can get LVEF >90%
• lower resting heart rate because large and contractile heart means larger SV at rest so vagal tone reduces heart rate cos don’t need higher CO at rest. This means can have greater increase in HR
• also have lower heart rate for a given work load
• can sustain higher workload for longer duration and recover easier as higher CO
o environment
• high altitude decreases max SV and CO
• lower pO2 arterial blood (due to lower atmospheric pressure), lower O2 delivery, hypoxia at lower workloads
• hypoxia decreases inotropy
• Reduced O2 delivery also means skeletal muscles switch to anaerobic metabolism earlier
• Increased temp
• More CO diverted to skin so max CO and O2 consumption reached sooner, reduced endurance
• Dehydration
• Decrease volume and CVP so less CO
• Heat exhaustion – fatigue, muscle weak, nausea, mental confusion
o Gender
• Males higher max oxygen consumption as max CO 25% more
• Cos of increases skeletal and cardiac muscle mass causing increased VR and SV
age - see age cards
