L21 Metabolism Exercise and metabolism

Overview

This lecture covers how the body supplies ATP during exercise and how that supply changes with intensity, duration, and training. It moves from the three energy systems (phosphagen, anaerobic glycolysis, aerobic) and how their relative contribution shifts with exercise intensity/duration, through acute and chronic cardiorespiratory responses that support aerobic metabolism, to the measurement of substrate use via indirect calorimetry and how carbohydrate/fat/protein use shifts with intensity and duration. It then covers fat metabolism and its enhancement with training, glucose transport (GLUT4) regulation by exercise, common misconceptions about lactate, and finishes with the clinical/health benefits of exercise on lipids and blood glucose, followed by a structured summary of structural, biochemical, and systemic training adaptations.

Energy Systems and Exercise Intensity/Duration

Three bioenergetic systems supply ATP during exercise, each with a trade-off between power (rate of ATP production) and capacity (total ATP available):

System	Maximal power (mol ATP/min)	Maximal capacity (total mol ATP)
Phosphagen (ATP-CP)	4.4	0.7
Anaerobic glycolysis (muscle glycogen)	2.4	1.6
Aerobic CHO (muscle glycogen)	1.0	84.0
Fat (aerobic)	0.4	4000

So the fastest systems (phosphagen, then anaerobic glycolysis) have the smallest total capacity, while aerobic fat metabolism is slowest but has by far the largest capacity.

The proportional contribution of each system to total energy supply changes with exercise intensity and duration (shorter/higher intensity → more anaerobic; longer/lower intensity → more aerobic):

• ATP-CP: spikes sharply to its peak almost immediately (~10 s efforts), then declines rapidly to near zero by ~1’40”.
• Anaerobic glycolytic: rises to a peak around 45 s–1’40”, then gradually declines.
• Aerobic: starts near zero, rises steadily, overtakes anaerobic glycolysis around 1’40”–3’30”, and plateaus as the dominant contributor by ~27 minutes.

Slide 6 flag: the table accompanying this graph lists, for the 27 min/10 km column, %Anaerobic = 97 and %Aerobic = 3. This is inconsistent with the adjacent graph (aerobic dominant by 27 min) and with the preceding trend across shorter distances (%Aerobic rising: 10, 30, 60, 80). It may be a slide typo with the columns swapped (intended ~3% anaerobic / 97% aerobic). Transcribed here exactly as printed on the slide.

Aerobic Capacity: VO2 and VO2max

• $\dot{V}{O}_2$ = volume of oxygen consumed per unit time (L/min or mL/kg/min).
• $\dot{V}{O}_{2max}$ = maximal aerobic capacity, i.e. the maximal rate of oxygen consumption. More oxygen used means more ATP produced aerobically.
• $\dot{V}{O}_{2max}$ is correlated with endurance capacity, and is inversely correlated with cardiovascular and other chronic disease risk and with all-cause mortality.
• In an incremental exercise test, oxygen uptake rises progressively with workload from a resting baseline and plateaus at $\dot{V}{O}_{2max}$ (with a slight decline at exhaustion), even as the protocol continues to increase demand (e.g. by holding speed constant and progressively increasing treadmill grade).
• Typical $\dot{V}{O}_{2max}$ values (mL/kg/min) span a wide range: heart failure patients lowest (~16, males), non-athletes moderate (~39–41), and elite endurance athletes highest — distance runners highest of all groups shown (~68–78), with rowers, cyclists, and swimmers also high (~60–74); sprinters and weightlifters lower than endurance specialists (~40–52). Males generally show higher values than females within each category.

$\dot{V}{O}_{2max}$ is not just a performance marker — its inverse association with cardiovascular disease risk and all-cause mortality gives it direct clinical relevance.

Acute and Chronic Cardiorespiratory Responses

Acute responses to exercise:

• Cardiac output: $\dot{Q}=HR\times SV$. At rest ≈ 5 L/min; at maximal exercise, 20–25 L/min.
• Heart rate and stroke volume both increase.
• Breathing rate and depth both increase.
• Blood flow to muscle: ~20% at rest → ~80%+ at maximal exercise.
• Oxygen extraction: ~25% at rest → 75–85% at maximal exercise.

Chronic (training) adaptations:

• Increased: plasma volume, stroke volume, maximal cardiac output, capillarisation and blood flow to muscle, oxygen extraction (partly via muscle mitochondrial adaptation), red blood cell mass and O2 delivery.
• Decreased: resting heart rate, blood pressure.

Rest-to-Exercise Transition and Recovery

• At the onset of exercise, oxygen uptake rises with a delay, taking roughly 1–4 minutes to reach steady state (“oxygen deficit” — considered a misnomer for this lag).
• During this lag, anaerobic energy systems contribute to total ATP production while aerobic metabolism ramps up.
• As exercise progresses, catecholamines, heart rate, cardiac output, vasodilation, and blood flow to muscle all increase to support the rising aerobic demand.
• Trained individuals reach steady-state $\dot{V}{O}_2$ faster than untrained individuals, incurring a smaller oxygen deficit; untrained individuals lag further behind and accumulate a larger deficit before reaching the same steady-rate $\dot{V}{O}_2$.

Slide 14 contains minor source typos ("Aanaerobic", "ouput"), transcribed here as printed; intended meaning is "anaerobic" and "output".

Recovery — Excess Post-Exercise Oxygen Consumption (EPOC):

• $\dot{V}{O}_2$ remains elevated after exercise stops in order to: replenish fuel stores (creatine phosphate, glycogen, intramuscular triglycerides) and return the body to homeostasis.
• EPOC magnitude is intensity-dependent: light exercise produces a small deficit and a modest recovery $\dot{V}{O}_2$; moderate-to-heavy aerobic exercise produces a larger deficit with recovery showing both a fast and a slow decline component; all-out maximal exercise (aerobic + anaerobic) produces the largest deficit and the largest/longest recovery $\dot{V}{O}_2$.
• Resting metabolic rate can remain elevated for up to 24 hours after exercise, depending on intensity and duration.

Indirect Calorimetry and Substrate Use

Indirect calorimetry infers which fuel is being oxidised from the ratio of CO2 produced to O2 consumed.

• Respiratory exchange ratio (RER or R), representing the (cellular) respiratory quotient (RQ): $R=\dot{V}C{O}_2/\dot{V}{O}_2$.
• Fat oxidation (palmitic acid, $C_{16}{H}_{32}{O}_2$): $C_{16}{H}_{32}{O}_2+23O_2\to 16C{O}_2+16H_{2}O$, giving $R=16/23=0.70$.
• Glucose oxidation ($C_6{H}_{12}{O}_6$): $C_6{H}_{12}{O}_6+6O_2\to 6C{O}_2+6H_{2}O$, giving $R=6/6=1.00$.
• Interpreting R: 0.70 = 100% fat oxidised; 0.85 = 50% fat/50% carbohydrate; 1.00 = 100% carbohydrate oxidised; R > 1.00 indicates a contribution from anaerobic metabolism.
• Measured via respiratory gas analysis: expired air passes through a flow meter/breathing valve into a sampling chamber, where it is split to separate electronic O2 and CO2 analysers, both feeding data to a microcomputer interface — used to track gas-exchange values (e.g. $\dot{V}E$, HR, $\dot{V}{O}_2$, $\dot{V}C{O}_2$, ventilatory ratios) across an incremental exercise test and determine ventilatory/gas-exchange thresholds.

Slide 16 flag: the six small sub-graphs of gas-exchange variables against time/workload are low-resolution; general shapes (progressive rise with workload) are legible but precise values are not readable.

Effect of Intensity and Duration on Fuel Selection

By intensity (rest → maximal $\%\dot{V}{O}_{2max}$):

• Carbohydrate (CHO) contribution to total energy expenditure rises from ~28% at rest to ~100% at maximal intensity.
• Lipid contribution falls from ~72% at rest to near 0% at maximal intensity; CHO and lipid contributions cross around 60–70% $\dot{V}{O}_{2max}$.
• RER rises from ~0.8 at rest to ~1.0 at maximal intensity, staying high from ~60% $\dot{V}{O}_{2max}$ onward.
• Breaking down fuel sources at increasing intensity (25% → 65% → 85% $\dot{V}{O}_{2max}$): plasma FFA contribution falls from dominant (~80%) at low intensity to a minor share at high intensity, while muscle glycogen contribution rises from a small share to dominant (~60%) at high intensity. Muscle triglycerides and plasma glucose contribute smaller, more stable shares throughout.

By duration (rest → 150 min at a constant intensity):

• CHO contribution rises sharply to a peak (~68%) around 20–30 minutes, then declines steadily to ~35% by 150 minutes.
• Lipid contribution falls to a low (~30%) around 20–30 minutes, then rises steadily to ~58% by 150 minutes, crossing CHO again around 120 minutes.
• RER rises quickly early on then stays roughly flat to slightly declining through 150 minutes.
• Over several hours, the proportion of energy expenditure from muscle glycogen narrows toward zero, while the proportion from plasma FFA widens substantially; blood glucose and muscle triglyceride contributions stay comparatively stable.

Underlying mechanism: increasing exercise duration shifts fuel use from carbohydrate toward fat, driven by an increased rate of lipolysis — breakdown of triglyceride (TG) into glycerol and free fatty acids (FFA) — as glycogen levels decrease. Lipolysis is stimulated by decreasing blood insulin levels, which disinhibits hormone-sensitive lipase.

Training Effects on Fat Metabolism

• At a fixed submaximal intensity (40% $\dot{V}{O}_{2max}$) sustained over 180 minutes, trained individuals show a consistently lower RQ than untrained individuals throughout the exercise duration, indicating greater reliance on fat oxidation. Both groups’ RQ rises to an early peak then declines, but the trained curve sits below the untrained curve at every time point.
• Training enhances fat metabolism via several mechanisms: increased O2 availability; increased mitochondrial density and enzyme content (Krebs cycle enzymes, beta-oxidation enzymes); increased intramuscular triglyceride (IMTG) stores; and increased enzyme activity/hormone sensitivity supporting lipolysis.

Adipocyte–capillary fatty acid trafficking: circulating triglyceride/fatty acids (from liver and intestine) in the capillary are acted on by lipoprotein lipase at the capillary wall, releasing fatty acids that enter the adipocyte; inside the adipocyte, fatty acids combine with α-glycerophosphate to re-form triglyceride for storage. Hormone-sensitive lipase then acts on this stored triglyceride to release fatty acids back into the capillary, which travel to other tissues for oxidation. This describes a storage/mobilisation cycle for adipose fatty acids.

Fuel Use During Exercise: Influence of Stores

• Carbohydrate: muscle glycogen (depleted rapidly by anaerobic glycolysis) and blood glucose (maintained via liver glycogenolysis and gluconeogenesis).
• Fat: intramuscular triglycerides and plasma FFA (from adipose tissue lipolysis, enhanced by exercise duration and glycogen depletion). Fat oxidation requires some glucogenic metabolism to proceed: pyruvate → oxaloacetate (OAA); OAA + acetyl-CoA → citric acid.
• Protein: normally only a small contribution to total energy production (~2%), but this can increase to 5–15% with prolonged or intensive exercise, especially if glycogen is depleted.

Exercise, GLUT4, and Glucose Regulation

• Glucose enters muscle cells via the GLUT4 transporter, regulated both acutely and chronically by exercise.
• Acute mechanism: translocation of GLUT4-containing vesicles to the plasma membrane. This occurs via two converging pathways — (1) insulin binding its receptor → insulin signalling pathway (insulin receptor → IRS-1 → PI-3-kinase → PDK → Akt → GSK3) and (2) chemical/mechanical effects of muscle contraction → ATP/AMP/Ca2+ changes → AMPK, p38 MAPK, PKC, NOS → NO. Both pathways converge on translocation of GLUT4 vesicles to the membrane, enabling glucose uptake; contraction and insulin effects are additive.
• Chronic mechanism: repeated muscle contraction (exercise training) increases synthesis of GLUT4 protein, via signalling through ↑AMP:ATP → LKB1 → AMPK, and Ca2+ → calmodulin → calcineurin/CaMKs/p38 MAPK, converging (with ATF2, MEF2) on PGC-1α, which drives fibre-type transformation, mitochondrial biogenesis, and increased GLUT4 protein expression.
• Exercise improves overall glucose regulation via: increased glucose delivery from the circulation (increased blood flow); greater muscle mass as an uptake site; more GLUT4 transporters per given stimulus; additive contraction and insulin effects; and increased muscle glucose phosphorylation via increased hexokinase activity.

Anaerobic Exercise and Lactate: Myths

• Lactate production during exercise is not because of insufficient oxygen delivery to muscle — “anaerobic exercise” refers to the energy systems used, not to inadequate O2 availability.
• Lactate/lactic acid is not the source of the increased acidity seen during high-intensity exercise:
  • The reaction pyruvate → lactate (via NADH/NAD+) actually takes up H+.
  • ATP hydrolysis releases H+.
  • More H+ is released via ATP hydrolysis during high-intensity exercise than lactate production could ever release.
• Lactate is an energy source for resting muscle and a gluconeogenic precursor for the liver.
• Lactate does not cause fatigue or post-exercise muscle pain — it leaves the muscle within minutes.

Common misconception to unlearn: lactate/lactic acid does not cause exercise-induced muscle acidosis or delayed soreness — the H+ driving acidity comes predominantly from ATP hydrolysis, not lactate production.

Clinical/Health Benefits of Exercise

Lipids:

• Comparing a single 30-min walk at 60% $\dot{V}{O}_{2max}$ before breakfast versus three 10-min walks at 60% $\dot{V}{O}_{2max}$ before each main meal (matched energy expenditure, same participants, against a control workday-activity condition):
  • Both walking conditions reduced postprandial plasma triglycerides compared to control, especially in the evening.
  • Fat oxidised increased by ~5 g over 11 hours with the walking conditions.
  • Fat storage was reduced by 4–5% in the exercise trials versus control.

Blood glucose:

• In a cross-over trial (15 with impaired glucose tolerance [IGT], 30 with type 2 diabetes) comparing control (no exercise), 45 min resistance training, and 45 min cycling at 50% max workload: both exercise conditions significantly reduced prevalence of hyperglycaemia over 24 hours relative to control (by 35% with resistance training and 33% with cycling, respectively) across IGT, oral-glucose-lowering-medication, and insulin-treated subgroups.
• In diet-controlled diabetics (cross-over, control vs. an acute HIIT session 90 min after breakfast: 10 × 60 s at ~90% HRmax with 60 s rest), exercise improved glucose control and reduced time spent in hyperglycaemia by 65%.
• Recent meta-analyses on “exercise snacking” (low-to-moderate intensity walking, >5×/day, >3 min each) found lower fasting glucose. Interrupting prolonged sitting with walking every 15–20 minutes lowered postprandial glucose and insulin (lesser reductions seen with standing or resistance exercise breaks), with a greater effect in obese individuals.

Slide 32 flag: the forest plot's individual numeric SMD/confidence-interval values are too small to read reliably; the overall direction (favouring exercise snacking, i.e. lower fasting glucose) is clear from the pooled diamond's position left of the null line.

Summary of Training Adaptations to (Endurance) Exercise

Structural (muscle):

• Increased fibre size, especially Type 1 fibres.
• Conversion of Type IIx to Type IIa fibres, increasing oxidative capacity.
• Increased capillary density and blood flow, increasing O2 delivery and fuel use.
• Increased IMTG stores and increased mobilisation of IMTG.
• Increased glycogen stored.
• Increased glucose and fatty acid transporter proteins.

Biochemical:

• Decreased basal and glucose-stimulated insulin levels — fit individuals release less insulin for a given carbohydrate load, and the insulin released is more effective.
• Increased enzyme number and activity, improving glucose and fat metabolism.
• Increased mitochondria, increasing oxidative capacity of muscle.

Systemic:

• Improved cardiovascular function: stronger heart, greater blood/stroke volume, lower resting heart rate, enhanced capillarisation, reduced blood pressure, enhanced peripheral and brain blood flow.
• Increased oxygen uptake and functional capacity at submaximal and maximal workloads (increased fitness).
• Increased FFA metabolism — greater ability to store, mobilise, and use FFA.
• Decreased LDL/VLDL cholesterol, increased HDL cholesterol.
• Increased hormone sensitivity (e.g. insulin), giving better blood glucose control.
• Maintenance of muscle mass — supports functionality with aging, plays a role in glucose tolerance, and is a major determinant of basal metabolic rate (energy expenditure and energy balance).
• Increased gut microbiome α-diversity and altered taxa, with numerous downstream effects: gut integrity, enhanced immunity, reduced inflammation, metabolic effects.
• Decreased comorbidity risks, e.g. cardiovascular disease, hypertension, visceral obesity, systemic inflammation, lipid abnormalities, cognitive decline, cancer, all-cause mortality.

Self-test

1. List the three bioenergetic systems used during exercise and, for each, state whether it has high power/low capacity or low power/high capacity.
2. How does the proportional contribution of the ATP-CP, anaerobic glycolytic, and aerobic systems change as exercise duration increases from ~10 seconds to ~27 minutes?
3. Define $\dot{V}{O}_2$ and $\dot{V}{O}_{2max}$.
4. Why is $\dot{V}{O}_{2max}$ clinically relevant beyond athletic performance?
5. Write the equation for cardiac output and give the approximate resting and maximal-exercise values.
6. List the acute cardiorespiratory responses to exercise (four parameters and their direction of change, plus the at-rest vs. maximal-exercise percentages given for blood flow to muscle and oxygen extraction).
7. List the chronic cardiovascular training adaptations, distinguishing those that increase from the one that decreases.
8. What is the “oxygen deficit” and why is it described as a misnomer? How does it differ between trained and untrained individuals?
9. Define EPOC and explain how its magnitude relates to exercise intensity.
10. What are the two main purposes served by the elevated $\dot{V}{O}_2$ during EPOC?
11. Give the RER for 100% fat oxidation and 100% carbohydrate oxidation, and derive them from the respective oxidation equations.
12. What does an RER greater than 1.00 indicate?
13. Describe how the relative contribution of carbohydrate versus fat to total energy expenditure changes as exercise intensity increases from rest to maximal $\dot{V}{O}_{2max}$.
14. Describe how the relative contribution of carbohydrate versus fat to total energy expenditure changes as exercise duration increases from rest to 150 minutes at a constant intensity.
15. What triggers increased lipolysis with increasing exercise duration, and what is released?
16. How does training affect RQ during prolonged submaximal exercise, and what does this indicate?
17. List four mechanisms by which training enhances fat metabolism.
18. Describe the cycle of triglyceride storage and mobilisation between the capillary and the adipocyte, naming the two enzymes involved.
19. What proportion of total energy production does protein normally contribute, and under what circumstances can this increase, and to what range?
20. Describe the two mechanisms (acute and chronic) by which exercise increases GLUT4-mediated glucose uptake into muscle.
21. List the ways exercise improves overall glucose regulation.
22. Why is lactate production during high-intensity exercise not due to insufficient oxygen delivery to muscle?
23. Explain why lactate/lactic acid is not the main source of increased H+ (acidity) during high-intensity exercise, and identify what is.
24. State two further reasons lactate should not be blamed for exercise-related fatigue or pain.
25. In the postprandial triglyceride study, what change was seen in plasma triglycerides and fat storage after adopting short walks before meals versus a no-exercise control?
26. In the exercise-snacking and sitting-interruption research, what glucose-related benefits were reported, and which population showed a greater effect?
27. List the structural, biochemical, and systemic categories of endurance training adaptation, giving two examples from each.
28. Integrative: explain how the shift in fuel source with increasing exercise duration (carbohydrate to fat) connects to the hormonal/enzymatic changes described for lipolysis, and to the training-induced RQ differences seen at 40% $\dot{V}{O}_{2max}$.
29. Integrative: a patient with impaired glucose tolerance wants to lower fasting glucose with minimal disruption to their day. Based on the exercise-snacking and sitting-interruption findings, what pattern of activity would be supported by this lecture’s evidence?

Answers

Reveal answers

1. Phosphagen (ATP-CP): high power (4.4 mol ATP/min), low capacity (0.7 mol ATP total). Anaerobic glycolysis: high-ish power (2.4), low-ish capacity (1.6). Aerobic CHO: lower power (1.0), high capacity (84.0). Fat: lowest power (0.4), highest capacity (4000).
2. ATP-CP dominates almost immediately (~10 s) then declines rapidly to near zero by ~1’40”. Anaerobic glycolysis peaks around 45 s–1’40” then gradually declines. Aerobic starts near zero, rises steadily, overtakes anaerobic glycolysis around 1’40”–3’30”, and becomes dominant by ~27 min. [Note: the slide’s printed table for the 27 min column (97% anaerobic/3% aerobic) is flagged as possibly a typo/swap, inconsistent with the graph and trend.]
3. $\dot{V}{O}_2$ = the volume of oxygen consumed per unit time (L/min or mL/kg/min). $\dot{V}{O}_{2max}$ = the maximal rate of oxygen consumption (maximal aerobic capacity); more oxygen used means more ATP produced aerobically.
4. Because $\dot{V}{O}_{2max}$ is inversely correlated with cardiovascular and other chronic disease risk and with all-cause mortality, not just with endurance performance.
5. $\dot{Q}=HR\times SV$. Resting ≈ 5 L/min; maximal exercise = 20–25 L/min.
6. Heart rate ↑, stroke volume ↑, breathing rate ↑, breathing depth ↑; blood flow to muscle ~20% (rest) → ~80%+ (max); oxygen extraction ~25% (rest) → 75–85% (max).
7. Increase: plasma volume, stroke volume, maximal cardiac output, capillarisation, blood flow to muscle, oxygen extraction, red blood cells/O2 delivery. Decrease: resting heart rate, blood pressure.
8. The oxygen deficit is the lag in oxygen uptake at the start of exercise (steady state takes ~1–4 min to reach); it’s a misnomer because anaerobic systems fill the gap so total ATP production is not actually deficient. Untrained individuals take longer to reach steady-rate $\dot{V}{O}_2$ and incur a larger deficit than trained individuals.
9. EPOC (excess post-exercise oxygen consumption) is the elevation of $\dot{V}{O}_2$ above baseline after exercise stops. Its magnitude increases with exercise intensity: light exercise gives a small deficit/small recovery $\dot{V}{O}_2$; moderate-heavy aerobic exercise gives a larger deficit with fast and slow recovery components; all-out maximal exercise gives the largest deficit and longest recovery $\dot{V}{O}_2$.
10. Replenishing fuel stores (creatine phosphate, glycogen, intramuscular triglycerides) and returning the body to homeostasis.
11. Fat (palmitic acid): $C_{16}{H}_{32}{O}_2+23O_2\to 16C{O}_2+16H_{2}O$, $R=16/23=0.70$. Glucose: $C_6{H}_{12}{O}_6+6O_2\to 6C{O}_2+6H_{2}O$, $R=6/6=1.00$.
12. It indicates a contribution from anaerobic metabolism.
13. CHO contribution rises from ~28% at rest to ~100% at maximal intensity; lipid contribution falls from ~72% to near 0%, crossing CHO around 60–70% $\dot{V}{O}_{2max}$; RER rises from ~0.8 to ~1.0, staying high from ~60% onward.
14. CHO rises sharply to a peak (~68%) at 20–30 min then declines to ~35% by 150 min; lipid falls to a low (~30%) at 20–30 min then rises to ~58% by 150 min, crossing CHO again around 120 min; RER rises quickly early then stays roughly flat/slightly declining.
15. Decreasing blood insulin levels disinhibit hormone-sensitive lipase, increasing the rate of lipolysis, which breaks down triglyceride into glycerol and free fatty acids.
16. Trained individuals show a consistently lower RQ than untrained individuals throughout prolonged submaximal exercise, indicating greater reliance on fat oxidation.
17. Increased O2 availability; increased mitochondria (Krebs cycle and beta-oxidation enzymes); increased IMTG stores; increased enzyme activity/hormone sensitivity for lipolysis.
18. Circulating triglyceride/FA (from liver/intestine) is acted on by lipoprotein lipase at the capillary wall, releasing fatty acids that enter the adipocyte and combine with α-glycerophosphate to re-form triglyceride for storage; hormone-sensitive lipase then acts on the stored triglyceride, releasing fatty acids back to the capillary for oxidation in other tissues.
19. Normally only ~2% of total energy production; can increase to 5–15% with prolonged/intensive exercise, especially if glycogen is depleted.
20. Acute: translocation of existing GLUT4-containing vesicles to the plasma membrane, via converging insulin-signalling (insulin receptor→IRS-1→PI-3-kinase→PDK→Akt→GSK3) and contraction-signalling (ATP/AMP/Ca2+→AMPK, p38 MAPK, PKC, NOS→NO) pathways. Chronic: increased synthesis of GLUT4 protein via AMPK and calcium-calmodulin/CaMK/p38 MAPK signalling converging on PGC-1α, which also drives fibre-type transformation and mitochondrial biogenesis.
21. Increased glucose delivery via increased blood flow; greater muscle mass as an uptake site; more GLUT4 per given stimulus; additive contraction and insulin effects; increased muscle glucose phosphorylation via increased hexokinase activity.
22. Because “anaerobic exercise” refers to which energy systems are being used, not to a lack of oxygen available to the muscle.
23. Pyruvate → lactate (via NADH/NAD+) actually takes up H+, and lactate leaves the muscle within minutes; the H+ that drives acidity is released by ATP hydrolysis, and more H+ is released this way during high-intensity exercise than lactate production could ever release.
24. Lactate is used as an energy source by resting muscle and as a gluconeogenic precursor by the liver; it does not cause fatigue or post-exercise pain and clears from the muscle within minutes.
25. Both walking patterns (1×30 min or 3×10 min at 60% $\dot{V}{O}_{2max}$) reduced postprandial plasma triglycerides compared to control, increased fat oxidised by ~5 g over 11 hours, and reduced fat storage by 4–5% versus control.
26. Exercise snacking (frequent short low-moderate intensity walks) was associated with lower fasting glucose; interrupting prolonged sitting with walking every 15–20 min lowered postprandial glucose and insulin (less so with standing/resistance breaks); the effect was greater in obese individuals.
27. Structural: e.g. increased fibre size (Type 1), increased capillary density/blood flow. Biochemical: e.g. decreased basal/glucose-stimulated insulin, increased mitochondria. Systemic: e.g. improved cardiovascular function, decreased LDL/VLDL and increased HDL cholesterol.
28. As exercise duration increases, falling glycogen and declining insulin disinhibit hormone-sensitive lipase, increasing lipolysis and shifting fuel use from carbohydrate toward fat — the same enzyme (hormone-sensitive lipase) and lipolytic pathway that training enhances (via more enzyme activity/hormone sensitivity), which is reflected functionally as a lower RQ (greater fat reliance) in trained versus untrained individuals across a bout of submaximal exercise.
29. Frequent short bouts of low-to-moderate intensity walking through the day (exercise snacking, >5×/day, >3 min each, and/or breaking up prolonged sitting with walking every 15–20 min) — the lecture’s evidence associates this pattern with lower fasting and postprandial glucose, with a greater effect in obese individuals.