VO2/PO Relationship In Type 2 Diabetic Subjects.

Abstract

The ability to perform physical activity of prolonged duration and adequate intensity (i.e. exercise tolerance) is instrumental to obtain the well-known health benefits that are associated with physical training in Type 2 diabetes (T2D). During whole-body physical activity exercise tolerance is compromised as the oxygen cost (VO2) of energy production becomes progressively higher (i.e. “excess” VO2) at power outputs (PO) above the lactate threshold (LT). This loss of muscle efficiency, of which type I fibers fatigue and/or increased type II fibers recruitment are putative causes, impairs exercise tolerance. PURPOSE: We tested the hypothesis that a strength training intervention (ST), by increasing maximal force (Fmax) and reducing the recruitment of high-threshold motor units at a given exercise intensity, will reduce the “excess” VO2 during a cycling incremental exercise. METHODS: 11 male patients (mean±SD age 56±8 yrs, BMI 29±4 kg/m2), with uncomplicated T2D on oral hypoglycemic drugs were tested Pre and Post a 4-months ST intervention (3 times per week, 60 min). VO2/PO relationship during an incremental cycling test to exhaustion was modelled using a double-linear fit: the slopes of the VO2/PO relationship below (S1) and above (S2) the LT were calculated. Parameters were compared with Wilcoxon singed-rank tests. RESULTS: Fmax, VO2max and POmax significantly increased following ST (20±5, 7±7 and 10±10% respectively). No “excess” VO2 was present before (S2 not different from S1: 10.5±1.1 vs 9.9±1.7 mlmin-1W-1) yet it became evident following ST (S2 significantly higher than S1: 14.1±3.1 vs 11.8±4.0 mlmin-1W-1). CONCLUSIONS: Contrarily to our hypothesis, the “excess” VO2, typically displayed by healthy age-matched controls, was absent in our T2D patients. We speculate that this could be due to the acceleration of the age-related selective atrophy of type II muscle fibers that is known to occur in T2D. A 4-months ST that improved muscle Fmax, VO2max and POmax, was associated with the appearance of an “excess” VO2. We speculate that this is the result of the recovered ability to recruit type II muscle fibers towards force production in the heavy-intensity domain of an incremental cycling exercise. The practical implications of the above findings for exercise prescription in T2D require further evaluation.