pubmed-article:1909689 | pubmed:abstractText | The effects of smoking on the kinetics of oxygen uptake (VO2), carbon dioxide production (VCO2), ventilation (Ve) and heart rate (HR) in the transition from rest to steady-state submaximal exercise was investigated in 6 female and 4 male smokers (32 +/- 8 yrs). The subjects underwent two counter-balanced treadmill tests at 60% of their maximal VO2, lasting 10 min each: one following a 24-hr smoking abstinence, and one immediately after smoking three cigarettes without prior abstinence. Physiological variables were measured at rest and every 30 sec throughout each test. The time required for a given variable to rise from its respective resting baseline to half of its steady-state value (t1/2) was calculated for VO2, VCO2, Ve and HR. Smoking abstinence was associated with t1/2 values of 32 +/- 8, 42 +/- 12, 43 +/- 10, and 30 +/- 9 sec for VO2, VCO2, Ve, and HR, respectively. Smoking significantly (p less than 0.01) lengthened those values to 51 +/- 12, 58 +/- 11, 54 +/- 8, and 41 +/- 10 sec. Concurrently, smoking raised the baseline (resting) values of HR (p less than 0.01) and of Ve, VCO2, O2 pulse (O2P), and both systolic and diastolic blood pressures (p less than 0.05). During steady-state exercise only HR values were elevated by smoking (p less than 0.01), while O2P values were lowered (p less than 0.05). These findings indicate that smoking considerably retards physiological responses to submaximal exercise. | lld:pubmed |