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Abstract
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 (greater than or equal to 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 less than 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 less than 0.05), and the end-tidal partial pressure of CO2 (PCO2) was reduced from 37.0 to 33.7 mm Hg (P less than 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.