The effects of exercise, heat-induced hypo-hydration and rehydration on blood–brain-barrier permeability, corticospinal and peripheral excitability

Abstract

Purpose The effects of low-intensity exercise, heat-induced hypo-hydration and rehydration on maximal strength and the underlying neurophysiological mechanisms are not well understood. Methods To assess this, 12 participants took part in a randomised crossover study, in a prolonged (3 h) submaximal (60 W) cycling protocol under 3 conditions: (i) in 45 °C (achieving ~ 5% body mass reduction), with post-exercise rehydration in 2 h (RHY2), (ii) with rehydration across 24 h (RHY24), and (iii) a euhydrated trial in 25 °C (CON). Dependent variables included maximal voluntary contractions (MVC), maximum motor unit potential (M MAX ), motor evoked potential (MEP RAW ) amplitude and cortical silent period (cSP) duration. Blood–brain-barrier integrity was also assessed by serum Ubiquitin Carboxyl-terminal Hydrolase (UCH-L1) concentrations. All measures were obtained immediately pre, post, post 2 h and 24 h. Results During both dehydration trials, MVC (RHY2: p < 0.001, RHY24: p = 0.001) and MEP RAW (RHY2: p = 0.025, RHY24: p = 0.045) decreased from pre- to post-exercise. MEP RAW returned to baseline during RHY2 and CON, but not RHY24 ( p = 0.020). MEP/M MAX ratio decreased across time for all trials ( p = 0.009) and returned to baseline, except RHY24 ( p < 0.026). Increased cSP ( p = 0.011) was observed during CON post-exercise, but not during RHY2 and RHY24. Serum UCH-L1 increased across time for all conditions ( p < 0.001) but was not significantly different between conditions. Conclusion Our findings demonstrate an increase in corticospinal inhibition after exercise with fluid ingestion, but a decrease in corticospinal excitability after heat-induced hypo-hydration. In addition, low-intensity exercise increases peripheral markers of blood–brain-barrier permeability. Graphical abstract

Bibliographic Information