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Exercise and Thermoregulation (Skeletal Muscle Fibre Types (Anaerobic…
Exercise and Thermoregulation
Heat Loss
Radiation:
Objects emit heat as electromagnetic waves
Your body radiates heat to objects around you
Follows a gradient
60% heat loss
Conduction:
Molecule to molecule transferring through touching
Follows temp gradient from warmest to coolest, some substances conduct more rapidly than others e.g. air vs water
Convection:
Heat loss through movement of air or fluid.
Hot air is less dense so rises and is replaced by cool air.
Convection = carrying away of warm molecules
Maintains temp gradient for conduction to occur.
Evaporation:
Moisture evaporates from the skin, vaporisation process draws heat away from the skin.
Sweat secreted by sweat glands onto skin
Cools the skin and maintains gradient of heat loss from core to skin.
Evaporation of sweat NOT sweat itself is what cools the skin.
Heat Gain
Radiation: Warmer objects emit heat to cooler ones i.e the sun
Conduction: Warmer substances conduct heat to cooler ones
Convection: Air or fluid movement carries heat to cooler substances
Metabolism:
Heat produced even while we rest.
Around 70% of this arises from metabolism of internal organs i.e kidney, brain, liver etc
Exercise:
Increases ATP usage which produces vast amounts of heat.
Around 75% of energy released during exercise ends up as heat e.g. why we shiver when we are cold. More muscle mass = larger rate of heat production
Nonshivering Thermogenesis:
Infants tend not to have a well developed shiver mechanism BUT have
B.A.T
B.A.T has high density of mitochondria and is able to produce large amounts of heat through metabolism of fats and glucose
Process stimulated by adrenaline, thyroid hormone and the SNS via hypothalamus pathway.
B.A.T thought to be scarce in adults but is now considered present
Circadian Rhythm:
Resting bodies show a rhythmic daily temp cycle with a high at 4pm and a low at 4am
Not related to environment or behaviour
Persists in coma patients
Gradually reset on timezone shift
Largely attributed to melatonin (pineal gland)
Decline in physical activity during the evening is also attributed because of the decline in heat production.
Temperature Homeostasis:
Peripheral thermoreceptors detect
Input to hypothalamus, output via sympathetic nerves to adrenal medulla, sweat glands, skin arterioles, skeletal muscles.
Cerebral cortex = voluntary motor responses act on skeletal muscles
Central thermoreceptors = same effectors.
Hypothermia:
Mild hypothermia commonly occurs during sedation and GA due to promotion of heat loss
Theatres are normally cool to place reliance on heat conservation
Patient is unable to use behavioural thermoregulation, relies on physiological mechanisms
Anaesthetics + opioids such as morphine promote vasodilation, impair hypothalamic thermoregulation depress overall sympathetic outflow
Generally regarded as negative, positives = drug metabolism is decreased, metabolic rate decreased by 8% per degree, greater capacity for oxygen limited tissues to maintain healthy state, decreased release of pro inflammatory cytokines.
Thermoregulation (Exercise):
Exercise = large amount of heat produced
CBT increases
Triggers reflex heat loss mechanisms
Sweating increases as does vasodilation
If not effective enough, CBT can climb dangerously.
Heat Exhaustion:
Small changes in CBT can cause it
Largely attributed to hypotension
Increased sweating causes dehydration and vasodilation
Both of these decrease blood pressure
Leads to; headaches, dizziness and fainting.
Heatstroke:
Breakdown of heat regulation systems
DANGEROUS
Usually follows on from heat exhaustion
Usual treatment is internal cooling and fluid replacement
Temperature Acclimatisation:
Acclimatising to new hot environment
Associated with earlier onset of sweating
Increased volume of sweat
Decreased salt content of sweat, aldosterone effect on sweat gland.
Fever
Increased temperature due to increase in set point
Regulation still occurs but set point has moved upwards
Common cause = infection
Chills occur when set point is reset upwards, individual is suddenly too cold.
Vasoconstriction and shivering are initiated to increase temperature to new set point
Fever breaks = set point is suddenly returned to lower value and individual is suddenly too hot.
Infection:
Endogenous pyrogens are released from macrophages
Circulating EP activates hypothalamic thermoreceptors
Stimulate vagal afferents
Local release of prostaglandins, causes resetting of hypothalamus to higher temp
Increase temp = increased immune activity
Aspirin inhibits release of prostaglandins
Glycolysis
Aerobic
= Mitochondrion
Efficient 36ATP from 1 G
Long lasting (1-2 hrs)
Slow release
Anaerobic
= Cytosol, produces lactic acid
Inefficient 2 ATP from 1 glucose
Short duration (2-3mins)
Rapid release
2 pathways = efficiency and duration balanced with rate
Fatty Acid Oxidation:
High yield
Long duration
Long latency
Feeds into oxidative phosphorylation
ATP Source
Weightlifting: CrP
A fast kilometer run: Anaerobic glycolysis
Marathon: Aerobic glycolysis and largely fatty acid oxidation, longer the run = more fatty acid % contribution.
Oxygen Debt:
Increased oxygen consumption after energy cessation
Larger in strenuous exercise than in endurance exercise.
Recovery of energy stores
Processing of lactic acid
CrP:
Short burst high intensity exercise
Need to invest ATP to regenerate CrP
CP + ADP <----> C + ATP
Myosin ATPase in contraction
Ca2+ATPase in relaxation
Lactic Acid:
The Cori Cycle = generation of 2 Lactate from glucose or glucose from 2 lactate in either liver or muscle.
Exercise
Involves:
Motor commands
Increased CBT
Increased arterial H+
Increased plasma adrenaline and potassium
Contraction of muscles
Local chemical changes
Central Command:
Parallel activation of locomotor and autonomic circuits in CNS
Acts on CVS and Respiratory System
Feedforward signals
Increased central command = increased input to cardiorespiratory system = increased response proportional to muscle activation
Temp, [H+], Adrenaline and K+:
Increase in ventilation is stimulated by increase in CBT
Increased [H+] acts via chemoreceptors to increas ventilation
Adernaline is released during exercise and increases cardiorespiratory activity
K+ is released from muscles during contraction and stimulates increased ventilation.
Muscle Feedback: Exercise Pressor Reflex
Muscle mechanoreceptors - feedforward
Muscle chemoreceptors - feedback
Both send input to CNS
Ventilatory Response to Exercise
Sudden increase in ventilation at exercise onset
Gradual increase during exercise
Cessation = decrease
Increased Ventilation
Arterial PO2 remains constant as venous PO2 decreases with increased O2 consumption at muscles. Ventilation increases proportionally to consumption rate.
Arterial PCO2 remains stable at moderate exercise, falls with intense exercise.
Venous CO2 increases with increased CO2 production by muscles, ventilation increases higher than CO2 production.
Arterial [H+] increases with intense exercise
Decreased arterial CO2 so no longer contributes to H+
Attributed to accumulation of lactic acid from increased anaerobic glycolysis
Arterial PO2
Transit time = how long an RBC spends in pulmonary capillary
During moderate exercise transit time decreases because of increased CO
If TT remains > 0.25s the O2 equilibrium will still be reached.
Blood/O2 Supply During Exercise
Increase CO, control blood vessels to send it to skeletal muscles
Increase SNS activity to increase global systemic vasoconstriction
Local metabolites and mechanical compression then override the constriction at the site of the muscles and cause dilation = redistribution.
Mean Arterial Blood Pressure
CO increases, TPR falls (vasodilation) but not enough to offset the CO increase so MABP increases.
Baroreceptor Reflex:
Barosensitive cells in NTS excite cells in central ventrolateral medulla
Barosensitive cells in CVLM inhibit the rostral ventrolateral medulla
Inhibited RVLM stimulates less sympathetic nerve activity
MABP returns to more normal value.
However:
Inhibitory NTS cells prevent response
Central command excites the inhibitory cells, prevents the decrease in SNS activity
Central command stimulates the RVLM increasing SNS activity.
Increase CO = Increase Venous Return
Enhanced by respiratory pump
Enhanced by skeletal muscle pump, further increased by increased blood flow.
Valasalva Maneuver
Resistance training
Closure of glottis + increase in thoracic pressure
IVC collapses
Decrease in EDV, SV, CO, MABP, Blood flow to brain
Leads to dizziness, seeing spots, fainting
Recovery = normalisation of intrathoracic pressure, increases MABP above pre-exercise values.
Skeletal Muscle Fibre Types
Type I Oxidative
Slow twitch
Slower movement
Higher fatigue resistance
Low force
Many mitochondria
High capillary density
Low glycolytic enzymes
Strength Training:
Increased strength + capacity for rapid ATP generation
Low reps/short duration
High intensity
Detectable response in 3 weeks
Type II Glycolytic
A and X
Rapid movement
Fatigues rapidly
Many (A) and few (X) mitochondria
High (A) and low (X) capillary density
Intermediate - High glycolytic enzymes present
Anaerobic Training
Myofibrillar Hypertophy:
Increased actin and myosin
Increased size of muscle fibres (not number)
Tension generation is proportional to myofibrillar CSA
Increased protein synthesis, mechanical stress = stimulus
Satellite cell proliferation; myogenic stem cells residing under basal lamina of skeletal muscle = undergo division and fuse with muscle fibres (increase size)
Microtrauma:
Damage during maximal loads
Stimulates satellite cells
Contractile proteins span the damaged area
Combine with increased protein synthesis = more tissue added = increased contractile strength.
Sarcoplasmic Hypertrophy:
Increased volume or SR
Increases anaerobic ATP synthesis - increases substrates (CrP, ATP, Cr and Glyc), increase quantity + activity of enzymes, increase capacity to generate blood lactate.
Increased Lactate Threshold
Aerobic Training
Results in increased aerobic capacity
Increase VO2 max
Lower intensity, more reps.
CVS Adaptations:
Limiting factor = CO
Ventricular walls are remodelled = moderate hypertrophy + increased chamber size
Decreases resting HR and increases CO (aerobic exercise capacity).
Angiogenesis: increased skeletal muscle + pulmonary vasculature = increases SA , decreases distance for diffusion of O2 and CO2
Increased strength of respiratory muscles.
Cellular Adaptations:
Increased myoglobin
Increased glycolytic and oxidative enzymes: increase ATP synthesis
Mitochondrial biogeneisis: increased number and size of mitochondria: increased capacity to consumption O2 at a higher rate.
VO2 Max:
Maximal rate or O2 consumption = maximal rate of exertion
Ability to generate ATP
Indicates aerobic fitness and can increase with training
Muscle Atrophy
Denervation: nerve supply to a muscle or NMJ becomes compromised
Disuse: muscle not used
Both conditions = decrease in contractile proteins = decrease in muscle size
Myostatin inhibits myogenesis, being targeted to combat diseases that cause muscle atrophy e.g. muscular dystrophy
Blood Doping
Method of increasing [RBC] and therefore aerobic capacity.
Recombinant EPO (synthetic)
Homologous: blood received from a compatible donor
Autologous: blood harvested from individual in advance of event and reintroduce