Preserved heart rate variability in first-degree relatives of subjects with Type 2 diabetes mellitus without metabolic disorders.

AIMS: To investigate the influence of a family history of Type 2 diabetes mellitus (T2DM) on resting heart rate variability in the absence of concomitant metabolic disorders. METHODS: We studied 55 first-degree relatives (FDRs) of subjects with T2DM and 36 control subjects without any known family history of diabetes. FDRs were recruited from a University Hospital out-patient diabetes clinic. The protocol included: oral glucose tolerance test (30, 60, 90 and 120 min after ingestion of 75 g glucose) blood glucose, plasma insulin, cholesterol and subfractions, triglycerides, leptin and C-reactive protein. Heart rate variability (HRV) at rest was determined by spectral analysis of interbeat intervals recorded during 10 min in the supine position. RESULTS: HRV was lower in FDRs compared with control subjects (P < 0.05). Multiple regression analysis identified cholesterol (P = 0.014) and triglycerides (P = 0.014) as significant independent predictors (model r = 0.40; P < 0.001) of HRV. Since FDRs had higher values for anthropometric and metabolic variables known to alter HRV, we performed an ancova adjusted for cholesterol and triglycerides and also another analysis in which the groups were comparable for anthropometric and metabolic characteristics. Comparison of FDRs and comparable control subjects revealed no significant difference in HRV (P > 0.05). CONCLUSIONS: A family history of T2DM, in the absence of concomitant metabolic disorders, does not impair heart rate variability.

Subacute effects of a maximal exercise bout on endothelium-mediated vasodilation in healthy subjects.

We evaluated vascular reactivity after a maximal exercise test in order to determine whether the effect of exercise on the circulation persists even after interruption of the exercise. Eleven healthy sedentary volunteers (six women, age 28 +/- 5 years) were evaluated before and after (10, 60, and 120 min) a maximal exercise test on a treadmill. Forearm blood flow (FBF) was measured by venous occlusion plethysmography before and during reactive hyperemia (RH). Baseline FBF, analyzed by the area under the curve, increased only at 10 min after exercise (P = 0.01). FBF in response to RH increased both at 10 and 60 min vs baseline (P = 0.004). Total excess flow for RH above baseline showed that vascular reactivity was increased up to 60 min after exercise (mean +/- SEM, before: 526.4 +/- 48.8; 10 min: 1053.0 +/- 168.2; 60 min: 659.4 +/- 44.1 ml 100 ml(-1) min(-1) . s; P = 0.01 and 0.02, respectively, vs before exercise). The changes in FBF were due to increased vascular conductance since mean arterial blood pressure did not change. In a time control group (N = 5, 34 +/- 3 years, three women) that did not exercise, FBF and RH did not change significantly (P = 0.07 and 0.7, respectively). These results suggest that the increased vascular reactivity caused by chronic exercise may result, at least in part, from a summation of the subacute effects of successive exercise bouts.

Subacute effects of a maximal exercise bout on endothelium-mediated vasodilation in healthy subjects

We evaluated vascular reactivity after a maximal exercise test in order to determine whether the effect of exercise on the circulation persists even after interruption of the exercise. Eleven healthy sedentary volunteers (six women, age 28 ± 5 years) were evaluated before and after (10, 60, and 120 min) a maximal exercise test on a treadmill. Forearm blood flow (FBF) was measured by venous occlusion plethysmography before and during reactive hyperemia (RH). Baseline FBF, analyzed by the area under the curve, increased only at 10 min after exercise (P = 0.01). FBF in response to RH increased both at 10 and 60 min vs baseline (P = 0.004). Total excess flow for RH above baseline showed that vascular reactivity was increased up to 60 min after exercise (mean ± SEM, before: 526.4 ± 48.8; 10 min: 1053.0 ± 168.2; 60 min: 659.4 ± 44.1 ml 100 ml-1 min-1 . s; P = 0.01 and 0.02, respectively, vs before exercise). The changes in FBF were due to increased vascular conductance since mean arterial blood pressure did not change. In a time control group (N = 5, 34 ± 3 years, three women) that did not exercise, FBF and RH did not change significantly (P = 0.07 and 0.7, respectively). These results suggest that the increased vascular reactivity caused by chronic exercise may result, at least in part, from a summation of the subacute effects of successive exercise bouts.

Exercise stress testing in healthy subjects during cholinergic stimulation after a single dose of pyridostigmine.

OBJECTIVE: The evaluation, by exercise stress testing, of the cardiorespiratory effects of pyridostigmine (PYR), a reversible acetylcholinesterase inhibitor. METHODS: A double-blind, randomized, cross-over, placebo-controlled comparison of hemodynamic and ventilation variables of 10 healthy subjects who underwent three exercise stress tests (the first for adaptation and determination of tolerance to exercise, the other two after administration of placebo or 45mg of PYR). RESULTS: Heart rate at rest was: 68+/-3 vs 68+/-3bpm before and after placebo, respectively (P=0.38); 70+/-2 vs 59+/-2bpm, before and after pyridostigmine, respectively (P<0.01). During exercise, relative to placebo: a significantly lower heart rate after PYR at, respectively, 20% (P=0.02), 40% (P=0.03), 80% (P=0.05) and 100% (P=0.02) of peak effort was observed. No significant differences were observed in arterial blood pressure, oxygen consumption at submaximal and maximal effort, exercise duration, respiratory ratio, CO2 production, ventilation threshold, minute ventilation, and oxygen pulse. CONCLUSION: Pyridostigmine, at a dose of 45mg, decreases heart rate at rest and during exercise, with minimal side effects and without interfering with exercise tolerance and ventilation variables.