[Determining the extent of intensive physical performance in patients with coronary heart disease]

Intensive physical exercise improves cardiac perfusion, skeletal muscle function and risk factors in patients with coronary artery disease (CAD). Otherwise, overdosed intensity can induce training adaptation as well as cardiac events. Therefore, we tested whether exercise intensity corresponding to an equilibrium between lactate production and elimination from the blood during incremental exercise tests represented the blood lactate [Lac-]B steady-state intensity during constant physical training. Randomized into two groups with 30 CAD patients each (T1: 25 male, 5 female; 59 +/- 7 years; T2: 26 male, 4 female; 60 +/- 9 years), the patients initially performed two successive incremental exercise tests. In the first test, workload was increased stepwise until exhaustion or symptom limitation (maximal workload: T1 142 +/- 48 watts, T2 145 +/- 45 watts) with the corresponding [Lac-]B accumulation of up to 6.7 +/- 2.6 (T1) or 6.5 +/- 2.0 (T2) mmol/l, respectively. After a seven minute active rest the second test began with 25 watts, increased with 5 (maximum workload in first test < 100 watts) or 10 watts per minute, respectively. During lower intensities in the second test, [Lac-]B initially decreased to an individual lactate minimum intensity (workload at LMI 83 +/- 32 in T1 or 86 +/- 29 in T2 watts, respectively; [Lac-]B at LMI 4.6 +/- 2.2 and 4.9 +/- 1.8 mmol/l, respectively) and then increased again. To check if the individual LMI represented the [Lac-]B steady-state workload in constant workload exercise, the patients performed 30 min constant load tests with the LMI (CT1) or a 30 min constant load test with an intensity 10% above the LMI (CT2), respectively. The workload in CT1 was 83 +/- 32 watts with a mean exercise time of 29.0 +/- 1.7 min. After 10 min of exercise the [Lac-]B steady state was reached at 3.3 +/- 1.4 mmol/l with no further increase in the last 20 min. The mean workload in CT2 was 95 +/- 31 watts with an exercise time of 23.3 +/- 8.3 min (p < 0.01). [Lac-]B increased from 4.4 +/- 1.7 mmol/l after 10 min to 4.7 +/- 2.0 mmol/l at the end (p < 0.01). Fifty percent of patients stopped CT2 before the 30 minute end. The results indicates that the LMI, estimated during lactic acidosis in two successive incremental tests, represented the individual lactate steady-state intensity also during constant load exercise. Therefore, training regimens for CAD patients could be deduced from LMI.