2026-03-02
Homeostasis
optimum temperature
optimum pH
optimal glucose levels
etc
Adaptations
overload principle
specificity
reversibility
individuality
Direct: measure heat produced during exercise - Human Calorimetry Chamber
Indirect: measure O2 consumption (VO2) typically about 0.25mL/kg/s of VO2 during exercise 0.05mL/kg/s of VO2 during rest
Maximum VO2 measured by exercising to exhaustion get up to 1mL/kg/s
corresponds to about 2000 Watts of power
training will increase your VO2 max
cardiovascular adaptations giving better O2 delivery
muscle mitocondrial O2 utilisation
athletes using large muscle masses for extended periods tend to have highest VO2 max
as well as measuring O2 levels we also monitor CO2 gives us the RER \[ RER = \frac{V_{CO_2}}{V_{O_2}} \] This gives information on type of food being used
for fats, RER = 0.7
for glucose, RER = 1.0
Fats, e.g. palmitate, C16H32O2 + 23 O2 -> 16 CO2 + 16 H2O \[ \frac{16}{23} = 0.70 \] Glucose, C6H12O6 + 6 O2 -> 6 CO2 + 6 H2O \[ \frac{6}{6} = 1.0 \]
for long distance, endurance, RER lets us deduce that mostly fats are burned
for high-powered activities like sprinting, mostly carbohydrates
muscle triglycerides: provide ~ 30% of energy initially but fades to ~10% gradually over four hours
plasma FFA: provide ~ 20% initially but this grows to 50% over four hours
blood glucose: provides 10% initially, this grows to 40% after four hours
muscle glycogen: provides ~ 40% initially but fades out over about 3 hours
decrease in CHO use leads to a decrease inperformance and to the onset of fatigue
See this video for a discussion of energy use in sled dogs.
As exercise intensity increases
progressive decrease in fats as fuel source
progressive increase in CHO as fuel source
Training adaptation - push this crossover point to higher intensities
Leads to sparing of precious CHO stores
Pushes back onset of fatigue
Only ATP can be used to directly cause muscle contraction
Breakdown of ATP allows crossbridge formation between actin and myosin (enzyme ATPase)
Amount of ATP in muscle is extremely low
During exercise as ATP utilisation goes up, need to replace it
\[ ATP_{prod} = ATP_{util} \] ATP producing pathways turns on by the energy charge in the cell \[ Energy\; Charge = \frac{[ATP] + {1\over2} [ADP]}{[ATP] + [ADP] + [AMP]} \] At rest, the energy charge in muscle is about 0.85 As energy charge decreases, ATP producing pathways are turned on while ATP utilising pathways are turned off
Oxidative production of ATP occurs in mitochondria.
This is vast majority of ATP production.
Activities lasting seconds need energy immediately Access stores of ATP in the cell
\[ ATP + H_2O\; \rightarrow\;ADP + P_i \qquad ATP_{ase} \]
\[ CP + ADP\; \rightarrow \; ATP + C \qquad creatine\; kinase \] No \(O_2\) in either process
About 3 or 4 times more CP than ATP in cell.
Carbohydrate can be broken down anaerobically
\[C_6H_{12}O_6\; \rightarrow\; 2 ATP + 2\; lactate \] Or aerobically
\[C_6H_{12}O_6 + 6O_2\; \rightarrow\; 30ATP + 6CO_2 + 6H_2O\] (note, for the same glucose molecule we get 15 times more ATP when broken aerobically) Limited amount of carbohydrate in the body, aerobic metabolism helps preserves carbohydrate stores.
Fats can also be broken down aerobically \[Palmitate + 23O_2\;\rightarrow\;108ATP + 16CO_2\]
Carbohydrates stored as Glycogen
Glycogen = strings of glucose attached to each other
When glucose needed, peeled off from glycogen
Total of 2000kCal can be depleted during endurance exercise This isn’t very much (gets depleted).
Adipose Tissue
Intensity and duration of exercise
at low intensities use fats
at high intensities use carbohydrates
at high intensities use mostly type II muscle fibres
Type of activity
Crossover Concept
Nutritional status
Muscle Fibres
glucose molecule stripped off by glycogen phosphorylase.
prompted by release of epinephrine or by Ca++ in muscle.
at high exercise intensities, muscle glycogen can drop from 90mM/kg to less 20mM/kg in minutes.
provides glucose for blood glucose levels
necessary to avoid exercise induced hypoglycemia
muscle uptake from blood is up to 50mM/min
normal liver glucose levels are about 4mM/L (about 5L of blood in human body)
increase CHO content in muscles prior to exercise
can get up to 250 mM/kg of muscle
(compare to 90 mM/kg normally)
increase CHO intake in week prior to exercise
roughly double it to ~0.6kg/day
rest for day or so before exercise
consumption of very dilute CHO drink during exercise
athletes at 70% VO2 max can exercise for ~4 hours rather than 3 hours before fatigue
gives addition source of CHO thus sparing liver glycogen
sedentary individuals can double their cell mitochondrial content through training
takes several weeks
means using more CHO aerobically rather than anaerobically
as we’ve seen, this is more more efficient
spares muscle CHO content
also observe a lower RER for individuals after training
lower RER means greater fat usage
this happens at all VO2 % levels
exercise intensity and fibre recruitment determine CHO utilisation
we have limited CHO stores (mostly in muscle)
liver glycogenolysis maintains blood glucose
carbohydrate loading increase muscle glucose levels before exercise
carbohydrate feeding maintains blood glucose during exercise
free fatty acids are immediate source of energy
fats must be converted to FFA’s before being used
FFA’s are hydrocarbon chains that can readily be oxidised in mitochondria
FFA’s stored in the form of triglycerides
triglycerides stored in adipose tissue (mostly) or skeletal muscle
FFA for direct ATP production
triglycerides are storage form
vast bulk of fat storage in adipose tissue ( > 100,000 Cal)
some fat storage in muscles (~ 3000Cal)
fats are preferred fuel at low exercise intensities
training adaptation is better use of fats
proteins made from amino acids
to be used as fuel (contribute ~10%), proteins must be broken down to constituent AA’s
some AA’s used directly as fuel, others converted to CHO and fat
Nitrogen balance - protein intake
typical adult diet ~ 60g protein / day
Muscular
Respiratory
Cardiovascular
Endocrine
Immune
\[H^+ + HCO_3\;\rightarrow\;H_2CO_3\;\rightarrow\;CO_2\; +\;H_2O \] - stops muscles and blood getting too acidic
increase tidal volume
increase breathing rate
at rest
maximal exercise
most efficient to increase tidal volume
initially neural control
later humoral (blood chemistry) control
\[Cardiac\;Output\;=\;Heart\;Rate\;\times\;Stroke\;Volume\]
reduce parasympathetic nerve activity
increase sympathetic nerve activity
increase epinephrine
heart rate from 40bpm to 180bpm
stroke volume 100 to 150 mL / beat
endurance athletes can get up to 50 L/min (at 5L/min \(O_2\) consumption)
measures efficacy of blood in delivering \(O_2\)
get about 6mL of \(VO_2\) for every 100mL of blood at rest
increases to 20mL of \(VO_2\) for every 100mL of blood at \(VO_2\:max\)
systolic blood pressure can double during intense exercise
diastolic pressure doesn’t change much
lower heart rate at rest and at submaximal exercise
greater stroke volume at rest and submaximal exercise
greater maximal cardiac output (due to increased stroke volume)
increased arteriovascular \(O_2\) difference
maximum heart rate doesn’t change
endurance training
strength training
get neural adaptations first, follwed by muscle hypertrophy
genetics, nutrition, environmental factors all play role
percentage strenght gain same for men and women
muscle protein synthesis > protein breakdown
resistance training + high protein diet
double protein intake to 1.6kg / kg body weight
ingest protein in first hour post training
causes diverse, but mostly in the muscle
depends on type of muscle fibre
depletion of ATP and PCr
increased muscle acidity
decrease in muscle and liver glycogen
decrease in intra-muscular calcium
higher body temperature
greater mental alertness
greater fat mobilisation
greater time to exhaustion
also interacts with \(Ca^{2+}\) from SR
dieting and weight control
heart disease
diabetes
cancer
successful aging
mental health
low fitness
smoking
systolic BP > 140mmHg
Cholesterol > 6.2 mM / L
BMI > 27
culprit is adipose cells that store fat
measures of body composition
atherosclerosis
LDL is major culprit here
heart attacks and stroke
exercise reduces both systolic and diastolic BP
physical activity addresses many of the risk factors
insulin resistance
insulin receptor in cell wall opens GLUT4 glucose channel
in diabetes, signal between insulin receptor and glucose channel is compromised
single bout of exercise reduces blood glucose
regular exercise increases glucose sensitivity in muscle
lower risk of some cancers, and helps treatment
has shown exercise reduces risk for breast, colon, prostate, lung cancers
exercise enhances natural immunity
increase levels of anti-oxidants
lowers obesity
retards growth factors implicated in cancer such IGF-1
as we’ve seen, exercise addresses many health issues that arise in aging
balance, strength, flexibility, endurance
\(VO_2\;max\) declines with age, exercising mitigates this
loss of calcium from bones
bone is similar to muscle in that when overloaded it will adapt and strengthen
weightlifting especially beneficial
increase cognitive function
decrease risk of dementia
decrease risk of Alzheimer’s
decrease risk of Parkinson’s
reduce depression, stress, anxiety
regular exercise
healthy diet
quality sleep
active social life
stress management
mental stimulation
blood flow can increase by up to 20% during exercise
pretty much all brain areas
increased blow (and CSF) flow reduces build-up of \(\beta\) amyloid plaques (AD)
exercise promotes dopamine, benefits people with Parkinson’s
Exercise Physiology: Theory and Application to Fitness and Performance. S.K. Powers and E.T. Howley. 10th edition. McGraw Hill publishers.
Exercise Physiology: Nutrition, Energy, and Human Performance. W.D. McArdle, F.I. Catch and V.L. Catch. 7th edition. Lippincott Williams & Wilkins publishers.
Biochemistry for Sport and Exercise Metabolism. D. McLaren and J. Morton. 1st edition. Wiley-Blackwell
Science of Exercise (University of Boulder, Colorado) - https://www.coursera.org/learn/science-exercise/