The Dallas Bed Rest and Training Study: Revisited after 50 years

In 1966, a seminal study in exercise science was conducted - the Dallas Bed Rest and Training Study. With the primary results published as a 78-page supplement to Circulation in 1968, it reported the changes in cardiorespiratory performance from extreme changes in physical activity (1). Much of our current knowledge about the adaptive capacity of the cardiovascular system derives from this study. Now at the 50^th anniversary of the initial publication, with 2 subsequent evaluations of the study participants over a 40 year span, here we highlight some of the key lessons learned from this period of study.

For the initial evaluations in 1966, 5 healthy 20-year old male volunteers were assessed at baseline, spent 3 weeks at complete bed rest with no weight bearing allowed (similar to clinical treatment of acute MI at the time), and then underwent 8 weeks of intensive endurance training. Cardiopulmonary function was evaluated by determining maximal oxygen uptake (VO_2max) during stress testing to exhaustion, the gold standard measure of integrated cardiorespiratory capacity reflecting the capacity of the circulatory and respiratory systems to deliver oxygen to skeletal muscle during exercise (2), measured at baseline, after bed rest, and after endurance training, with results summarized in the Table.

Table.

Group average results from treadmill maximal cardiopulmonary exercise tests over the 40 year interval

Variable	1966			1996		2006
	Baseline	After bed rest	After Training	Baseline	After Training	Baseline
VO2max (L/min)	3.3	2.4	3.9	2.9	3.3	2.4
CO (L/min)	20.0	14.8	22.8	21.4	21.7	18.9
HR (bpm)	193	197	190	181	171	174
SV (mL/beat)	104	75	120	121	129	109
AVDO2 (mL O2/100mL)	16.2	16.5	17.1	13.8	15.2	12.7
SBP (mmHg)	204	153	201	208	192	176
DBP (mmHg)	81	63	74	96	103	82

VO_2max-maximum oxygen uptake; CO-cardiac output; HR-heart rate; SV-stroke volume; AVDO2-arteriovenous oxygen difference; SBP-systolic blood pressure; DBP-diastolic blood pressure; are values are group means

Average VO_2max declined 27% after bed rest with a subsequent 45% increase with training. As shown in the Table, average maximal cardiac output declined by 26% after bed rest followed by a 40% increase with training, with no significant changes across the evaluations in maximal AVDO₂ or heart rate. Thus, changes in VO_2max were attributable to changes in maximal cardiac output due to changes in maximal stroke volume that declined 31% with bed rest followed by a 48% increase with training.

Additional important observations were the impact of bed rest and exercise training on submaximal exercise performance. For example, a submaximal workload of 1.5_L/m (~ 100 Watts on a bike) would represent 45% of the observed baseline maximal workload, 63% after bed rest, and 38% after training. These changes in relative work amounts are important because the cardiovascular responses to endurance exercise are determined by the percent of VO_2max achieved with exercise, and not the absolute workload attained. The average baseline heart rate at a submaximal work load of 1.5 L/m was 129 beats per minute (bpm), after bed rest was 164 bpm, and after training 115 bpm, nearly a 50 bpm difference at the same workload; likewise, at the same submaximal workload, blood pressure was higher after bed rest and lower after training.

These findings must be considered in the context of myocardial oxygen demand during exercise, determined by heart rate, left ventricular wall tension (intracardiac pressure and chamber radius), and contractility. Thus, at any submaximal workload, myocardial oxygen demands are higher after bed rest and lower after exercise training.

There were important clinical implications from this study that changed how patients were treated, almost immediately. For example, for patients with MI, strict bed rest that underpinned clinical care at the time was then understood to be harmful due to adverse effects on cardiovascular performance, transitioning care to early ambulation and use of cardiac rehabilitation.

These same 5 volunteers were studied 30 years later (1996) at baseline and after endurance training, with no bed rest exposure evaluated, with results previously published (3, 4), summarized in the Table. Contrasted with the 27% decline in VO_2max with bed rest in the 1966 study, baseline VO_2max had declined by 12% over the 30-year interval. Thus, 3 weeks of bed rest at age 20 reduced cardiovascular capacity more than 30 years of aging. Compared with the original study, training at the 30-year follow up was less intense and titrated slowly over 6 months instead of 8 weeks due the age of the volunteers and risk for injury; each achieved the same final weekly duration of exercise (250 minutes per week).

In the 1966 study, compared with baseline, VO_2max increased with training by 18%. In the 30-year follow-up, VO_2max increased by 14% with training and achieved levels similar to the 1966 baseline evaluations. Thus, endurance training in middle aged men effectively reversed the effects of 30 years of aging on cardiovascular capacity. However, post-training VO_2max 15% lower at the 30-year follow up.

The same 5 volunteers were studied again 10 years later (2006), and at the age of 60, had developed comorbidities typical of an aging population (5). Three had hypertension, two had paroxysmal atrial fibrillation, and one had disabling back pain that compromised his exercise capacity, ultimately found to be due to metastatic renal cell carcinoma. At this evaluation, only baseline cardiopulmonary testing was performed with no training component.

As summarized in the Table, average VO_2max had declined an additional 17% over the 10-year interval, and 27% over 40 years, with the rate of decline increasing from 13 ml/year over the first 30 years to 50 ml/year over the final 10 years. It is also notable that average VO_2max was the same after bed rest in 1966 as it was at the 40-year baseline evaluation; i.e. bed rest at the age of 20 was as detrimental as 40 years of aging. Intriguingly, reductions in stroke volume accounted for reductions in VO_2max with bedrest, while reduction in oxygen extraction (reflected by AVDO₂) had a greater contribution and endurance exercise training improved both with aging. This difference highlights the importance of strength training with aging, especially at more advanced age, to limit sarcopenia and its associated decline in peripheral oxygen uptake.

The Dallas Bed Rest and Training Study and its follow up used VO_2max (1) to evaluate the effects of extremes in physical activity and of age on integrated cardiorespiratory performance. Bed rest was found to be extremely harmful and endurance training beneficial across the spectrum of age. The original study not only demonstrated the extraordinary adaptive capacity of the cardiovascular system and the compelling adverse effects of sedentary behavior, but it also had immediate clinical impact sustained to present day minimizing sedentary time in the management of acute and chronic medical conditions.