Effects of prolonged bed rest on cardiovascular oxygen transport during submaximal exercise in humans

Abstract

The hypothesis was tested that prolonged bed rest impairs O2 transport during exercise, which implies a lowering of cardiac output Qc and O2 delivery (QaO2). The following parameters were determined in five males at rest and at the steady-state of the 100-W exercise before (B) and after (A) 42-day bed rest with head-down tilt at -6 degrees: O2 consumption (VO2), by a standard open-circuit method; Qc, by the pressure pulse contour method, heart rate (fc), stroke volume (Qh), arterial O2 saturation, blood haemoglobin concentration ([Hb]), arterial O2 concentration (CaO2), and QaO2. The VO2 was the same in A and in B, as was the resting fc. The fc at 100 W was higher in A than in B (+17.5%). The Qh was markedly reduced (-27.7% and -22.2% at rest and 100 W, respectively). The Qc was lower in A than in B [-27.6% and -7.8% (NS) at rest and 100 W, respectively]. The CaO2 was lower in A than in B because of the reduction in [Hb]. Thus also QaO2 was lower in A than in B (-32.0% and -11.9% at rest and at 100 W, respectively). The present results would suggest a down-regulation of the O2 transport system after bed rest.

Metabolic and cardiovascular responses during sub-maximal exercise in humans after 14 days of head-down tilt bed rest and inactivity

“…By contrast, other studies, performed over longer periods of HDTBR, showed significant decreases of _ Q at rest in upright position. After 42-day of bed rest, _ Q was about 28% less than in the control condition (Ferretti et al 1998) and, after 60 and 113 days of bed rest, it decreased by 16 and 8%, respectively (Spaak et al 2005). In the first case, f H remained the same and did not compensate for the large drop of SV (-28%).…”

“…In fact, the decrease in stroke volume reduces drastically the maximal cardiac output and the maximal oxygen uptake after HDTBR (Ferretti et al 1997;Capelli et al 2006). Conversely, cardiac output during steady state sub-maximal exercise seems to be maintained-only slightly reduced at rest-because heart rate is able to compensate for the lower stroke volume (Ferretti et al 1998;Spaak et al 2005). Therefore, the ability to maintain blood pressure and to perform low intensity dynamic exercise seems not to be affected by HDTBR (Ferretti et al 1998;Spaak et al 2005).…”

“…Conversely, cardiac output during steady state sub-maximal exercise seems to be maintained-only slightly reduced at rest-because heart rate is able to compensate for the lower stroke volume (Ferretti et al 1998;Spaak et al 2005). Therefore, the ability to maintain blood pressure and to perform low intensity dynamic exercise seems not to be affected by HDTBR (Ferretti et al 1998;Spaak et al 2005). This is at variance with the observations made during actual space flight, whereby the relationship between cardiac output and exercise intensity is shifted downward more markedly than in simulated microgravity, suggesting an actual impairment of the cardiovascular response during sub-maximal exercise in space (Shykoff et al 1996).…”

Feedback Respiratory Training to Enhance Chest Expansion and Pulmonary Function in Chronic Stroke: A Double-Blind, Randomized Controlled Study

“…Decreased motor performance occurring after a stroke limits patient activity and prolongs bed rest, and is known to decrease cardiopulmonary function in association with oxygen transport capacity 2) . For patients with stroke, cardiopulmonary function is one of the important issues in preservation of life 3) .…”

The Effects of Combination of Inspiratory Diaphragm Exercise and Exspiratory Pursed-lip Breathing Exercise on Pulmonary Functions of Stroke Patients

“…Stroke patients' respiratory function is affected by the cardiopulmonary performance, both directly and indirectly, as they experience a decline in cardiovascular function and pulse rate, which affects oxygen delivery, and a deterioration in the movement of the chest wall on the paralyzed side and its electrical activities 1) . The respiratory efficiency and the changes in breathing mechanism reflect the extent of damage in the movement of the chest wall, its asymmetry and the degree of muscular paralysis of stroke patients.…”