Dietary nitrate (NO3−) is converted to nitrite (NO2−) and can be further reduced to the vasodilator nitric oxide (NO) amid a low O2 environment. Accordingly, dietary NO3− increases hind limb blood flow in rats during treadmill exercise; however, the evidence of such an effect in humans is unclear. We tested the hypothesis that acute dietary NO3− (via beetroot [BR] juice) increases forearm blood flow (FBF) via local vasodilation during handgrip exercise in young adults (n = 11; 25 ± 2 years). FBF (Doppler ultrasound) and blood pressure (Finapres) were measured at rest and during graded handgrip exercise at 5%, 15%, and 25% maximal voluntary contraction (MVC) lasting 4 min each. At the highest workload (25% MVC), systemic hypoxia (80% SaO2) was induced and exercise continued for three additional minutes. Subjects ingested concentrated BR (12.6 mmol nitrate (n = 5) or 16.8 mmol nitrate (n = 6) and repeated the exercise bout either 2 (12.6 mmol) or 3 h (16.8 mmol) postconsumption. Compared to control, BR significantly increased FBF at 15% MVC (184 ± 15 vs. 164 ± 15 mL/min), 25% MVC (323 ± 27 vs. 286 ± 28 mL/min), and 25% + hypoxia (373 ± 39 vs. 343 ± 32 mL/min) and this was due to increases in vascular conductance (i.e., vasodilation). The effect of BR on hemodynamics was not different between the two doses of BR ingested. Forearm VO2 was also elevated during exercise at 15% and 25% MVC. We conclude that acute increases in circulating NO3− and NO2− via BR increases muscle blood flow during moderate‐ to high‐intensity handgrip exercise via local vasodilation. These findings may have important implications for aging and diseased populations that demonstrate impaired muscle perfusion and exercise intolerance.
Previous transcranial magnetic stimulation (TMS) studies showed exercise-induced depression of motor evoked potentials (MEP). The purpose of the present study was to evaluate changes in MEP size and central motor conduction time (CMCT) after various kinds of exercise of daily life and sports. Changes of both central and peripheral motor conduction were recorded immediately after predominantly aerobic (climbing stairs and jogging) and anaerobic (press-ups, dumb-bell holding, and 400 m-run) exercise. Strength exercise resulted in a significant decrease of MEP amplitudes. Exhausting press-ups reduced the mean MEP amplitude by 33% as compared to pre-exercise value, exhausting dumb-bell holding reduced the mean MEP amplitude by 66%. Aerobic exercises (climbing 600 steps and jogging 50 minutes) did not significantly change MEP amplitudes. The compound motor action potentials (registered after supramaximal peripheral electrical stimulation) remained unchanged after each paradigm. CMCT was not significantly altered by any of the exercises under investigation. Peripheral motor conduction time (PMCT) was slightly lengthened by 4% after isometric dumb-bell holding. PMCT and total motor conduction time were decreased after aerobic exercises, probably due to an increase of temperature of the lower extremities. In conclusion, TMS is a suitable technique for objective evaluation of central fatigue. The present study is the first to show its possible use in sports medicine, indicating that only exhaustive or strength exercises result in reduced MEPs.
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