Exercise‐induced arterial hypoxaemia in healthy human subjects at sea level.

Abstract

SUMMARY1. We determined the incidence of exercise-induced arterial hypoxaemia and its determinants in sixteen highly trained, healthy runners who were capable of achieving and sustaining very high metabolic rates (maximal 02 uptake = 72 + 2 ml kg-' min-or 4-81 + 0-131 min'). Arterial blood gases and acidbase status were determined at each load of a progressive short-term exercise test and repeatedly during constant-load treadmill running while breathing air and during inhalation of mildly hypoxic, hyperoxic, and helium-enriched gases.2. 5. In view of the correction of hypoxaemia with mild hyperoxia and the very high ratios of alveolar ventilation to pulmonary blood flow (PA/C = 4-6) achieved during heavy exercise, we think it unlikely that non-uniformity of the VA/QC distribution or veno-arterial shunt could explain the hypoxaemia observed in most of our subjects. By exclusion, we suggest that hypoxaemia may be attributed to a diffusion limitation secondary to very short red cell transit times in at least a portion of the pulmonary circulation. These excessively short transit times may occur at high metabolic rates 6 PHY 355 J. A. DEMPSEY, P. G. HANSON AND K. S. HENDERSON if pulmonary capillary blood volume has achieved its maximum expansion at a time when pulmonary blood flow continues to increase.6. Considerable individual variations were present in the hyperventilatory response to heavy work. These variations were inconsistently related to corresponding levels of metabolic acidosis and in many cases a compensatory hyperventilation was minimal or absent in the face of substantial acidosis and hypoxaemia. The findings that tidal breaths during heavy exercise often exceeded the maximum flow-volume curve and that hyperventilation was consistently obtained with helium inhalation, suggest that the hyperventilatory response to heavy work is determined to a significant extent by the mechanical load imposed on the chest wall secondary to increased pulmonary impedance.

Exercise-induced Arteriovenous Intrapulmonary Shunting in Dogs

“…Our findings in the exercising dog, that is, that exercise recruits anatomic arteriovenous shunts, despite a previous inert gas study that has not found physiological pulmonary shunt in the dog (32), is consistent with previous human work demonstrating I-P shunt as assessed by contrast echocardiography (1-3), even though prior gas exchange-dependent techniques have not documented substantial right-to-left shunt (4)(5)(6)(7)(8). Indeed, we would suggest that the magnitude of the exercise-induced anatomic arteriovenous shunting in the human may be greater than in the dog (32), because of the larger relative increases in cardiac output, pulmonary vascular pressures, and (a-a)Do 2 typically observed in humans with exercise.…”

“…Despite an absence of right-to-left I-P shunt during exercise as determined by functional, gas exchange-dependent techniques (4)(5)(6)(7)(8), there is substantial research documenting anatomic arteriovenous anastomoses in the isolated lung. Studies have demonstrated direct vascular anastomoses between pulmonary arteries and veins in many mammals including cats (9), dogs (9)(10)(11), and healthy humans (9,12,13).…”

“…oxygen (4)(5)(6)(7)(8), that has failed to detect substantial right-to-left physiological I-P shunt during exercise.…”

Does exercise-induced hypoxemia modify lactate influx into erythrocytes and hemorheological parameters in athletes?

“…During sea-level exercise, some endurance-trained athletes experience arterial hypoxemia [exercise-induced hypoxemia (EIH)] that can be defined as a decrease in both oxygen arterial partial pressure (Pa O 2 ) and arterial hemoglobin saturation during exercise (8). Miyachi and Katayama (21) have reported repeated episodes of EIH during training sessions when endurance athletes performed very intense exercise, a result suggesting that athletes develop frequent episodes of mild hypoxemia during training.…”

Doping and Respiratory System

“…It might be worthwhile to discuss the possible actions on the most important functional respiratory parameters. Taking the maximal oxygen consumption (V'O 2 max) as the target of most physical performances, it is known that in the high level endurance athletes, their blood saturation may decrease during heavy or extreme exercise [5][6]. A very good analysis on the possible mechanisms underlying the human aerobic performance and the limit to V'O 2 was carried out by Lindstedt SL and Careley KE [7].…”