Extreme exercise Flashcards
energy delivery (specifically oxygen)
at onset of exercise there is lag before oxygen delivery increases
-leads to oxygen deficit and oxygen debt
during the initial two minutes of exercise the body relies on ____ and ____ glycolysis
“stored energy”
anaerobic glycolysis
glycolysis producing ATP
rather inefficient,
every glucose –> only produce 2 ATP for one
(anaerobic)
anaerobic glycolysis and oxidative phosphorylation
much slower generate large amounts of (30) ATP for the cell per glucose molecule
ATP in the cells always
5 ATP
phosphatecreatine (PCr) in the cells always
10-50 molar
“stored energy” used at the beginning:
- ATP –> ADP + Phosphate + Energy (ATP used up so..)
- ADP + PCr –[Creatine kinase]–> ATP + Creatine
PCr used up tho so ADP accumulates___
ADP+ADP–Adenylate kinase–> ATP+AMP
Built up of ADP, AMP and phosphate from energy stores =
stimulate metabolic pathways involved in energy productions (krebs cycle etc ) via negative feedback
Anaerobic phase (non oxidative) of energy release: USING GLYCOLYSIS
-2 ATP / glucose molecule
- muscles fibres store glycogen about 300-400g
- substrate enters glycolysis at 2 points
-glycogenolysis = glucose-1-phosphate
-converted to glucose-6-phosphate
-uptake of glucose from blood by GLUT4, glucose enters glycolysis pathway
==> 2 pyruvate molecules formed produced.
pyruvate converted to lactic acid/lactate
-H+ from lactic acid lowers cells pH and leads to muscle fatigue
aerobic phase (oxidative) of energy release
- oxygen delivery to tissue increases, energy production via oxidative phosphorylation is stimulated
- slower but mote efficient = 30 ATP / glucose molecule
- glucose sourced from blood(GLUT4), following breakdown of glycogen from liver
- lactate is converted back into pyruvate feeds oxidative phosphorylation
- TypeIIX fibres release lactate into circulation (can enter other muscles or to liver to generate fresh glucose)
extended periods of exercise:
lactate and alanine: used by liver –> new glucose
During exercise: lactate can be released from non exercising muscles. body acts to redistribute glycogen stores
-mobilisation of non-muscle lipids (increase in circulating fatty acids) taken up by muscle
-breakdown of triaglycerols stored in muscle
muscle fatigue:
inability to maintain a described power output
-decline in force and velocity of muscle shortening
muscle fatigue: central fatigue
minor factor in trained exercise
‘this is starting to hurt’ ‘mind over matter’
muscle fatigue: peripheral fatigue
at the level of the muscle fibre- various factors
muscle fatigue: high-freq fatigue
alteration in cell Na/K (inside high Na low K normally) balance
-particularly relevant to type 2 fibres
muscle fatigue: low-freq fatigue
reduced release of Ca2+ from sarcoplasmic reticulum (more apparent at low frequency stimulation, type1 fibres)
muscle fatigue: ATP depletion
Intense stimulation can cause large drops in ATP near sites of cross-bridge formation and ATPases.
normally 5 mM to 2mM,
muscle fatigue: lactic acid build up
high rates of lactate production lead to cellular acifdifcaiton
muscle fatigue: glycogen depletion
losing good source of glucose production
considerations for maintaining aerobic activity:
1) uptake of oxygen by lungs - pulmonary ventilation
2) oxygen delivery to muscle - blood flow and O2 content in blood
2) oxygen extraction by muscle - depends on oxygen delivery and diffusion gradient
maximal oxygen uptake VO2 Max
As work done (power output) increases reach a point where Oxygen delivery can’t meet the demand. Oxygen consumption plateaus.
SO VO2 max =maximal oxygen uptake is an index of ability to generate aerobic power
to increase VO2 max or adapt the body:
1) intensity of activity must be higher than a critical threshold
2) each period of activity must be of a sufficient duration
3) repetition of activity
4) rest period to allow adaptions to occur
training increases the
ability to deliver oxygen to tissues
maximum rate of oxygen uptake =
optimal cardiac output X diffusion gradient for oxygen in muscle
maximising oxygen content in arterial blood: possible options
1) increase maximal alveolar ventilation
2) increase pulmonary diffusing capacity
3) improve ventilation/perfusion matching
4) increase haemoglobin concentration (ISSUES, more RBC increased velocity of blood)
maximising cardiac output.
cardiac output =
heart rate X stroke volume
- HR fixed, so increase stroke volume
- max CO can increase by ~40%
- – increased plasma volume
maximising oxygen extraction:
- formation of new microvesseld mainly capillaries in muscles
- -allows an increase blood flow to muscle
- -Increased surface area for diffusion
- -Reduced distance for diffusion to muscle fibres
increase in mitochondrial content in skeletal muscle fibres
- -promotes oxygen extraction form blood
- -increased capacity to oxidise fat
high altitude training: 3 models
- Live high train high
- live low train high
- live high train low
Live high train high (LHTH)
- effectiveness is not conclusive
- popular
- less oxygen so can’t train at same intensity as you would at sea level,
- increased chance of mountain sickness
- heat acclimatisation
live low train high (LLTH) OR Intermittent hypoxic training (IHT)
live in normal conditions, training subjected to hypobaric conditions
- no haematological benefits, but may see benefits from muscle adaptions
- used as a preacclimisation technique before ascending to reduce risk of AMS
live high train low (LHTL)
BEST OPTION?
- need to live at 2000m for 14-16 hours per day for 19-20 days to sustain erythropoietic (RBC production) effects
- Athletes gain benefits of physiological adaptations and can maintain normal intensity of training.
- Studies show mixed results.
- Disadvantage – travel time to and from altitude
ergogenic aids:
a perfomance enhancer that gives you a mental or physical eye while exercising or competing
-range from caffeine and sports drinks to illegal substances
beetroot juice supplementation
enhanced skeletal muscle function
