Eighty-seven male Sprague-Dawley rats (245-300 g) were randomly assigned to one of two experimental groups. The first group consumed a diet high in fat and low in carbohydrate (LCD), whereas the second group ate a normal diet (ND). After either 1 or 5 wk on the diets, rats from each group were killed either before or after an exhausting run on a rodent treadmill (35 m X min-1, 0% grade). The LCD animals ran significantly longer before exhaustion at both week 1 (44.9 +/- 5.1 vs. 41.6 +/- 4.2 min) and week 5 (47.1 +/- 3.6 vs. 35.5 +/- 3.1 min) (P less than 0.05). Adaptations to the LCD included lower muscle and liver glycogen content, decreased rate of glycogen breakdown during exercise, decreased lactate production, and elevated blood ketone levels. In addition to these substrate changes, the LCD caused increased enzyme activities of muscular 3-hydroxyacyl-CoA dehydrogenase (35-110%) and citrate synthase (15-20%). These data indicate that rats exposed to a high-fat diet are capable of prolonged intense exercise in spite of limited glycogen stores. This improved capacity for exercise appears to be partially the result of muscular adaptations to the diet, which apparently increase the ability to oxidize fat and concomitantly spare glycogen.

A common belief among many clinicians and trainers is that intensive simultaneous training for muscle strength and cardiovascular endurance is counterproductive. To test this premise, 14 healthy, untrained men trained four days per week for 20 weeks on a bicycle ergometer for endurance (END Group, n = 4), on an isokinetic device for increased torque production (ITP Group, n = 5), or on both devices (COMBO Group, n = 5). The ITP and COMBO groups had equal torque gains throughout the study (234 +/- 45 and 232 +/- 23 N.m, respectively). After 11 weeks, both END and COMBO groups had similar gains in maximal oxygen consumption (VO2max) (in milliliters per kilogram of body weight per minute). During the last half of the study, however, the END Group had a significant gain in VO2max (p less than .05) of 4.7 +/- 1.2 mL.kg-1.min-1, whereas the COMBO Group had a nonsignificant gain (p greater than .05) of 1.8 +/- 0.6 mL.kg-1.min-1. In harmony with this finding, the END Group showed a significant increase (p less than .05) in citrate synthase activity (15.5 +/- 7.9 mumol.g-1.min-1), whereas the COMBO Group had no significant increase. The authors concluded that simultaneous training may inhibit the normal adaptation to either training program when performed alone. The extent of the interference probably depends on the nature and intensity of the individual training program. [Nelson AG, Arnall DA, Loy SF, et al: Consequences of combining strength and endurance training regimens.

The purpose of this study was to test the hypothesis that increased availability of fatty acids could increase endurance by slowing the rate of glycogen depletion. Rats were given corn oil by stomach tube, and 3 h later an injection of heparin was given to raise their plasma free fatty acids (FFA). The rats with raised FFA were able to run approximately 1 h longer than otherwise comparable control animals before becoming exhausted (181 +/- 8 vs. 118 +/- 8 min, P less than 0.001). At the point of exhaustion, both groups were hypoglycemic and had low muscle glycogen concentrations. The fall in blood glucose occurred less rapidly in the animals with raised FFA; these rats also had significantly higher blood glycerol and beta-hydroxybutyrate concentrations than the controls. Glycogen concencentration decreased less rapidly in all three types of skeletal muscle and in liver in the animals with raised FFA than in the controls. We conclude that increased availability of fatty acids delays the development of exhaustion in rats subjected to prolonged running. It appears likely that the carbohydrate-sparing effect of fatty acids is largely responsible for the increase in endurance.

Following a strenuous bout of exercise, glycogen repletion occurred most rapidly in the fast-twitch red type of muscle, least rapidly in fast-twitch white, and at an intermediate rate in slow-twitch red muscle. There was a linear correlation between glycogen synthase I activity and the rate of glycogen synthesis in the three types of muscle. This finding helps explain the differences between the rates of glycogen resynthesis in the three muscle types, and supports the view that glycogen synthase activity is the most important factor determining the rate of glycogen synthesis when substrate supply is adequate. There was an inverse correlation between muscle glycogen concentration and percent glycogen synthase I. Plasma insulin concentration was low and norepinephrine and glucagon concentrations were elevated in the postexercise period. The finding that rapid glycogen synthesis occurred despite a hormonal milieu conducive to glycogenolysis provides evidence that a low glycogen concentration is a potent stimulus to glycogen synthesis that overrides the effects of low insulin, and high norepinephrine and glucagon levels.

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.