[Exercise effort training for COPD: physiological basis and results]. / Le réentraînement à l'effort des BPCO: bases physiologiques et résultats.

INTRODUCTION: In the last decade pulmonary rehabilitation has become a well accepted treatment for patients with chronic obstructive pulmonary disease (COPD) suffering from persistent dyspnea and fatigue, despite appropriate medical treatment. STATE OF ART: Patients with COPD frequently have muscular dysfunction that can be corrected by appropriate exercise training programmes. Muscle function as measured by strength and endurance tests exercise capacity and also the health status and quality of life are improved by exercise and endurance training. However, integration of exercise training in a multidisciplinary management programme is necessary to take account of all aspects of the illness. PERSPECTIVES: Methods of exercise training need to be adapted for patients with severe COPD who are unable to undertake endurance training and for patients who obtain little benefit. CONCLUSIONS: Pulmonary rehabilitation, thanks to its multidisciplinary nature, seems to be an effective modality of management for patients with COPD. However, the improvements in physical ability, quality of life and general health require an exercise training programme that is adapted for the individual patient.

Contractile properties and histochemical characteristics of the rat diaphragm after prolonged triamcinolone treatment and nutritional deprivation.

The influence of decreased muscle mass and reduced food intake on diaphragm structure and contractility in male Wistar rats was determined after triamcinolone acetate treatment (TR: 0.5 mg per kg per day for 4 weeks) and two degrees of undernutrition (PW: pair-weight, which resulted in a similar (41%) reduction of body weight as TR; PF: pair-fed, which resulted in a moderate (13%) reduction of body weight) and a free-fed control group (FF, with an increase (9%) in body weight). energy intake of TR decreased, but based on daily measurements of food intake and body weight, energy expenditure of the TR rats was increased compared with the other groups. Body (BW) and muscle weights were reduced in proportion to the extent of undernutrition in the nutritionally deprived rates (i.e. BW and diaphragm weight of PF animals were reduced 215 and 16% respectively compared with FF, v. a. 48% and 41% reduction in the PW group). Triamcinolone-induced atrophy was limited to type II fibres (30% of type IIa and 45% of type IIx/b, p < 0.05), while severe chronic undernutrition (PW) induced a generalized fibre type atrophy in the diaphragm (23% type I, 38% type IIa and 49% type IIx/b, p < 0.05), and moderate undernutrition (PF) caused only significant type IIa atrophy (20%, p < 0.05). A leftward shift of the diaphragmatic tension-frequency relationship and a decreased fatiguability of the TR and PW bundles were observed (p < 0.01), while the PF bundles were not significantly different compared with FF. These results suggest that triamcinolone and severe undernutrition cause similar alterations in in vitro contractility of the diaphragm. The effects of triamcinolone treatment on diaphragm structure may be partly explained by the reduced food intake, but the atrophy pattern induced by severe undernutrition (PW) was different.

Low load inspiratory muscle training increases diaphragmatic fiber dimensions in rats.

The effects of 8 wk of inspiratory resistive loading (30 min/d, 3 x/wk) on diaphragm mass, contractile properties, fatigue, and fiber dimensions were studied in 10 male Wistar rats. They were conditioned to breathe through a Hans-Rudolph device. Half of them had to overcome a moderate inspiratory resistance (MR; n = 5), whereas the others only had to overcome the small resistance (SR; n = 5) of the inspiratory valve of the device. Results were compared with control rats (C; n = 5) moving and breathing freely. At the end of training, animals submitted to MR and SR generated mean inspiratory pressures of -2.5 +/- 1.1 and -0.2 +/- 0.05 cm H2O, respectively. TI/Ttot was 0.60 +/- 0.06 and 0.57 +/- 0.05, respectively. Body and diaphragm weight were unaffected by loading. Little or no change in in vitro diaphragmatic twitch kinetics, force generation, and fatigability was found between the three groups. Nevertheless, cross-sectional area of all fiber types increased in the two loaded groups compared with control animals. This increase reached statistical significance for type I fibers in the MR group (846 +/- 74 microm2) compared with the C and SR groups (589 +/- 32 and 683 +/- 96 microm2, respectively, p < 0.05). For IIa fibers both training groups were significantly different from the control group (SR: 768 +/- 99 and MR: 790 +/- 108 versus C: 592 +/- 37 microm2, p < 0.05). A hypertrophy of type IIx/b fibers was seen in MR compared with control animals (C: 1,555 +/- 136, SR: 1,845 +/- 338, MR: 2,053 +/- 326 microm2, p < 0.05). No differences were present in fiber type proportions between the three groups. We conclude that in our training setup, 8 wk of intermittent long-term inspiratory loading stressed the diaphragm already with a small resistance resulting in hypertrophy of predominantly type IIa fibers. A higher resistance resulted in hypertrophy of all fiber types.

Intermittent inspiratory muscle training induces fiber hypertrophy in rat diaphragm.

The effects of 8 wk of moderate load intermittent inspiratory resistive loading on diaphragm contractility, and histochemistry of the diaphragm, scalenes, and gastrocnemius were studied in rats. A resistance was placed in the inspiratory port of a Hans-Rudolph valve, through which each animal breathed during 30 min/d, 5 times/wk (loaded group, n = 10). These rats were compared with animals breathing through the same device without inspiratory resistance (control group, n = 10). During loading, animals generated mean inspiratory pressures of -3.2 +/- 1.7 cm H2O with a TI/Ttot of 0.69 +/- 0.06, resulting in a tension-time index of 0.050. At the end of training, the diaphragm mass increased in loaded animals (0.17 +/- 0.01% body mass) compared with control animals (0.15 +/- 0.01%, p < 0.01), while scalene and gastrocnemius mass remained unchanged. Diaphragmatic force as well as fatigue resistance were similar in both groups, whereas time to peak tension was significantly (p < 0.01) shorter in loaded rats (18.8 +/- 1.7 ms) compared with control rats (21.2 +/- 1.8 ms), half-relaxation time remaining unchanged. Finally, hypertrophy of diaphragmatic type IIa (+19%, p < 0.01) and IIx/b (+12%, p < 0.05) was present in the loaded group. Histochemistry of the scalenes remained unchanged, whereas type IIx/b hypertrophy (+12%, p < 0.001) was observed in the gastrocnemius internus. We speculate that the latter was due to multiple escape maneuvers. We conclude that intermittent inspiratory muscle training: (1) caused fast twitch fiber hypertrophy in the diaphragm; (2) did not produce any effect in the scalenes.

Effects of nandrolone decanoate on respiratory and peripheral muscles in male and female rats.

Thirty male and 18 female adult rats received weekly an intramuscular injection of either saline (control; C), 1.5 mg/kg (low-dose; LD) nandrolone decanoate or 7.5 mg/kg (high-dose; HD) nandrolone decanoate during 5 wk. Compared with respective C, growth rate was stunted in male HD rats from 2 wk of treatment on, whereas it was enhanced in female LD and HD rats after 1 wk. Mass of all muscles studied varied proportionally to body weight, except for the gastrocnemius (males: 0.49 +/- 0.04 vs. C: 0.52 +/- 0.03%, not significant; females: 0.17 +/- 0.01 vs. C: 0.15 +/- 0.01%, P < 0.05). In vitro contractile and fatigue properties of the diaphragm remained unchanged, except for a decrease in twitch kinetics (time to peak tension: C, 21 +/- 2; LD, 19 +/- 1; HD, 19 +/- 2 ms, P < 0.05; half-relaxation time: C, 26 +/- 5, LD, 25 +/- 5, HD, 23 +/- 3 ms, P < 0.01). Histochemistry of the diaphragm and the gastrocnemius revealed a significant increase in type IIx/b dimensions. In the gastrocnemius, type I fiber dimensions also increased. A pair-fed study, including another 24 female rats, showed that the changes in oral food intake only partly accounted for the observed anabolic effects.

Corticosteroid treatment and nutritional deprivation cause a different pattern of atrophy in rat diaphragm.

Triamcinolone (TR) causes type IIb fiber atrophy in the rat diaphragm, which is associated with changes in contractile properties. We investigated whether this is a direct effect of TR or the result of an accompanying loss of body and diaphragm weights. For 6 wk, adult rats received saline intramuscularly, TR (0.5 mg/kg im), or nutritional depletion (ND) that resulted in a similar (approximately 40%) reduction in body weight as TR. In these animals, the half-relaxation time of the diaphragm bundles increased, the force-frequency relationship shifted leftward, and the resistance to fatigue was increased. No histological changes were found in the ND diaphragm, in contrast to severe myogenic alterations in the TR diaphragm. Type IIb fiber cross-sectional area (CSA) in the TR diaphragm was reduced by 51%, whereas type I and IIa CSAs were unaffected. In the ND animals, the CSAs of type I, IIa, and IIb fibers were reduced by 31, 33, and 52%, respectively. Similar changes occurred in the deep part of the m. gastrocnemius. In conclusion, myogenic changes and selective type IIb fiber atrophy were caused by TR, whereas ND induced generalized fiber type atrophy without histological changes.