The interplay of central and peripheral factors in limiting maximal O₂ consumption in man after prolonged bed rest

Abstract

The effects of bed rest on the cardiovascular and muscular parameters which affect maximal O2 consumption (VO2,max) were studied. The fractional limitation of VO2,max imposed by these parameters after bed rest was analysed. The VO2,max, by standard procedure, and the maximal cardiac output (Q̇max), by the pulse contour method, were measured during graded cyclo‐ergometric exercise on seven subjects before and after a 42‐day head‐down tilt bed rest. Blood haemoglobin concentration ([Hb]) and arterialized blood gas analysis were determined at the highest work load. Muscle fibre types, oxidative enzyme activities, and capillary and mitochondrial densities were measured on biopsy samples from the vastus lateralis muscle before and at the end of bed rest. The measure of muscle cross‐sectional area (CSA) by NMR imaging at the level of biopsy site allowed computation of muscle oxidative capacity and capillary length. The VO2max was reduced after bed rest (−16.6%). The concomitant decreases in Q̇max (−30.8%), essentially due to a change in stroke volume, and in [Hb] led to a huge decrease in O2 delivery (−39.7%). Fibre type distribution was unaffected by bed rest. The decrease in fibre area corresponded to the significant reduction in muscle CSA (−17%). The volume density of mitochondria was reduced after bed rest (−16.6%), as were the oxidative enzyme activities (−11%). The total mitochondrial volume was reduced by 28.5%. Capillary density was unchanged. Total capillary length was 22.2% lower after bed rest, due to muscle atrophy. The interaction between these muscular and cardiovascular changes led to a smaller reduction in VO2max than in cardiovascular O2 transport. Yet the latter appears to play the greatest role in limiting VO2max after bed rest (>70% of overall limitation), the remaining fraction being shared between peripheral O2 diffusion and utilization.

Fundamental questions about genes, inactivity, and chronic diseases

“…Skeletal muscles become weaker with less endurance for light physical effort (1). In addition, metabolic pathways adapt to inactivity by decreasing mitochondrial concentration in skeletal muscles (38), lowering the capacity to oxidize fatty acids. Whole body insulin sensitivity declines within the first 3 days of inactivity, whether it is bed rest (65,87) or active individuals stopping daily exercise (15,73).…”

Myofibrillar distribution of succinate dehydrogenase activity and lipid stores differs in skeletal muscle tissue of paraplegic subjects

“…These results are in agreement with a recent study by Nielsen et al (48), who showed that SS mitochondrial content decreased by 33% after 2 wk of muscle immobilization by whole leg casting, whereas central IMF mitochondrial content remained unchanged. In contrast, Feretti et al (22) reported a 17% decrease in IMF mitochondria, with no significant decrease in SS mitochondrial content, in young subjects after 37 days of bed rest. The difference in mode of disuse and activity level could explain the observed discrepancies.…”

“…It is known that with inactivity (14, 50, 52), immobilization (22,48), and denervation (26,43), muscle oxidative capacity is reduced. The latter has at least partly been attributed to a change in muscle fiber type composition toward more type 2 fibers (54) and in particular type 2x fibers (12,13,57).…”

Energetics of Muscular Exercise

“…Moreover, in this experimental model, only the duration of the bed rest period varies among studies, allowing a precise evaluation of the time courses of the functional modifications induced by bed rest. _ V O 2max decreases after bed rest (Bringard et al 2010;Capelli et al 2006;Convertino et al 1982;Ferretti et al 1997a;Greenleaf et al 1989;Kashihara et al 1994;Saltin et al 1968;Stremel et al 1976;Trappe et al 2006), even of very short duration (Smorawinski et al 2001). The size of the _ V O 2max decrease is larger the longer is the bed rest duration, being fast in the first days, and progressively slower as bed rest proceeds.…”

“…This explains why F Q ¼ 0:7 instead of 0.5, so that we necessarily have F p ¼ 0:3, partly attributable to F t , partly to F m . According to Ferretti et al (1997a), the differences in _ V O 2max would be minimal, if we assume, on one extreme, R t ¼ R p , and on the other extreme, R m = R p , and that it makes no difference to assume R t and R m in series or in parallel. Direct experimental assessment of the parameters of Eq.…”