Effects of acute leg ischemia during cycling on oxygen and carbon dioxide stores

• Published in: Journal of rehabilitation research and development Vol. 45; no. 7; pp. 1091 - 1102
• Main Authors: Loeppky, Jack A, Gurney, Burke, Icenogle, Milton V
• Format: Journal Article
• Language: English
• Published: United States Department of Veterans Affairs 01-01-2008; Superintendent of Documents
• Subjects: Adult; Carbon dioxide; Carbon Dioxide - metabolism; Changes; Chronic illnesses; Chronic obstructive pulmonary disease; Exercise; Exercise - physiology; Exercise Test; Exercise Therapy - methods; Feasibility Studies; Female; Gases; Health aspects; Humans; Inflation; Injuries; Ischemia; Ischemia - physiopathology; Leg; Leg - blood supply; Leg - physiology; Male; Middle Aged; Oxygen Consumption; Physical Endurance; Physical fitness; Physiological aspects; Resistance Training; Risk factors; Ventilation; Veterans; Young Adult; United States
• ISSN: 0748-7711; 1938-1352
• DOI: 10.1682/JRRD.2007.11.0198

This study estimated changes in whole body oxygen stores (O(2)s) and carbon dioxide stores (CO(2)s) during steady state exercise with leg ischemia induced by leg cuff inflation. Six physically fit subjects performed 75 W steady state exercise for 15 min on a cycle ergometer. After 5 min of exercise, cuffs on the upper and lower legs were inflated to 140 mmHg. Cuffs were deflated after 5 min and exercise continued for another 5 min. O(2 )uptake (VO(2)) and CO(2) output (VCO(2)) significantly increased during the first 30 s after inflation, significantly decreased between 60 and 90 s, and then rose linearly until deflation. VO(2) and VCO(2) significantly increased further after cuff deflation, peaking between 30 and 60 s and then returned to near baseline exercise levels. Model-estimated changes in total O(2)s and CO(2)s were compared with time-integrated store changes from VO(2) and VCO(2). During 5 min after cuff deflation, VO(2) and VCO(2) exceeded the model-estimated change in stores by 273 and 697 mL, respectively. These results reflect the O(2) cost repayment of the anaerobic component and lactate buffering to neutralize circulating metabolites caused by the preceding ischemia.