No abstract

The force-velocity (F-V) relationships of canine gastrocnemius-plantaris muscles at optimal muscle length in situ were studied before and after 10 min of repetitive isometric or isotonic tetanic contractions induced by electrical stimulation of the sciatic nerve (200-ms trains, 50 impulses/s, 1 contraction/s). F-V relationships and maximal velocity of shortening (Vmax) were determined by curve fitting with the Hill equation. Mean Vmax before fatigue was 3.8 +/- 0.2 (SE) average fiber lengths/s; mean maximal isometric tension (Po) was 508 +/- 15 g/g. With a significant decrease of force development during isometric contractions (-27 +/- 4%, P < 0.01, n = 5), Vmax was unchanged. However, with repetitive isotonic contractions at a low load (P/Po = 0.25, n = 5), a significant decrease in Vmax was observed (-21 +/- 2%, P < 0.01), whereas Po was unchanged. Isotonic contractions at an intermediate load (P/Po = 0.5, n = 4) resulted in significant decreases in both Vmax (-26 +/- 6%, P < 0.05) and Po (-12 +/- 2%, P < 0.01). These results show that repeated contractions of canine skeletal muscle produce specific changes in the F-V relationship that are dependent on the type of contractions being performed and indicate that decreases in other contractile properties, such as velocity development and shortening, can occur independently of changes in isometric tension.

This study was designed to test the hypothesis that epinephrine (E) and norepinephrine (NE) increase net muscle lactate output (L) of in situ gastrocnemius-plantaris muscle group during contractions. Plasma [E] and [NE] were measured before and after the surgical isolation of the muscle and at 10-min intervals during the 60-min experiments. Plasma [E] and [NE] were increased threefold by intravenous infusions of E (n = 3) or NE (n = 3) at a rate of 1.5 micrograms X kg body wt-1 X min-1. Arterial and muscle venous blood samples for O2 and lactate concentrations were also obtained. The infusions began at min 11 and repetitive isometric contractions (4 tw/s) began at min 31. The presurgery plasma [E] and [NE] averaged 0.34 and 0.52 ng/ml, respectively, and rose to 1.12 and 1.19 ng/ml 10 min after surgery. Arterial and venous lactate concentrations (CaL and CvL) increased continuously during E infusion but remained constant during NE infusion. Maximal L during the first 10 min of contractions was significantly increased compared with an identical earlier study without infusions. O2 uptake was not changed by the infusions. It is concluded that E causes CaL to rise and that both E and NE increase maximal net lactate output during contractions.

This study was designed to investigate the effects of naloxone on athletic performance in humans. Two groups of elite middle-distance runners performed a maximal or a submaximal exercise protocol following the double-blind intravenous injection of either naloxone (0.15 mg X kg body wt-1) or saline. The maximal test (group M) was comprised of a short-duration treadmill run to maximal intensity; the submaximal test (group S), a prolonged submaximal treadmill run to exhaustion. O2 uptake, heart rate, ventilation, and perceived exertion were determined during each test. Perception of pain was assessed after exercise by use of a modified McGill pain questionnaire. No significant differences between placebo and naloxone treatments were found in any of the measured variables at the usually accepted 5% (P = 0.05) confidence level; however, evidence suggesting differences (i.e., P = 0.1 to 0.05) in these important respects was observed. In group M, maximal exercise performance measured by maximal O2 consumption was not different between placebo and naloxone; results suggest that VE was increased (P = 0.08) following naloxone, but only at the final work stage. In group S, exercise performance time was reduced following naloxone (P = 0.09), whereas the affective component of pain was increased (P = 0.06); no differences in the measured physiological variables were observed. These results suggest the following: 1) the opiate receptor-endorphin system may alter the perception of pain associated with prolonged high-intensity submaximal exercise with a resultant significant effect on performance; and 2) it may play a role in the control of ventilation during maximal exercise.

Blood flow through the gastrocnemius-plantaris muscle of the dog in situ was increased by a pump in the arterial supply during a 30-min period of 1/s isotonic tetanic contractions. Compared with a control series of experiments with normoxemia and spontaneous flow, the pump increased flow 84%, from 1.51 +/- 0.08 to 2.78 +/- 0.15 ml.g-1.min-1. The perfusion pressure was increased from 125 to 196 mmHg. The pump hyperemia increased maximal O2 uptake (VO2) at 5 min of contractions by 31%, from 8.97 +/- 0.44 to 12.89 +/- 0.30 mumol.g-1.min-1. The extraction was decreased, and venous PO2 (PVO2) was increased. Fatigue, measured as a drop in power production from the highest level at 10 s to 30 min, was 49% during pump hyperemia and 54% in the control conditions. VO2 decreased 30% from the 5-min value to the 30-min value with pump hyperemia and 28% over the same time in the control conditions. At maximal VO2, the ratio VO2/PVO2 was increased by pump hyperemia compared with control conditions, suggesting an increased O2 diffusing conductance of the muscles. We conclude that the elevated perfusion pressure of pump hyperemia increased flow to raise maximal VO2 mainly in areas of the muscle that had restricted flow under control conditions.