Author(s): ACTON, J., ALSHARIF, N.S., COCKSEDGE, S.P., PEDEN, D.P., FERGUSON, R.A., MITCHELL, E.A., BAILEY, S.J., Institution: LOUGHBOROUGH UNIVERSITY, Country: UNITED KINGDOM, Abstract-ID: 2511

INTRODUCTION:
Impaired mitochondrial respiratory function [increased uncoupled leak respiration through complex I (CIL) or lower coupled respiration through complexes I+II (CI+IIP)] following high-intensity exercise has been reported in some, but not all previous studies. Therefore, the purpose of the current study was to determine the effect of severe-intensity cycling exercise on mitochondrial respiratory function compared to resting values.
METHODS:
Thirteen recreationally active (V̇O2peak, 48.0 ± 6.6 ml/kg/min) male participants reported to the laboratory on three separate occasions. Initially, participants performed a 30 W/min linear ramp incremental cycle test until the limit of tolerance (Tlim), to determine the gas exchange threshold (GET) and V̇O2peak. On visit two, participants were familiarised to a constant-load cycling exercise test at a work-rate equivalent to the GET, plus 70% of the difference between V̇O2peak and GET (70%Δ), until Tlim. Time taken to reach Tlim was recorded to the nearest second and 80% of this time was calculated and termed 80%Tlim. On the final visit, muscle biopsies were taken from the m. vastus lateralis, at rest and following performance of the 70%Δ constant load exercise test to 80%Tlim. Mitochondrial respiratory variables in permeabilised muscle fibres were assessed using high-resolution respirometry. Specifically CIL, coupled respiration through complex I (CIP) and complexes I+II (CI+IIP), and noncoupled maximal electron transfer system capacity through complexes I+II (CI+IIE), complex II (CIIE) and complex IVE were determined. The following flux control ratios (FCRs) were subsequently calculated Leak control ratio (LCR; CIL/CI+IIE), phosphorylation control ratio (PCR; CI+IIP/CI+IIE), inverse respiratory control ratio (INV-RCR; CIL/CI+IIP), substrate control ratio (SCR; CIp/CI+IIP) and complex IV reserve control ratio (CIVres; CI+IIP/CIVE). All samples were analysed in quadruplicate and analysis order was counterbalanced. Citrate synthase activity was used as a validated surrogate of mitochondrial content. Paired T-tests were used to assess the difference between the mitochondrial respiratory variables at rest and post exercise.
RESULTS:
Mass-specific CIP¬ (12%), CI+IIP (9%) and CI+IIE (9%) respiration was greater post exercise compared to rest (all P =0.048). There were no differences between time points for CIL, CIIE and CIVE and the FCRs (P > 0.05). There were no differences in CS activity or in mitochondrial respiration parameters or FCRs between time-points when mass-specific respiration was corrected to CS activity (P > 0.05).
CONCLUSION:
Mitochondrial respiratory function was not impaired following acute severe-intensity cycling exercise to 80% of Tlim. These findings conflict with some previous research and could be explained by this study counterbalancing the order in which the resting and post-exercise biopsies were analysed, thus mitigating the potential carry over effect of chemical inhibitors.