Peak Blood Lactate Levels and Peak Performance Markers in Two Groups of MS Patients Performing an Exhaustive Bicycle Ergometry

Abstract

In the present work, two groups of MS patients were characterized by analyzing their peak performance in an exhaustive, incremental bicycle spiroergometry. The groups differed regarding the disease course (primary- or secondary-progressive MS in group P vs. relapsing-remitting MS in group R) and the grade of disability according to the expanded disability status scale (EDSS; 4–6 in group P vs. 0–3.5 in group R). The main objective was to determine and compare the peak blood lactate response to exercise and the maximal workload and to investigate their interrelation. In group P (n=41), subjects reached a mean peak blood lactate level of 4.1 mM/l and a mean maximal workload of 1.5 W/kg. In group R (n=25), the mean peak blood lactate level was 6.5 mM/l and the mean maximal workload was 2.1 W/kg. Spiroergometric peak performance in both groups was significantly lower than predicted for healthy, untrained individuals. Group R reached significantly higher values in all performance markers than group P, and peak blood lactate was correlated with maximal workload in both groups. The peak blood lactate response was lower than normal in both groups, but the effect was more pronounced in group P: Only 5 out of 41 subjects in this group reached the blood lactate level expected at volitional exhaustion (≥ 8 mM/l for men and ≥ 6 mM/l for women). Less than half of the subjects reached the level of 4 mM/l, which is still routinely used in exercise tests as a fixed marker for aerobic capacity. A reduced peak blood lactate response to exercise has previously been described in other chronic diseases but is, to our knowledge, a novel finding for MS patients. As exercise interventions and exercise tests are becoming more common in MS, these results call into doubt if the lactate performance tests and lactate thresholds used for healthy individuals can simply be transferred to MS patients. Our results also raise the question which processes limit the exercise capability of the subjects in this study. After reviewing the literature, it seems probable that central manifestations of the disease cause a pathologic lack of neuromuscular activation and feedback. This aberrant motor processing, combined with the resulting atrophy and changes in the muscles’ energy metabolism and fiber composition, presumably limits the exercise capacity and the muscular lactate production in MS patients. A habitual lack of physical activity, which is frequently seen not only in MS, might contribute to the limitation of exercise capability by causing a “physiologic” lack of neuromuscular activation, resulting in further muscular deconditioning.