Average capillary pressure (Pc) close to the venous end (fluid equilibrium point) of the exchange vessels (denoted Pc,v), arterial (PA) and venous pressure, and the rate of net transcapillary fluid flux were continuously recorded in sympathectomized muscle during 30 min of graded exercise and for 30 min in the post-exercise period. Regional changes in colloid osmotic pressure (pi pl) and total osmolality in plasma, the latter reflecting work-induced interstitial hyperosmolality, were measured at intervals. In the control state at rest with a Starling fluid equilibrium, Pc,v averaged 17.6 +/- 0.8 mmHg. Exercise caused a rapid transcapillary plasma fluid loss, the net driving pressure for which in the initial phase of heavy work was 58 mmHg (transcapillary fluid flux divided by the capillary filtration coefficient). This comprised an increase in Pc,v of 16 mmHg, a nonprotein osmotic force (Posm) related to exercise-induced tissue hyperosmolality corresponding to 46 mmHg and an opposing force established by a raised pi pl of 4 mmHg. A theoretical analysis indicated that the main fraction of the osmotic fluid loss passed through transcellular ultrapores and only a minor part through conventional small pores. In spite of the fact that Pc remained high throughout the exercise period, the outward fluid flux gradually declined and a Starling equilibrium was re-established 23 min after the commencement of heavy exercise. This was explained by a gradual decline of Posm and apparently also by a secondary increase in tissue pressure (Pif) and/or a decrease in interstitial colloid osmotic pressure (pi if). Net fluid absorption occurred in the post-exercise period as a result of a gradual decrease in Pc, reversed transcapillary Posm and also maintained high Pif and/or low pi if. Exercise (even light) abolished normal Pc autoregulation, implying that the filtration component of net transcapillary fluid flux becomes distinctly modulated if PA is altered.