1. The purpose of this study was 1) to characterize the decrease observed in mean firing rates of motor units in the first 8-15 s of isometric constant-force contractions and 2) to investigate possible mechanisms that could account for the ability to maintain force output in the presence of decreasing motor unit firing rates. 2. The decrease in mean firing rates was characterized by investigating myoelectric signals detected with a specialized quadrifilar needle electrode from the first dorsal interosseus (FDI) and the tibialis anterior (TA) muscles of 19 healthy subjects during a total of 85 constant-force isometric contractions at 30, 50, or 80% of maximal effort. The firing times of motor units were obtained from the myoelectric signals with the use of computer algorithms to decompose the signal into the constituent motor unit action potentials. Time-varying mean firing rates and recruitment thresholds were also calculated. 3. Motor units detected from the TA muscle were found to have a continual decrease in their mean firing rates in 36 of 44 trials performed during isometric ankle dorsiflexion at force values ranging from 30 to 80% of maximal effort and a duration of 8-15 s. Likewise, motor units detected in the FDI muscle displayed a decrease in firing rate in 32 of 41 trials performed during constant-force isometric index finger abduction for contractions ranging from 30 to 80% of maximal effort. In 14 contractions (16% of total), firing rates were essentially constant, whereas in 3 contractions (4%), firing rates appeared to increase. 4. Motor units with the higher recruitment thresholds and lower firing rates tended to display the greater decreases in firing rate over the constant-force interval, whereas motor units with lower recruitment thresholds and higher firing rates had lesser rates of decrease. Furthermore, increasing contraction levels tended to intensify the decrease in the motor unit firing rates. 5. Three possible mechanisms were considered as factors responsible for the maintaining of force output while motor units decreased their firing rates: motor unit recruitment, agonist/antagonist interaction, and twitch potentiation. Of these, motor unit recruitment was discarded first because none was observed during the 8-15 s duration of any of the 85 contractions. Furthermore, contractions outside the physiological range of motor unit recruitment (at 80% of maximal effort) revealed the same decreasing trend in firing rates, ruling out recruitment as the means of sustaining force output. 6. The role of agonist or antagonist muscle interaction was investigated with the use of the muscles controlling the wrist joint. Myoelectric signals were recorded with quadrifilar needle electrodes from the wrist extensor muscles while myoelectric activity in the wrist flexor muscles was concurrently monitored with surface electrodes during constant-force isometric wrist extension at 50% of maximal effort. Firing rates of the motor units in the wrist extensor muscles simultaneously decreased while the flexor muscl...

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The plasma catecholamine and serum cortisol responses to cardiac arrest (ventricular fibrillation), cardiopulmonary resuscitation (CPR), and ventricular defibrillation were examined in 10 intact (sham-operated controls) and 10 bilaterally adrenalectomized dogs. One hour after surgery, the cardiac ventricles were electrically fibrillated, and 30 s later Standard American Heart Association CPR was begun. After 12 min of CPR, the ventricles were defibrillated. Cardiac arrest per se results in a massive increase in plasma epinephrine and norepinephrine concentrations and indicates that the adrenal medullas are the predominant source of this response. Although the epinephrine response was virtually nonexistent in the adrenalectomized dogs, the norepinephrine response was approximately 30% of that in the sham-operated control animals. Thus there is an adrenomedullary, and perhaps a sympathetic neural, component to the sympathochromaffin response to cardiac arrest. Resuscitation from experimental cardiac arrest tended (P greater than 0.05 less than 0.1) to be lower in the adrenalectomized dogs (1 of 10) than in the animals with intact adrenal glands (6 of 10).

The purpose of this study was to attain a better understanding of how the adipocyte transports and metabolizes glucose with and without the influence of exercise training. Rates of 2-deoxyglucose and glucose oxidation, using [1-14C]-and [6-14C]glucose, were measured in adipocytes from exercise-trained and sedentary control female rats of the same age. The trained animals were exercised by swimming, 6 h/day, 5 days/wk for 10 wk. The fat cells of the sedentary rats were significantly larger (P less than 0.005) than the trained animals and had very low rates of glucose uptake and [1-14C]- and [6-14C]glucose oxidation. The adipocytes of the trained rats were very responsive to insulin with 2-deoxyglucose rates seven times higher than those of the control animals and [1-14C]- and [6-14C]-glucose oxidation rates 14- and 13-fold (respectively) larger than control values. Comparisons of the data from exercised animals to younger sedentary rats indicates that glucose oxidation remains normal in the adipocytes of the trained animals whereas glucose transport is greatly improved. If the older sedentary controls are compared to younger animals, it can be seen that as the cell enlarges it loses its ability to take up or metabolize glucose. The combination of a loss in glucose transporting capacity with cellular enlargement and an increase in glucose uptake with exercise training suggests that movement of glucose across the cell membrane may be a limiting factor in glucose utilization in fat cells.