Vascular and metabolic response to cycle exercise in sedentary humans: effect of age

We measured leg blood flow (LBF), drew arterial-venous (A-V) blood samples, and calculated muscle O(2) consumption (VO(2)) during incremental cycle ergometry exercise [15, 30, and 99 W and maximal effort (maximal work rate, WR(max))] in nine sedentary young (20 +/- 1 yr) and nine sedentary old (70 +/- 2 yr) males. LBF was preserved in the old subjects at 15 and 30 W. However, at 99 W and at WR(max), leg vascular conductance was attenuated because of a reduced LBF (young: 4.1 +/- 0.2 l/min and old: 3.1 +/- 0.3 l/min) and an elevated mean arterial blood pressure (young: 112 +/- 3 mmHg and old: 132 +/- 3 mmHg) in the old subjects. Leg A-V O(2) difference changed little with increasing WR in the old group but was elevated compared with the young subjects. Muscle maximal VO(2) and cycle WR(max) were significantly lower in the old subjects (young: 0.8 +/- 0.05 l/min and 193 +/- 7 W; old: 0.5 +/- 0.03 l/min and 117 +/- 10 W). The submaximally unchanged and maximally reduced cardiac output associated with aging coupled with its potential maldistribution are candidates for the limited LBF during moderate to heavy exercise in older sedentary subjects.     

Vascular and metabolic response to isolated small muscle mass exercise: effect of age

To determine the effect of age on quadriceps muscle blood flow (QMBF), leg vascular resistance (LVR), and maximum oxygen uptake (QVO2 max), a thermal dilution technique was used in conjunction with arterial and venous femoral blood sampling in six sedentary young (19.8 +/- 1.3 yr) and six sedentary old (66.5 +/- 2.1 yr) males during incremental knee extensor exercise (KE). Young and old attained a similar maximal KE work rate (WRmax) (young: 25.2 +/- 2.1 and old: 24.1 +/- 4 W) and QVO2 max (young: 0.52 +/- 0.03 and old: 0.42 +/- 0.05 l/min). QMBF during KE was lower in old subjects by approximately 500 ml/min across all work rates, with old subjects demonstrating a significantly lower QMBF/W (old: 174 +/- 20 and young: 239 +/- 46 ml. min-1. W-1). Although the vasodilatory response to incremental KE was approximately 142% greater in the old (young: 0.0019 and old: 0.0046 mmHg. min. ml-1. W-1), consistently elevated leg vascular resistance (LVR) in the old, approximately 80% higher LVR in the old at 50% WR and approximately 40% higher LVR in the old at WRmax (young: 44.1 +/- 3.6 and old: 31.0 +/- 1.7 mmHg. min. ml-1), dictated that during incremental KE the LVR of the old subjects was never less than that of the young subjects. Pulse pressures, indicative of arterial vessel compliance, were approximately 36% higher in the old subjects across all work rates. In conclusion, well-matched sedentary young and old subjects with similar quadriceps muscle mass achieved a similar WRmax and QVO2 max during incremental KE. The old subjects, despite a reduced QMBF, had a greater vasodilatory response to incremental KE. Given that small muscle mass exercise, such as KE, utilizes only a fraction of maximal cardiac output, peripheral mechanisms such as consistently elevated leg vascular resistance and greater pulse pressures appear to be responsible for reduced blood flow persisting throughout graded KE in the old subjects.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

Changes in cardiac output during sustained maximal ventilation in humans

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.     

Sustained maximal ventilation after endurance exercise in athletes

Although impaired respiratory muscle performance that persists up to 5 min after exercise is stopped has been demonstrated during exhaustive exercise in normal young men, it is not known whether impaired respiratory muscle function follows endurance exercise to exhaustion in highly trained athletes. To study the effects of exercise on sustained maximal voluntary ventilation immediately after exercise, eight elite cross-country skiers performed a 4-min maximal sustained ventilation (MSV) test before and immediately after exhaustive exercise. Subjects were encouraged to maintain maximal ventilation (VE) throughout the MSV test. To encourage greater effort, rapid visual feedback of VE was provided on a computer terminal along with a target VE based on their 12-s maximum voluntary ventilation (MVV). The subjects (7 males, 1 female) were 18.5 +/- 0.9 yr old (mean +/- SD) and exercised for 62.5 +/- 16.7 min at 77 +/- 5% of their maximum oxygen consumption during which average VE was 106.7 +/- 24.2 l/min BTPS. The mean MVV was 196.0 +/- 29.9 l/min or 107% of their age- and height-predicted MVV. Before exercise the MSV was 86% of the MVV or 176.7 +/- 30.5 l/min, whereas after exercise the MSV was 90% of the MVV or 180.3 +/- 28.9 l/min (P = NS). The total volume of gas expired during the 4-min MSV was 706.7 +/- 121.9 liters before and 721.2 +/- 115.5 liters after exercise (P = NS). In this group of athletes, exhaustive exercise produced no deleterious effects on the ability to perform a 4-min MSV test immediately after exercise.     

Effects of preexercise snack feeding on endurance cycle exercise

We studied the effects of ingesting either a snack food (S) (260 kcal) or placebo (P) 30 min before intermittent cycle exercise at 70% maximal O2 consumption on endurance performance and muscle glycogen depletion in eight healthy human males. Immediately before exercise there were significantly greater increases in plasma glucose (PG) (S +28 +/- 9.7; P +0.1 +/- 0.8 mg/dl) and insulin (S +219 +/- 61.5; P -7 +/- 5.5 pmol/l) (P less than 0.05) following S feeding compared with P. These differences were no longer present by the end of the first exercise period. There were no differences in endurance times (S 52 +/- 6.4; P 48 +/- 5.6 min) or in the extent of muscle glycogen depletion following exercise (S 56 +/- 14.7; P 50 +/- 15.5 micrograms/mg protein) between the two groups. PG was maintained at base-line (prefeeding) concentrations following S, whereas there was a tendency for PG to steadily decrease after P. Total grams of carbohydrate oxidized during exercise did not differ between the two groups (S 120; P 118 g). These results demonstrate that the ingestion of a mixed-macronutrient snack 30 min before exercise does not impair endurance performance nor increase the extent of muscle glycogen depletion during high-intensity cycle exercise in untrained adult male subjects.     

Adaptations in beta-adrenergic cardiovascular responses to training in older women.

To determine whether endurance exercise training can alter the beta-adrenergic-stimulated inotropic response in older women, we studied 10 postmenopausal healthy women (65.4 +/- 0.9 yr old) who exercised for 11 mo. Left ventricular (LV) function was evaluated with two-dimensional echocardiography during infusion of isoproterenol after atropine. Maximal O(2) consumption increased 23% in response to training (from 1.35 +/- 0.06 to 1.66 +/- 0.07 l/min; P = 0.004). Training had no effect on baseline LV function, end-diastolic diameter, LV wall thickness, or LV mass. The increase in LV systolic function in response to isoproterenol was unaffected by training. Furthermore, neither the systolic shortening-to-end-systolic wall stress relationship nor the end-systolic wall stress-to-end-systolic diameter relationship during isoproterenol infusion changed with training. We conclude that older postmenopausal women can increase their maximal O(2) consumption with exercise training without eccentric LV hypertrophy or enhancement of beta-adrenergic-mediated LV contractile function. These observations provide an explanation for the finding that maximal cardiac output and stroke volume are not increased in older women in response to training.     

Aging attenuates vascular and metabolic plasticity but does not limit improvement in muscle VO(2) max

The interactions between exercise, vascular and metabolic plasticity, and aging have provided insight into the prevention and restoration of declining whole body and small muscle mass exercise performance known to occur with age. Metabolic and vascular adaptations to normoxic knee-extensor exercise training (1 h 3 times a week for 8 wk) were compared between six sedentary young (20 +/- 1 yr) and six sedentary old (67 +/- 2 yr) subjects. Arterial and venous blood samples, in conjunction with a thermodilution technique facilitated the measurement of quadriceps muscle blood flow and hematologic variables during incremental knee-extensor exercise. Pretraining, young and old subjects attained a similar maximal work rate (WR(max)) (young = 27 +/- 3, old = 24 +/- 4 W) and similar maximal quadriceps O(2) consumption (muscle Vo(2 max)) (young = 0.52 +/- 0.03, old = 0.42 +/- 0.05 l/min), which increased equally in both groups posttraining (WR(max), young = 38 +/- 1, old = 36 +/- 4 W, Muscle Vo(2 max), young = 0.71 +/- 0.1, old = 0.63 +/- 0.1 l/min). Before training, muscle blood flow was approximately 500 ml lower in the old compared with the young throughout incremental knee-extensor exercise. After 8 wk of knee-extensor exercise training, the young reduced muscle blood flow approximately 700 ml/min, elevated arteriovenous O(2) difference approximately 1.3 ml/dl, and increased leg vascular resistance approximately 17 mmHg x ml(-1) x min(-1), whereas the old subjects revealed no training-induced changes in these variables. Together, these findings indicate that after 8 wk of small muscle mass exercise training, young and old subjects of equal initial metabolic capacity have a similar ability to increase quadriceps muscle WR(max) and muscle Vo(2 max), despite an attenuated vascular and/or metabolic adaptation to submaximal exercise in the old.     

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of fitness on arm vascular and metabolic responses to upper body exercise

We investigated arm perfusion and metabolism during upper body exercise. Eight average, fit subjects and seven rowers, mean +/- SE maximal oxygen uptake (VO2 max) 157 +/- 7 and 223 +/- 14 ml O2. kg(-0.73).min(-1), respectively, performed incremental arm cranking to exhaustion. Arm blood flow (ABF) was measured with thermodilution and arm muscle mass was estimated by dual-energy X-ray absorptiometry. During maximal arm cranking, pulmonary VO2 was approximately 45% higher in the rowers compared with the untrained subjects and peak ABF was 6.44 +/- 0.40 and 4.55 +/- 0.26 l/min, respectively (P < 0.05). The arm muscle mass for the rowers and the untrained subjects was 3.5 +/- 0.4 and 3.3 +/- 0.1 kg, i.e., arm perfusion was 1.9 +/- 0.2 and 1.4 +/- 0.1 l blood.kg(-1).min(-1), respectively (P < 0.05). The arteriovenous O2 difference was 156 +/- 7 and 120 +/- 8 ml/l, respectively, and arm VO2 was 0.98 +/- 0.08 and 0.60 +/- 0.04 l/min corresponding with 281 +/- 22 and 181 +/- 12 ml/kg, while arm O(2) diffusional conductance was 49.9 +/- 4.3 and 18.6 +/- 3.2 ml.min(-1).mmHg(-1), respectively (P < 0.05). Also, lactate release in the rowers was almost three times higher than in the untrained subjects (26.4 +/- 1.1 vs. 9.5 +/- 0.4 mmol/min, P < 0.05). The energy requirement of an approximately 50% larger arm work capacity after long-term arm endurance training is covered by an approximately 60% increase in aerobic metabolism and an almost tripling of the anaerobic capacity.     

Human muscle metabolism during sprint running

Biopsy samples were obtained from vastus lateralis of eight female subjects before and after a maximal 30-s sprint on a nonmotorized treadmill and were analyzed for glycogen, phosphagens, and glycolytic intermediates. Peak power output averaged 534.4 +/- 85.0 W and was decreased by 50 +/- 10% at the end of the sprint. Glycogen, phosphocreatine, and ATP were decreased by 25, 64, and 37%, respectively. The glycolytic intermediates above phosphofructokinase increased approximately 13-fold, whereas fructose 1,6-diphosphate and triose phosphates only increased 4- and 2-fold. Muscle pyruvate and lactate were increased 19 and 29 times. After 3 min recovery, blood pH was decreased by 0.24 units and plasma epinephrine and norepinephrine increased from 0.3 +/- 0.2 nmol/l and 2.7 +/- 0.8 nmol/l at rest to 1.3 +/- 0.8 nmol/l and 11.7 +/- 6.6 nmol/l. A significant correlation was found between the changes in plasma catecholamines and estimated ATP production from glycolysis (norepinephrine, glycolysis r = 0.78, P less than 0.05; epinephrine, glycolysis r = 0.75, P less than 0.05) and between postexercise capillary lactate and muscle lactate concentrations (r = 0.82, P less than 0.05). The study demonstrated that a significant reduction in ATP occurs during maximal dynamic exercise in humans. The marked metabolic changes caused by the treadmill sprint and its close simulation of free running makes it a valuable test for examining the factors that limit performance and the etiology of fatigue during brief maximal exercise.     

Ascorbic acid does not affect the age-associated reduction in maximal cardiac output and oxygen consumption in healthy adults.

Maximal aerobic capacity (Vo(2max)) decreases progressively with age, primarily because of a reduction in maximal cardiac output (Q(max)). This age-associated decline in Vo(2max) may be partially mediated by the development of oxidative stress that can suppress beta-adrenergic-receptor responsiveness and, consequently, reduce Q(max). To test this hypothesis, Vo(2max) (indirect calorimetry) and Q(max) (open-circuit acetylene breathing) were determined in 12 young (23 +/- 1 yr, mean +/- SE) and 10 older (61 +/- 1 yr) adults following systemic infusion of either saline (control) and/or the powerful antioxidant ascorbic acid (acute: bolus 0.06; drip 0.02 g/kg fat-free mass) and following chronic 30-day oral administration of ascorbic acid (500 mg/day). Plasma ascorbic acid concentration was not different between young and older adults and was increased similarly, independent of age [change (Delta) acute = 1,055 +/- 117%; Delta chronic = 62 +/- 19%]. Oxidized low-density lipoprotein concentration was greater (P < 0.001) in older (57 +/- 5 U/l) compared with young (34 +/- 3 U/l) adults and was reduced in both groups (P < 0.02) following acute (Delta = -6 +/- 2%) but not chronic (P = 0.18) ascorbic acid administration. Control (baseline) Vo(2max) and Q(max) were positively related (r = 0.76, P < 0.001) and were lower (P < 0.05) in older (34 +/- 2 ml.kg(-1).min(-1); 16.1 +/- 1.1 l/min) compared with young (43 +/- 3 ml.kg(-1).min(-1); 20.2 +/- 0.9 l/min) adults. Following ascorbic acid administration, neither Vo(2max) (young acute = 41 +/- 2; young chronic = 42 +/- 2; older acute = 34 +/- 2; older chronic = 34 +/- 2 ml.kg(-1).min(-1)) nor Q(max) (young acute = 20.1 +/- 0.9; young chronic = 19.1 +/- 0.8; older acute = 16.2 +/- 1.1; older chronic = 16.6 +/- 1.4 l/min) was changed. These data suggest that ascorbic acid administration does not affect the age-associated reduction in Q(max) and Vo(2max).     

Effect of graded erythrocythemia on cardiovascular and metabolic responses to exercise

The effects of graded induced erythrocythemia on cardiovascular and metabolic responses to intense treadmill running were studied in four highly trained endurance runners. Three autologous infusions of 1 unit (U) whole blood (450 ml/U) were administered sequentially 2-7 days apart. Maximal O2 consumption (VO2max) increased from 5.04 l/min at control (C) to 5.24 l/min after 2 U (R2) and 5.38 l/min after 3 U (R3). Cardiac output during treadmill running at 91% control VO2max was 28.2 l/min at C, 29.8 l/min at R2, and 33.1 l/min at R3. Corresponding heart rates were unchanged, and stroke volume was increased at R3. Peak lactate concentration was reduced, and arterial acid-base status improved at R2 and R3 after standardized bouts of intense exercise. Arterial blood pressures and electrocardiograms during exercise were not affected by erythrocythemia. We conclude that the reinfusion of up to 3 U of autologous blood into highly trained endurance runners who have normal hematology does not adversely affect their cardiovascular response to maximal exercise. In addition, the increases in VO2max following reinfusion of 2 U, and again after 3 U, suggest that the aerobic power of the working muscles was not surpassed at these levels of erythrocythemia.     

Cardiac adaptation to endurance exercise in rats

Endurance exercise is widely assumed to improve cardiac function in humans. This project has determined cardiac function following endurance exercise for 6 (n = 30) or 12 (n = 25) weeks in male Wistar rats (8 weeks old). The exercise protocol was 30 min/day at 0.8 km/h for 5 days/week with an endurance test on the 6th day by running at 1.2 km/h until exhaustion. Exercise endurance increased by 318% after 6 weeks and 609% after 12 weeks. Heart weight/kg body weight increased by 10.2% after 6 weeks and 24.1% after 12 weeks. Echocardiography after 12 weeks showed increases in left ventricular internal diameter in diastole (6.39 ± 0.32 to 7.90 ± 0.17 mm), systolic volume (49 ± 7 to 83 ± 11 μl) and cardiac output (75 ± 3 to 107 ± 8 ml/min) but not left wall thickness in diastole (1.74 ± 0.07 to 1.80 ± 0.06 mm). Isolated Langendorff hearts from trained rats displayed decreased left ventricular myocardial stiffness (22 ± 1.1 to 19.1 ± 0.3) and reduced purine efflux during pacing-induced workload increases. 31P-NMR spectroscopy in isolated hearts from trained rats showed decreased PCr and PCr/ATP ratios with increased creatine, AMP and ADP concentrations. Thus, this endurance exercise protocol resulted in physiological hypertrophy while maintaining or improving cardiac function. (Mol Cell Biochem 251: 51–59, 2003)     

Plasma adrenocorticotropin and cortisol responses to brief high-intensity exercise in humans

The purpose of this study is to examine plasma cortisol and adrenocorticotropin (ACTH) levels following a brief high-intensity bout of exercise. Each subject (n = 6) performed a 1-min bout of exercise on a cycle ergometer at 120% of his maximum O2 uptake. Blood samples were collected at rest, immediately following the exercise bout, and at 5, 15, and 30 min postexercise. Mean (+/- SE) plasma ACTH levels increased significantly (P less than 0.05) from 2.2 +/- 0.4 pmol/l at rest to 6.2 +/- 1.7 pmol/l immediately following exercise. Mean (+/- SE) plasma cortisol levels increased significantly from 0.40 +/- 0.04 mumol/l at rest to 0.52 +/- 0.04 mumol/l at 15 min postexercise. These data show that brief high-intensity exercise results in significant increases in plasma cortisol and ACTH levels. Furthermore, the temporal sequence between the two hormones suggests that the increase in plasma cortisol levels following brief high-intensity exercise is the result of ACTH-induced steroidogenesis in the adrenal cortex.     

Physiological factors associated with the lower maximal oxygen consumption of master runners

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.     

Controlled 5-mo aerobic training improves heart rate but not heart rate variability or baroreflex sensitivity.

Endurance-trained athletes have increased heart rate variability (HRV), but it is not known whether exercise training improves the HRV and baroreflex sensitivity (BRS) in sedentary persons. We compared the effects of low- and high-intensity endurance training on resting heart rate, HRV, and BRS. The maximal oxygen uptake and endurance time increased significantly in the high-intensity group compared with the control group. Heart rate did not change significantly in the low-intensity group but decreased significantly in the high-intensity group (-6 beats/min, 95% confidence interval; -10 to -1 beats/min, exercise vs. control). No significant changes occurred in either the time or frequency domain measures of HRV or BRS in either of the exercise groups. Exercise training was not able to modify the cardiac vagal outflow in sedentary, middle-aged persons.     

Aerobic power and insulin action improve in response to endurance exercise training in healthy 77-87 yr olds.

Previous studies have demonstrated that frail octogenarians have an attenuated capacity for cardiovascular adaptations to endurance exercise training. In the present study, we determined the magnitude of cardiovascular and metabolic adaptations to high-intensity endurance exercise training in healthy, nonfrail elderly subjects. Ten subjects [8 men, 2 women, 80.3 yr (SD2.5)] completed 10-12 mo (108 exercise sessions) of a supervised endurance exercise training program consisting of 2.5 sessions/wk (SD 0.2), 58 min/session (SD 6), at an intensity of 83% (SD 5) of peak heart rate. Primary outcomes were maximal attainable aerobic power [peak aerobic capacity (Vo(2peak))]; serum lipids, oral glucose tolerance, and insulin action during a hyperglycemic clamp; body composition by dual-energy X-ray absorptiometry, and energy expenditure using doubly labeled water and indirect calorimetry. The training program resulted in an increase in Vo(2peak) of 15% (SD 7) [22.9 (SD 3.3) to 26.2 ml.kg(-1).min(-1) (SD 4.0); P < 0.0001]. Favorable lipid changes included reductions in total cholesterol (-8%; P = 0.002) and LDL cholesterol (-10%; P = 0.003), with no significant change in HDL cholesterol or triglycerides. Insulin action improved, as evidenced by a 29% increase in glucose disposal rate relative to insulin concentration during the hyperglycemic clamp. Fat mass decreased by 1.8 kg (SD 1.4) (P = 0.003); lean mass did not change. Total energy expenditure increased by 400 kcal/day because of an increase in physical activity. No change occurred in resting metabolism. In summary, healthy nonfrail octogenarians can adapt to high-intensity endurance exercise training with improvements in aerobic power, insulin action, and serum lipid and lipoprotein risk factors for coronary heart disease; however, the adaptations in aerobic power and insulin action are attenuated compared with middle-aged individuals.     

Mitochondrial capacity is affected by glycemic status in young untrained women with type 1 diabetes but is not impaired relative to healthy untrained women

In this study, we examined whether glycemic status influences aerobic function in women with type 1 diabetes and whether aerobic function is reduced relative to healthy women. To this end, we compared several factors determining aerobic function of 29 young sedentary asymptomatic women (CON) with 9 women of similar age and activity level with type 1 diabetes [DIA, HbA1c range = 6.9-8.2%]. Calf muscle mitochondrial capacity was estimated by (31)P-magnetic resonance spectroscopy. Capillarization and muscle fiber oxidative enzyme activity were assessed from vastus lateralis and soleus muscle biopsies. Oxygen uptake and cardiac output were evaluated by ergospirometry and N(2)O/SF(6) rebreathing. Calf muscle mitochondrial capacity was not different between CON and DIA, as indicated by the identical calculated maximal rates of oxidative ATP synthesis [0.0307 (0.0070) vs. 0.0309 (0.0058) s(-1), P = 0.930]. Notably, HbA1c was negatively correlated with mitochondrial capacity in DIA (R(2) = 0.475, P = 0.040). Although HbA1c was negatively correlated with cardiac output (R(2) = 0.742, P = 0.013) in DIA, there was no difference between CON and DIA in maximal oxygen consumption [2.17 (0.34) vs. 2.21 (0.32) l/min, P = 0.764], cardiac output [12.1 (1.9) vs. 12.3 (1.8) l/min, P = 0.783], and endurance capacity [532 (212) vs. 471 (119) s, P = 0.475]. There was also no difference between the two groups either in the oxidative enzyme activity or capillary-to-fiber ratio. We conclude that mitochondrial capacity depends on HbA1c in untrained women with type 1 diabetes but is not reduced relative to untrained healthy women.     

Cardiovascular responses to voluntary and nonvoluntary static exercise in humans.

We have measured the cardiovascular responses during voluntary and nonvoluntary (electrically induced) one-leg static exercise in humans. Eight normal subjects were studied at rest and during 5 min of static leg extension at 20% of maximal voluntary contraction performed voluntarily and nonvoluntarily in random order. Heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were determined, and peripheral vascular resistance (PVR) and stroke volume (SV) were calculated. HR increased from approximately 65 +/- 3 beats/min at rest to 80 +/- 4 and 78 +/- 6 beats/min (P < 0.05), and MAP increased from 83 +/- 6 to 103 +/- 6 and 105 +/- 6 mmHg (P < 0.05) during voluntary and nonvoluntary contractions, respectively. CO increased from 5.1 +/- 0.7 to 6.0 +/- 0.8 and 6.2 +/- 0.8 l/min (P < 0.05) during voluntary and nonvoluntary contractions, respectively. PVR and SV did not change significantly during voluntary or nonvoluntary contractions. Thus the cardiovascular responses were not different between voluntary and electrically induced contractions. These results suggest that the increases in CO, HR, SV, MAP, and PVR during 5 min of static contractions can be elicited without any contribution from a central neural mechanism (central command). However, central command could still have an important role during voluntary static exercise.