Abstract

The effects of induced metabolic alkalosis (ALK) on the regulation and integration of ATP producing pathways during exercise have not been clearly elucidated. PURPOSE To examine the effects of ALK on the rate of skeletal muscle phosphocreatine (PCr) degradation during a step increase in work rate from light to moderate (MOD) then to heavy (HVY) exercise. METHODS Healthy, active male volunteers (n = 10, age = 26±4; mean ± SD) performed a single trial of isotonic wrist flexion (0.5 Hz, 70° ROM) in control (CON) and in ALK (0.3g/kg of NaHCO3, 90 min prior to testing). Prior to the trials, each subject performed an incremental ramped wrist flexion exercise protocol (0.12 W/min) to determine the work rate corresponding to the intracellular pH threshold (IT). The exercise trials consisted of wrist flexion for 9 min at MOD (75% IT) and HVY (125% IT) exercise. Relative [PCr]and intracellular H+ were measured using 31P-MRS. The initial fundamental PCr response was modeled using a mono-exponential equation and non-linear least-squares regression techniques. RESULTS The time constant of PCr degradation (τPCr) during transition to MOD was similar in CON (52±12 s) and ALK (52±17 s). During HVY the τPCr in CON (57±9 s) and ALK (64±14 s) were not different, however, the relative magnitude of the PCr slow component was reduced (p< 0.05) in ALK (0.034±0.031) compared to CON (0.062±0.028). During the final 3 min of HVY exercise, intracellular [H+] was lower (p< 0.05) in ALK (246±117 nmol/l) compared to CON (291±129 nmol/l). CONCLUSIONS Induced alkalosis during dynamic wrist flexion exercise was associated with similar PCr kinetics during the initial fundamental response in MOD and HVY, but the PCr slow component was reduced in ALK, which may be explained by an attenuated rise in intracellular [H+]. Supported by NSERC

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