1 Fatigue During Muscular Exercise Brooks Chapter 33

2 Muscular Fatigue Inability to maintain a given exercise intensity. Several causes for fatigue. Fatigue is task specific. Can have impairment within the active muscle. –peripheral fatigue Fatigue can also be due to central factors. –psychological –environmental (heat)

3 Muscular Fatigue Depends on the training and activity status of the individual. Can be due to depletion of key metabolites in the muscle. Can be due to accumulation of metabolites. Identifying the cause of fatigue is not simple.

4 Identifying Fatigue The inability to maintain a given exercise intensity. An athlete is rarely completely fatigued. – they adopt a lower power output Often fatigue can be related to a specific cause or site. (  glycogen,  Ca 2+ ) The causes of fatigue can also be general and involve several factors (dehydration).

5 Compartmentalization in physiological organization make it difficult to identify the site of fatigue. –eg. ATP depleted at myosin head, but adequate elsewhere? The effect of exercise at an absolute, or relative, exercise intensity will be more severe on an untrained individual.

6 Heat and humidity will affect endurance performance. –  sweat, heat gain, dehydration, electrolyte shift –redistribution of CO in the heat –uncouple oxidation and phos in mitochondria less ATP with same VO 2 –irritant to CNS, affect psychological perception of exercise –fatigue is cumulative over time previous day dehydration will influence current performance –glycogen depletion  endurance performance

7 Metabolite Depletion ATP and CP the immediate source of ATP is CP CP in muscle is limited when CP is depleted, muscle ATP is  must match use with restoration otherwise you can not maintain exercise the greater the work load, the greater the CP depletion CP depletion leads to muscle fatigue

8 CP levels decline in two phases: drop rapidly, then slowly ( Fig 33, 1a ). –both severity of the first drop and extent of the final drop are related to work intensity Fatigue in maximal cycling coincides with CP depletion. –tension developed related to CP level, therefore CP related to fatigue

9 ATP ATP is well maintained up to maximum effort. –due to compartmentalization –down regulation by muscle cells for protection –muscle cell shuts off contraction, with ATP depletion, in favor of maintaining ion gradients –free energy of ATP declines 14% in physiological pH range also depends on ATP/ADP ratio consequence: less energy available for work with given VO 2 flux fatigue also influences ATP binding in X-bridge cycle

10 Glycogen Glycogen depletion in skeletal muscle is associated with fatigue. With moderate activity glycogen is depleted uniformly from different fiber types. With low resistance activity there is selective recruitment and depletion of glycogen from slow twitch (type I) fibers. With high resistance type II fibers are depleted. Thus glycogen can be depleted from specific fibers.

11 Blood Glucose During short intense exercise bouts, blood glucose  above pre-ex levels as the CNS stimulates hepatic glycogenolysis. During prolonged exercise glucose production may be limited to gluconeogenesis because of hepatic glycogen depletion. Thus glucose production may fall below that required by working muscle and other essential tissues.

12 Lactic Acid Accumulation During short term high intensity exercise –lactic acid production exceeds removal –strong organic acid: pH  –it is the H + rather than the lactate ion that  pH H + accumulation within muscle –inhibit PFK and slow glycolysis –displace Ca 2+ from troponin (inhibit contraction) –main stimulate pain receptors

13 H + in blood –reacts in the brain and causes pain, nausea –inhibits combination of O 2 with Hb in the lung –reduces hormone sensitive lipase in adipose tissue limits release of FFA It is still uncertain if  pH stops exercise.

14 Phosphates Phosphagen depletion during exercise results in phosphate (P i, or HPO 4 2- ) accumulation. Phosphate behaves like H + and inhibits glycolysis (PFK) and interferes with Ca 2+ binding. Phosphate and H + produce hydrogen phosphate which is a very harmful metabolite that accumulates in working muscle.

15 Calcium Ion There are several reasons why Ca 2+ may be involved in muscle fatigue: Ca 2+ from the SR during EC may be taken up by mito –interferes with mitochondrial function reduced ability of SR to release Ca 2+ during twitches –less forceful contraction actin-myosin sensitivity to Ca 2+ is reduced –less forceful contraction Ca 2+ re-uptake by SR is slowed –prolongs contraction, slows relaxation

16 O 2 Depletion and Muscle Mitochondrial Density The depletion of O 2 stores, or inadequate O 2 delivery to muscle, can result in fatigue. –impaired circulation –high altitude –strenuous exercise Adequate O 2 supply is essential to support maximal aerobic work.

17 Inadequate O 2 supply or utilization can be represented by: –  CP levels –  lactate production –both Thus inadequate O 2 can result in at least 2 fatigue causing effects.

18 Skeletal muscles contain a greater mito respiratory capacity than can be supplied by the circulation.  mito density in response to endurance exercise will provide benefits other than VO 2. –  capacity to oxidize fatty acids as a fuel –minimize mito damage during exercise free radical accumulation more mitos, reduced effect of free radicals

19 Disturbances to Homeostasis The continuation of exercise depends on the integrated functioning of many systems. Any factor that upsets this integrated function can cause fatigue. Some important factors that maintain homeostasis include: ions (K +, Na +, Ca 2+ ), blood glucose, FFA, plasma volume, pH, core temp, hormone levels.

20 Central and Neuromuscular Fatigue In the linkage between afferent inputs and the performance of a task, several sites require adequate functioning. A decrement at any site will  performance (fatigue). Therefore it is possible to have muscular fatigue when the muscle itself is not impaired.

21 It is very difficult to obtain data on CNS function during exercise. The relationship between central and peripheral functions should not be overlooked. Physiological signals can lead to psychological inhibition. –eg. painful inputs affect willingness to continue activity

22 Setchenov Phenomenon The exhausted muscle of one limb recovers faster if the opposite limb is exercised moderately during recovery. –repeated by other researchers –not due to  muscle blood flow –it is attributed to afferent input having a facilitatory effect on the brain’s reticular formation and motor centers.

23 Psychological Fatigue We have a very limited understanding of how afferent input during exercise (pain, breathing, nausea, motivation) can influence the physiology of the CNS. Through training or intrinsic mechanisms, some athletes learn to minimize the influence of distressing afferents and approach performance limits of the musculature. Some athletes (altitude) will slow down to reduce discomforting inputs to a tolerable level. Training at high intensities allows athletes to select a proper race intensity.

24 Heart as a Site of Fatigue No direct evidence that exercise is limited by fatigue of the heart muscle. Well oxygenated during exercise. Heart gets first choice at CO. Can use lactate or FFA as fuel. During severe dehydration –major fluid and electrolyte shift –K +, Na +, Ca 2+ can affect e-c coupling cardiac arrhythmia is possible

25 VO 2 max and Endurance Relationship between max O 2 consumption and upper limit for aerobic metabolism. 1. VO 2 max limited by O 2 transport –CO and arterial content of O 2 2. VO 2 max limited by the respiratory capacity of contracting muscles. Currently we can conclude that VO 2 max is a parameter set by maximal O 2 transport, while endurance is also determined by muscle respiratory capacity.

26 Muscle Mass Muscle mass influences VO 2 max. Once a critical mass of muscle is utilization VO 2 is independent of muscle mass. –VO 2 when cycling with 1 leg is < than with 2 –2 x VO 2 of 1 leg is much greater than 2 legs –VO 2max when cycling and arm cranking is not greater than just cycling alone. VO 2max  as active muscle mass  to a point beyond which O 2 delivery is inadequate to supply working muscle.

27 Muscle Mitochondria Correlation observed between VO 2 max and mito activity Mito and VO 2 max with training and detraining –muscle mito  30%, VO 2  19% –VO 2 persistent longer during detraining than muscle respiratory capacity –illustrates independence of these factors The maximal ability of muscle mito to consume O 2 is several times the ability to supply O 2. –hence, VO 2 max is limited by arterial O 2 transport

28 Arterial O 2 Transport Arterial O 2 transport (T aO 2 ) is equal to the product of cardiac output (Q) and arterial O 2 content(C aO 2 ). T aO 2 = Q(C aO 2 ) Attempts to raise arterial O 2 content by breathing  O 2 conc or blood doping raise VO 2max.

29 VO 2max and Performance Maximal capacities of cardiac output, arterial O 2 transport, VO 2max and physical performance are all interrelated. Despite these correlations, VO 2max is a poor predictor of performance among elite athletes. This is due to the importance of peripheral, as opposed to central, factors in determining endurance.

30 Catastrophy Theory Physiological processes are highly controlled and often redundant in function. Successes and failures in integrated functions involve multiple cells, tissues, organs, and systems. Catastrophy theory: the failure of one enzyme system, cell, tissue organ or system places a burden on related systems, such that they may fail simultaneously.

31 Future of Fatigue Technology is making available new devices that will further investigation of fatigue. NMR –nuclear magnetic resonance spectroscopy –radio freq signal emitted by a particular atomic species –determine concentrations of: ATP, CP, Pi, water, fat, metabolites without breaking the skin

32 PET Positron emission tomography. Great potential for studying regional blood flow and metabolism. NIRS Near infrared spectroscopy. Noninvasively and continuously monitor the state of oxygenation of iron containing compounds (myoglobin).

33 Fatigue and Physical Training  To date there is no formal training theory that quantitatively and accurately prescribes the pattern, duration and intensity of exercise to elicit a specific physiological adaptation.  Without accurate quantification of a training dose, the results from training studies to date remain qualitative and argumentative.

34  A training model developed by Banister et al. (1975) uses a unit of measure called a training impulse (TRIMP) to accurately quantify a training dose. This training theory proposes that a precisely measured quantity of training above that currently practiced will improve physical, physiological, and biochemical indices of adaptation and growth.

35  An individual’s daily training is quantified by calculating a training impulse [w(t)], which represents the integrated effect of duration (D) and intensity (Y) of exercise.  Exercise performance may be predicted by transforming a daily TRIMP score [w(t)] into separate daily scores of a hypothesized fitness [g(t)] and fatigue [h(t)].

36  The time course of the difference between fitness and fatigue represents the time course of predicted physical performance p(t), due to the training. Thus fitness and fatigue grow and decay exponentially throughout a period of training.  During a taper period fatigue decays much faster than fitness, and the predicted performance increases.

37  An effective training format is one that has an “on” stimulus of 28 days, in which the exercise has the proper intensity and duration to induce a positive exponential growth response in physiological and biochemical variables.  A 7 – 14 day taper at the end of the 28 day training program, will then allow fatigue to decay faster than fitness.  The end of the taper period provides a time when there is a maximal separation between fitness and fatigue, and performance reaches a peak.

38 12 Week Training Program

39 Fitness/Fatigue Graph