L289 Exercise Physiology - Oxygen, Heat and Fluids Flashcards
O2 uptake is ______ dependent
Intensity-dependent
Describe O2 uptake + ex intensity relationship
Linear increase until reach plateau - VO2max
Equation for VO2 max
- VO2 = Q x (CaO2 – CvO2) = CO x AVO2 difference
Describe O2 uptake at the beginning of exercise
• O2 deficit: lag between O2 uptake needed for workload and actual O2 uptake
- In this time, anaerobic energy sources help supplement energy needs
CO + intensity relationship
↑ intensity, ↑CO
With increasing intensity, describe the BF to muscle, kidneys, heart, skin, brain and gut.
- ↑BF to muscle, heart, ↑/= BF to brain
- ↓BF to kidneys, gut
- ↑ then ↓ to skin
Why does BF to kidneys and gut decrease?
- Compensatory VC to redistribute BF where needed
Why does BF to skin increase then decrease?
- Initially ↑BF with ↑ intensity to lose heat
- Until the point where muscle requires BF going to skin - skin then VC ∴ potential for overheating
Hierarchy of BF importance during ex
brain > muscle > skin
What does the hierarchy of BF importance mean for BF to the muscle?
muscle can have ↓BF (VC) if brain perfusion is at risk
small muscle group vs dynamic body ex effect on BP
Small muscle group exercise → ↑↑ BP cw. dynamic all body exercise - because of the ↑ VC
↑BF during exercise is called…
ex hyperaemia
4 plausible mechanisms for exercise hyperaemia
- Metabolic vasodilators from contracting skeletal muscle, endothelium and/or RBCs
- Muscle pump
- “Conducted vasodilation”
- Functional sympatholysis
Muscle pump during ex: important for maintaining what?
VR cw BF
Explain conducted vasodilation
- Local relaxation of smooth muscle through smooth muscle gap junctions
- Relaxation is conducted proximally
Explain functional sympatholysis
- SNS-mediated VC is desensitised in response to metabolic vasodilators
- ↑SNS activity at rest → significant ↑ VC at muscle, but ↑SNS activity during exercise → less significant ↑ VC at muscle
What occurs to HR and systole during incremental ex?
↑HR, ↑SV that plateaus
Explain the increased and levelled off SV during incremental ex
• ↑HR during exercise → shortened diastole
- Because systole relatively fixed
∴ ↑ SV eventually level off, due to impact on diastolic filling
During ex, SBP and DBP mimic what?
SBP mimics CO and DBP mimics peripheral resistance
Therefore, what happens to SBP and DBP during ex?
- ↑CO → ↑SBP
- DBP maintained/falls slightly if TPR falls
What happens to MAP during ex, and why?
exercise → ↑MAP: because of ↑SBP + ↓DBP (i.e. systole becomes larger component of equation)
Why can MAP and HR increase simultaneously during ex?
Because baroreceptors reset to a higher level in exercise
CV responses to prolonged exercise
• CV drift: = ↑HR and ↓SV over time
Which comes first is chicken or egg debate!
Reasons for CV drift during prolonged exercise (4)
- Hyperthermia
- Dehydration
- ↑ plasma [adrenaline]
- Peripheral displacement of BV due to cutaneous vasodilation
Peripheral displacement of BV due to cutaneous vasodilation: how might this cause CV drift?
- Skin circulation is quite compliant esp. venous circulation
∴ blood going to skin can ↓ systemic circulation flow → ↑HR
Neural control of the circulation: interaction between..
• Central command
- Powerful pre-anticipatory control over body before exercise
• FB from peripheral sensors
- Mechanical and chemical muscle sensors, baroreceptors, thermoreceptors etc.
Explain the early increase in HR during ex
Early ↑HR during exercise due to withdrawal of vagal (PNS) control and thus SNS domination of control
- Remembering basal HR actually driven by SNS
Mechanisms of ↑CO following training (4)
- Expanded blood volume
- ↑ heart size(↑ LV mass and chamber size)
- ↑ adrenergic sensitivity?
- Microvascular adaptations - ↑capillary density and recruitment
Ventilation during incremental exercise: describe relationship
• Linear increases between VO2 and Ve
- Initial gradient b/n rest VO2 and VT1 in response to CO2 from aerobic resp. - 2nd ↑ gradient b/n VT1 and VT2 in response to need to buffer lactic acid - 3rd ↑↑ gradient after VT2 in response to ↑↑ CO2 from aerobic resp. and metabolism → hyperventilation
Pulmonary gas exchange during exercise: describe
• ↑CO during exercise → transit time ↓ as blood velocity ↑
When can pulmonary gas exchange become a problem?
- At altitude with ↓PO2
2. Well trained athletes with ↑↑CO
Main driver for respiration
CO2 - not hypoxia!
↑ ventilation during exercise is called …
Exercise hyperpnea
Mechanisms of exercise hyperpnea (5)
- Motor cortical activation
- Muscle afferents (spindles, type III & IV)
- CO2 flux to the lung
- Increased K+, H+, lactate?
- Elevated catecholamines and temperature
Exercise ventilation following training (5)
- Reduced blood lactate/H+
- Lower plasma K+
- Lower plasma catecholamines
- Reduced activation of muscle afferents?
- Reduced central drive?
Main mechanism of heat loss during ex and when in particular
Evaporation of sweat -at high temperatures in particular
Skin BF and CO at rest in heat
Skin already VD and CO increased (CO matches exercising at 5-6 mets at cooler temperature)
Skin BF and CO with exercise in heat
- Almost immediately ↓ skin BF because blood needed somewhere else
- ∴ ability to dissipate heat decreased
Exercise-induced dehydration affects which body fluid compartments?
Exercise-induced dehydration affects all body fluid compartments
- Plasma volume reasonable well protected, but marked IC and EC dehydration occurs
Dehydration and heat stress effect on performance
Both impair performance
Heat production during ex directly determined by…
ex intensity
VO2 max closely correlates with…
O2 delivery
