R. Jorge Zeballos

Exercise and hypoxia increase sickling in venous blood from an exercising limb in individuals with Sickle cell trait

PURPOSE The association between sickle cell trait (SCT) and complications related to exercise may be explained if exercise-induced sickling interferes with capillary blood flow and causes tissue ischemia and functional abnormalities. To test this hypothesis, we measured sickling and blood gas values in venous and arterial blood of an exercising limb in subjects with SCT and in controls. SUBJECTS AND METHODS The study consisted of 15 subjects with hemoglobin AS (SCT group) and 15 subjects with hemoglobin AA (control group). Each performed two maximal arm crank exercise tests, one at 1,270 meters and one at simulated 4,000 meters. RESULTS At 1,270 meters, axillary venous sickling increased significantly (p less than 0.05) from (mean +/- SD) 1.0 +/- 1.0% at rest to 2.3 +/- 2.6% during peak exercise. At simulated 4,000 meters, sickling increased significantly (p less than 0.001) from 1.5 +/- 1.2% to 8.5 +/- 7.1%. A wide range of sickling during peak exercise was observed (1% to 25%). One minute after exercise at simulated 4,000 meters, venous sickling remained elevated (7.2 +/- 7.8%) despite high levels of oxygen saturation. Arterial sickling (less than 1%) was present in only two subjects. There was no significant difference in oxygen consumption (29.4 +/- 3 versus 30.7 +/- 4 mL/kg/minute) between the subjects with SCT and the controls, nor was there a correlation between exercise performance and sickling (r less than 0.2). CONCLUSION We conclude that exercise at 1,270 meters slightly, albeit significantly, increased sickling in blood from an exercising limb and that simulated 4,000 meters dramatically potentiated this effect. Sickling in the effluent blood of an exercising limb does not appear to measurably affect overall maximal arm crank exercise performance.

Cardiopulmonary and gas exchange responses to acute strenuous exercise at 1,270 meters in sickle cell trait

The impact of strenuous exercise and environmental hypoxia on sickle cell trait (SCT) remains controversial. To determine if these factors induce cardiopulmonary and gas exchange abnormalities in SCT, healthy, young black male volunteers, 25 with SCT (HbAS) and 16 control subjects (HbAA), were evaluated during incremental and steady-state exercise tests using a cycle ergometer at 1,270 meters and 24 degrees C. Peak incremental exercise values for power (242 +/- 7 versus 253 +/- 10 watts), oxygen consumption (3.08 +/- 0.1 versus 3.26 +/- 0.14 liters/minute), heart rate (188 +/- 2 versus 189 +/- 3 beats/minute), minute ventilation (129 +/- 4.6 versus 144 +/- 7.7 liters/minute), oxygen pulse (16.4 +/- 0.5 versus 17.3 +/- 0.8 ml/beat), and respiratory exchange ratio (1.31 +/- 0.01 versus 1.33 +/- 0.02) revealed no significant differences (p less than 0.05) between the SCT and control groups, respectively. Peak incremental exercise values for arterial oxygen tension (82 +/- 1.7 versus 82 +/- 2.2 mm Hg), arterial carbon dioxide tension (32 +/- 0.7 versus 31 +/- 0.9 mm Hg), and alveolar-arterial oxygen pressure differences (19 +/- 1.4 versus 21 +/- 1.9 mm Hg) were similar for the SCT and control groups, respectively. Steady-state exercise results corroborate incremental exercise findings. It is concluded that cardiopulmonary and gas exchange responses to a brief period of strenuous exercise performed at low altitude at 24 degrees C in a well-characterized SCT sample of recruits were within normal limits and comparable to those of a carefully selected control sample.

Effect of moderate inspiratory hypoxia on exercise performance in sickle cell trait

In previous work (Weisman IM, Zeballos RJ, Johnson BD: Cardiopulmonary and gas exchange responses to acute strenuous exercise at 1,270 meters in sickle cell trait. Am J Med 1988; 84: 377-383), no significant differences in cardiopulmonary and gas exchange responses to acute, strenuous exercise were observed between volunteers with sickle cell trait (SCT) and control subjects at an altitude of 1,270 meters. The current study was designed to evaluate the effect of a greater hypoxic stimulus on the response of healthy, black male basic recruits, 11 with SCT (HbAS) and 11 control subjects, to acute strenuous exercise. Simulated 2,300-meter and simulated sea-level conditions were achieved by adjustment of the fraction of inspired oxygen (simulated condition of 2,300 meters equal to 18 percent; simulated sea-level condition equal to 24 percent) at the same barometric pressure (656 mm Hg). For each simulated condition, the subjects performed an incremental exercise test to exhaustion on a cycle ergometer. One steady-state exercise test with radial arterial access for arterial blood gases was performed under each condition on Day 2. Peak incremental exercise values for oxygen consumption (2.9 versus 2.81 liters/minute), heart rate (189 versus 187 beats/minute), oxygen pulse (15.4 versus 15.1 ml/beat), and anaerobic threshold (1.59 versus 1.62 liters/minute), at the simulated 2,300-meter height revealed no significant differences between men with SCT and control subjects, respectively. A 5 to 9 percent decrement in exercise performance at the simulated 2,300-meter level compared with exercise performance at the simulated sea-level condition was noted for both groups. Steady-state exercise values for arterial oxygen tension (64 versus 65 mm Hg), arterial oxygen saturation (90 versus 90 percent), alveolar-arterial oxygen pressure difference (22 versus 21 mm Hg), and physiologic dead space to tidal volume ratio (12 versus 11) at the simulated condition of 2,300 meters were similar for the SCT and control groups, respectively. It is concluded that in a moderate hypoxic environment, the cardiopulmonary and gas exchange responses of persons with SCT during brief episodes of exhaustive exercise were comparable to those of control subjects.