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The Dallas Bed Rest and Training Study, 2019, Mitchell et al.
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A Longitudinal Study of Adaptive Changes in Oxygen Transport and Body Composition (1968)
BENGT SALTIN; GUNNAR BLOMQVIST; JERE H. MITCHELL; ROBERT L. JOHNSON, JR.; KERN WILDENTHAL; CARLETON B. CHAPMAN; Eugene Frenkel; Walter Norton; Marvin Siperstein; Wadi Suki; George Vastagh; Abraham Prengler
The effects of a 20-day period of bed rest followed by a 55-day period of physical training were studied in five male subjects, aged 19 to 21. Three of the subjects had previously been sedentary, and two of them had been physically active. The studies after bed rest and after physical training were both compared with the initial control studies.
Effects of Bed Rest
All five subjects responded quite similarly to the bed rest period. The total body weight remained constant; however, lean body mass, total body water, intracellular fluid volume, red cell mass, and plasma volume tended to decrease. Electron microscopic studies of quadriceps muscle biopsies showed no significant changes. There was no effect on total lung capacity, forced vital capacity, one-second expiratory volume, alveolar-arterial oxygen tension difference, or membrane diffusing capacity for carbon monoxide. Total diffusing capacity and pulmonary capillary blood volume were slightly lower after bed rest. These changes were related to changes in pulmonary blood flow. Resting total heart volume decreased from 860 to 770 ml.
The maximal oxygen uptake fell from 3.3 in the control study to 2.4 L/min after bed rest. Cardiac output, stroke volume, and arterial pressure at rest in supine and sitting positions did not change significantly. The cardiac output during supine exercise at 600 kpm/min decreased from 14.4 to 12.4 L/min, and stroke volume fell from 116 to 88 ml. Heart rate increased from 129 to 154 beats/min. There was no change in arterial pressure. Cardiac output during upright exercise at submaximal loads decreased approximately 15% and stroke volume 30%. Calculated heart rate at an oxygen uptake of 2 L/min increased from 145 to 180 beats/min. Mean arterial pressures were 10 to 20 mm Hg lower, but there was no change in total peripheral resistance. The A-V 02 difference was higher for any given level of oxygen uptake. Cardiac output during maximal work fell from 20.0 to 14.8 L/min and stroke volume from 104 to 74 ml. Total peripheral resistance and A-V 02 difference did not change. The Frank lead electrocardiogram showed reduced T-wave amplitude at rest and during submaximal exercise in both supine and upright position but no change during maximal work.
The fall in maximal oxygen uptake was due to a reduction of stroke volume and cardiac output. The decrease cannot exclusively be attributed to an impairment of venous return during upright exercise. Stroke volume and cardiac output were reduced also during supine exercise. A direct effect on myocardial function, therefore, cannot be excluded.
Effects of Physical Training
In all five subjects physical training had no effect on lung volumes, timed vitalometry, and membrane diffusing capacity as compared with control values obtained before bed rest. Pulmonary capillary blood volume and total diffusing capacity were increased proportional to the increase in blood flow. Alveolar-arterial oxygen tension differences during exercise were smaller after training, suggesting an improved distribution of pulmonary blood flow with respect to ventilation. Red cell mass increased in the previously sedentary subjects from 1.93 to 2.05 L, and the two active subjects showed no change.
Maximal oxygen uptake increased from a control value of 2.52 obtained before bed rest to 3.41 L/min after physical training in the three previously sedentary (+33%) and from 4.48 to 4.65 L/min in the two previously active subjects (+4%). Cardiac output and oxygen uptake during submaximal work did not change, but the heart rate was lower and the stroke volume higher for any given oxygen uptake after training in the sedentary group.
In the sedentary subjects cardiac output during maximal work increased from 17.2 L/min in the control study before bed rest to 20.0 L/min after training (+16.5%). Arterio-venous oxygen difference increased from 14.6 to 17.0 ml/100 ml (+16.5%). Maximal heart rate remained constant, and stroke volume increased from 90 to 105 (+17%). Resting total heart volumes were 740 ml in the control study before bed rest and 812 ml after training.
In the previously active subjects changes in heart volume, maximal cardiac output, stroke volume, and arteriovenous oxygen difference were less marked.
Previous studies have shown increases of only 10 to 15% in the maximal oxygen uptake of young sedentary male subjects after training. The greater increase of 33% in maximal oxygen uptake in the present study was due equally to an increase in stroke volume and arteriovenous oxygen difference. These more marked changes may be attributed to a low initial level of maximal oxygen uptake and to an extremely strenuous and closely supervised training program.
Link (Circulation)
BENGT SALTIN; GUNNAR BLOMQVIST; JERE H. MITCHELL; ROBERT L. JOHNSON, JR.; KERN WILDENTHAL; CARLETON B. CHAPMAN; Eugene Frenkel; Walter Norton; Marvin Siperstein; Wadi Suki; George Vastagh; Abraham Prengler
The effects of a 20-day period of bed rest followed by a 55-day period of physical training were studied in five male subjects, aged 19 to 21. Three of the subjects had previously been sedentary, and two of them had been physically active. The studies after bed rest and after physical training were both compared with the initial control studies.
Effects of Bed Rest
All five subjects responded quite similarly to the bed rest period. The total body weight remained constant; however, lean body mass, total body water, intracellular fluid volume, red cell mass, and plasma volume tended to decrease. Electron microscopic studies of quadriceps muscle biopsies showed no significant changes. There was no effect on total lung capacity, forced vital capacity, one-second expiratory volume, alveolar-arterial oxygen tension difference, or membrane diffusing capacity for carbon monoxide. Total diffusing capacity and pulmonary capillary blood volume were slightly lower after bed rest. These changes were related to changes in pulmonary blood flow. Resting total heart volume decreased from 860 to 770 ml.
The maximal oxygen uptake fell from 3.3 in the control study to 2.4 L/min after bed rest. Cardiac output, stroke volume, and arterial pressure at rest in supine and sitting positions did not change significantly. The cardiac output during supine exercise at 600 kpm/min decreased from 14.4 to 12.4 L/min, and stroke volume fell from 116 to 88 ml. Heart rate increased from 129 to 154 beats/min. There was no change in arterial pressure. Cardiac output during upright exercise at submaximal loads decreased approximately 15% and stroke volume 30%. Calculated heart rate at an oxygen uptake of 2 L/min increased from 145 to 180 beats/min. Mean arterial pressures were 10 to 20 mm Hg lower, but there was no change in total peripheral resistance. The A-V 02 difference was higher for any given level of oxygen uptake. Cardiac output during maximal work fell from 20.0 to 14.8 L/min and stroke volume from 104 to 74 ml. Total peripheral resistance and A-V 02 difference did not change. The Frank lead electrocardiogram showed reduced T-wave amplitude at rest and during submaximal exercise in both supine and upright position but no change during maximal work.
The fall in maximal oxygen uptake was due to a reduction of stroke volume and cardiac output. The decrease cannot exclusively be attributed to an impairment of venous return during upright exercise. Stroke volume and cardiac output were reduced also during supine exercise. A direct effect on myocardial function, therefore, cannot be excluded.
Effects of Physical Training
In all five subjects physical training had no effect on lung volumes, timed vitalometry, and membrane diffusing capacity as compared with control values obtained before bed rest. Pulmonary capillary blood volume and total diffusing capacity were increased proportional to the increase in blood flow. Alveolar-arterial oxygen tension differences during exercise were smaller after training, suggesting an improved distribution of pulmonary blood flow with respect to ventilation. Red cell mass increased in the previously sedentary subjects from 1.93 to 2.05 L, and the two active subjects showed no change.
Maximal oxygen uptake increased from a control value of 2.52 obtained before bed rest to 3.41 L/min after physical training in the three previously sedentary (+33%) and from 4.48 to 4.65 L/min in the two previously active subjects (+4%). Cardiac output and oxygen uptake during submaximal work did not change, but the heart rate was lower and the stroke volume higher for any given oxygen uptake after training in the sedentary group.
In the sedentary subjects cardiac output during maximal work increased from 17.2 L/min in the control study before bed rest to 20.0 L/min after training (+16.5%). Arterio-venous oxygen difference increased from 14.6 to 17.0 ml/100 ml (+16.5%). Maximal heart rate remained constant, and stroke volume increased from 90 to 105 (+17%). Resting total heart volumes were 740 ml in the control study before bed rest and 812 ml after training.
In the previously active subjects changes in heart volume, maximal cardiac output, stroke volume, and arteriovenous oxygen difference were less marked.
Previous studies have shown increases of only 10 to 15% in the maximal oxygen uptake of young sedentary male subjects after training. The greater increase of 33% in maximal oxygen uptake in the present study was due equally to an increase in stroke volume and arteriovenous oxygen difference. These more marked changes may be attributed to a low initial level of maximal oxygen uptake and to an extremely strenuous and closely supervised training program.
Link (Circulation)
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A 30-Year Follow-Up of the Dallas Bed Rest and Training Study I. Effect of Age on the Cardiovascular Response to Exercise (2001)
Darren K. McGuire; Benjamin D. Levine; Jon W. Williamson; Peter G. Snell; C. Gunnar Blomqvist; Bengt Saltin; Jere H. Mitchell
Background—Cardiovascular capacity declines with aging, as evidenced by declining maximal oxygen uptake (V 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, V max decreased 11% (3.30 versus 2.90 L/min). Likewise, V max decreased when indexed to total body mass (43 versus 31 mL · kg 21 · min21 ) 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.
Link | PDF (Circulation)
A 30-Year Follow-Up of the Dallas Bed Rest and Training Study II. Effect of Age on Cardiovascular Adaptation to Exercise Training (2001)
Darren K. McGuire; Benjamin D. Levine; Jon W. Williamson; Peter G. Snell; C. Gunnar Blomqvist; Bengt Saltin; Jere H. Mitchell
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, V increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, V 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 V 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.
Link | PDF (Circulation)
Darren K. McGuire; Benjamin D. Levine; Jon W. Williamson; Peter G. Snell; C. Gunnar Blomqvist; Bengt Saltin; Jere H. Mitchell
Background—Cardiovascular capacity declines with aging, as evidenced by declining maximal oxygen uptake (V 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, V max decreased 11% (3.30 versus 2.90 L/min). Likewise, V max decreased when indexed to total body mass (43 versus 31 mL · kg 21 · min21 ) 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.
Link | PDF (Circulation)
A 30-Year Follow-Up of the Dallas Bed Rest and Training Study II. Effect of Age on Cardiovascular Adaptation to Exercise Training (2001)
Darren K. McGuire; Benjamin D. Levine; Jon W. Williamson; Peter G. Snell; C. Gunnar Blomqvist; Bengt Saltin; Jere H. Mitchell
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, V increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, V 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 V 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.
Link | PDF (Circulation)
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A Forty-Year Follow-Up of the Dallas Bed Rest and Training Study: The Effect of Age on the Cardiovascular Response to Exercise in Men (2009)
McGavock, Jonathan M.; Hastings, Jeffrey L.; Snell, Peter G.; McGuire, Darren K.; Pacini, Eric L.; Levine, Benjamin D.; Mitchell, Jere H.
Background. In 1966, five 20-year-old men underwent a comprehensive physiological evaluation of the capacity for adaptation of the cardiovascular system in response to 3 weeks of bed rest and 8 weeks of heavy endurance training; these same participants were reevaluated before and after training at the age of 50. The aim of the present study was to reexamine these same men 40 years following the original assessments.
Methods and Results. In all three studies, minute ventilation and expired gases were analyzed during exercise testing with Douglas bag collection. Cardiac output (CO) was determined using the acetylene rebreathing technique. Compared with the original 30-year interval, the decline in maximal oxygen uptake (VO2max ) (−11% vs −25%), maximal CO (+6% vs −11%), and maximal stroke volume (+10% vs −10%) were greater between 50 and 60 years of age. The annualized decline in VO 2max (55 mL/min/y) between ages 50 and 60 was approximately fourfold higher than the decline between 20 and 50 years (12 mL/min/y).
Conclusions. In the original five participants of the Dallas Bed Rest and Training Study, VO 2max declined after 40 years of living due to a balanced decrease in central and peripheral determinants of oxygen uptake. The rate of decline in VO 2max and its components accelerated after the age of 50 years secondary to age and clinical comorbidities. The net proportional decline in VO 2max for a period of 40 years of life was comparable with that experienced after 3 weeks of strict bed rest at the age of 20 (27% vs 26%, respectively).
Link | PDF (The Journals of Gerontology: Series A)
McGavock, Jonathan M.; Hastings, Jeffrey L.; Snell, Peter G.; McGuire, Darren K.; Pacini, Eric L.; Levine, Benjamin D.; Mitchell, Jere H.
Background. In 1966, five 20-year-old men underwent a comprehensive physiological evaluation of the capacity for adaptation of the cardiovascular system in response to 3 weeks of bed rest and 8 weeks of heavy endurance training; these same participants were reevaluated before and after training at the age of 50. The aim of the present study was to reexamine these same men 40 years following the original assessments.
Methods and Results. In all three studies, minute ventilation and expired gases were analyzed during exercise testing with Douglas bag collection. Cardiac output (CO) was determined using the acetylene rebreathing technique. Compared with the original 30-year interval, the decline in maximal oxygen uptake (VO2max ) (−11% vs −25%), maximal CO (+6% vs −11%), and maximal stroke volume (+10% vs −10%) were greater between 50 and 60 years of age. The annualized decline in VO 2max (55 mL/min/y) between ages 50 and 60 was approximately fourfold higher than the decline between 20 and 50 years (12 mL/min/y).
Conclusions. In the original five participants of the Dallas Bed Rest and Training Study, VO 2max declined after 40 years of living due to a balanced decrease in central and peripheral determinants of oxygen uptake. The rate of decline in VO 2max and its components accelerated after the age of 50 years secondary to age and clinical comorbidities. The net proportional decline in VO 2max for a period of 40 years of life was comparable with that experienced after 3 weeks of strict bed rest at the age of 20 (27% vs 26%, respectively).
Link | PDF (The Journals of Gerontology: Series A)
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so they’ve claimed 30yrs of deterioration from 2weeks bed rest, based on 2/3 people with no interim checks over 30yrs?
2/3yr follow up would be interesting as might this if large enough number meant matched pairs wasn’t necessary but those numbers would need to be huge to account for so many possibilities in luck and lifestyle and poverty and so on?
As I understand it, the deterioration from the bed rest was temporary and easily reversed by the exercise regime.