Dominique Desplanches

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

1 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. 2 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. 3 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. 4 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%). 5 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. 6 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.

Effect of endurance training on mRNA expression of uncoupling proteins 1, 2, and 3 in the rat.

Endurance exercise training has been shown to decrease diet‐induced thermogenesis (DIT) in rats and humans. In rodents, most thermogenesis is thought to occur in brown adipose tissue via activation of the uncoupling protein‐1 (UCP1) and in skeletal muscle. Since the level of UCP1 mRNA in rat BAT was reported to be unmodified by exercise training, the newly described uncoupling proteins UCP2 and UCP3 could be responsible for the decreased DIT in trained rats. UCP3 mRNA levels in endurancetrained rats were found to be reduced by 76% and 59% in tibialis anterior and soleus muscles, respectively. UCP2 mRNA levels were also decreased in tibialis anterior and in heart by 54% and 41%, respectively. Neither white adipose tissue UCP2 nor brown adipose tissue UCP1, UCP2, and UCP3 mRNA levels were modified. The results of this study show that a need for a higher metabolic efficiency is associated with decreased mRNA expression of the uncoupling proteins in skeletal and heart muscles, which would decrease energy dissipation in these tissues. The down‐regulation of UCP3 and UCP2 expressions might also contribute to the rapid weight gain known to occur when exercise training ceased.—Boss, O., Samec, S., Desplanches, D., Mayet, M.‐H., Seydoux, J., Muzzin, P., Giacobino, J.‐P. Effect of endurance training on mRNA expression of uncoupling proteins 1, 2, and 3 in the rat. FASEB J. 12, 339–335 (1998)

Effects of training in normoxia and normobaric hypoxia on human muscle ultrastructure.

AbstractThe adaptive response of skeletal muscle to training in normoxia and in severe normobaric hypoxia was studied. The first group of five male subjects trained for 3 weeks on a bicycle (2 h/day, 6 days/week) in normoxia (Control training, Con T). A second group of five subjects trained in an ambient FIO2 decreasing progressively from 12.7% to a final level of 10.0% (hypoxic training, Hyp T). Fourteen months later, these subjects trained in normoxia at the same absolute power (normoxic training, Nor T). Peak oxygen consumption (n

EFFECT OF VOLUNTARY EXERCISE ON H2O2 RELEASE BY SUBSARCOLEMMAL, AND INTERMYOFIBRILLAR MITOCHONDRIA

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Oxidative stress, apoptosis and proteolysis in skeletal muscle repair after unloading

nO2 max) was measured in normoxic and hypoxic conditions. Biopsies from the vastus lateralis muscle were analysed for fibre size, capillary and ultrastructural composition. Nor T had no effect on muscle tissue or n

Angio‐adaptation in unloaded skeletal muscle: new insights into an early and muscle type‐specific dynamic process

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