Exam 2- Lecture 8 Flashcards
When are respiratory centers in the brain stain active?
they are spontaneously active
Central Chemoreceptors
Very sensitive to H+
pH surrounding chemosensitive cells; the H+ level is related to CO2 levels
Peripheral Chemoreceptors
Sensitive to O2 (and CO2 and H+, but to a lesser extent)
what is the primary controller of ventilation at rest?
PaCO2 sensed at the central chemoreceptor
At rest, when does ventilation increase?
as PaCO2 increases
What neural mechanisms are involved in the regulation of ventilation at the onset of exercise?
central command and feedback from exercising muscle
what is central command?
neural projections from the rostral brain (activated as part of the voluntary decision to move) that result in simultaneous activation of locomotion and the initial ventilatory and cardiovascular responses to exercise
what is the evidence of central command in humans?
partial curarization of exercising muscles results in addition increase in ventilation
Curare decreases muscle strength
brain increases “effort” in an attempt to maintain exercise goal
Increased central command results in greater minute ventilation
What do mechanically sensitive group III/IV afferents in skeletal muscle do?
they project to reparatory and CV brainstem sites and can also initiate hypernea
what are group III/IV afferents associated with?
collagen structures in the muscle- they are sensitive to mechanical events during contractions
low level dynamic exercise stimulates group III/IV muscle afferents
in human, when does minute ventilation abruptly increase?
at onset of passive exercise
passive exercise activates muscle mechanoreceptors (group III/IV)
Chemical feedback during phase II and III of exercise ventilation
becomes more important as exercise continues in duration and intensity
what do peripheral chemoreceptors do?
fine tune the ventilatory response
explain increased neural feedback from chemosenstive muscle receptors during heavy exercise
contribute to higher minute ventilation
they are sensitive to products of cellular metabolism
involved in CV regulation during exercise
discuss the relationship between metabolite driver afferent activity and the respiratory system regulation during heavy exercise
metabolite driver afferent activity during heavy exercise is more important for CV regulation than reparatory system regulation during heavy exercise
3 words used interchangeably
ventilatory threshold
lactate threshold
anaerobic threshold
Ventilatory equivalent for oxygen
Ratio of minute ventilation to volume of O2
what is the ventilatory equivalent for oxygen in adults during stead state exercise
about 25/1 (up to 55% of VO2max)
ventilatory threshold
as intensity increases >60% VO2max, there is a short increase in minute ventilation without a corresponding increase in VO2
minute ventilation increases from 25 up to 35-40
“excess ventilation” represented by the elevated ventilatory equivalent for O2 is a response to an number of inputs including:
- arterial metabolic acidosis
- a response to increases in interstitial potassium, catecholamines, and increased neural feedback from exercising muscles
- increased central command
want does ventilatory threshold correspond in time to?
lactate threshold
what is lactate threshold?
- the exercise VO2 above which there is a sustained rise in blood lactate
- the point where lactate increases more than 1 mM over pre-exercise values
Glycolysis and blood lactate:
lactate is continuously being formed by cells and removed from the circulation (taken up by the liver and other cells for energy)
when production»_space; removal, we observe an exponential accumulation of lactate in the blood
what can be used to identify lactate threshold?
ventilatory threshold
OBLA
- oxygen uptake at which there is a sustained blood lactate level of >4.0 mM
- signals development of metabolic acidosis
- occurs later than lactate threshold
Anaerobic threshold
- used interchangeably with LT
- level of exercise VO2 able which aerobic energy production is supplemented by anaerobic mechanisms and is reflected by an increase in lactate as well as lactate/pyruvate ratios in blood or muscle
how is anaerobic threshold determined?
by determining the ventilatory threshold (Ve/VO2 breakpoint)
What is responsible for OBLA/LT?
- oxygen demand is greater than oxygen supply is mitochondria
- activation of fast twitch muscle fibers (high capacity to make lactate)
- decrease rate of lactate removal from blood
what are LT and OBLA of interest in exercise testing?
- relationship of LT/OBLA to work rate or %VO2max provides a method for estimating the capacity to sustain a given intensity of steady state exercise
what signals non-steady state exercise?
progressive accumulation of lactate
physiologic implications of exercising above the LT
- acceleration of metabolic/cellular acidosis
- results in enzymatic and contractile processes inhibition
- acidosis/fatigue correlation - exercise intensity at onset of blood lactate
- good predictor of performance in aerobic activity
what occurs to OBLA with exercise intensity training?
shifts higher (absolute and relative)
what is the lower limit for LT in a normal 40 yo male/female?
male: 44% of vo2max (mean 55%)
female: 47% (mean 58%)
what is the functional consequence of low LT or OBLA?
- persons with low LT have difficulty maintaining level of activity needed for everyday work/home life
- symptoms of fatigue and dyspnea
Does ventilation limit VO2 max?
- generally, no
- no desaturation (hypoxemia) during maximal exercise
- Ve/VO2 relationship doesn’t decrease during maximal exercise
- PaCO2 actually decreases during maximal exercise –> hyperventilation
Energy cost of breathing
rest: low
moderate exercise: 3-5% of VO2
maximal exercise: 8-11% of VO2
elite athletes: 15%
General cardiovascular responses at the onset of exercise
- increased HR (vagal withdrawal)
- increase sympathetic vasoconstrictor activity in viscera
- increase stroke volume
- increase blood pressure
- increase cardiac output
- large increase in blood blow to active muscle
how does central command primarily play a role in heart rate during exercise?
inhibits parasympathetic (vagal) activity to the heart and thus rapidly raises HR
how does central command secondarily play a role in heart rate during exercise?
raises sympathetic drive to visceral vasculature and skin thus redistributing cardiac output to active muscle
(greater effect on skin SNA than muscle SNA)
Exercise pressor reflex
phenomenon that neural feedback from exercising muscle causes CV and ventilatory adjustments during exercise
what are the key points of exercise pressor reflex?
- stimulation of muscle mechanoreceptors can increase HR, ventilation, and sympathetic outflow to the periphery
- stimulation of muscle chemosensitive receptors has a particularly strong effect on raising sympathetic outflow to the periphery, including to the heart, active and inactive skeletal muscles and viscera
- chemosensitive receptors can also influence ventilation
evidence for exercise pressor reflex
- in anesthetized animals, electrical stimulation of group III//IV afferents from muscle cause increase in BP, HR, and sympathetic activity (and increases in ventilation)
- in humans, passive cycling or electrically-stimulated static contractions (no central command) causes pressor (BP) responses –> something else has to be signaling it
exercise pressor mechanosensitive receptors
- group III/IV very important at the onset of dynamic exercise
- muscle mechanoreflex
- fire in response to an increase in muscle tension during contraction
exercise pressor chemosensitive receptors
- in Group III but mostly IV
- become activated as exercise increases in intensity or duration
- muscle chemoreflex or muscle metaboreflex
chemosensitive receptors sensitive to what metabolites released from the muscle?
- extracellular ATP
- potassium, phosphate, bradykinin, prostaglandins, H+, lactic acid
what is going on during sustained exercise?
- CV system has established higher HR, BP, and sympathetic nerve activity to visceral vascular beds
- metabolic vasodilation in active muscles (large blood flow)
- vasodilation in skin as heat load rises
- reduced peripheral vascular resistance
- increased SNA to active and inactive muscle if the intensity of activity is moderate to heavy
The goals of CV adjustments that are constantly going on during dynamic exercise
- maintain adequate oxygen delivery to active muscle
2. regulate body temperature (heat loss mechanisms)
factors that affect the magnitude of CV adjustments:
- changes in intensity of the exercise
- duration of the exercise
- heat load
what mechanisms tell the brainstem that CV adjustments are needed as exercise continues or increases in intensity?
- central command
- exercise pressor reflexes
- other peripheral input baroreflexes (arterial, cardiopulmonary)
- All interact to control CV function as exercise continues past the first 20 seconds
role of exercise pressor reflex during sustained exercise
- if blood flow is limited to active muscles or if oxidative capacity is less than normal (peripheral vascular disease, congestive heart failure, COPD), muscle chemo reflexes may be strongly activated at low levels of exertion resulting in excessive BP, sympathetic and ventilatory response to exercise
two major controllers of CV responses during dynamic exercise are:
- central command
2. exercise pressor reflexes from exercising muscle
when might chemosensitve receptors play an important role?
in moderate to heavy exercise
especially static exercise
what is congestive heart failure characterized by?
- poor ventricular function leading to inadequate cardiac output
- results in poor exercise tolerance
- ADLs may be exhausting because workload > OBLA & dyspena and muscle fatigue
what do patients with congestive heart failure show?
exaggerated pressor, sympathetic activity and ventilatory response
what is the pathophysiologic hypothesis of exercise intolerance in CHF?
excessive activation of chemosensitive afferents contributes to exaggerated hemodynamic responses and to the dyspnea and fatigue experienced in CHF patients
exercise training in patients with CHF
- improvements in skeletal muscle abnormalities and oxidative capacity in patients with CHF or COPD associated with exercise training decrease degree of dyspnea and muscle fatigue associated with low level activity
- exercise training may improve the ability to function during daily life and thus raise QoL
