Isocapnia blocks exercise-induced reductions in ocular tension

Previous reports suggest that isometric exercise (2-min handgrip at 50% maximal voluntary contraction [MVC]) substantially lowers intraocular pressure (IOP). The authors questioned whether the mechanism for lowered IOP in exercise is secondary to hyperventilation. Accordingly, in this study 11 subjects, with elevated IOP (≥18 mm Hg) and otherwise healthy, did 2 min of handgrip exercise at 50% MVC with and without carbon dioxide supplementation to maintain isocapnic conditions. Compared with a control experiment that involved neither exercise nor CO₂ addition, exercise induced a fall in IOP from 18.3 to 15.6 mm Hg (P < 0.001). This statistically significant decline in IOP persisted for 15 min after the exercise session. At the point of minimum IOP (1 min after the end of exercise), the minute ventilation was elevated from 6.5-8.1 l/min (P < 0.05), and the end-tidal partial pressure of CO₂ (PCO₂) was reduced from 37.0 to 33.7 mm Hg (P < 0.05) with respect to control values. By contrast, adding CO₂ sufficient to maintain isocapnic conditions (experimental end-tidal PCO₂ = 38.9 versus 38.5 mm Hg in the control study; P = not significant) abolished the exercise-induced ocular hypotension (experimental IOP = 17.8 versus 18.1 mm Hg in the control study; P = not significant). It was concluded that prevention of hypocapnia during isometric handgrip exercise blocks the subsequent fall in IOP, suggesting both that isometric exercise per se has no direct influence on IOP and that therapy for ocular hypertension could involve manipulation of blood gases.