Diet- but not exercise-induced iso-energetic deficit induces compensatory appetitive responses.

Although physical exercise and dietary restriction can be both used to induce energy deficits, they have been suggested to favor different compensatory appetitive responses. While dietary restriction might favor increased subsequent energy intake and appetite sensations, such compensatory responses have not been observed after a similar deficit by exercise. The present work provides a first overview of the actual evidences discussing the effects of iso-energetic deficits induced by exercise versus dietary restriction on subsequent energy intake, appetite sensations, and on the potentially involved hedonic and physiological mechanisms.

Reduced fibre size, capillary supply and mitochondrial activity in constitutional thinness' skeletal muscle.

AIM: Constitutional thinness (CT) is a rare condition of natural low body weight, with no psychological issues, no marker of undernutrition and a resistance to weight gain. This study evaluated the skeletal muscle phenotype of CT women by comparison with a normal BMI control group. METHODS: Ten CT women (BMI < 17.5 kg/m2 ) and 10 female controls (BMI: 18.5-25 kg/m2 ) underwent metabolic and hormonal assessment along with muscle biopsies to analyse the skeletal muscular fibres pattern, capillarity, enzymes activities and transcriptomics. RESULTS: Constitutional thinness displayed similar energy balance metabolic and hormonal profile to controls. Constitutional thinness presented with lower mean area of all the skeletal muscular fibres (-24%, P = .01) and percentage of slow-twitch type I fibres (-25%, P = .02, respectively). Significant downregulation of the mRNA expression of several mitochondrial-related genes and triglycerides metabolism was found along with low cytochrome c oxidase (COX) activity and capillary network in type I fibres. Pre- and post-mitochondrial respiratory chain enzymes levels were found similar to controls. Transcriptomics also revealed downregulation of cytoskeletal-related genes. CONCLUSION: Diminished type I fibres, decreased mitochondrial and metabolic activity suggested by these results are discordant with normal resting metabolic rate of CT subjects. Downregulated genes related to cytoskeletal proteins and myocyte differentiation could account for CT's resistance to weight gain.

Soluble Milk Proteins Improve Muscle Mass Recovery after Immobilization-Induced Muscle Atrophy in Old Rats but Do not Improve Muscle Functional Property Restoration.

OBJECTIVES: Effect of 3 different dairy protein sources on the recovery of muscle function after limb immobilization in old rats. DESIGN: Longitudinal animal study. SETTING: Institut National de la Recherche Agronomique (INRA). The study took part in a laboratory setting. INTERVENTION: Old rats were subjected to unilateral hindlimb immobilization for 8 days and then allowed to recover with 3 different dietary proteins: casein, soluble milk proteins or whey proteins for 49 days. MEASUREMENTS: Body weight, muscle mass, muscle fibre size, isometric, isokinetic torque, muscle fatigability and muscle oxidative status were measured before and at the end of the immobilization period and during the recovery period i.e 7, 21, 35 and 49 days post immobilization. RESULTS: In contrast to the casein diet, soluble milk proteins and whey proteins were efficient to favor muscle mass recovery after cast immobilization during aging. By contrast, none of the 3 diary proteins was able to improve muscle strength, power and fatigability showing a discrepancy between the recovery of muscle mass and function. However, the soluble milk proteins allowed a better oxidative capacity in skeletal muscle during the rehabilitation period. CONCLUSION: Whey proteins and soluble milk proteins improve muscle mass recovery after immobilization-induced muscle atrophy in old rats but do not allow muscle functional property restoration.

Endurance but not resistance training increases intra-myocellular lipid content and ß-hydroxyacyl coenzyme A dehydrogenase activity in active elderly men.

AIM: Endurance and resistance training (ET and RT, respectively) in older subjects have been proven beneficial against metabolic or cardiovascular disorders and against sarcopaenia respectively. Like ET, RT may also increase muscle oxidative capacities. In addition, it could be questioned whether RT, similarly to ET, is able to increase muscle energetic stores such as intra-myocellular lipids (IMCL) and glycogen contents. To evaluate a possible ET- and RT-induced parallel increase in oxidative capacity and energetic stores, active elderly men (72 ± 2 years) were submitted to a 14-week training programme (three times week(-1) ) combining lower body endurance and upper body resistance. METHODS: Muscle samples were collected in ET vastus lateralis (VLat) and RT deltoid (Del) muscles before and after training. IMCL and glycogen contents were assessed by histochemistry (Oil Red O and periodic acid-Schiff staining, respectively) and by biochemical assay for glycogen. Citrate synthase (CS, marker of mitochondrial citric acid cycle), ß-hydroxyacyl coenzyme A dehydrogenase (ß-HAD, beta-oxidation) and phosphofructokinase (PFK, glycolytic pathway) activities were determined and so was the capillary interface index (LC/PF). RESULTS: Both training regimens significantly increased CS and LC/PF in ET-VLat and RT-Del. IMCL content and ß-HAD activity increased (P < 0.05) only in ET-VLat, whereas PFK activity increased (P < 0.05) only in RT-Del. Glycogen content was not significantly altered in response to training in both muscles. CONCLUSION: Unlike RT, which induced an increase in PFK, ET is able to increase IMCL content and ß-oxidation capacity in active elderly men, even though both training may improve CS activity and LC/PF.

[Exercise therapy and myopathies]. / Thérapie par l'exercice et myopathies.

Since the first consensus papers published early in the 2000s, a growing number of recent publications has shown that adapted physical activity is not only safe in the context of myopathy but also potentially effective as a therapeutic tool. After a short recall of the different exercise modalities, the mechanical strain they induce and the expected muscular benefits, the present paper reviews the different studies related to exercise therapy in myopathic patients and provides a critical analysis of the topic. Myopathies are rare diseases with many different etiologies and a large number of training modalities which could be useful for the different muscular challenges have been proposed. We have chosen to focus on several specific training modalities and to discuss the results from the most recent papers. The purpose of this review is to, firstly, update physical training guidelines for patients with myopathy and, secondly, highlight some common pitfalls associated with this strategy. This is particularly important for medical and allied professionals involved in prescribing and managing exercise therapy protocols.

Comparison of muscle mechanical and histochemical properties between young and elderly subjects.

We examined age-related human muscle fiber changes and their relation with maximal power scaled to muscle volume (specific power). Fiber type distribution and cross sectional area (CSA) were determined from m. vastus lateralis in 7 young (YS; 29.6 +/- 5 years) and 7 elderly subjects (ES; 74.3 +/- 3 years). Muscle volume and mean CSA of the thigh were anthropometrically measured. Muscle power was assessed by a series of accelerations on a cycle ergometer. Specific power was 35 % lower in ES than YS. Area ratios of IIa/I and IIx/I fibers were lower in ES than YS. By including single fiber power data from the literature to the present results, the decline in the specific power between YS and ES was 34 %, when data of both IIa and IIx fibers were considered. The decrease of the specific power with age on the whole muscle would be compatible with the age-induced changes in the muscle histochemical characteristics.

Effect of endurance training on muscle microvascular filtration capacity and vascular bed morphometry in the elderly.

AIM: Exercise training is a strong stimulus for vascular remodelling and could restore age-induced vascular alterations. The purpose of the study was to test the hypothesis that an increase in vascular bed filtration capacity would corroborate microvascular adaptation with training. METHODS: We quantified (1) microvascularization from vastus lateralis muscle biopsy to measure the capillary to fibre interface (LC/PF) and (2) the microvascular filtration capacity (K(f)) in lower limbs through a venous congestion plethysmography procedure. Twelve healthy older subjects (74 +/- 4 years) were submitted to a 14-week training programme during which lower-limbs were trained for endurance exercise. RESULTS: The training programme induced a significant increase in the aerobic exercise capacity of lower limbs (+11% V(O2peak); P < 0.05; +28% Citrate Synthase Activity; P < 0.01). K(f) was largely increased (4.3 +/- 0.9 10(-3) mL min(-1) mmHg(-1) 100 mL(-1) post-training vs. 2.4 +/- 0.8 pre-training, mean +/- SD; P < 0.05) and microvascularization developed as shown by the rise in LC/PF (0.29 +/- 0.06 post- vs. 0.23 +/- 0.06 pre-training; P < 0.05). Furthermore, K(f) and LC/PF were correlated (r = 0.65, P < 0.05). CONCLUSION: These results demonstrated the microvascular adaptation to endurance training in the elderly. The increase in K(f) with endurance training was probably related to a greater surface of exchange with an increased microvessel/fibre interface area. We conclude that measurement of the microvascular filtration rate reflects the change in the muscle exchange area and is influenced by exercise training.

Evaluation of in vivo dose measurements for patients undergoing electron boost treatments.

This study evaluated p-type silicon diodes for use in in vivo dosimetry in clinical electron beams. A calibrated p-type silicon diode detector was used to measure the dose received by the patient in the centre of the field. Readings were corrected for energy, temperature and stand-off of the electron applicator from the patient surface. The mean difference between measured and prescribed dose was 1.04% (95% CI 0.72 to 1.36 %).

An inhibition of post-ganglionic motor transmission in the mammalian vas deferens by D-lysergic acid diethylamide.

1. Under certain conditions D-lysergic acid diethylamide (LSD), 10(-9)-10(-6) g/ml., exerted an immediate, prolonged and slowly reversible inhibitory effect upon the post-ganglionic motor transmission in desheathed guinea-pig vas deferens preparations.2. The most critical factor influencing this action of LSD appeared to be the train length. With short trains of less than 4 or 5 pulses the twitch inhibition produced by LSD was often total. With longer trains (5-20 pulses), the degree of inhibition declined with increase in train length. These results suggest the existence of two components in the motor response to post-ganglionic stimulation, distinguished by their susceptibility to LSD.3. The inhibition of the LSD-susceptible component was related to the dose of LSD in the range 10(-9)-10(-6) g/ml., reaching a maximum at 0.5-1 x 10(-6) g/ml. The response remnants elicited by trains of more than 5 pulses under these conditions could not be reduced further by a ten- to twenty-fold increase in LSD concentration to 10(-5) g/ml. and were in fact slightly potentiated.4. The inhibition of post-ganglionic motor transmission by LSD was not explicable on the basis of an alpha-adrenoceptor blockade because it was not associated with any reduction in motor responses to noradrenaline.5. The use of propranolol excluded mediation of the LSD-inhibition by beta-adrenoceptors.6. The LSD effect was not due to a non-specific smooth muscle depression because it was not associated with any reduction in motor responses to acetylcholine, ATP or bradykinin.7. The inhibitory effect of LSD on post-ganglionic transmission resembled that of noradrenaline in that it was antagonized by phentolamine; another alpha-adrenoceptor blocking agent, phenoxybenzamine, was less effective than phentolamine in this respect.8. The LSD-inhibition was obtained in preparations taken from reserpinized guinea-pigs.9. The inhibition of motor transmission in the vas deferens by LSD was confirmed in rats, Meriones shawii and rabbits.10. The inhibition of post-ganglionic transmission by LSD was unrelated to its ability to antagonize 5-hydroxytryptamine (5-HT), to which the longitudinal muscle of the guinea-pig vas deferens is insensitive. The more potent 5-HT antagonists, methysergide and BOL 148 were either virtually inactive or considerably weaker than LSD.

Inhibition of post-ganglionic motor transmission in vas deferens by indirectly acting sympathomimetic drugs.

1. Using field stimulation with short trains of pulses (< 10 per train), the post-ganglionic motor transmission in the mammalian vas deferens has been further analysed pharmacologically.2. In preparations taken from guinea-pigs, rats and rabbits the effects of the indirectly sympathomimetic drugs, tyramine and cocaine, could be explained entirely on the basis of the actions of released, endogenous noradrenaline.3. Tyramine produced a contraction in vasa taken from normal rats but not from normal guinea-pigs. The tyramine contraction was due to release of endogenous noradrenaline because it was not seen in preparations taken from reserpinized rats and because it was abolished in normal vasa by phenoxybenzamine or phentolamine, thus denying the supposed inaccessibility, to alpha-blockers, of the motor alpha-adrenoceptors activated by endogenous noradrenaline.4. Phenoxybenzamine or phentolamine failed to block post-ganglionic motor transmission in rat and in guinea-pig vasa.5. Tyramine strongly inhibited motor transmission in vasa taken from normal but not from reserpinized guinea-pigs.6. Tyramine produced inhibition of motor transmission in phenoxybenzamine-treated preparations taken from normal but not from reserpinized rats.7. Cocaine inhibited motor transmission in guinea-pig and in rat vasa. This effect was not due to a local anaesthetic or to a smooth-muscle depressant action because it did not occur in preparations taken from reserpinized animals.8. The inhibitory effect of tyramine or cocaine was not abolished by beta-adrenoceptor blockade with propranolol.9. Whereas reserpinization abolished the tyramine- and cocaine-inhibitions, it did not affect the inhibitory actions of noradrenaline or of PGE(2).10. Indomethacin and sodium meclofenamate, which suppress prostaglandin synthesis, did not affect the twitch-inhibiting actions of noradrenaline, tyramine or cocaine.11. These results provide further support for the conclusion that post-ganglionic motor transmission to the vas deferens is non-adrenergic in these species and assign to endogenously released noradrenaline an inhibitory role upon motor transmission.

Evidence for the release of two atropine-resistant spasmogens from Auerbach's plexus.

1. Two atropine-resistant response-components of nervous origin have been detected in plexus-containing preparations of the longitudinal muscle from the guinea-pig ileum, by alternate field stimulation with equal numbers of pulses at 50 Hz (response A) and at 5 Hz (response B). With trains of ten or more pulses, response A is always larger than B; the ratio of A/B (1.2-21.3) is subject to animal variation.2. Both responses are abolished by tetrodotoxin and are absent from plexus-free preparations.3. Neither response is reduced by ganglion-block with (+)-tubocurarine, dimethyltubocurarine or hexamethonium, or by ganglion-paralysing doses of nicotine; the contribution of excited preganglionic endings to these responses is therefore negligible.4. Neither response is due to a release of histamine, 5-hydroxytryptamine (5-HT) or prostaglandins, since both A and B persist in the presence of mepyramine, methysergide and the prostaglandin-antagonist SC-19220 (1-acetyl-2(8-chloro-10,11-dihydrodibenz [b,f] [1,4]oxazepine-10-carbonyl) hydrazine).5. The two response-components are affected differentially by a number of drugs.6. Histamine, 0.1 mug/ml., reduces response A to the level of B; this selective inhibition of the histamine-sensitive component in A is specifically antagonized by nicotine, 1-2.5 x 10(-5) g/ml.7. 5-HT, 0.1 mug/ml., and strychnine, 20-40 mug/ml., also reduce response A to the level of B, but these selective inhibitions are not antagonized by nicotine.8. Diphenhydramine, 10 mug/ml., produces equality of the two responses by depressing A and potentiating B.9. The inhibitory effects of the foregoing drugs are not due to catecholamine release, since they persist after alpha + beta adrenoceptor blockade with phentolamine and pronethalol, and after previous reserpinization of the guinea-pigs.10. In atropinized plexus-containing preparations of the longitudinal muscle from the guinea-pig descending colon, the responses elicited at 50 Hz and at 5 Hz are virtually equal and both appear to be of Type B since they are not inhibited by histamine, 5-HT or strychnine; diphenhydramine produces strong contractions.