Defects in MT-CYB are also documented in patients with multisystem disorders in cases of exercise intolerance accompanied by deafness, mental retardation, retinitis pigmentosa, cataract, growth retardation, and epilepsy [9], [10].
Circulatory disturbance of the kidney is an alternative mechanism, as most renal biopsies in cases of exercise-induced AKI show no uric acid crystallization.
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Skeletal muscle physiology suggests that glucose supplementation might improve muscle performance in case of prolonged exercise and this situation is analogous to the gravid uterus during delivery.
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Moreover, it would be expected that, in case of continuing the exercise until severe fatigue appears, post values will overcome pre values changing the sense of the differences, as described earlier by other authors12,13,25.
For example, in case of strong physical exercise the concentration of lactate in human blood may rise to values as high as 19.5 mM (in blood plasma) respectively 7.0 mM (in erythrocyte cytoplasm) [ 34] indicating that the lactate production by the anaerobic skeletal muscle clearly exceeds its rate of re-conversion to glucose in the liver and its utilization rate in the heart muscle.
False-negative results are more likely with submaximal exercise (in the case of exercise-induced stress), single-vessel disease and moderate stenosis (50 70%) [ 78].
However, the difference reached statistical significance only in the case of exercise at 25%% of Wmax and after 30 min of exercise at 55%% of Wmax (p < 0.03).
Depletion of the cellular ATP buffer with this high percentage requires very intense muscle contractions and has only been reported in case of very high-intensity exercise (Forbes et al. 2009; Schmitz et al. 2010; Walter et al. 1999).
