Nutrition and sports lecture notes - NUTRITION AND SPORTS LECTURE 1: AN INTRODUCTION INTO THE FIELD - Studeersnel (2023)



Sports nutrition (science) is the application of nutrition principles for the purpose ofimproving training, recovering and performance.

Recent developments and future‘Customized nutrition’: eating strategies for athletes must take account of each athlete’sphysiological and biochemical characteristics as well as the training load and competitiongoals.Sports nutrition is now more about using nutrition strategies to modulate training-inducedmuscle adaptations. – ‘periodized nutrition’


Performance testing - Real competition - Simulated competition (time trial, Loughborough Soccer Passing Test (LSPT), Leuven Tennis Performance Test) - Determinants of performance: speed, strength (power), coordination, flexibility and endurance.

Measures of sporting performance - Validity (accuracy). Resembles the performance that is simulated. Correlation, prediction. - Reliability (precision). CV, ICC, Pearson’s r. - Sensitivity. To detect small but important differences (smallest difference you can measure).In practice: aspects to control.

External factors to control when doing performance testing - Familiarization (‘experience’). How well do you know what you should do? Crucial! - Verbal encouragement - Music - Feedback - Additional measurements - Diet - Exercise

Dietary intakeOvernight fast vs. pre-event meals, CHO (glycogen), energy, protein, hydration status,caffeine intake/withdrawal. Alcohol consumption, other supplement use.

Dietary standardizationApproach: consider the advantages/disadvantages. Match the level of dietary control.

Exercise standardization - Training status subjects - Habitual training (changes) - Last exercise bout - Experimental exercise intensity o Relative vs absolute intensity


Three different levels of nutrition influenceExercise nutrition: nutrition has a direct impact on exercise performance.Support recovery nutrition: support training sessions with good food.General health nutrition: to stay healthy.

Balanced diet - Diet that supports a healthy and active lifestyle. - Sufficient energy intake  RED-S syndrome (not enough energy to support sports, but just basic functions). - Adequate macronutrients - Sufficient fluid intake - Adequate micronutrients  varied diet (supplementation if needed).

Sport-specific nutrition - Optimize performance and recovery - Macronutrients/fluid  to meet training/competition goals - Timing of nutrient intake - Normal foods - Sport nutrition products

Supplements: Final winning edge (what can I add as the final 1/2 % to enhance performance) - Ergogenic supplements - To “supplement” your diet  not main focus - Be critical, backed-up by science - Discuss with experts (does it work for me?)

(Sport) supplements - ‘Sport nutrition products’ and ‘dietary/ergogenic supplements’.


For very high force contractions lasting only a few seconds, the initial energy source is fromthe ATP stores. This is a very important signal to activate all different processes.

After 2 minutes, maximal dynamic exercise becomes predominantly aerobic.

Substrate level phosphorylation: phosphocreatine + anaerobic glycolysisOxidative phosphorylation: oxidative metabolism


Weightlifters (explosive power)

Energy: ATP that is already availableType 1 fibers  Slow twitch/red fibers: fatigue fibers, canproduce energy for quite a long type before becomingfatigue.Type 2 fibers  fast twitch/white fibers.Color depends on capillary/mitochondrial density.


Almost exclusively depending on the anaerobicmetabolism. - Phosphagen system  relatively low capacity, high power. High active from start onward. o ATP o Mostly phosphocreatine breakdown - Glycolytic system (duration is a little bit longer).  Larger capacity, power is lower. Starts later.Energy peak after already a few seconds (about 4 seconds, phosphocreatine system).

PCr breakdownActivation  decrease ratio ATP/ADP becauseof ATP breakdown.Inhibition  increase ratio ATP/ADP due toincreased aerobic ATP production or decreasedATP utilization.

The complete resynthesis of phosphocreatineafter very high intensity exercise normallytakes roughly 4 minutes (when there is enoughoxygen present). Quite short recovery time!Phosphocreatine resynthesis during recoveryfrom exercise is inhibited by a lack of oxygen.

ATP resynthesis from glycogen metabolismGlycogenolysisGlycolysis - Reach maximum not until 5 seconds (quite slow). - Maintained up to 30 seconds. - Rate lower (2x) size higher (4x) compared to PCr: power output lower.

PCr metabolism is higher from the start and starts to decrease after a few seconds. Glycolyticmetabolism takes a little longer but increases and stays stable for a longer time.

Fatigue: exercise < 10 seconds - Maximum power reached after 3-4 seconds. - Performance depends on maximum speed achieved early in exercise: o PCr availability o Maintenance of force pH depended. - Metabolites implicated. o Pi, H+ and lactate - Dietary consequences

Creatine is 95% stored in our muscles. Endogenous production liver. Diet (meat,supplements!).Taking creatin leads to weight gain (osmotic effect  water).Supports high intensity exercise  muscle mass/function. Allows you to train harder!

Middle distance athlete

The average intensity of exercise (%VO2 max) for an elite middle-distance runner during a1500-meter race will be about 120% VO2.The net production of ATP by substrate-level phosphorylation in glycolysis is 2 from bloodglucose and 3 from glycogen.

(Anaerobic) glycolysisFrom glycogen, you only need 1 ATP input and fromblood glucose, you need 2 ATP input.Glycogen is the preferred starting point, because itcan produce 50% more ATP per time.This whole process takes place in the cytosol, nooxygen is needed.During this whole process, NAD is produced. To keepthe glycolysis running, you need NAD. In pyruvic acid lactic acid, NADH  NAD, so the glycolysis cankeep running. We pay the price: H+ (proton)production, acidification.

Glycogen phosphorylase (important for the breakdown to glucose-1-phosphate). Regulatedby adrenalin and calcium. Decreased by H+.The rate limiting step is regulated by PFK. When F-6-P, ADP increases. Decreased by ATP/PCr,but also H+.

  • First step in mitochondrion.
  • Balance between aerobic (oxidative phosphorylation) and anaerobic metabolism (substrate phosphorylation).
  • Irreversible reaction (only goes in one direction).PDH controlled by two enzymes: PDK (when activated, inhibits PDH) and Calcium.

Fat oxidationFatty acids have a different starting point. Can be in themuscles, but mostly adipose tissue.There is no anaerobic fat metabolism, only aerobic.Always in the mitochondria.

As soon as you start doing exercises  massive increasesin fatty acids.CPT-1 (carnitine) rate limiting enzyme.

Dominant pathway: Acetyl-CoA.If you’re fasted, dominant pathway: Fatty acetyl-CoA.

(de)activation lipolysis - Increase fatty acids due to increased lipolysis: elevation (nor)adrenaline, glucagon, growth hormone, cortisol. - Inhibition lipolysis: lactate accumulation, increase insulin after CHO intake.

High fat oxidation will reduce/limit the oxidation of the glycolytic system.

Factors influencing substrate utilization (see ppt slide 58)

Fatigue endurance athlete‘Hitting the wall’ - Muscle glycogen depletion  shift to fat oxidation. fat oxidation can only meet energy 50-60% VO2max. - Hepatic glycogen depletion: hypoglycemia (prolonged exercise)  brain.

Game player

  • Intermittent sprinting, limited recovery
  • Endurance

Intermittent HI exercise – multiple sprints - Power output falls - Rates of muscle glycogen breakdown, PCr hydrolysis and lactate accumulation all decline. o Recovery time (PCr – 4 min; glycolysis much longer) - Relative contribution of aerobic metabolism increases (PDH activity (first enzyme of the aerobic carbohydrate metabolism). - Plasma glucose well maintained. with repeated sprints: PCr and aerobic, contribution anaerobic glycolysis rapidly decrease


RED-S syndrome  relative energy deficiency in sports.

Energy expenditureEnergy requirement/need: BMR x PAL(physical activity level)  doesn’t work for anathlete.ER = general EE + exercise EE - General EE = (BMR x PAL) x h/ - Exercise EE = (MET x BW) x h

MET score  how much a certain activity requires compared to your basalmetabolic rate.

Physical activity level (PAL)PAL = TEE/BMR

Exercise Energy: MET metabolic equivalents.MET ~ PAL - Per activity: ratio of work metabolic rate to a standard BMR of 1 - 1 standard MET = 1 kcal/kg/h - General values: individual differences, skill, pace, fitness level - Moderate intensity MET 3-

Energy balanceAmount of dietary energy added to or lost from the body’s energy stores after the body’sphysiological systems have completed their work for the day.Energy balance = energy intake – total energy expenditure (EB = EI – TEE)Energy deficit when EI < TEE

Energy balance not the best concept: methodological issues in estimating energy balance,adaptation (if negative energy balance, which creates new energy balance, by reducingBMR).

Energy availabilityAmount of energy remaining for body functions after accounting for energy expended fromphysical activity.  what is necessary for cellular maintenance, bone development, growth,thermoregulation, reproduction etc.The advantage of EA is that it doesn’t fluctuate over time.

EA = energy intake – exercise EE ( per kg FFM)


EI insufficient to support EE required for health, function, and daily living after taking intoaccount the extra energy cost for exercise and sports.

Female athlete triad: the combination of disordered eating (DE) and irregular menstrualcycles eventually leading to a decrease in endogenous estrogen and other hormones,resulting in low bone mineral density (BMD).

Treatment - Increase EI, reduce exercise load. o Energy rich supplement; rest day - Oral contraceptives may be considered for athletes requiring contraception, these may mask the low EA, menstrual dysfunction and perpetuate bone loss. - BMD (bone mineral density): calcium and vitamin D - Psychological factor is generally present: treatment should be provided by a mental health professional knowledgeable about the management of Eds in athletes.



Humans can cope better with extreme heat than with extreme cold.Dealing with heat: vasodilation, sweat loss, behavior  very powerful acclimatization.Dealing with cold: vasoconstriction, shivering, behavior (exercise for heat production,clothing)  poor acclimatization.

Exercise: coping with the heat - Body core temperature and exercise - Impact on performance  heat has effect on different things. - (Early) fatigue from: cardiovascular collapse, hydration & fluid imbalance, metabolic changes, psychological factors (unpleasant).Risk factors heat strain: exercise, solar radiation, no wind, insulation, high temperature &humidity  acclimatization.

Exercise, body temperature and performance (loss)  exercising in the heat will reduceperformance to some extent.

Four ways the body loses heat. 1. Convection: moving air removes radiated heat (warm air just above your skin) 2. Conduction: direct transfer of heat by contact 3. Radiation: emission of electromagnetic radiation (everything with a temperature above the zero point will radiate heat)All these three are bidirectional. 4. Evaporation: loss of heat by evaporation of water (sweat respiration). Strongest way to lose heat.

Heat balance has three parts: heat production/gain, heat loss, heat storage.Heat balance  M(etabolism) +- S(torage) +- R(adiation) +- C(onduction/convection) –E(vaportion) = 0.R & C = dry heat lossE (sweat) = wet heat loss

When heat is stored in the body, body core temperature will increase.

Measuring the human heat balance - Metabolism  indirect calorimetry - Storage  change in body temperature - Radiation  difference skin and ambient temperature - Convection  air flow (wind)! - Conduction  difference skin and ambient temperature (very limited) - Evaporation  body weight change, corrected for fluid loss.

  • Environmental conditions (heat acclimation, altitude)
  • Intensity/duration (very important aspect)
  • Fitness level
  • Body composition (%BF)
  • Medication (diuretics, increases urine loss)

Fluid balance (sweat rate): pre-exercise BW – post exercise BW (+fluid-urine)

Fluid: electrolytesElectrolytes - Sodium and chloride main electrolytes - Sweat is hypotonic  interindividual variation - Extreme conditions up to 7 gram salt loss  acclimatization reduces Na lossHyponatremia  low blood sodium levels (< 130 mmol/L) - Symptoms: headache, nausea, dizziness and muscle weakness. In extreme conditions even lethal symptoms: encephalopathy, pulmonary edema. - Overdrinking!

Hyperhydration – pre-exercise - Euhydration – sodium containing fluid. - Hyperhydration has no thermoregulatory advantages, it only delays dehydration.Fluid overloading: urine production, stomach/gut problems, body weight.

Glycerol hyperhydration  adding to your drink. Kind of expander, will allow your body tokeep a higher water content. - Osmotic pressure/expands extra-intracellular space. - Advantage? /hyponatremia/complaints

Rehydration and recoveryVoluntary fluid intake depends on physiological thirst, perceived thirst. These are alsoaffected by different factors.

Issues in (post-exercise) rehydration - Practical issues - Voluntary intake: 30-70% of their sweat loss  people often fail to rehydrate. - Difficult after high levels of hypohydration or interval between exercises short. - Gastrointestinal physiology: gastric emptying, intestinal absorption.

When to drink? - Prevent a fluid loss of 2-3% of BW (small advantage of lower BW in some sports). - Thirst sensation: delayed compared to other physiological indicators of hypohydration. - Overdrinking: when GI problems, hyponatremia.What to drink? Sodium - Water ingestion: dilution of plasma osmolality and sodium content. Results in increased diuresis (urination) and reduced thirst.

  • So, adding sodium to your drink: water absorption (more water is maintained), maintains osmolality, palatability. ORS 90 mmol/L.

Caffeine and alcohol are potential diuretics.For caffeine there is no clear evidence  increased voluntary intakeAlcohol: increases urinary losses ( ADH) - Effect of low dose alcohol is blurred when dehydrated. - Interfering with ability/interest post exercise nutrition.

Hydration guidelinesBefore exercise - Stay well-hydrated. - Pay attention to thirst. - Drink at least 2 hours 5-10 ml per kg  pale yellow urine - HyperhydrateDuring exercise - Strength/power athletes drink to sweat loss. - Endurance: drink to thirst or prevent > 2-3% BW loss - Cold drink (thermoregulation)After exercise - 150% of fluid loss - Add sodium (and glucose, palatability) - Slower drinking? - Palatable is key! - (Solid foods/sodium replacements)

Skeletal muscle structure - Fibers  cylindrical, multinucleated muscle cells. - Fasciculus  bundle up to 150 muscle fibers. - Epimysium  connective tissue surrounding muscle. - Perimysium  connective tissue surrounding fasciculus. - Endomysium  connective tissue surrounding muscle fiber. - Network of arteries, veins and capillaries around endomysium.

Fiber structure - Sarcolemma  membrane enclosing muscle fiber. Plasma membrane and basement membrane. - Myofibril  basic unit of muscle fiber. - Transverse tubule  invagination of sarcolemma. - Sarcoplasmic reticulum  muscular smooth endoplasmic reticulum, regulating intracellular calcium and structural integrity. - Terminal cisternae  enlargement of SR around t-tubule. - Triad  T-tubule + 2 terminal cisternae, - Nuclei  fibers are also multinucleated (muscle cells are a fusion of multiple cells). - Satellite cells  little cytoplasm located between plasma and basal membrane (= extracellular matrix). Precursor cells: differentiation and augmentation of existing fiber. Satellite cells can differentiate. - Mitochondria  powerhouse of the cell.

Fiber arrangement & forceThe way the fibers are arranged in the muscle, decides the effect on force/function of themuscle.Fusiform versus pennateIncreasing the angle of pennation: decreases force exerted by each fiber (by cosinus of angleof pennation).However, total muscle force is increased by increased fiber packing (more fibers/muscle).

Muscles move in vertical (dottedline) direction, muscle fibers movein diagonal direction.

Muscle only contracts from origin toinsertion. The bigger the angle, theless the power of contraction.Because there is then a muscleforce that the body cannot use.Why would the body do something like this? You can pack muchmore muscle fibers (total sum) this way!

Muscle cross sections - Anatomical cross-sectional area. Does not reflect the number of muscle fibers because of pennation.

  • Physiological cross-sectional area. Total cross-sectional area of all muscle fibers. PSCA = muscle volume/fiber length. Gives a better reflection of muscle force.

PCSA & muscle functionShort fiber length (relative to muscle length): increases maximum force but decreases musclerange of motion (because short length) and contraction velocity (mm change in musclelength/second).

Ultrastructure of skeletal muscleSarcomeres are the functional units of myofibril. Runs from Z-to-Z line.

Sliding-filament theoryActin and myosin fibers (partly) overlap  possibilities for cross-bridge formation. Musclefiber shortens because the myosin and actin filaments slide past each other.

Sarcomere length versus tension: there is maximal tension at optimal overlap of actin andmyosin filaments.The more cross-bridges, the more tension (active force).Even without cross-bridge formation, even if you stretch the muscle too much, there will be aforce  elastic recoil of the muscle (passive force).

Skeletal muscle functioningMuscle contraction results in movement of body parts across a bony lever system. Forcegenerated at the outer end of lever depends on muscle force, but also the relative length ofeffort distance (i., between joint axis and muscle attachment) and resistance distance (i.,between joint axis and outer end of lever.). Mechanical advantage = effort distance / resistance distance.

Role of calciumTropomyosin covers up myosin-binding sites  calcium can bind with troponin, resulting in ashift of tropomyosin  this exposes the myosin-binding sites.

Mechanical energy versus chemical energyMovement of bones is the result of mechanical energy exerted by contraction of the skeletalmuscle. Contraction of the skeletal muscle requires conversion of chemical energy (ATP) tomechanical energy (contraction).

CapillarizationDegree of capillarization: 200-500 capillaries/mm^2 muscle tissue. Compared to other tissue,very highly capillarized. Necessary for oxygen delivery (diffusion), removal metabolicproducts and removal of heat.Capillary to muscle fiber ratio determines exercise endurance capacity.

Skeletal muscle has a rich vascular network, blood flow is rhythmic: vessels compressedduring contraction phase; vessels open. During relaxation phase.During sustained contractions > 60% capacity: anaerobic processes supply ATP.


Muscle innervationSkeletal muscle contractions are under voluntary control. Stimulation originates in motorcortex.Alfa-motor neurons cause release of acetylcholine which stimulate muscle contraction (vianicotinic receptor).

Excitation-contraction coupling  excitation results in calcium release from SR, initiatingcross bridge cycling.

One motor neuron typically innervates more than one muscle fiber. - Motor unit: one motor neuron and all the muscle fibers it innervates. Basic unit of contraction in a muscle.

Size of motor unitsThe smaller the motor units, the more finetuned you can do movements. So, less fibers,more finetuned (e., your hand, compared to your leg).Fine movements versus rapid, concurrent force generation.

Recruitment of muscle fibersDifferent motor neurons innervate different muscle fibers (motor unit). However, one motorunit only contains fibers of the same type!Just like different muscle fiber types, there are also different motor unit types. Contractileproperties of motor units correspond to enclosed fiber types.

Depending on required muscle force, different subtypes of fibers are activated.When needing high muscle force for exercise, you start of using the type 1 muscle fibers. Ifthat isn’t enough for the effort that you’re doing, type 2a and type 2x fibers are added.So, at high level of effort/intensity, you use all your different types of fibers!

Resistance training increases muscle strength by: increasing the physiological cross sectionalarea of the muscle and improving motor neuron functioning.

Summation of contractionsForce of muscle action dependent on: - Number of muscle fibers contracting (recruitment). - Frequency of fiber contraction (tetanus). Next contraction starts before muscle fiber it is fully relaxed  summation.

Training and fiber recruitment: Training improves force and speed of torque. Associated withstronger and faster muscular electrical activity. Training resulted in faster movement andmore force in this movement.Also associated with an increased firing frequency of motor units.Neural changes are the first adaptations of muscle function to exercise training, at later stagealso muscle growth.

Muscle plasticity & trainingEndurance training: low intensity, high repetitive - Preferential activation of (only) slow twitch (type 1) fibers. - Improvement of aerobic plasticity. - Muscles completely rely on your oxidative energy system.Strength training: high intensity, low repetitive - Activations of (eventually) all fiber subtypes. - Improvement of muscle strength.Different responses to training.

Increasing aerobic capacity: capillarizationExercise increases the capillarization of muscle tissue. - >40% increase in the number of capillaries per muscle fiber. - Angiogenesis (formation new blood vessels)  Important role for vascular endothelial growth factor (VEGF).Increase in capillarization means larger supply of oxygen for aerobic ATP production.

Mitochondria  important for oxidative phosphorylation (aerobic energy metabolism).Oxidative phosphorylation (primary oxygen consuming process in mitochondria): electrontransport chain. - Ex vivo assessment of mitochondrial function  high resolution respirometry. Measures disappearance of oxygen from the medium. The higher training status, the higher your aerobic capacity of the muscle cells, the more energy you can generate from oxidative phosphorylation. - In vivo mitochondrial oxidative functioning. o Post-exercise recovery of phosphocreatine  depending on oxidative metabolic pathways  reflects mitochondrial oxidative functioning. The resynthesis of phosphocreatine is completely “payed for” by oxidative phosphorylation. Increasing oxidative phosphorylation. The higher your mitochondrial capacity, the faster the resynthesis of phosphocreatine occurs.

Training and mitochondria: 6 weeks of endurance training increases mitochondrial volumedensity in vastus lateralis muscle.Training and mitochondrial density: endurance training increases mitochondrial density(number (mitochondrial biogenesis) increases!).Increasing mitochondrial capacity requires increased expression of mitochondrial proteins(i., enzymes involved in oxidative phosphorylation).

Endurance training increases mitochondrial activity. This is related to improved performance.


Suggested mechanisms that link exercise to adaptations in mitochondrial biogenesis andfunction: - Increased [Ca2+] in cytosol/mitochondria.

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