Training and Detraining Effects of a Combined-strength and Aerobic Exercise Program on Blood Lipids in Patients With Coronary Artery Disease :

Skeletal muscle is characterized by its ability to dynamically adapt to variable levels of functional demands. During periods of insufficient training stimulus, muscular detraining occurs. This may be characterized by a decreased capillary density, which could take place within 2--3 wk of inactivity. Arterial-venous oxygen difference declines if training stoppage continues beyond 3--8 wk. Rapid and progressive reductions in oxidative enzyme activities bring about a reduced mitochondrial ATP production. The above changes are related to the reduction in VO(2max) observed during long-term training cessation. These muscular characteristics remain above sedentary values in the detrained athlete but usually return to baseline values in recently trained individuals. Glycolytic enzyme activities show nonsystematic changes during periods of training cessation. Fiber distribution remains unchanged during the initial weeks of inactivity, but oxidative fibers may decrease in endurance athletes and increase in strength-trained athletes within 8 wk of training stoppage. Muscle fiber cross-sectional area declines rapidly in strength and sprint athletes, and in recently endurance-trained subjects, whereas it may increase slightly in endurance athletes. Force production declines slowly and in relation to decreased EMG activity. Strength performance in general is readily maintained for up to 4 wk of inactivity, but highly trained athletes' eccentric force and sport-specific power, and recently acquired isokinetic strength, may decline significantly.

Detraining can be defined as the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining is characterized, among other changes, by marked alterations in the cardiorespiratory system and the metabolic patterns during exercise. In highly trained athletes, insufficient training induces a rapid decline in VO2max, but it remains above control values. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume resulting from a rapid blood volume loss, and maximal cardiac output is thus reduced. Cardiac dimensions are also reduced, as well as ventilatory efficiency. Consequently, endurance performance is also markedly impaired. These changes are more moderate in recently trained subjects in the short-term, but recently acquired VO2max gains are completely lost after training stoppage periods longer than 4 wk. From a metabolic viewpoint, even short-term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio. This may result from a reduced insulin sensitivity and GLUT-4 transporter protein content, coupled with a lowered muscle lipoprotein lipase activity. These metabolic changes may take place within 10 d of training cessation. Resting muscle glycogen concentration returns to baseline within a few weeks without training, and trained athletes' lactate threshold is also lowered, but still remains above untrained values.

Eighteen hospitalized patients with severe chronic heart failure (ejection fraction [mean +/- SEM] 21% +/- 1%) underwent 3 weeks of exercise training (interval bicycle ergometer and treadmill walking training exercises) and 3 weeks of activity restriction in a random-order crossover trial. Before and after exercise training and after activity restriction, a 6-minute walking test was performed to determine the maximum distance walked, hemodynamic and cardiopulmonary responses, norepinephrine levels, and ratings of leg fatigue and dyspnea while walking. A ramp test on bicycle ergometer (increments of 12.5 W/min) was performed before and after exercise training and activity restriction to determine peak oxygen uptake. After training, the maximum distance walked was increased by 65% (from 232 +/- 21 m at baseline to 382 +/- 20 m; p < 0.001), whereas after activity restriction (253 +/- 19 m) there was no significant difference compared with baseline. No significant differences in hemodynamic and cardiopulmonary parameters (with the exception of the ventilatory equivalent for carbon dioxide and perceived exertion) or norepinephrine levels were observed during walking tests. Improvement in maximum distance walked correlated significantly with training-induced increase in peak oxygen uptake measured during bicycle ergometry (r = 0.47, p < 0.05). The lower the maximum distance walked at baseline, the more pronounced the training-induced prolongation of maximum distance (r= -0.73; p < 0.001). These data support the value of exercise training in patients with severe chronic heart failure for improving maximum distance walked, as documented by the 6-minute walking test. The impairment of walking test performance during activity restriction suggests a need for long-term exercise training programs.