EXERCISE PHYSIOLOGY Dr Nicolas Theron Tel : (051)4476559
Cardio-respiratory fitness Heart and blood vessels Lungs Oxygen transport and utilization Neuromuscular function Metabolism
Muscle Classification Type I Slow twitch (endurance) Mitochondria Red Type II Fast twitch (explosive) Few mitochondria White
Muscle Types
ENERGY METABOLISM Anaerobic metabolism Oxygen dependent or independent i.e. whether O 2 is present or not No evidence for skeletal muscle anaerobiosis (oxygen depletion) during exercise So called anaerobic metabolism can occur under fully aerobic conditions (lactate increases progressively from low intensity exercise) Lactic acid not found at physiological ph
Oxygen Independent Metabolism (Anaerobic) ATP (Adenosine Triphosphate) CrP (Creatine Phosphate) Glycogen
Oxygen Dependent Metabolism (Aerobic) Glycogen Glucose FFA (Free Fatty Acids) Aninoacids (Proteins)
Power Systems Energy Metabolism
% Energy cost 60 50 40 30 20 Fat Glucose Glycogen Protein 10 0 30min 240min
Body Energy Stores ATP 5,5kJ PCr 18,4kJ, energy for 10s Glygogen (Glycolytic rate is maximal for 6s then it slows), energy for 40s Regulate to preserve life Carbohydrates energy for 2h Fat energy for 60h (running at 93kJ/min I.e.4min/km)
BELIEFS I : Maximal exercise is limited by failure of adequate O 2 supply to the mitochondria In theory failure of O 2 delivery leads to fatigue
BELIEFS CONT. II :VO 2 max is a reliable predictor of athletic performance ( Hill (1925) / Hill and Lupton (1923) / Hill, Long and Lupton (1924) Hill postulated that fatigue during maximal exercise resulted from skeletal muscle anaerobiosis and lactic acid He also thought lactic acid was the stimulus for contraction and that relaxation occurred when it was buffered.
BELIEFS CONT. III : During exercise of progressive intensity a point can be identified where anaerobiosis occurs i.e. the anaerobic threshold, ventilatory turn point or Owle s point ( Wasserman & Mc Throy 1964) O 2 /ventilation graph exponential CO 2 /ventilation graph linear PaCO 2 normal i.e. metabolic H + ions from glycolysis and lactate from co-efflux
Ventilatory Turn Point
BELIEFS CONT. IV : O 2 consumption begins to plateau During exercise with a progressive increase in intensity, O 2 consumption plateau s (increase in intensity, no increase in O 2 use) i.e. no increase in cardiac output
BELIEFS CONT. V : Oxygen debt (Wyndham et al 1959) EPOC Due to increased metabolic rate Correlates with body temperature, not blood lactate
Oxygen debt
BELIEFS CONT. ALL have no concrete scientific basis due to lack of sophisticated testing methods used in original studies
Oxygen Delivery Ventilation MVV greater than exercise demands Diffusion - O 2 saturation remains normal during maximal exercise O 2 carrying capacity of blood Female athletes, blood doping and EPO Cardiac Output no angina during maximal exercise
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL I) ABSENCE OF A PLATEAU PHENOMENON VO 2 max lower while cycling than running in the same subjects (even in triathletes trained in both disciplines) or when running down hill. (Meyers et al 1990 / 1989, Hartling 1989, Liefeldt 1991, Astrand and Saltin 1961, Schineider 1990)
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL II ) ABSENCE OF MUSCLE RIGOR The end point of anaerobiosis should be depletion of ATP and thus muscle rigor This has never occurred a in living athlete
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL III) ABSENCE OF PASTEUR EFFECT (anoxia increases glycolysis - lactate prodution in yeast ) Glycolysis does not accelerate continuously Cheetham 1986 / Boobis 1987 showed glycolysis maximal in first 6 seconds then fell off. Spriet 1987, ischaemia with a tourniquet - electrical stimulation - again glycolysis fell - contractions reduced before ATP fell - ATP did not drop below 60 % - Rigor did not develop i.e. The muscle contractible function probably regulates the metabolic function
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL IV) REDOX STATE Mitochondinal NAD + / NADH should reduce Graham and Saltin 1989 found it increased
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL V) FATIGUE AT HIGH ALTITUDE Opposite of what we would expect At altitude HR & CO lower but ventilation rate higher IEMG activity lower thus a central fatigue
FATIGUE AT HIGH ALTITUDE Operation Everest Studies Max work = 120 Watts HR = 118 bpm CO = 16 l/min po 2 = 18 kpa Lactate low Ventilation high 120 Watts at sea level the same i.e. the heart does not try to increase the CO
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL VI) VO 2 max IS A POOR PREDICTOR OF ATHLETIC PERFORMANCE Strength training increases endurance performance without increasing VO 2 max Efficiency of movement changes O 2 consumption Elite athletes run longer at a greater %VO 2 max During maximum endurance activity you only recruit 20 % of your muscle (If more hyperthermia & hypotension will develop)
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL VII) Chronic Disease CCF, Renal Failure, COPD, FM Abnormal skeletal muscle found in all patients Heart transplant patients post surgery max work load and VO 2 max do not improve, lactate remains low and histology does not improve 12 months of rehab improves the response
STUDIES : INCOMPATIBLE WITH THE ANAEROBIC METABOLISM MODEL In conclusion: a model of aerobic fatigue must be put forward Benefit - it would protect against muscle rigor
Old Fatigue Model 1880 O 2 limitation / Lactic acid (Substrate deficiency & CV fitness) 1920 Hypoglycaemia 1960 Muscle glycogen depletion 1970 Hyperthermia 1986 Liver glycogen 1987 PO 4- accumulation 1990 Altered cellular function
Cardiovascular / Anaerobic model First organ to suffer would be the heart No anaerobiosis / hypoxia / ischaemia Prolonged exercise Heat / Altitude / Chronic disease Poor predictor of performance Energy supply depletion Recruitment Biomechanical Psychological
New Model Muscle contractile function is regulated ATP use is restricted? Central / Peripheral How blood flow (hypotention) mechanical arrest increased H +, PO 4- &Mg 2+ Hypoxia Hyperthermia Hypoglycaemia Central, BCAA (Tryptophan)
LACTATE 70% of lactate is used as fuel Main fuel for Creb s cycle, not pyruvate Dependent on arrival & disappearance No association to muscle pain or cramping Altitude / Chronic disease / Mc Ardle s syndrome (glycogen phosphorylase deficiency) Ventilatory threshold and early fatigue but no lactate or acidosis
Fluids Dehydration is not a problem Over-hydration can be fatal (25 % of participants in ultra distance events are over-hydrated) (Aspirin and NSAID s add to fluid retention) (Slower participants who drink a lot) Salt is not necessary if you don t drink too much
Iron Man Study 2000 Race time was inversely proportional to serum sodium concentrations Faster finishers were more dehydrated, as much as 8% Average weight loss of 3,7kg was found, which had not normalized 12h after the race Fluid overload (hyponatraemia) resulted in fatigue
Fluid Replacement 6-8% CHO hypotonic solution with 20mmol/l Na +, and 3mmol/l K + is best 500ml 2h before race 200-400ml just prior to start 150-200ml every 15-20 minutes (sachet/cup holds 100-150ml) I.e. 800ml/h and thus end slightly dehydrated
Exercise Associated Muscle Cramps Hyperthermia Dehydration Salt imbalances (serum electrolytes) Metabolic abnormalities Cramps in cold environments (swimmers) Field studies found no difference in serum electrolytes or hydration statuses between controls and athletes with EAMC (Nicol, 1996) Cramps only active muscle Night cramps
New Theory A neuro-physiological model explains EAMC the best Fatigue is the biggest cause of cramping Muscle contractions in a shortened position will result in cramping (At any time)
Mechanisms of Cramps If the inhibition is reduced the muscle cannot relax During fatigue Reduced Golgi tendon activity Inner range of motion No tension on tendon
Exercise Associated Muscle Treatment Adequate training and tapering Go slow and get slower Stretch the muscle immediately should it cramp Optimal fluid and energy replacement to avoid fatigue Cramps
Thank you