Energetics and Fatigue Flashcards
What are the definitions of: Neural Drive Excitation Contraction Energy Supply
Neural drive: the delivery of AP by the nervous system to the neuromuscular junction
Excitation: the processes between the AP arriving at the neuromuscular junction, passing along and into the muscle fibres and releasing calcium
Contraction: the processes between the release of calcium and the production of force
Energy Supply: The provision of chemical energy that is necessary for the contraction to continue
Describe the cycle of ATP?
ATP is hydrolysed which provides the cross bridges within a myofibril the kinetic energy to perform the power stroke. The remaining ADP and Pi is then resynthesised (which requires more energy) and the process begins again.
Phophocreatine slide:
what is the enzyme used to breakdown PCr?
To what extent do PCr levels drop during maximal exercise?
Creatine Kinase
Resting levels of PCr - 80mmol/kg dry mass (dm)
66% decrease after 10 seconds max sprint - 35mmol/kg dm
after 30 seconds max sprint - 15 mmol/kg dm
Describe the process of anaerobic and aerobic CHO metabolism and how this may link with fatigue?
1) muscle glycogen, under the action of enzyme phosphorylase, is broken down into a singular glucose 6 phosphate molecule
- another method is by the transfer of blood glucose into the cell, but this costs energy
2) Glucose 6-p goes through glycolysis: a 10 reaction process that produces 3 ATP and 2 pyruvate
- Phophofructokinase (PFK) is known as the rate limiting enzyme
3) The 2 pyruvate molecules are passed into the mitochondria, if there is available oxygen, and produce 36 ATP molecules.
- thus a greater ATP yield during aerobic metabolism
At high intensities, there is a heavy flow of ATP which produces lots of pyruvate. Due to the lack of oxygen available, the pyruvate is turned to lactic acid which immediately dissociates to form H+ and lactate
H+ is the bad guy. More H+ = acidosis which inhibits several physiological functions.
Describe Bogdanis et al. (1998) paper looking at the contributions to energy pathways during sprint exercise
Muscle biopsy study, where participants performance 10s sprints and then 20s sprints. Muscle biopsy allowed the measurement of byproducts that deduce the contribution of an energy system.
first 10s
stored ATP contributes 10% of total energy
PCr contributes 30%
Glycogen 60%
second 10s
Rate of ATP production has dropped by 50%
PCr contribution drops by 2/3
Glycogen contributions drop by 1/3
Describe the graph Boobis (1984) reported, when measuring power output during a 30s sprint?
What is fatigue index?
Peak power occurs within 1-3 seconds
Power declines subsequently to peak power
Fatigue index= % fall in power from peak to end power
de Ruiter et al. (1999) reported what differences to the force-velocity and power relationships between a fresh and fatigued muscle?
Jones et al. (2006) also reported these findings when undergoing sustained isometric contractions
The whole curve shifts down toward the origin in the fatigued state
Isometric force and max shortening velocity drastically decline
Increased curvature of the relationship in the fatigued state
Using magnetic resonance spectroscopy, what were the metabolic changes with fatigue reported by Jones et al. (2009) and Kent-Braun (1999) during sustained contractions?
Jones et al. (2009) showed:
- Small drop in ATP (ATP is tightly regulated and not allowed to drop drastically)
- A steep decline in PCr in the first few seconds. With an decreasing contribution with increasing time
- Steep increases to Pi and lactate
Kent-Braun (1999)
- Muscle pH drops linearly
- pH drop is due to increase H+ that are produced via the breakdown of lactic acid
- strong correlation between increased H+ and drop in force
What is the evidence to suggest central fatigue impacts drops in performance?
What is the key mechanism of central fatigue?
A study superimposing evoked tetanic contractions at 50Hz showed that with increasing fatigue, when ETC were delivered, there was a transient increase in force. Thus the voluntary contraction must therefore be submaximal. Suggesting some failure of maximal activation
Kawakami et al., 2000 used 100 repeated contractions, with a superimposed twitch on every 10th voluntary effort to assess neuromuscular activation. The results showed that with increasing contraction number, the %VA decreased. In fact, 25-50% of the decline in force was attributed to reduced activation.
central fatigue is attributed to extensive afferent feedback influence spinal and supraspinal neural drive
What evidence is there to show that reduced muscle excitation impacts drops in performance?
What is the mechanism for this?
Allen et al., 2008 reported for type 2 fibres- Ca release into the sarcomore decreases with increasing fatigue, although there is a temporary increase first.
Type 1 fibres are more resistant to fatigue. It takes longer for decreases to Ca release.
Mechanisms: Pi binds to stored Ca in sarcoplasmic rectilium. Pi is a byproduct of high turnover of ATP. Pi binds to Ca and prevents the release of calcium into the fibres.
What evidence is there to show that impaired contraction impacts drops in performance?
Debold et al. (2006) reported the S shaped relationship between force and Ca to shift to right when fatigued. Cross bridges become less sensitive and responsive to Ca. It takes far more Ca for the same amount of force because of this shift.
Mechanisms: It is though that the metabolic byproducts (ADP, Pi, H+) appear to inhibit cross bridge function. Leading to a decline in the number of cross bridges formed and also the force per cross bridge also drops.
What evidence is there to suggest that impaired ATP and PCr supply impact drops in performance?
ATP drops only a small and tolerable amount in early exercise
PCr however, drops lots more as exercise progresses, such that PCr is increasingly depleted. The bogdanis study shows that PCr contribution during the latter 10-s of a 20-s sprint drops by 66%.
This is because PCr can supply the largest rate of energy, however, has the smallest reserve.
Further, a study was able to show that isometric force and PCr follow a similar drop and recovery following exercise, suggesting the recovery of PCr is important to the restoration of function.
What evidence is there to suggest that impaired glycogen supply impacts drops in performance?
Bogdanis was able to show that glycolysis is reduced with fatigue: 33% lower during the second 10-s of exercise vs the first 10-s. however, muscle glycogen stores remain relatively high (>75%) following 20s sprint.
Mechanisms: Glytolytic flux (rate of anerobic glycolysis) seems to be impaired by H+ causing acidosis and inhibition of glycolytic enzymes (PFK).
This impairment to the rate of glycolysis flow is more important than the drop in glycogen muscle stores.
