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Alan Richardson

on 22 March 2017

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Transcript of Fatigue

Inorganic Phosphate Accumulation
Direct action on cross bridge cycling.

Pi release coupled to the powerstroke
accumulation would reverse this step

Metabolic Acidosis
& the Nervous System
Effect of acidosis may also be indirect

Extracellular acidosis activates group III-IV afferents (nerves) and hence is involved in the sensation of discomfort in fatigue

Training which induces high Blac levels - learn to cope with the acidosis induced discomfort without loosing pace/power/technique

Training to cope with high acidotic levels??

Lactate Accumulation
When production exceeds clearance

Accumulation of H+ ions causes acidosis within the muscle

Buffers (e.g. sodium bicarbonate) minimise disrupting influence of H+

Without buffers H+ would lower pH to 1.5 – killing cells

H+ concentration buffered so that pH falls no lower than 6.4 at exhaustion

Fatigue in Sprint Activities
Dr Alan Richardson
Sport & Exercise Science, University of Brighton

Sprint Performance
Dr Alan Richardson
Ability to maintain a high velocity for the race duration
ATP resynthesis is generated rapidly and without oxygen from a high energy phosphate compound
Crucial during transition from low to high energy demand
4 – 6 times more CP in the cell than ATP
ATP and CP together can support exercise for up to 20sec
So what could we do?
ATP depleted less rapidly than CP
As CP reduces, ability to replace ATP is hindered
Repeated MVCs - fatigue coincides with CP depletion
Basis for creatine supplementation

What does the evidence say?
In conclusion, CrS significantly increased skeletal muscle TCr, CrP, and free Cr contents, and these remained significantly elevated 2 wk after cessation of supplementation. Each had returned to control levels by 4 wk after CrS. Despite these muscle adaptations, peak power and work output during five bouts of maximal 10-s cycle sprints were unchanged by CrS, either acutely or for up to 4 wk after supplementation, in comparison to the placebo group. Thus CrS did not increase maximal intermittent sprinting performance.
A significant (P < 0.05) increase in performance (+7%) at the end [4-6 s] of the later sprints (4-7 and 8-10) was observed combined with a lower production of blood lactate (-1 mmol x L(-1)) with Cr supplementation. The concentration of Cr was increased significantly in urine (P < 0.001) and serum (P = 0.005), whereas creatinine (Crn) was increased in serum (P < 0.001). Crn in urine and Crn clearance did not change significantly with Cr intake. There were no significant changes in the analyzed blood enzyme activities. A significant gain of body weight (pre-Cr 76.5 +/- 1.7 kg to 77.9 +/- 1.7 kg post-Cr) with Cr supplementation was measured, but no accompanying increase of muscle mass in a limited volume of the lower limb was observed by MRI.
Breakdown of glucose via glycolytic enzymes
Glucose stored as glycogen
When glycogen serves as the source of glucose for energy = glycogenolysis
When glycolysis begins with glycogen there is a net gain of 3 ATP rather than 2 as occurs when glycolysis begins with glucose itself

Anaerobic glycolysis:
Glucose + 2 ADP + 2 H+  2 Pyruvate + 2 ATP

Anaerobic glycogenolysis:
Glycogen + 3 ADP + 3 H+  2 Pyruvate + 3 ATP

H+ + NaHCO3 Na + H2O + CO2

Lactate buffered by bicarbonate.
Excess CO2 stimulates pulmonary ventilation
H+ + HCO3 H2CO3 H2O + CO2
With Sodium Bicarbonate Supplementation
Energy Systems
Repeated Sprint Performance
Directed Study
Consider your sport:
Is there fatigue?
Does this have any consequence to performance?
What physiologically is causing a decline in exercise tolerance?
I will be asking you next week to discuss you sport with us all

And yes I will pick on people
- Repeated Sprint Recovery
What is repeated sprint activity? - Relevance
Repeated ANAEROBIC bouts
Term sprint often used in literature as an easier method to use within research - questionable specificity
Recovery from a single sprint
Assessing Maximal Accumulated Oxygen Deficit
But how do we know our
anaerobic capacity
if we utilise aerobic metabolism at the same time....?
Using linear relationship between exercise intensity and VO2.

VO2 measured at 4-submax workloads and extrapolation of running speed @ 120% VO2max

2nd visit – run to exhaustion at 120% VO2max

MAOD calculated as difference between O2 demand for the exercise intensity and actual VO2 during the exercise

Over the 30 s,
aerobic contribution =16%,
glycolytic contribution =56%,
ATP-PC contribution =28%
A Single Wingate Test
Blood Lactate Responses to a Wingate
Blood lactate can give an indication of the underlying metabolism
Response slow - Peak BLa ~5min after test completion
Recovery From Multiple Sprints
ATP-PC Recovery
Elite sprinters resynthesise ATP rapidly – 1000 fold increase within several seconds

50% resynthesised with 30s aerobic recovery and total restoration within 5 min

Causes of Fatigue
What is Fatigue?
Intracellular pH below 6.9 inhibits action of PFK slowing rate of glycolysis and ATP production

At 6.4 no further glycolysis takes place

H+ may also displace Ca in muscle fibre, interfering with actin-myosin cross bridge cycling

Low muscle pH is the major limiter of performance and the main cause of fatigue in max. exercise of 20 – 30s duration

Central Fatigue Limiting Performance?
Lactic Acid is NOT the cause of fatigue!
Patients fatigue very easily – constantly tired

Cannot produce myophosphorylase to breakdown glycogen to glucose (preventing very little glycolytic activity) – and therefore cannot accumulate lactate
McArdle's Patients
Lactic acid exists within the body for a very short period in very small quantities

Becomes H+ and Lactate.

Lactic Acid and H+ are not the same thing!
When ATP provision cannot
be maintained
Pairs of ADP molecules
generate AMP
AMP further deaminated
Reduces amount of ADP for
Increased Ammonia
– peripherally induces PFK activity
– increasing glycolytic flux
– increasing La accumulation
Transported systemically to brain
- disrupts activity of vital neurotransmitter
activity (e.g. GABA and glutamate)
Brain may act as a safety device only activating a small proportion of that available , even when trying to recruit our 'maximum'

Stimulation whether noise, verbal or electrical can induce increases in force production acutely.

A very well discussed bone of contention within the literature!

Central Governor???
ATP Provision
Total Anaerobic ATP production during final sprint reduced to 35% of levels for first sprint
Gaitanos et al. (1993). J Appl Physiol 75: 712

30 s of passive recovery b/w 6 s cycling sprints

Anaerobic Sources of ATP in 10 x 6 s sprints
Glycolytic Contribution to Repeated Sprints
In 4 subjects, 0% contribution from glycolysis in 10th sprint

Peak power measured pre and post (0s) 30s sprint, then a second 30 s sprint was performed either 1.5, 3 or 6 mins after the first (on 3 separate occasions).

Restoration of peak power followed closely the pattern of CP replenishment, even though pH was still relatively low – around 6.7.

Increasing Aerobic Contribution to Repeated Sprints
Aerobic contribution to single 6s sprint is low (<10%)
As sprints are repeated level of aerobic ATP provision increases
During recovery VO2 remains elevated to:
Replenish MbO2 stores
Resynthesize CP
Metabolise lactate
Remove accumulated Pi
If subsequent sprints before VO2 falls back to resting levels, VO2 of successive sprint will be elevated..
Cumulative response

Increasing Aerobic Contribution
Conclusions .......
Lactate or lactic acid is not the cause of fatigue!

Decrease in pH prevents enzymatic processes – e.g PFK

Metabolic acidosis may induce nervous pain

Inorganic Phosphates may reduce crossbridge cycling efficency

Ammonia can accumulate during heavy exercise causing a number of serious detrimental issues with fuel and muscle metabolism.

The brain may act as a safety device to prevent us from producing our true 'maximal'

Directed Study
This will help you with the lab report!
Write a short (4 line review of Bogdanis paper) and write notes as you go through the Glaiser review.

These will help you write and find other articles required to do the anaerobic based lab report.

Bogdanis, G.C., Nevil, M.E., Boobis, L.H., Lakomy, H.K.A, Nevil, A.M. (1995). Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. Journal of Physiology, 482(2), 467-480.

Glaister, M. (2005). Multiple Sprint Work. Sports Medicine, 35(9), 757-777.
Baldari, C., Videira, M., Madeira, F., Sergio, J. & Guidetti, L. (2004). LActate removal during recovery related to the individual anaerobic and ventilatory thresholds of soccer players. Eur J Appl Physiology, 9, 224-230.

Bogdanis, G.C., Nevil, M.E., Boobis, L.H., Lakomy, H.K.A, Nevil, A.M. (1995). Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. Journal of Physiology, 482(2), 467-480.

Crisafulli, A., Valentina, O., Melis, F., Tocco, F. & Concu, A. (2003). Hemodynamics during active and passive recovery from a asingle bout of supramaximal exercise. Eur J Appl Physiology, 89, 209-216

Glaister, M. (2005). Multiple Sprint Work. Sports Medicine, 35(9), 757-777.
Useful Texts for the Lab Report
Directed Study
Consider what physiological and perceptual variables have between used to evaluate recovery from repeated sprint activity.
List these and consider how these could be used within you lab report.
Find an article that uses these variables.
What kind of changes do they see with repeated sprints?
e.g. VO2 - increased in subsequent sprints. Lactate elevated 3mins post final sprint?
Abstract The aim of this study was to compare the lactate (La) removal during active recovery at three different work rates below the individual anaerobic threshold (IAT). Recently, it has been recommended that exercise intensity should be determined in relation to the IAT instead of the percentage of maximal oxygen uptake (VO2max), especially for training and research purposes. Therefore, we defined the recovery work rates by calculating 50% of the threshold difference (DT) between the IAT and the individual ventilatory threshold (IVT) work rates, then choosing the IVT+50%DT, the IVT and the IVT50%DT. All these work rates fell within the range (30–70% VVO2max) previously reported for optimal La removal. After a 6-min treadmill run at 90% VV_ O2max, soccer players [n=12 male, age 22 (1) years] performed, in a random order, four 30-min recovery treatments: (1) run at IVT+50%DT, (2) at IVT, (3) at IVT50%DT, (4) passive recovery. La was obtained at 1, 3, 6, 9, 12, 15, 20, 25 and 30 min of recovery. The La removal curve was significantly affected by treatments (P<0.01) and recovery timing (P<0.01), with a significant interaction between them (P<0.01). Although they were more efficient than passive recovery, the studied work rates [between 39 (7) and 60 (4)% VVO2max) produced different lactate removal curves. IVT and IVT50%DT were significantly more efficient than IVT+50%DT, while no difference was found between IVT and IVT50%DT for any time point. In conclusion, both IVT50%DT and IVT were efficient individual work rates for La removal, and no further La decrease occurred after 20 min.
Active Vs Passive Recovery from Sprint Activity
Faster recovery of intracellular pH.
pH recovers quicker in Type I than Type II fibres.
Lactate clearance – Cori Cycle
Increased pyruvate dehydrogenase (PDH) activation?
Increased Krebs cycle substrate - pyruvate?
Intensity specific - LT?
Increased mean power, reduced fatigue index. As glycolytic energy production is improved.
Type of Recovery?
Maintenance of blood pressure

Prevents blood pooling

re-oxidation of myoglobin and hemoglobin

Increased removal
of muscle lactate
and H+

Increased aerobic contribution to energy supply - activation of PDH?

Increased CP resynthesis?

Reoxidation of lactate in muscle, non working muscles, liver and heart.

Increased blood
flow and O2 transport

Mechanisms explaining improvement

Lactate clearance – Active vs Passive

Performance changes – Mean Power or Work Done – Glycolytic energy

Performance changes – Peak Power – PCr + ATP degradation & resynthesis

Training state and recovery – Sport type important?
pH changes, lactate clearance, sympathetic changes

VO2 increases with repeated sprints

Write down the key parts of this lecture that would help with writing you lab report. What issue could you consider discussing?....

Key Points for Lab Report
As recovery periods are shortened, responses regress to those of continuous high intensity exercise

Shorter recovery periods associated with higher VO2, RPE, RER, HR and fatigue
20 x 5 s multiple sprint protocol with 10 s rest – HR responses identical to continuous HIE

Glaister et al. (2005). J Strength Cond Res 19: 831

Duration of recovery

Recovery of ph

Next Week
Looking at more of the Active Vs Passive Literature

Considering how to analyse the data from the labs for the lab report.
Thigh O2 uptake

At onset of intense exercise – delay in VO2 by working muscles

Oxygen bound to myoglobin (MbO2) can buffer initial oxygen demand of exercise MbO2 rapidly desaturated in response to rapid drop in intracellular partial pressure of oxygen

During recovery MbO2 are fully replenished within 20 s
Therefore unlikely that O2 availability from myoglobin is limiting factor during repeated sprint


Answers on Student Central
25 marks each
Creatine is a now widely used dietary supplement in sporting populations. Describe the physiological rationale regarding why creatine supplementation might be effective, and who may benefit most from its use. Provide evidence based conclusions about its effectiveness.

Explain the degradation in power output during repeated 10 x 6sec anaerobic bouts. Discuss how variations in recovery would cause physiological changes to allow repeated maximal performance.

Inorganic Phosphate Clearance
Key Considerations of Recovery
Recovery and Training State
Lactate Clearance
Consider why would active recovery be better than passive?? - What are the mechanistic processes occuring
As repeated sprints continue, aerobic sources become predominant energy yield.

Replenishment of energy closely related to sprint performance indicators
- PCr and Peak Power %

Clearance of waste products and resynthesis of energy providers essential during recovery
- these mechanism improve with training.
Purpose: To compare active versus passive recovery on performance and metabolism during a test of repeated-sprint ability.

Methods: Nine males performed four repeated-sprint cycle tests (six 4-s sprints, every 25 s) in a randomized, counterbalanced order: two tests with active recovery (~32% VO2max) and two with passive recovery. Muscle biopsies were taken during the four tests from the vastus lateralis pretest, immediately posttest, and following 21 s of recovery to determine phosphocreatine ([PCr]), creatine, and muscle lactate concentration ([MLa-]).

Results: Active recovery resulted in a greater power decrement than passive recovery (7.4 ± 2.2 vs 5.6 ± 1.8%, P = 0.01) and lower final peak power (14.9 ± 1.5 vs 15.3 ± 1.5 W·kg-1, P = 0.02). However, there was no significant difference in work decrement or total work. The percent of resting [PCr] was lower and approached significance posttest (32.6 ± 10.6 vs 45.3 ± 18.6%; P = 0.06; effect size (ES) = 0.8) and following 21 s of recovery (54.6 ± 9.6 vs 71.7 ± 14.1%; P = 0.06; ES = 1.2) during active recovery. The [MLa-] was significantly higher posttest during active recovery (71.7 ± 12.3 vs 55.2 ± 15.7 mmol·kg-1 dm; P = 0.048; ES = 1.2); however, no significant differences were evident following 21 s of recovery (55.0 ± 11.3 vs 48.4 ± 16.7 mmol·kg-1 dm, P = 0.07; ES = 0.5).

Conclusions: Despite no differences in the majority of performance measures, active recovery resulted in a significantly lower final peak power, a greater peak power decrement, a higher [MLa-], and a strong trend towards lower [PCr], suggesting a potential suboptimal effect of active recovery during repeated-sprint exercise.
Moderate to low intensity Active Recovery better for lactate removal
- Can be too hard and can be too little (Passive)
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