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Metabolic Response to Exercise

• Foss ch. 3• Brooks - Exercise Phys. Ch. 10

– selected sections - Brooks Ch. 5-7

• Outline• Fuel utilization - crossover concept• Recovery

– Glycogen re-synthesis– lactate– performance

• Lactate shuttles• Endurance Training effects

– lactate, Glycolysis, mitochondria

• Anaerobic Threshold??

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Measurement of Metabolic Response

• Evaluation provides info about absolute and relative intensity of exercise bout (fig 10.1a)

– absolute VO2 (L/min or ml/Kg/min)– % of VO2 max– % of HR max– multiples of Metabolic Rate (MET’s)

• 1kcal/Kg/hour at rest

• determination of metabolic response allows estimation of – Total energy cost– Nutritional requirements– Efficiency calculations– Estimation of workload indicates

metabolic system utilization, and the potential for fatigue

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Substrate Utilization• Brooks p 133• Power output is the most important

factor determining fuel utilization• Crossover concept

– post absorptive and resting• lipid used predominantly

– with increasing intensity• fuel mix switches from lipid to CHO

• Fig 7-12• training - displaces absolute intensity

at which crossover occurs – epinephrine suppression– inc lactate clearance– inc mitochondria – prolong onset of glycogen breakdown,

depletion and fatigue

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Fuel Utilization• Fig 7-11• Glucose - fatty acid cycle• FFA breakdown inhibits glycolysis• PDH is inhibited by Acetyl-CoA

from Beta oxidation• PFK is inhibited by inc citrate from

Beta oxidation and ATP– in highly trained and glycogen depleted

this is accentuated– Fig 7-10 - higher FFA utilization with

higher mitochondrial enzyme activity following training

• Hexokinase is inhibited by its product G6P, which builds up if glycolysis is not active.

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Recovery from Exercise• Ch. 3 - Foss• process of recovery from exercise

involves transition from catabolic to anabolic state– breakdown of glycogen and fats to

replenishment of stores– breakdown of protein to protein

synthesis for muscle growth and repair

• Our discussion of recovery will include;– oxygen consumption post exercise– Replenishment of energy stores– Lactate metabolism(energy or glycogen)

– Replenishment of oxygen stores– intensity and activity specific recovery– guidelines for recovery

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Recovery Oxygen• Recovery O2 - Net amount of oxygen

consumed during recovery from exercise– excess above rest in Litres of O2

• Fast and Slow components– Based on slope of O2 curve– first 2-3 min of recovery - O2 consumption

declines fast– then declines slowly to resting

• Fig 3.1• Fast Component - first 2-3 minutes

– restore myoglobin and blood oxygen– energy cost of elevated ventilation– energy cost of elevate heart activity– replenishment of phosphagen

• volume of O2 for fast component = area under curve– related to intensity not duration

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Recovery Oxygen

• Slow Component– elevated body temperature

• Q10 effect - inc metabolic activity

– cost of ventilation and heart activity– ion redistribution Na+/K+ pump– glycogen re-synthesis– effect of catecholamines and thyroid hormone– oxidation of lactate serves as fuel for many of

these processes

• duration and intensity do not modify slow component until threshold of combined duration and intensity– After 20 min and 80% – We observe a 5 fold increase in the volume of

the slow component

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Energy Stores• Both phosphagens (ATP, CP) and glycogen

are depleted with exercise

• ATP/CP - recover in fast component– measured by sterile biopsy, MRS

– rate of PC recovery indicative of net oxidative ATP synthesis (VO2)

– study of ATP production• 20-25 mmol/L/min glycogen and all fuels

• during exercise– CP can drop to 20%, ATP to 70 %

– CP lowest at fatigue, rises immediately with recovery

• Fig 3.2 - very rapid recovery of CP– 30 sec 70%, 3-5 min 100% recovery

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Phosphagen Recovery(cont.)• Fig 3.3

– occlusion of blood flow - no phosphogen recovery

– ** requires aerobic metabolism– estimate 1.5 L of oxygen for ATP-PC recovery

• Energetics of Recovery• Fig 3.4

– breakdown carbs, fats some lactate– produce ATP which reforms CP– high degree of correlation between phosphagen

depletion and volume of fast component oxygen

• Fig. 3.5– Strong correlation between phosphagen

depletion and volume of the fast component of recovery oxygen - sea level and altitude

• anaerobic power in an athlete related to phosphagen potential - Wingate test

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Glycogen Re-synthesis• Requires 1-2 days and depends on

– type of exercise and amount of dietary carbohydrates consumed

• Two types of exercise investigated– continuous endurance (low intensity)– intermittent exhaustive (high intensity)

• Continuous - (low- moderate intensity)

• Fig 3.6 - diet effect– minor recovery in 1-2 hours, does not

continue with fasting– complete re-synthesis requires high

carbohydrate diet ~ 2 days

– Recovery does not occur without high carbohydrate diet

– depletion of glycogen related to fatigue– Fig 3.7 - heavy training

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Glycogen Re-synthesis • Intermittent (high intensity) exercise• Fig 3.8

– significant re-synthesis in 30 min-2 hrs• does not require food intake

– complete re-synthesis does not require high carbohydrate intake

• only ~ 24 hrs for 100 % recovery

– rapid recovery in first few hours

• Continuous vs. intermittent– amount of glycogen depleted

• Much higher with long duration

– precursor availability• lactate, pyruvate and glucose available after

high intensity exercise

– Muscle fiber type involved in activity• re-synthesis is faster in type II fibers which

are utilized with higher intensity activity

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Lactate Recovery• Blood lactate levels are fairly

constant with rising intensity until a threshold of intensity is reached(10.1b)

– After threshold, you observe a sharp rise in [lactate] along with intensity

– [Lactate] is influenced by the duration of exercise and rest interval between repeated bouts

– Fig 10-2 - lactate turnover

• fig 3.10 - exhaustive exercise – ~25 min for 1/2 recovery (passive)– passive recovery - minimal activity

• Fig 3-11 active vs passive recovery• Fig 3-12 intensity of active recovery

– untrained 30- 45% VO2 Max– trained up to 50-60% - in some studies– glycogen re-synthesis is slowed with

higher intensity active recovery

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Recovery• fig. 3.13(fate of lactate)

• Fig 3.14 (lactate vs slow component)

– close association between the slow component of O2 recovery and the removal of lactate - but not exact

• restoration of O2 stores– fast component - 10-80 seconds

• Ion concentrations– pH - rapid return after light exercise

– heavy exercise dec. From 7-6.4

– ~20 min for recovery

– close correlation to lactate and fatigue– Recovery of Maximum Voluntary

Contraction correlates with Pi (both factors are restored in ~5 min)

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Performance Recovery• How quickly do we regain

performance? - force, power, MVC• Guidelines Table 3.2

– Dependant on • energy system utilized

• Intensity of exercise and type of recovery

• Aerobic fitness (VO2 max) is an important influence as well– good correlation between fast recovery

of muscle function and VO2 max

• why?– Fast component requires O2

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Lactate Shuttles• Intracellular lactate shuttle (Brooks p 69)

– Within one cell– evidence of LDH in mitochondria of

muscle, liver and other cells– evidence that mito in liver and heart

oxidize lactate more than pyruvate– lactate- more than pyruvate - is link

between glycolytic and oxidative met• Fig 5-13, 14 (Brooks)

– rapid glycolysis -creates a rise in cytosolic lactate

– lactate enters mitochondria via MCT pyruvate/lactate carrier (Brooks p79)

– oxidized to pyruvate in mito– continues through TCA (Krebs)– NADH formed inside mitochondria, as

well as recycled in cytosol

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Intercellular Lactate Shuttle

• Between different cells (Brooks p 78)

• Lactate actively oxidized - preferred fuel in heart and slow twitch muscle

• produced in Type IIb fibers– transported directly between cells in

same muscle

– or through blood circulation to type I fibers or heart muscle cells

• Fig 5-20 (Brooks)

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Muscle as Consumer of Lactate

• P 202 - 209 (Brooks)

• Similar to discussions in Foss• EPOC - Excess post-exercise oxygen

consumption- instead of Recovery Oxygen

• Causes for excess oxygen used in recovery

– 13 % increase in BMR / degree Celsius• similar to Q10 effect

– Fig 10-11 - uncoupling of mitochondria - inc ATP needs

– Calcium- accumulates with contraction - mitochondria may sequester Ca++- ATP required to remove it, which may alter net oxidative phosphorylation

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Endurance Training• Table 6-1, 6-2

– With endurance training, we observe • a doubling of enzyme activity

– TCA and ETC - in all muscle fiber types

• a doubling of mitochondrial content

• Table 6-3– improvements in oxidative capacity

correlate well with running endurance• ~ 90 percent correlation

– Correlation between oxidative capacity and VO2 max is not as strong

• ~ 70 percent correlation• ~ 10- 15 % increase in VO2 max with

training vs. ~100% for oxidative capacity

• With an increased mitochondrial content– The given rate of O2 consumption can

occur at a much higher ATP/ADP ratio – Fig 6-13– This reduces carbohydrate breakdown

in favor of lipid metabolism

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Anaerobic Threshold??• Brooks p 215

• Historically, the non linear rise in blood lactate at ~60% VO2 Max was termed the anaerobic threshold– does not however provide info about

anaerobic metabolism– reflects balance between lactate entry

and removal from blood (turnover)– Lactate inflection point is now the

preferred term

• Inflection often corresponds to ventilatory threshold – (non linear rise in ventilation) (talk test)

• However; Fig 10-17 – Patients with McArdles syndrome

• lack of phospohorylase - unable to breakdown glycogen

– Have normal ventilatory threshold• Association, therefore, is not causal

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Lactate Inflection Point• Many factors may influence either

the production or removal of lactate• Type II b fiber recruitment - increases

with intensity - results in higher lactate production

• Sympathetic NS activity increases with intensity of exercise– vasoconstriction (many tissues)

– Leads to reduced oxidation of circulating lactate - ie. less removal

• *local factors (paracrines) in muscle – Stimulate vasodilation – raising % of Cardiac Output to muscle

• Epinephrine and glucagon– stimulate glycogenolysis and glycolysis– higher lactate production

• increased Calcium with contraction - activates glycogenolysis - (Fig 10-18)

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Learning Objectives• Understanding of metabolic influences in

glucose fatty acid cycle

• Distinction between fast and slow components of recovery oxygen– What contributes to the volume of each

component

• Pathways for recovery of energy stores - – Phosphagens, glycogen

• Recovery of resting lactate concentrations– Active vs passive recovery

• Performance recovery– Force, power, MVC

• Lactate shuttles– Oxidative use of lactate - intra vs inter cellular

• Training impacts on fuel use and recovery

• Influences on lactate inflection point