NEUROMUSCULAR FATIGUE

1. NEUROMUSCULAR FATIGUE • In Exercise Physiology, neuromuscular fatigue can be defined as a transient decrease in muscular performance usually seen as a failure to maintain or develop a certain expected force or power.

2. Importance of Neuromuscular Fatigue • Does O2 delivery alone limit exercise performance? • Is it just O2 transport and O2 fuel utilization? • Have we adequately explored other areas relating to muscle contractile function? • TD Noakes – South Africa • Only 50% of VO2 max trials result in a plateau – is there really a plateau? • Is fatigue biochemical or CNS controlled anticipatory response?

3. Loss of Strength with Fatigue • Any volitional loss of strength during a sustained exercise is the basis of fatigue.

4. Effect of Fatigue on Reflexes and Coordination • A reflex arc is fatigable. • If a reflex arc is stimulated repeatedly – it will eventually fail to elicit any type of expected reflex response. • The more interneurons and synapses involved, the more quickly it may become fatigued. • Coordination can be viewed the same way • Irradiation of motor impulses to neighboring motor nerve centers – coordination is lost.

5. Effect of Fatigue on Industrial Workers • How much work can be done in an 8-hour time period without fatigue? • Static work is more fatiguing than dynamic work • Blood flow • Rest periods

6. Basic Nature of Fatigue • Relationship between intensity of work and endurance appears to be a fundamental characteristic of performance… • Is there some equation that can be universally applied to calculate the highest sustainable workload? • Physical Working Capacity at Fatigue Threshold • PWCFT

7. Central versus Peripheral • Where does fatigue occur? • Central fatigue • Proximal to the motor unit • Peripheral fatigue • Residing within the motor unit

8. Central Fatigue • Brain and spinal cord; CNS fatigue • Studies that used voluntary exhaustion and then additional electrical stimulation • After voluntary exhaustion, electrical stimulation evoked sizable force production • Central location of fatigue

9. Peripheral Fatigue • Fatigue occurring within the local motor unit; local fatigue • Studies that fatigued a muscle with electrical stimulation to the point of no muscle twitch • Muscle action potentials were relatively unaffected • Peripheral location of fatigue (but not at the NMJ)

10. So, where does fatigue occur? • In both central and peripheral locations. • The location of fatigue is intensity-dependent • Lower-intensity, longer duration fatigue will primarily occur centrally • Higher-intensity, short duration fatigue will primarily occur peripherally • Example  Why does pedaling rate decrease during the Wingate test? • Example  Why can’t we do another repetition after a 5RM lift? • Example  Why do we slow down during the course of a 1600 m race? Do we slow down?

11. What Causes Fatigue? • There are two hypotheses: • The Accumulation hypothesis • The Depletion hypothesis • The origin of fatigue is exercise-dependent and may be due to either accumulation, depletion, or both.

12. Accumulation Hypothesis • There is a buildup of metabolic by-products in the muscle fiber • Lactic acid (lactate) • Hydrogen ions (H+) • Ammonia • Inorganic phosphate • Lactate is the primary marker associated with the accumulation hypothesis • If you exercise at a high enough intensity, H+ accumulation interferes with force production • Applies to maximal exercise for 20 sec  3 minutes

13. Four Factors Associated with the Decrease in Force Production Due to H+ Accumulation • H+ interferes with Ca++ release from the sarcoplasmic reticulum. • H+ interferes with actin-myosin binding affinity • H+ interferes with ATP hydrolysis • H+ interferes with ATP production

14. 1. Ca++ release from the sarcoplasmic reticulum • Lactic acid (H+) accumulation disrupts the release of Ca++ from the sarcoplasmic reticulum, in part, by changing the membrane potential (ICF vs. ECF) • When Ca++ is not released as effectively, less is available to bind with troponin-C.

15. 2. Actin-myosin binding affinity • Actin and myosin do not bind as readily or as “tightly” in an increased acidic cellular environment (i.e., microenvironment).

16. 3. ATP hydrolysis • H+ accumulation decreases the effectiveness of mATPase. • Why?

17. 4. ATP production • H+ accumulation interferes with enzymes that catalyze reactions that produce ATP. • What is the rate limiting step in glycolysis? • Allosteric inhibition:

18. Acid Removal • What are the two primary ways to clear H+ accumulation? • Increased blood flow • Buffering • What is the body’s primary blood buffer?

19. Depletion Hypothesis • 2 aspects to the depletion hypothesis: • Neural depletion • Depletion of acetylcholine • Depletion of energy substrates • Phosphagen depletion • Glycogen depletion

20. Neural Depletion • Neural fatigue that is caused by a depletion of the stimulatory neurotransmitter ACh. • You can induce neural depletion in an excised muscle, but can this happen in vivo? • Two possible instances where it might have occurred: • East German woman completing the final lap of a marathon • Ironman Triathalon competition in Hawaii (same occurance)

21. Depletion of Energy Substrates • 2 aspect of substrate depletion: • Phosphagen depletion • Glycogen depletion

22. Phosphagen Depletion • 2 aspects to phosphagen depletion: • Reduction in ATP • Small ATP stores in skeletal muscle • Enough to provide 2 – 3 seconds of maximal muscular contraction • Used quickly • Depletion of phosphocreatine (PC) • Enough PC stored to provide up to 20 – 30 seconds of maximal muscular contraction • Nearly completely depleted during maximal exercise

23. Glycogen Depletion • Glycogen is a polymer of glucose that is created with glycogen synthase • Glycogen is stored in relatively large amounts in skeletal muscle. • About 2,000 kcals of energy stored in the form of glycogen (skeletal muscle) • Where are the two primary locations for glycogen storage in the body? • It takes approximately 100 kcals to run a mile, so we have enough glycogen stored for about 20 miles of running. • Glycogen depletion occurs during long-term activities that are done at a medium to moderate intensity • When this occurs, the body is forced to use alternative energy sources (that are not as powerful as glucose metabolism) • Example: “Hitting the runner’s wall” • What about glycogen supercompensation??

24. Muscle Temperature Effect on Fatigue • Optimal deep muscle temperature between 80 - 86 F • At 103, the endurance time decreased 65% • Due to metabolite accumulation or temperature effects of protein/enzyme function (titration). • At 68, the endurance time decreased 80% • Due to interference with neuromuscular transmission

25. Electromyographic Observations of Fatigue • EMG Amplitude (submaximal workloads) • Increases linearly with exhaustion • PWCFT • EMG Amplitude (maximal workload) • Remains constant or decreases with exhaustion • “Muscle Wisdom” hypothesis • EMG Frequency (max and submax) • Decreases… • Why?

27. Assignment for next week • Read handout • deVries & Housh • Read Enoka, 2003 pgs. 374-389. • Prepare for questions next week over this lecture.

28. Course Projects • Pick one of the five neuromuscular disorders: • Parkinsonism • Muscular/Myotonic Dystrophy • Cerebral Palsy • Low Back Pain • Peripheral neuropathy (generic)

29. Course Projects • Give a 50-min lecture on the neuromuscular disorder that you chose • Etiology • Pathology • Common signs / symptoms • How does it affect motor unit function? • Describe how we could investigate this disorder with surface EMG and MMG: • Collect pilot data and report your results on 4 or 5 healthy subjects • Extrapolate your findings to the diseased subjects

30. Course Projects • Lectures given on: • April 18 • April 25 • May 2 • Choice must be made by next week.