Exercise performance is impaired by increased respiratory work, yet the mechanism for this is unclear. This experiment assessed whether neural drive to an exercising muscle was affected by cortically-driven increases in ventilation. On each of five days, eight subjects completed a 2 min maximal voluntary contraction (MVC) of the elbow flexor muscles, followed by 4 min of recovery, while transcranial magnetic stimulation tested for suboptimal neural drive to the muscle. On one day, subjects breathed without instructions under normocapnia. During the 2-min MVC ventilation was ~3.5 times that at rest. On another day, subjects breathed without instruction under hypercapnia. During the 2-min MVC, ventilation was ~1.5 times that on the normocapnic day. On another two days under normocapnia, subjects voluntarily matched their breathing to the uninstructed breathing under normocapnia and hypercapnia using target feedback of the rate and inspiratory volume. On a fifth day under normocapnia, the volume feedback was set to each subject’s vital capacity. On this day, ventilation during the 2-min MVC was ~ twice that on the uninstructed normocapnic day (or ~ 7 times rest). The experimental manipulations succeeded in producing voluntary and involuntary hyperpnea. However, maximal voluntary force, fatigue and voluntary activation of the elbow flexor muscles were unaffected by cortically- or chemically-driven increases in ventilation. Results suggest that any effects of increased respiratory work on limb exercise performance are not due to a failure to drive both muscle groups optimally.