SPRINT Flashcards

1
Q

what are the determinants of sprint success?

A
  • rate of anaerobic energy expenditure
  • running economy
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2
Q

rate of anaerobic expenditure - Metabolism

A

phosphocreatine, glycolysis and oxidative phosphorylation - made up of enzymes, metabolites, and buffer capacity

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3
Q

rate of anaerobic expenditure - Morphology

A

muscle fibre type, muscle fibre size, sarcoplasmic reticulum, and muscle conduction velocity

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4
Q

how is energy available for work? (highest energy potential to lowest)

A

change in G (free energy)
ATP
Phosphocreatine
Anaerobic glycolysis
carbohydrate oxidation
fat oxidation
protein breakdown

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5
Q

Gaitanos et al., 1993 - metabolism during 6s sprint

A
  • 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
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6
Q

Nevill et al., 1989 - metabolism during 30s sprint

A
  • 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
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7
Q

Phosphocreatine (PCr)

A
  • 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
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8
Q

Bogdanis et al., 1995 - PCr resynthesis

A

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

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9
Q

Casey and Greenhoff, 2000 - creatine supplementation, skeletal muscle metabolism and performance

A

-> 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

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10
Q

Bracken et al., 2005 - Sprinting and alkalising agents

A
  • ingestion of oral alkalising agent like sodium citrate or bicarbonate increase extracellular buffering capacity
  • bicarbonate and base excess concs increase with sodium citrate ingestion
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11
Q

Wilkes et al., 1983 - sprinting and alkalising agents

A
  • 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
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12
Q

Costill et al., 1984 - sprinting and alkalising agents

A
  • 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
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13
Q

Oral alkalising agents improve performance

A

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

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14
Q

Cox and Jenkins, 1994 - sodium citrate ingestion

A
  • 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
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15
Q

Oral alkalising agents research differences are due to:

A
  • 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)
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16
Q

Effects of Sprint Training on Exercise - Harmer et al., 1994

A
  • 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
17
Q

Harmer et al., 2000 - Sprint Training Protocol

A
  • 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
18
Q

Harmer et al., 2000 - Parameters Reduced Post-Match:

A
  • muscle and plasma lactate
  • H+ concs
  • anaerobic ATP production
  • glycogen
  • IMP accumulation
  • peak plasma K+
  • Plasma NA
19
Q

Burgomaster et al., 2005

A
  • 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%