Medical Implications of the Lactate and Ammonia Relationship in Anaerobic Exercise*

Abstract

The genesis of the modern ischemic forearm exercise test (IFET) employing the measurement of lactate and ammonia as countervailing metabolites is briefly reviewed, along with the application of the lactate ammonia exercise ratio in the diagnosis of myoadenylate deaminase deficiency and disorders of glycolysis and glycogenolysis. Two cases are presented to illustrate the response patterns elicited, their reproducibility, the types of parameters that can be quantified, and the role the IFET may play in the differential diagnosis of fitness failures. The role of the ammonia measurement is emphasized here because the lactate response is more familiar. The roles of hypoxanthine responses and of muscle ammonia measurements in the evaluation of cases are examined, and some pertinent and recently introduced analytic methods are cited. The applications of newer approaches, such as aspiration biopsy and N-14 NMR spectroscopy, are discussed, along with an example of the new clinical defects in enzymes and membrane carriers that should be anticipated during the utilization of the IFET.

Muscle function during fatigue in myoadenylate deaminase-deficient Dutch subjects

“…It has to be noted that, in contrast with the voluntary exercise protocols used thus far [4,8,14,15], only a small muscle was activated in the present study. The adductor pollicis muscle was chosen for practical reasons : it can easily be maximally activated by electrical stimulation of the nerve, and its force can be measured without interference of other muscles.…”

“…The main conclusion of the present work is that there were no significant differences in adductor pollicis muscle power output between the MAD-deficient and the control subjects before, during or after short-term maximal dynamic exercise. Some previous studies showed an effect of MAD deficiency on performance during exercise of rather moderate intensity [4,8,15], whereas others failed to show such an effect during more intensive exercise [14,16]. There are indications that MAD deficiency is a harmless polymorphism and not a disease in itself [11,23].…”

“…It has been shown repeatedly that muscle metabolism is different during exercise in MAD-deficient compared with normal muscle [4,8,[13][14][15][16], and in some studies the deficiency reduced muscle performance during exercise of moderate intensity [4,8,12], whereas others did not find a reduction of performance during high-intensity exercise [14,16]. These previous studies all used some form of voluntary exercise, which has the limitation that the performance to a large extent depends on the subject's motivation.…”

A non-ischemic forearm exercise test for the screening of patients with exercise intolerance

“…Methods: Twenty-six healthy subjects and 32 patients with exercise intolerance performed an isometric exercise at 70% of the maximal voluntary contraction during 30 seconds in non-ischemic conditions. 3,4,[11][12][13] The main variable methodologic factors are the intensity and duration of exercise, the contraction type, the assessment of the muscle work, the subjective sensation of fatigue and pain during the exercise, and the protocol of blood sampling. Results: A nearly fourfold lactate rise was induced by exercise in healthy subjects.…”

Metabolic myopathies: functional evaluation by different exercise testing approaches

“…The ischemic forearm exercise test allows also a presumptive diagnosis of MADD when a negligible increase in blood ammonia despite a normal rise in lactate occurs [50][51][52].…”