We examined the effect of intravenous ascorbate (VitC) administration on exercise-induced redox balance,
inflammation, exertional
dyspnea, neuromuscular
fatigue, and exercise tolerance in patients with
chronic obstructive pulmonary disease (
COPD). Eight
COPD patients completed constant-load cycling (∼80% of peak power output, 83 ± 10 W) to task failure after intravenous VitC (2 g) or saline (placebo, PL) infusion. All participants repeated the shorter of the two exercise trials (isotime) with the other infusate. Quadriceps
fatigue was determined by pre- to postexercise changes in quadriceps twitch torque (ΔQtw, electrical femoral nerve stimulation). Corticospinal excitability before, during, and after exercise was assessed by changes in motor evoked potentials triggered by
transcranial magnetic stimulation. VitC increased
superoxide dismutase (marker for
endogenous antioxidant capacity) by 129% and mitigated
C-reactive protein (marker for
inflammation) in the plasma during exercise but failed to alter the exercise-induced increase in lipid peroxidation (
malondialdehyde) and
free radicals [electron paramagnetic resonance (EPR)-spectroscopy]. Although VitC did, indeed, decrease neuromuscular
fatigue (ΔQtw: PL -29 ± 5%, VitC -23 ± 6%, P < 0.05), there was no impact on corticospinal excitability and time to task failure (∼8 min, P = 0.8). Interestingly, in terms of pulmonary limitations to exercise, VitC had no effect on perceived exertional
dyspnea (∼8.5/10) and its determinants, including oxygen saturation ([Formula: see text]) (∼92%) and respiratory muscle work (∼650 cmH2O·s·min-1) (P > 0.3). Thus, although VitC facilitated indicators for
antioxidant capacity, diminished inflammatory markers, and improved neuromuscular
fatigue resistance, it failed to improve exertional
dyspnea and cycling exercise tolerance in patients with
COPD. As
dyspnea is recognized to limit exercise tolerance in
COPD, the otherwise beneficial effects of VitC may have been impacted by this unaltered sensation.NEW & NOTEWORTHY We investigated the effect of intravenous
vitamin C on redox balance, exertional
dyspnea, neuromuscular
fatigue, and exercise tolerance in
chronic obstructive pulmonary disease (
COPD) patients. Acute
vitamin C administration increased
superoxide dismutase (marker of
antioxidant capacity) and attenuated
fatigue development but failed to improve exertional
dyspnea and exercise tolerance. These findings suggest that a compromised redox balance plays a critical role in the development of
fatigue in
COPD but also highlight the significance of exertional
dyspnea as an important symptom limiting the patients' exercise tolerance.