what are the determinants of sprint success?
- rate of anaerobic energy expenditure
- running economy
rate of anaerobic expenditure - Metabolism
phosphocreatine, glycolysis and oxidative phosphorylation - made up of enzymes, metabolites, and buffer capacity
rate of anaerobic expenditure - Morphology
muscle fibre type, muscle fibre size, sarcoplasmic reticulum, and muscle conduction velocity
how is energy available for work? (highest energy potential to lowest)
change in G (free energy)
ATP
Phosphocreatine
Anaerobic glycolysis
carbohydrate oxidation
fat oxidation
protein breakdown
Gaitanos et al., 1993 - metabolism during 6s sprint
- 1st bout of 6s maximal ex - PCr conc fell by 57% - muscle lactate increased to 28.6mmol/kg wt, confirming glycolytic activity
- 10th sprint no change in muscle lactate conc even tho MPO reduced to 73% of that of 1st sprint
- reduced glycogenesis - despite high plasma epinephrine conc after 9th sprint
- considerable reduction in contribution of anaerobic glycogenolysis to ATP production - suggested during 1st sprint power output supported by energy mainly derived from PCr degradation and an increased aerobic metabolism
Nevill et al., 1989 - metabolism during 30s sprint
- metabolic responses to 110% run unchanged across 8 week period
- sprint training resulted in 12% (P>0.05) and 6% (NS) improvement in peak and mean power output respectively
- increase in post-ex muscle lactate and plasma norepinephrine concs and decrease in post-ex blood. no change in skeletal muscle buffering capacity
Phosphocreatine (PCr)
- cytoplasmic PCr present in muscle cell at a conc of ~75mmol.kg dm-1 (x3 more than ATP)
- could support ATP resynthesis for ~6-8s of maximal-ex
- free energy of PCr hydrolysis (-43KJ mole-1) is greater than ATP (-31KJ mole-1) resulting in greater likelihood of change in G occurring from PCr to ADP to reform ATP
Bogdanis et al., 1995 - PCr resynthesis
modelling of the individual PCr resynthesis using a power function curve gave the average for t1/2 for PCr resynthesis of 56.6 ± 7.3s
Casey and Greenhoff, 2000 - creatine supplementation, skeletal muscle metabolism and performance
-> high energy phosphates are utilised in maximal-ex
-> creatine supplementation increases muscle creatine content and max and total external work
-> different creatine supplementation strategies can increase muscle creatine content
-> both physical exercise and CHO supplementation can influence effectiveness of creatine supplementation strategies
Bracken et al., 2005 - Sprinting and alkalising agents
- ingestion of oral alkalising agent like sodium citrate or bicarbonate increase extracellular buffering capacity
- bicarbonate and base excess concs increase with sodium citrate ingestion
Wilkes et al., 1983 - sprinting and alkalising agents
- raised extracellular pH and bicarbonate conc facilitates a greater trans-membrane flux of muscle lactate and H+ to extracellular fluid
- which may enhance the muscle contractile performance and delay onset of muscle fatigue during high intensity-ex
Costill et al., 1984 - sprinting and alkalising agents
- sodium bicarbonate ingestion caused greater muscle pH values before 5th bout of cycle ex compared to con
- suggests increased transmembrane flux of H+ from muscle to circulation
Oral alkalising agents improve performance
significant improvements in high intensity-ex have been reported in some (Goldfinch et al., 1988) but not all (Katz et al., 1984) studies involving administration of oral ingestion of alkalising agents
Cox and Jenkins, 1994 - sodium citrate ingestion
- no differences in performance
- exercise VCO2 and changes in venous blood (HCO3) were higher in citrate condition
- peak post-ex plasma lactate concs and post-ex venous blood pH significantly higher following citrate ingestionn
Oral alkalising agents research differences are due to:
- differences in oral alkalising agents (citrate vs bicarbonate)
- differences in dosages and how dose is applied (i.e. capsule vs powder)
- timing of ingestion (60-120 mins)
- subjects used (trained vs UT)
- experimental model employed (intensity, frequency of ex, mode, time of post-ex samples)
Effects of Sprint Training on Exercise - Harmer et al., 1994
- some changes in metabolites when exercise is continued to exhaustion either pre- or post-sprint training
- some changes in metabolites when exercise is matched either pre or post-sprint training
- sprint training reduces anaerobic ATP production resulting from high intensity-ex as aerobic metabolism is enhanced
Harmer et al., 2000 - Sprint Training Protocol
- pre train test 1 @130% VO2max to exhaustion
- post train test 1 @130% VO2max to Pre-T volume
- post train test 2 @130%VO2max to exhaustion
- 30s cycle sprint, 4 mins recovery
Harmer et al., 2000 - Parameters Reduced Post-Match:
- muscle and plasma lactate
- H+ concs
- anaerobic ATP production
- glycogen
- IMP accumulation
- peak plasma K+
- Plasma NA
Burgomaster et al., 2005
- PPO significantly increased but wasn’t due to increases in resting ATP or PCr concs
- 2 weeks sprint training increases muscle oxidative potential and doubles endurance capacity during intense cycle exercise
- resting muscle glycogen increased by 26%
- resting citrate synthase increased by 38%
