Resistive exercise versus resistive vibration exercise to counteract vascular adaptations to bed rest

Bed rest results in marked vascular adaptations, and resistive vibration exercise (RVE) has been shown to be an effective countermeasure. As vibration exercise has practical and logistical limitations, the use of resistive exercise (RES) alone has the preference under specific circumstances. However, it is unknown if RES is sufficient to prevent vascular adaptations to bed rest. Therefore, the purpose of the present study was to examine the impact of RES and RVE on the vascular function and structure of the superficial femoral artery in young men exposed to 60 days of bed rest. Eighteen healthy men (age: 31 ± 8 yr) were assigned to bed rest and randomly allocated to control, RES, or RVE groups. Exercise was applied 3 times/wk for 5–7 min/session. Resting diameter, blood flow, flow-mediated dilation (FMD), and dilator capacity of the superficial femoral artery were measured using echo-Doppler ultrasound. Bed rest decreased superficial femoral artery diameter and dilator capacity ( P < 0.001), which were significantly attenuated in the RVE group ( P < 0.01 and P < 0.05, respectively) but not in the RES group ( P = 0.202 and P = 0.696, respectively). Bed rest significantly increased FMD ( P < 0.001), an effect that was abolished by RVE ( P < 0.005) but not RES ( P = 0.078). Resting and hyperemic blood flow did not change in any of the groups. Thus, RVE abolished the marked increase in FMD and decrease in baseline diameter and dilator capacity normally associated with prolonged bed rest. However, the stimulus provided by RES alone was insufficient to counteract the vascular adaptations to bed rest.

Vascular adaptation to deconditioning and the effect of an exercise countermeasure: results of the Berlin Bed Rest study

Deconditioning is a risk factor for cardiovascular disease. The physiology of vascular adaptation to deconditioning has not been elucidated. The purpose of the present study was to assess the effects of bed rest deconditioning on vascular dimension and function of leg conduit arteries. In addition, the effectiveness of resistive vibration exercise as a countermeasure for vascular deconditioning during bed rest was evaluated. Sixteen healthy men were randomly assigned to bed rest (BR-Ctrl) or to bed rest with resistive vibration exercise (BR-RVE). Before and after 25 and 52 days of strict horizontal bed rest, arterial diameter, blood flow, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation were measured by echo Doppler ultrasound. In the BR-Ctrl group, the diameter of the common femoral artery decreased by 13 ± 3% after 25 and 17 ± 1% after 52 days of bed rest ( P < 0.001). In the BR-RVE group this decrease in diameter was significantly attenuated (5 ± 2% after 25 days and 6 ± 2% after 52 days, P < 0.01 vs. BR-Ctrl). Baseline blood flow did not change after bed rest in either group. After 52 days of bed rest, FMD and nitroglycerin-mediated dilatation of the superficial femoral artery were increased in both groups, possibly by increased nitric oxide sensitivity. In conclusion, bed rest deconditioning is accompanied by a reduction in the diameter of the conduit arteries and by an increased reactivity to nitric oxide. Resistive vibration exercise effectively attenuates the diameter decrease of leg conduit arteries after bed rest.

Vascular adaptation to 4 wk of deconditioning by unilateral lower limb suspension

Physical inactivity or deconditioning is an independent risk factor for atherosclerosis and cardiovascular disease. In contrast to exercise, the vascular changes that occur as a result of deconditioning have not been characterized. We used 4 wk of unilateral lower limb suspension (ULLS) to study arterial and venous adaptations to deconditioning. In contrast to previous studies, this model is not confounded by denervation or microgravity. Seven healthy subjects participated in the study. Arterial and venous characteristics of the legs were assessed by echo Doppler ultrasound and venous occlusion plethysmography. The diameter of the common and superficial femoral artery decreased by 12% after 4 wk of ULLS. Baseline calf blood flow, as measured by plethysmography, decreased from 2.1 ± 0.2 to 1.6 ± 0.2 ml·min−1·dl tissue−1. Both arterial diameter and calf blood flow returned to baseline values after 4 wk of recovery. There was no indication of a decrease in flow-mediated dilation of the superficial femoral artery after ULLS deconditioning. This means that functional adaptations to inactivity are not simply the inverse of adaptations to exercise. The venous pressure-volume curve is shifted downward after ULLS, without any effect on compliance. In conclusion, deconditioning by 4 wk of ULLS causes significant changes in both the arterial and the venous system.

Effect of hyperoxia and hypoxia on leg blood flow and pulmonary and leg oxygen uptake at the onset of kicking exercise

The purpose of this study was to examine the interactions of adaptations in O2 transport and utilization under conditions of altered arterial O2 content (CaO2), during rest to exercise transitions. Simultaneous measures of alveolar ([Formula: see text]O2alv) and leg ([Formula: see text]O2mus) oxygen uptake and leg blood flow (LBF) responses were obtained in normoxic (FiO2 (inspired fraction of O2) = 0.21), hypoxic (FiO2 = 0.14), and hyperoxic (FiO2 = 0.70) gas breathing conditions. Six healthy subjects performed transitions in leg kicking exercise from rest to 48 ± 3 W. LBF was measured continuously with pulsed and echo Doppler ultrasound methods, [Formula: see text]O2alv was measured breath-by-breath at the mouth and [Formula: see text]O2mus was determined from LBF and radial artery and femoral vein blood samples. Even though hypoxia reduced CaO2 to 175.9 ± 5.0 from 193.2 ± 5.0 mL/L in normoxia, and hyperoxia increased CaO2 to 205.5 ± 4.1 mL/L, there were no differences in the absolute values of [Formula: see text]O2alv or [Formula: see text]O2mus across gas conditions at any of the rest or exercise time points. A reduction in leg O2 delivery in hypoxia at the onset of exercise was compensated by a nonsignificant increase in O2 extraction and later by small increases in LBF to maintain [Formula: see text]O2mus. The dynamic response of [Formula: see text]O2alv was slower in the hypoxic condition; however, hyperoxia did not affect the responses of oxygen delivery or uptake at the onset of moderate intensity leg kicking exercise. The finding of similar [Formula: see text]O2mus responses at the onset of exercise for all gas conditions demonstrated that physiological adaptations in LBF and O2 extraction were possible, to counter significant alterations in CaO2. These results show the importance of the interplay between O2 supply and O2 utilization mechanisms in meeting the challenge provided by small alterations in O2 content at the onset of this submaximal exercise task.

Effects of acetylcholine and nitric oxide on forearm blood flow at rest and after a single muscle contraction

We tested the hypothesis that ACh or nitric oxide (NO) might be involved in the vasodilation that accompanies a single contraction of the forearm. Eight adults (3 women and 5 men) completed single 1-s-duration contractions of the forearm to raise and lower a weight equivalent to ∼20% maximal voluntary contraction through a distance of 5 cm. In a second protocol, each subject had a cuff, placed completely about the forearm, inflated to 120 mmHg for a 1-s period, then released as a simulation of the mechanical effect of muscle contraction. Three conditions were studied, always in this order: 1) control, with intra-arterial infusion of saline; 2) after muscarinic blockade with atropine; and 3) after NO synthase inhibition with N G-monomethyl-l-arginine (l-NMMA) plus atropine. Forearm blood flow (FBF), measured by combined pulsed and echo Doppler ultrasound, was reduced at rest with l-NMMA-atropine compared with the other two conditions. After the single contraction, there were no effects of atropine, butl-NMMA reduced the peak FBF and the total postcontraction hyperemia. After the single cuff inflation, atropine had no effects, whereasl-NMMA caused changes similar to those seen after contraction, reducing the peak FBF and the total hyperemia. The observation thatl-NMMA reduced FBF in response to both cuff inflation and a brief contraction indicates that NO from the vascular endothelium might modulate the basal level of vascular tone and the mechanical component of the hyperemia with exercise. It is unlikely that ACh and NO from the endothelium are involved in the dilator response to a single muscle contraction.