Current understanding about the nature of fatigue may be placing
inadequate emphasis on fatigue of cardiac muscle.
The mechanisms of the different types of short term and long term fatigue have implicated
temporary impairment of rate or level of neural excitation, local muscle contractility,
oxygen supply to the muscles, metabolic substrate activity and several other processes.
The duration and quantity of energy from ATP-CP, aerobic and anaerobic glycolysis,
triglyceride metabolism and so forth has been examined, as have changes in hormonal level,
accumulation of hydrogen ions associated with lactate metabolism and flux of calcium ions
across various cell membranes.
The focus has been placed on contributions made by the inability of the heart pump to
deliver adequate oxygenation or other biochemicals to the appropriate muscles and tissues
or on local failure at a neuromuscular or muscular level. A great deal of work has
concerned itself with the adequacy of the pumping, interface transferring and interface
uptake systems. In other words, much emphasis has been placed on fatigue of local muscular
or bioelectrical systems.
We are well aware of local muscle fatigue. We all know that muscle fatigues, but does this
also imply that cardiac muscle also fatigues? This would seem quite logical, because no
biological contractile tissue, be it smooth or striated muscle, is exempt from fatigue. Of
course, we may argue that if the cardiac muscle fatigues, then we might die or experience
cardiac failure - but does this negate the possibility that cardiac muscle may also suffer
fatigue.
If this is even partly true, then we may have to question if too much emphasis has been
placed on concepts such as VO2 max, lactate or OBLA thresholds. What role, if any, does
cardiac muscle fatigue (or even associated fatigue of the peripheral local muscle pumps
which facilitate venous return to the heart) play in limiting performance in endurance
activities?
Quote any relevant research in your commentary on this P&P.
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