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Previous investigators have reported that oxygen consumption (VO2) continues to rise after the initial 2- to 3-min transient period of exercise when work exceeds approximately 60% of VO2 max. The purpose of this investigation was to examine the possible causes of this slow rise in VO2. Eighteen subjects exercised for 20 min at 65% and at 80% of VO2 max on the bicycle ergometer. VO2, ventilation (VE), and respiratory exchange ratio were monitored by a continuous computer-based system. Blood lactate concentration and rectal temperatures were measured at 2- to 3-min intervals during the exercise. VO2 increased significantly from the 5th to 20th min of exercise in 81% of the tests at both levels of work intensity. The magnitude of the rise was not different for the two work loads. No evidence was found to support the lactacid explanation proposed for this rise. Increased temperature could account for 30% of the rise; the estimated cost of increased VE could account for 30 and 81% of the rise at the two work loads. The sum of these factors could account for 60 and 111% of the rise in VO2 at the 65 and 80% of VO2 max work loads.

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61-67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65-90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.

Groups of endurance-trained masters athletes (60 +/- 2 yr), older untrained men (62 +/- 1 yr), lean older untrained men (61 +/- 2 yr), endurance-trained young athletes (26 +/- 1 yr), and young untrained men (28 +/- 1 yr) were studied to obtain information on the separate effects of age, physical activity, and body fatness on glucose tolerance and insulin sensitivity. Each subject underwent an oral 100-g glucose tolerance test. Skinfold thickness was determined at six sites. The trained groups had a higher maximum O2 uptake capacity and lower sum of skinfolds than their sedentary peers. The lean older untrained group had a sum of skinfolds similar to that of the young untrained group. The masters athletes, young athletes, and young untrained men exhibited similar glucose tolerance whereas the two older untrained groups had an almost twofold greater total area under the glucose curve (P less than 0.05). The masters and young athletes had significantly blunted plasma insulin responses compared with the other three groups (P less than 0.05). The young and the lean older untrained groups had similar plasma insulin responses with significantly lower insulin levels than the older untrained group (P less than 0.05). These results provide evidence that regularly performed vigorous exercise can, in some individuals, prevent the deterioration of glucose tolerance and insulin sensitivity with age.

This study was undertaken to determine the effects of exercise intensity and duration on the time course and magnitude of recovery O2. Eighteen men exercised at 50, 65, and 80% of maximal O2 consumption (VO2max) for 5 and 20 min. Each exercise bout was preceded and followed by cycling at 150 kpm.min-1, which established the base-line VO2 used in this study. The magnitude of the rapid component of recovery O2 was proportional to exercise intensity and was not altered by exercise duration. The slow component of recovery O2 was not significantly altered by exercise intensity or duration at 50 and 65% of VO2max. However, after 20 min of exercise at 80% of VO2max, the slow component of recovery 02 was 5 times (p less than 0.01) larger than after the 5-min exercise at 80% of VO2max. End-exercise blood lactate level was also higher after the 20-min bout at 80% of VO2max; however, at most, 30% of the difference between the magnitude of the slow components of recovery O2 after the 5- and 20-min rides at 80% of VO2max could be accounted for by lactate metabolism. The Q10 effect of temperature on metabolism could account for 60-70% of the slow components of recovery O2 at all work rates and durations. It could also account for the remaining 70% of the increase in the slow component after the 20-min exercise at 80% of VO2max.

This study was undertaken to determine if patients who lack muscle phosphorylase (i.e., McArdle's disease), and therefore the ability to produce lactic acid during exercise, demonstrate a normal hyperventilatory response during progressive incremental exercise. As expected these patients did not increase their blood lactate above resting levels, whereas the blood lactate levels of normal subjects increased 8- to 10-fold during maximal exercise. The venous pH of the normal subjects decreased markedly during exercise that resulted in hyperventilation. The patients demonstrated a distinct increase in ventilation with respect to O2 consumption similar to that seen in normal individuals during submaximal exercise. However their hyperventilation resulted in an increase in pH because there was no underlying metabolic acidosis. End-tidal partial pressures of O2 and CO2 also reflected a distinct hyperventilation in both groups at approximately 70-85% maximal O2 consumption. These data show that hyperventilation occurs during intense exercise, even when there is no increase in plasma [H+]. Since arterial CO2 levels were decreasing and O2 levels were increasing during the hyperventilation, it is possible that nonhumoral stimuli originating in the active muscles or in the brain elicit the hyperventilation observed during intense exercise.

Seven endurance exercise-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Maximal O2 uptake (VO2 max) declined 7% (P less than 0.05) during the first 21 days of inactivity and stabilized after 56 days at a level 16% (P less than 0.05) below the initial trained value. After 84 days of detraining the experimental subjects still had a higher VO2 max than did eight sedentary control subjects who had never trained (50.8 vs. 43.3 ml X kg-1 X min-1), due primarily to a larger arterial-mixed venous O2 (a-vO2) difference. Stroke volume (SV) during exercise was high initially and declined during the early detraining period to a level not different from control. Skeletal muscle capillarization did not decline with inactivity and remained 50% above (P less than 0.05) sedentary control. Citrate synthase and succinate dehydrogenase activities in muscle declined with a half-time of 12 days and stabilized at levels 50% above sedentary control (P less than 0.05). The initial decline in VO2 max was related to a reduced SV and the later decline to a reduced a-vO2 difference. Muscle capillarization and oxidative enzyme activity remained above sedentary levels and this may help explain why a-vO2 difference and VO2 max after 84 days of detraining were still higher than in untrained subjects.

The effects of prolonged endurance training on maximal O2 uptake capacity (VO2max) and its determinants were studied in 11 older individuals (63 +/- 2 yr). The subjects were evaluated before training, after 6 mo of low-intensity (LI) training, and after an additional 6 mo of higher intensity (HI) training. VO2max was 25.4 +/- 4.6 ml X kg-1 X min-1 before training, 28.2 +/- 5.2 ml X kg-1 X min-1 after LI training (P less than 0.05), and 32.9 +/- 7.6 ml X kg-1 X min-1 after HI training (P less than 0.01), with an overall increase of 30%. The increase in VO2max in response to training appeared to be mediated primarily through an increase in maximal arteriovenous O2 difference (P less than 0.01), with little augmentation of maximal cardiac output (Q) (P greater than 0.05). At the same absolute work rates, stroke volume was higher (P less than 0.05); heart rate (HR), blood pressure (BP), and systemic vascular resistance were lower (P less than 0.05); and Q and arteriovenous O2 difference were unchanged after training. At the same relative work rates, arteriovenous O2 difference was higher (P less than 0.01); BP and systemic vascular resistance were lower (P less than 0.05); and HR, Q, and stroke volume did not change significantly. These findings show that older individuals can adapt to prolonged endurance training with a large increase in aerobic power.

This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).

One possible reason for the lower exercise heart rate after endurance exercise training is that the sympathetic drive to the heart is reduced. We have studied the relationship between plasma catecholamines and heart rate during exercise in the course of a 7-wk training program. Six untrained subjects exercised vigorously (on bicycle ergometers and by running) 30--50 min/day for 7 wk. Prior to the beginning of training and at weekly intervals thereafter, participants were subjected to a 5-min strenuous bicycle ergometer test. In the test prior to training, plasma epinephrine increased to 0.5 ng/ml and norepinephrine increased to 3.0 ng/ml. The major proportion of the training-induced decrement in catecholamine response was reached at the end of the 3rd wk when epinephrine increased to 0.17 ng/ml and norepinephrine increased to 1.5 ng/ml in response to the same test. Heart rate during exercise continued to decrease even after the catecholamine response had plateaued, implying that the reduced sympathetic response is not solely responsible for the reduced exercise heart rate.

This study was undertaken to evaluate the effects of endurance exercise training on O2 deficit and O2 debt, and on the time courses of the adjustment to, and recovery from, submaximal exercise of oxygen uptake (VO2) carbon dioxide production (VCO2), minute ventilation (VE), and heart rate (HR). Eight subjects participated in a 9-wk-long exercise program that increased their VO2max by 24%. It was found that O2 deficit and O2 debt were lower at the same absolute work rate and not significantly different at the same relative work rate after training. The increases in VO2, VCO2, VE, and HR at the onset of constant load submaximal work, and the decreases in VO2, VCO2, VE, and HR in recovery were more rapid at both the same absolute and the same relative work rates after training. These results show that the adaptations to endurance exercise training enable an individual to adjust to the energy requirement of constant load submaximal work more rapidly, resulting in a smaller O2 deficit. The rate of recovery is also more rapid after training, resulting in a smaller O2 debt.

One purpose of this study was to determine whether the half time of the oxygen consumption (VO2) response at the onset of exercise varies with work intensity. Fifteen subjects performed 5 min of bicycle ergometer exercise across a range of relative work loads with VO2 determined continuously via computer analysis. The results revealed that the half time of the VO2 response increased as work intensity increased. Our second purpose was to determine whether VO2 response kinetics are dependent on the maximum oxygen uptake (VO2max) of the subject. When VO2 response kinetics were compared at equal absolute work loads for a highly trained (n = 8, mean VO2max = 70.2 ml/kg.min) and an untrained (n = 7, mean VO2max = 49.7 ml/kg.min) group, the highly trained group had a more rapid VO2 response (P less than 0.05). The same tendency was evident at equal relative work loads but the differences were not significant. The more rapid adaptation of the highly trained subjects at absolute work loads may be caused by the enzymatic and circulatory adaptations which result from endurance training. The more rapid adjustment of VO2 at the onset of exercise may explain the slower phosphagen and glycogen depletion found in highly trained subjects following short-term work at equal absolute loads.

This investigation was undertaken to determine the effect of pedal frequency on submaximal exercise responses. Seven well-trained competitive cyclists were studied riding their road-racing bicycles on a motor-driven treadmill at 80% of maximum O2 consumption (VO2 max) using different gear ratios. Cyclists were also studied during a series of unloaded trials to assess the effects of varying rates of limb movements independent of external work load. Heart rate (HR) increased, whereas net HR (after subtracting the HR during unloaded cycling) decreased with increasing pedal frequency during loaded cycling. Expiratory flow (VE), O2 consumption (VO2), blood lactate, net VO2 (after subtracting the VO2 of unloaded cycling), and net VE (after subtracting the VE during unloaded cycling) were quadratically related to pedal frequency. The quadratic relationships evident after corrections were made for the additional work needed to move the legs more frequently may be explained at the lower pedaling rates by a less uniform pattern of blood flow caused by increasing the force requirement per pedal stroke and, at the higher pedal frequencies, by the recruitment of additional musculature to stabilize the trunk. The average of preferred frequency for the group, which was also the most economical pedaling rate judged by most of the variables was 91 rpm, although the preferred pedaling rate for each subject ranged from 72 to 102 rpm.

Sixteen highly trained masters endurance athletes, 59 +/- 6 yr, were compared with 16 young athletes, with whom they were matched on the basis of their training regimens, and with 18 untrained middle-aged men. On echocardiographic evaluation, both groups of athletes had a significantly greater left ventricular volume and mass than the untrained men; their were no significant differences in percent fiber shortening or velocity of fiber shortening among the three groups. Maximum O2 uptake (VO2max) averaged 15% less in the masters than in the young athletes (58.7 vs. 69 ml.kg-1.min-1). When expressed in terms of lean body mass to correct for differences in body fat content, VO2max of the masters athletes was about 60% higher than that of the middle-aged untrained men. Maximum heart rate was 14% lower in the masters athletes than in the young athletes (169 vs. 197 beats/min). The O2 pulse during maximum exercise (i.e., VO2max/heart rate at VO2max) was identical in the masters and young athletes. This finding suggests that the major factor responsible for the lower VO2max of the masters athletes, compared with the young athletes, is their slower heart rate.

Six patients with ischemic heart disease who had exercised intensely for longer than 1 yr appeared to have a disproportionately high capacity for endurance exercise relative to VO2 max. They were compared with healthy runners of the same age (mean 55 yr) with similar training programs (6-12 km/day, 5 day/wk). The trained patients had a significantly (P less than 0.05) lower maximal cardiac output (-17%) and VO2 max (-18%, 37 vs. 45 ml . kg-1 . min-1). Despite their lower VO2 max, the trained patients were able to run 8 km at the same speed as the normal runners (approximately 189 m/min). The trained patients' ability to keep pace with the normal subjects was apparently due to a very high lactate threshold (LT) relative to VO2 max. The patients' LT (lactate 1 mM above base line) occurred at a treadmill running speed of 176 m/min, which elicited 100% of their VO2 max, compared with a LT at 178 m/min and 84% of VO2 max in the normal subjects (P less than 0.01). Our results show that some individuals with VO2 max limited by impaired cardiac function can undergo adaptations to training that enable them to maintain close to a metabolic steady state during exercise that elicits VO2 max.

Five subjects who had been training vigorously for 2 mo worked 5 min on the cycle ergometer at 1,480 +/- 100 kpm/min and at 1,920 kpm/min on separate days. Plasma norepinephrine (NE), blood lactate, and heart rate were determined during the postexercise periods. The same subjects were also tested at 1,480 +/- 100 kpm/min after a 2-mo detraining period, when subjects did not train. At 1,920 +/- 80 kpm/min, plasma NE was 4 ng/ml at the end of exercise. The NE concentration increased slightly in the first min postexercise, then decreased with a half-time of 2.8 min between 1 and 11 min postexercise. Detraining for 2 mo did not markedly affect the rate of disappearance of NE in the postexercise period in these five subjects. Between 11 and 30 min postexercise (1,480 +/- 100 kpm/min), heart rate was 25 beats/min higher after detraining, while NE was not significantly different. These data provide evidence that more rapid recovery of heart rate in trained individuals during this period is not likely due to a more rapid recovery from the sympathetic response to exercise.

Plasma glucagon and catecholamines increase during prolonged submaximal exercise, but the magnitude of the increase is less in endurance-trained individuals than in untrained subjects. We have studied the rapidity at which this adaptation occurs. Six initially untrained healthy subjects exercised vigorously (on bicycle ergometers and by running) 30-50 min/day, 6 days/wk, for 9 wk. Prior to the beginning of training and at 3-wk intervals thereafter, participants were subjected to 90-min bicycle ergometer test work loads that elicited 58 +/- 2% of the subjects' initial maximal oxygen consumption. The major proportion of the training-induced decrement in plasma glucagon and catecholamine responses to exercise was seen after 3 wk of training. We conclude that the hormonal component of the training adaptation occurs very early in the course of a vigorous endurance training program.

This paper reports the effect of 12 mo of intense endurance exercise training on the plasma catecholamine response to exercise in 11 male patients [aged 50 +/- 8 yr (mean +/- SD)] with coronary artery disease. A substantial adaptation to training was attained as evidenced by a 42% increase in maximum O2 uptake capacity. At rest, heart rate was lower after training, but resting blood pressure and plasma catecholamines were unchanged. At the same absolute work rate, plasma norepinephrine and epinephrine levels, rate pressure product, and ischemic S-T segment depression were all significantly lower after training. A higher plasma norepinephrine level was attained at maximal exercise after training (2,049 +/- 654 before vs. 3,408 +/- 1,454 pg/ml after, P less than 0.025); this was associated with a higher systolic blood pressure (175 +/- 25 before vs. 188 +/- 22 mmHg after, P less than 0.025) and a higher rate-pressure product (25.3 X 10(3) +/- 4.5 X 10(3) before vs. 27.6 X 10(3) +/- 5.2 X 10(3) after, P less than 0.025). Despite the higher plasma norepinephrine level and rate pressure product, S-T segment depression at maximal exercise was unchanged. These findings suggest that some patients with coronary arterial disease can attain a higher myocardial O2 requirement, without electrocardiographic evidence of increased ischemia, after prolonged strenuous exercise training.

Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations to training which correlate with maximal oxygen uptake (VO2max) and reduced adiposity. Our study was undertaken to test the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon. Eight well-trained subjects stopped training for 10 days. There were no significant changes in VO2max (58.6 +/- 2.2 vs. 57.6 +/- 2.1 ml/kg), estimated percent body fat (12.5 +/- 0.7 vs. 12.5 +/- 0.8%), or body weight. The maximum rise in plasma insulin concentration in response to a 100-g oral glucose load was 100% higher after 10 days without exercise than when the subjects were exercising regularly. Despite the increased insulin levels, blood glucose concentrations were higher after 10 days without exercise. Insulin binding to monocytes also decreased with physical inactivity. One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial "trained" value. These results support our hypothesis.

Eight men were studied before and after a 12-wk exercise program to determine the effect of training on blood lactate levels during submaximal exercise. The training elicited a 26% increase in maximum O2 uptake (VO2max). Lactate concentrations at the same relative exercise intensities in the 55-75% of VO2max range were significantly lower after training. A significantly higher relative exercise intensity was needed to elicit a given lactate level in the 1.5- to 3.0-mM range after training. O2 uptake at the work rate required to raise blood lactate to 2.5 mM was 39% higher after training. A blood lactate of 2.5 mM was attained at 68 +/- 4% VO2max before and 75 +/- 3% of VO2max after training. Eight competitive runners required an even higher relative work rate (83 +/- 2% of VO2max) to attain a blood lactate of 2.5 mM. These data provide evidence that the adaptations to training that result in an increase in VO2max are, to some degree, independent of those responsible for the lower blood lactate levels during submaximal exercise.