A 30-year follow-up of the Dallas Bedrest and Training Study: I. Effect of age on the cardiovascular response to exercise.

BACKGROUND: Cardiovascular capacity declines with aging, as evidenced by declining maximal oxygen uptake (VO(2)max ), with little known about the specific mechanisms of this decline. Our study objective was to assess the effect of a 30-year interval on body composition and cardiovascular response to acute exercise in 5 healthy subjects originally evaluated in 1966. METHODS AND RESULTS: Anthropometric parameters and the cardiovascular response to acute maximal exercise were assessed with noninvasive techniques. On average, body weight increased 25% (77 versus 100 kg) and percent body fat increased 100% (14% versus 28%), with little change in fat-free mass (66 versus 72 kg). On average, VO(2)max decreased 11% (3.30 versus 2.90 L/min). Likewise, VO(2)max decreased when indexed to total body mass (43 versus 31 mL. kg(-1). min(-1)) or fat-free mass (50 versus 43 mL/kg fat-free mass per minute). Maximal heart rate declined 6% (193 versus 181 bpm) and maximal stroke volume increased 16% (104 versus 121 mL), with no difference observed in maximal cardiac output (20.0 versus 21.4 L/min). Maximal AV oxygen difference declined 15% (16.2 versus 13.8 vol%) and accounted for the entire decrease in cardiovascular capacity. CONCLUSIONS: Cardiovascular capacity declined over the 30-year study interval in these 5 middle-aged men primarily because of an impaired efficiency of maximal peripheral oxygen extraction. Maximal cardiac output was maintained with a decline in maximal heart rate compensated for by an increased maximal stroke volume. Most notably, 3 weeks of bedrest in these same men at 20 years of age (1966) had a more profound impact on physical work capacity than did 3 decades of aging.

A 30-year follow-up of the Dallas Bedrest and Training Study: II. Effect of age on cardiovascular adaptation to exercise training.

BACKGROUND: Aerobic power declines with age. The degree to which this decline is reversible remains unclear. In a 30-year longitudinal follow-up study, the cardiovascular adaptations to exercise training in 5 middle-aged men previously trained in 1966 were evaluated to assess the degree to which the age-associated decline in aerobic power is attributable to deconditioning and to gain insight into the specific mechanisms involved. Methods and Results-- The cardiovascular response to acute submaximal and maximal exercise were assessed before and after a 6-month endurance training program. On average, VO(2max) increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, VO(2max) increased 16% when indexed to total body mass (31 versus 36 mL/kg per minute) or fat-free mass (44 versus 51 mL/kg fat-free mass per minute). Maximal heart rate declined (181 versus 171 beats/min) and maximal stroke volume increased (121 versus 129 mL) after training, with no change in maximal cardiac output (21.4 versus 21.7 L/min); submaximal heart rates also declined to a similar degree. Maximal AVDO(2) increased by 10% (13.8 versus 15.2 vol%) and accounted for the entire improvement of aerobic power associated with training. CONCLUSIONS: One hundred percent of the age-related decline in aerobic power among these 5 middle-aged men occurring over 30 years was reversed by a 6-month endurance training program. However, no subject achieved the same maximal VO(2) attained after training 30 years earlier, despite a similar relative training load. The improved aerobic power after training was primarily the result of peripheral adaptation, with no effective improvement in maximal oxygen delivery.

Relationship between insulin sensitivity, hyperinsulinemia, and insulin-mediated sympathetic activation in normotensive and hypertensive subjects.

The adrenergic response to high physiological hyperinsulinemia was studied in 39 hypertensive subjects (28 men and 11 women) and 25 normal volunteers (15 men and 10 women), using the euglycemic clamp technique. Control studies using 0.45% saline infusions (sham studies) were also performed. Before and during the clamp procedure, plasma norepinephrine (NE) and epinephrine (E) were measured using a high performance liquid chromatographic method (HPLC). The association between the increment in NE and E levels and insulin sensitivity, steady-state insulin level during the clamps, waist to hip ratio (WHR), baseline NE levels and gender was studied. NE levels increased during the hyperinsulinemic period (mean increase 46 +/- 6 pmol P < .001 upsilon baseline and P < .01 upsilon sham studies). E levels did not differ between the insulin clamps and the sham studies. Insulin sensitivity was not significantly associated with the increment in NE. Hypertensive subjects had a higher NE increase than the normotensive individuals (55 +/- 7 upsilon 30 +/- 10 pmol, P = .03), but also had higher insulin levels during the clamps (839 +/- 43 upsilon 522 +/- 38 pmol, P < .001). Insulin levels accounted for most of the differences in NE increase between the normotensive and hypertensive groups. Gender, adiposity and WHR were also associated with NE increment. We conclude that the insulin mediated sympathetic activation is not affected in the presence of decreased insulin sensitivity for glucose utilization. The greater degree of sympathetic activation observed in hypertensive subjects is a function of the level of insulinemia obtained during the clamps.

Physical fitness and cardiovascular regulation: mechanisms of orthostatic intolerance.

We studied three groups of eight men each--high, mid, and low fit (peak O2 consumption 60.0 +/- 0.8, 48.9 +/- 1.0, and 35.7 +/- 0.9 ml.min-1.kg-1)--to determine the mechanism of orthostatic intolerance in endurance athletes. Tolerance was defined by progressive lower body negative pressure (LBNP) to presyncope. Maximal calf vascular conductance (Gmax) was measured. The carotid baroreflex was characterized using both stepwise R-wave-triggered and sustained (2 min) changes in neck chamber pressure. High-fit subjects tended to have lower LBNP tolerance than mid- and low-fit subjects but similar baroreflex responses. Subjects with poor LBNP tolerance had larger stroke volumes (SV) (120 +/- 6 vs. 103 +/- 3 ml) and greater decline in SV with LBNP to -40 mmHg (40 +/- 2 vs. 26 +/- 4%). Stepwise multiple linear regression analysis revealed that Gmax and steady-state gain of the carotid baroreflex contributed significantly toward explaining interindividual variations in LBNP tolerance. Thus endurance athletes may have decreased LBNP tolerance, but apparently not as a simple linear function of aerobic fitness. Orthostatic tolerance depends on complex interactions among functional characteristics that appear both related (Gmax and SV) and unrelated (baroreflex function) to fitness or exercise training.

Effects of active muscle mass size on cardiopulmonary responses to exercise in congestive heart failure.

Previous studies from this laboratory demonstrated that in healthy young men, cardiac output is closely coupled to oxygen uptake during dynamic exercise, regardless of its mode or relative intensity, whereas other physiologic responses such as heart rate, blood pressure and ventilation are inversely related to the size of the active muscle mass when expressed as functions of oxygen uptake. The purpose of the current investigation was to determine whether congestive heart failure alters the pattern of physiologic responses to various modes of arm and leg exercise in proportion to the size of the active muscle mass. Cardiopulmonary responses to four modes of dynamic work (one arm curl, one arm cycle ergometry, one leg cycle ergometry and two leg cycle ergometry) were characterized in terms of absolute and relative intensities (oxygen uptake and mode-specific percent of peak oxygen uptake, respectively) in middle-aged men with congestive heart failure and control groups of healthy subjects and patients after myocardial infarction without heart failure. Peak oxygen uptake was reduced to the greatest extent in patients with heart failure for large muscle mass work (-13% for curl, -32% for one arm and one leg cycle ergometry and -37% for two leg cycle ergometry; p less than 0.05 versus the normal group for the three modes of ergometry). This finding was paralleled by a markedly blunted slope for the cardiac output-oxygen uptake relation for leg but not arm exercise that was only partially compensated for by a widened arteriovenous oxygen difference. Blood pressure expressed as a function of oxygen uptake remained inversely related to active muscle mass size in all groups of subjects despite attenuation of systolic pressure for heavy large muscle mass effort in the group with heart failure. Pulmonary ventilation at a given metabolic rate was not influenced by active muscle mass size. Thus, saturation of capacity for systemic oxygen transport occurs in conjunction with blunted cardiac output reserve in patients with heart failure during exercise involving a smaller muscle mass than in healthy subjects. The basic inverse relation between size of the active muscle mass and blood pressure at a given metabolic rate is not altered by aging or reduced cardiac reserve. The muscle mass effect on ventilation seen in young healthy subjects disappears with aging.

Effects of 100% oxygen on performance of professional soccer players.

Supplemental oxygen is currently widely utilized in conjunction with athletic competition. To assess the utility of this practice, 12 professional soccer players performed two bouts of exhaustive exercise separated by 5 minutes of rest ("recovery period"). During the recovery period, the subjects breathed either room air or 100% oxygen, assigned by randomized, double-blind design. The entire procedure was repeated on each subject using the opposite gas. The administration of enriched oxygen during the recovery period had no effect on plasma lactate levels or on performance during the second period of exercise. The subjects were unable to identify which gas they received. In conclusion, data from this study indicate that using 100% oxygen applied for short periods offers no advantage on recovery from exhaustive exercise or on subsequent exercise performance.

Aerobic training exercises for individuals who had amputation of the lower limb.

The findings in ten subjects who had an amputation of the lower limb or limbs were studied before and after a fifteen-week aerobic conditioning program to determine if it improved cardiovascular fitness and reduced the effort of walking. Each subject exercised on an Air-Dyne ergometer (Schwinn, Chicago, Illinois) regularly during each week of the study period at 60 to 80 per cent of their estimated maximum heart rate. A test of maximum exercise on the ergometer and a test of walking on a treadmill were administered before and after training. After training, there was an increase of 25 per cent in the maximum capacity for exercise on the ergometer as well as significantly lower values for heart rate and consumption of oxygen during submaximum walking on the treadmill at various inclined grades. Aerobic conditioning was shown not only to improve cardiovascular fitness but also to increase the economy of walking in the subject who had an amputation of the lower limb or limbs.

Cardiovascular adaptations to intense swim training in sedentary middle-aged men and women.

Central and peripheral cardiovascular adaptations to 12 weeks of intense swim training were characterized in 12 previously sedentary middle-aged men and women. Peak oxygen uptake (VO2) during upright bicycle exercise improved from 29.2 +/- 5.6 to 34.7 +/- 6.7 ml/kg/min (mean +/- SD, p less than .01) because of similar increases in peak cardiac output (CO) and calculated arteriovenous oxygen difference (both p = .02). Peak supine VO2 was 10% higher after training (p less than .005) solely because of enhanced CO (p = .005). Peak heart rate decreased in both postures; therefore stroke volume at peak exercise was greater by 10% and 18% in the upright and supine postures, respectively (p = .05 and p = .005). There was an identical 18% rise (p = .01) in peak supine left ventricular end-diastolic volume index by radionuclide ventriculography but no change in left ventricular ejection fraction or end-systolic volume index (ESVI). Peak systolic blood pressure (SBP) was unchanged in the upright posture but was 8% higher (p = .002) during recumbency despite a similar total peripheral resistance and SBP/ESVI ratio. Maximal calf conductance (Gmax), assessed separately by venous occlusion plethysmography after local ischemic exercise to fatigue, was augmented 20% (p less than .02) by training, resulting in an 18% greater hyperemic blood flow (p = .05). Peak VO2, CO, and Gmax were unchanged in five nonexercising control subjects. We conclude that in middle-aged humans, intense swim training for 12 weeks produces adaptations that include a greater capacity for vasodilatation in skeletal muscle and an enhanced cardiac pump capacity.

Maximal vascular leg conductance in trained and untrained men.

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Maximal response of wheelchair-confined subjects to four types of arm exercise.

Maximal work capacity and aerobic fitness of wheelchair-confined subjects generally have been determined by one of three modes of exercise: wheelchair ergometry, wheelchair exercise on a treadmill (TM), and arm crank ergometry. In the present study, two new types of arm ergometers, the Cybex Upper Body Exercise ergometer (CUBE) and the Schwinn Air-Dyne ergometer (SAE), have been evaluated and compared with older methods for determining aerobic capacities of wheelchair-confined subjects. Seven persons with paraplegia with lesions ranging from T-3 to L-1 and one bilateral amputee each performed four exercise tests to volitional exhaustion, on separate days, utilizing four modes of exercise. These included wheelchair exercise on a treadmill and arm exercise using a Monark arm ergometer (MAE), a CUBE, or an SAE. Peak values for oxygen consumption, heart rate, and blood lactate were similar during each type of exercise. Significant (p less than 0.05) differences were observed only in the peak values for minute ventilation (CUBE greater than MAE, SAE greater than MAE). The similarity of the maximal responses observed in this study indicates that the CUBE and SAE are comparable to TM exercise and to the MAE in assessing the aerobic capacity of wheelchair-confined subjects.

Role of muscle mass and mode of contraction in circulatory responses to exercise.

The roles of the mode of contraction (i.e., dynamic or static) and the active muscle mass as determinants of the cardiovascular responses to exercise were studied. Six healthy men performed static handgrip (SHG), dynamic handgrip (DHG), static two-knee extension (SKE), and dynamic two-knee extension (DKE) to local muscular fatigue in approximately 6 min. Increases in mean arterial pressure were similar for each mode of contraction, 29 +/- 5 and 30 +/- 3 mmHg in SHG and DHG and 56 +/- 2 and 48 +/- 2 mmHg in SKE and DKE (P greater than 0.05) but larger for KE than HG (P less than 0.001). Cardiac output increased more for dynamic than for static exercise and for each mode more for KE than HG (P less than 0.001). Systemic resistance was lower for dynamic than static exercise and fell from resting levels by approximately 1/3 during DKE. The magnitude of the pressor response was related to the active muscle mass but independent of the contraction mode. However, the mode of contraction affected the circulatory changes contributing to the pressor response. Equalization of the pressor responses was achieved by proportionately larger increases in cardiac output during dynamic exercise.

The role of maximal oxygen uptake in exercise performance.

The maximal ability to deliver oxygen to the tissues of the body establishes the upper limit of endurance performance; however, the ability of the skeletal muscles to utilize a high oxygen load for a sustained period of time is also of great importance. The fatigue that limits endurance is due to a local limitation of oxygen or substrate, which leads to excessive anaerobic metabolism or decreased energy production. The peripheral adaptation from specific and intense training may further improve endurance performance.