Energy cost of breathing at depth: effect of respiratory muscle training.

INTRODUCTION: Respiratory muscle training against resistance (RRMT) increases respiratory muscle strength and endurance as well as underwater swimming endurance. We hypothesized that the latter is a result of RRMT reducing the high energy cost of breathing at depth. METHODS: Eight subjects breathed air in a hyperbaric chamber at 55 fsw, both before and after RRMT. They rested for 10 minutes, cycled on an ergometer for 10 minutes (100 W), rested for 10 minutes, and then, while still at rest, they voluntarily mimicked the breathing pattern recorded during the exercise (isocapnic simulated exercise ventilation, ISEV). RESULTS: Post-RRMT values of V(E) at rest, exercise and ISEV were not different from those recorded pre-RRMT. Pre-RRMT minute-ventilation (V(E)) during ISEV was not different from the exercise ventilation (49.98 +/- 10.41 vs. 47.74 +/- 8.44 L/minute). The end-tidal PCO2 during ISEV and exercise were not different (44.26 +/- 2.54 vs. 44.49 +/- 4.49 mmHg) or affected by RRMT. Oxygen uptake (VO2) was 0.32 +/- 0.08 L/ minute at rest, 1.78 +/- 0.15 during exercise pre-RRMT, and not different post-RRMT. During ISEV, VO2 decreased significantly from pre-RRMT to post-RRMT (0.46 +/- 0.06 vs. 0.36 +/- 0.11 L/minute). Post-RRMT delta VO2/delta V(E) was significantly lower during ISEV than pre-RRMT (0.0094 +/- 0.0021 L/L vs. 0.0074 +/- 0.0023 L/L). CONCLUSION: RRMT significantly reduced the energy cost of ventilation, measured as delta VO2/delta V(E) during ISEV, at a depth of 55 fsw. Whether this change was due to reduced work of breathing and/or increased efficiency of the respiratory muscles remains to be determined.

Respiratory muscle training improves swimming endurance at depth.

Respiratory muscle training (RMT) has been shown to improve divers swimming endurance at 4 feet of depth; however, its effectiveness at greater depths, where gas density and the work of breathing are substantially elevated has not been studied. The purpose of this study was to examine the effects of resistance respiratory muscle training (RRMT) on respiratory function and swimming endurance at 55 feet of depth (270.5 kPa). Nine male subjects (25.9 +/- 6.8 years) performed RRMT for 30 min/day, 5 d/ wk, for 4 wks. Pre- and Post RRMT, subjects swam against a pre-determined load (70% VO2 max) until exhausted. As indices of respiratory muscle strength, maximal inspiratory and expiratory pressures were measured before and immediately following the swims pre- and post-RRMT. These measurements showed that ventilation was significantly lower during the swims and, at comparable swim duration, that the respiratory muscles were considerably less fatigued following RRMT. The reduced ventilation was due to a lower breathing frequency following RRMT. The ventilatory changes following RRMT coincided with significantly increased swimming time to exhaustion (approximately 60%, 31.3 +/- 11.6 vs. 49.9 +/- 16.0 min, pre- vs. post-RRMT, p < 0.05). These results suggest respiratory muscle fatigue limits swimming endurance at depth as well as at the surface and RRMT improves performance.

Exercise delays the hypoxic thermal response in rats.

Exercise exacerbates acute mountain sickness. In infants and small mammals, hypoxia elicits a decrease in body temperature (Tb) [hypoxic thermal response (HTR)], which may protect against hypoxic tissue damage. We postulated that exercise would counteract the HTR and promote hypoxic tissue damage. Tb was measured by telemetry in rats (n = 28) exercising or sedentary in either normoxia or hypoxia (10% O2, 24 h) at 25 degrees C ambient temperature (Ta). After 24 h of normoxia, rats walked at 10 m/min on a treadmill (30 min exercise, 30 min rest) for 6 h followed by 18 h of rest in either hypoxia or normoxia. Exercising normoxic rats increased Tb ( degrees C) vs. baseline (39.68 +/- 0.99 vs. 38.90 +/- 0.95, mean +/- SD, P < 0.05) and vs. sedentary normoxic rats (38.0 +/- 0.09, P < 0.05). Sedentary hypoxic rats decreased Tb (36.15 +/- 0.97 vs. 38.0 +/- 0.36, P < 0.05) whereas Tb was maintained in the exercising hypoxic rats during the initial 6 h of exercise (37.61 +/- 0.55 vs. 37.72 +/- 1.25, not significant). After exercise, Tb in hypoxic rats reached a nadir similar to that in sedentary hypoxic rats (35.05 +/- 1.69 vs. 35.03 +/- 1.32, respectively). Tb reached its nadir significantly later in exercising hypoxic vs. sedentary hypoxic rats (10.51 +/- 1.61 vs. 5.36 +/- 1.83 h, respectively; P = 0.002). Significantly greater histopathological damage and water contents were observed in brain and lungs in the exercising hypoxic vs. sedentary hypoxic and normoxic rats. Thus exercise early in hypoxia delays but does not prevent the HTR. Counteracting the HTR early in hypoxia by exercise exacerbates brain and lung damage and edema in the absence of ischemia.

Role of nitric oxide in thermoregulation and hypoxic ventilatory response in obese Zucker rats.

To examine the role of nitric oxide (NO) on thermoregulation and control of breathing in obesity, awake obese and age-matched lean Zucker (Z) rats underwent a sustained hypoxic challenge. Body temperature (Tb), oxygen consumption (V O(2)) and ventilation (V E) were measured during room air and during 30-min of hypoxia (10% O(2)) after intraperitoneal administration of either 100 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS inhibitor, 25 mg/kg of 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, or equal volume of vehicle (dimethyl sulfoxide: DMSO) as control. Tb in obese rats during room air was significantly lower than that of lean rats. Hypoxia induced a more pronounced drop in Tb and V O(2) in lean rats than in obese rats. Tb in lean Z rats dropped significantly by approximately 0.2 degrees C after L-NAME and, more markedly, by approximately 1.1 degrees C after 7-NI compared with control during room air, whereas Tb in obese Z rats was unaffected. L-NAME and 7-NI attenuated hypoxia-induced hypothermia or hypometabolism in lean rats, but not in obese rats. Lean rats exhibited an abrupt increase in V E in response to hypoxia followed by a gradual decline in V E. In contrast, obese rats displayed an initial increase in V E that plateaued during sustained hypoxia. Both L-NAME and 7-NI induced marked decreases in V E during room air and hypoxia compared with control lean rats, whereas V E was virtually unaffected by either agent in obese rats. The present results suggest that the blunted thermoregulatory and ventilatory responses to hypoxia in obese Z rats may be attributed to reduced activity of NOS in the central nervous system.

Sporadic paroxysmal exercise induced dystonia: report of a case and review of the literature.

Sporadic paroxysmal exercise induced dystonia (PEID) is a rare condition. So far only fifteen cases have been reported in the world literature. It is characterised by dystonic posture on prolonged exercise, which gets relieved with rest. In general, these are refractory to medical treatment. We report one such case, along with review of the literature. The lower limbs were spared and only right shoulder was tucked up with the head turning to right side. The duration of exercise necessary to bring out the dystonic posture gradually diminished with time, a feature not reported previously.

Detection of the principal synthetic route indicative impurity in lamotrigine.

An analytical method has been developed for the detection of trace amounts of the principal synthetic route indicative impurity in lamotrigine (3,5-diamino-6-(2,3-dichlorophenyl)-1,2,4-triazine). A sample extract was preconcentrated by normal-phase high-performance liquid chromatography (HPLC) and analysed by subsequent on-line reversed-phase HPLC-thermospray mass spectrometry (TSP-MS). During the sample extraction and concentration step, carried out by semipreparative normal-phase chromatography, the preliminary separation of the impurity from the lamotrigine takes place. The organic solvent (dichloroethane-methanol, 90:10, v/v) is evaporated from the collected fraction and the material is redissolved in a smaller volume of the reversed-phase mobile phase. The collected fraction is then subjected to reversed-phase HPLC-TSP-MS. The influence of an ultrasonic extraction step has been examined. When the method was applied to lamotrigine tablets, a shake flask partitioning step using 1 mg/ml EDTA in water-dichloroethane was used instead of the ultrasonic extraction. Detection limit and recovery measurements showed that the route indicative impurity formed during the synthesis could be detected in the 50-100 ppb (w/w) range.

Clinical trial of pentazocine as analgesic in paediatric cases.

This study was undertaken with the objective of relieving pain which has been poorly understood and managed in peri-operative period specially in children. Here the analgesic efficacy of pentazocine was studied in 50 cases, aged between 5 and 9 years subjected to both major and minor surgeries. No premedication was given to assess the sole analgesic effect of the drug. Pentazocine was given during induction, dose being 0.5 mg/kg body weight intravenously. Subsequently small incremental doses were repeated after every 30-45 minutes during surgery. Satisfactory analgesia was obtained during intra- and postoperative period. No respiratory depression, no change in pulse, BP and no other complications were observed after administration of intravenous pentazocine.

Effect of emetine treatment on subcellular nucleic acid and protein metabolism.

The subcellular RNA and protein metabolism have been studied in emetine-treated rats. Emetine treatment for a period of 10 days reduced the incorporation in vivo of [14C]-leucine into proteins of nuclear fraction of liver. This was accompanied by a reduction in the nuclear protein content. The mitochondrial fraction of heart exhibited an increase in the protein content after emetine treatment. This was, however, not accompanied by an increased rate of incorporation into its protein. On the other hand, the nuclear fraction of heart of emetine-treated rats showed a diminution in the rate of incorporation into its protein without having been reduced in protein content. The mitochondrial and microsomal RNA of liver and the microsomal RNA of heart responded to emetine treatment by showing increased levels. The liver RNase activity was reduced after emetine treatment, while the heart RNase remained independent of the treatment. It has been suggested that both synthesis and breakdown of liver proteins are reduced by emetine treatment. The synthesis of liver nuclear proteins was supposedly affected more than was its breakdown by emetine. The synthesis of rapidly turningover proteins of heart nuclear fraction and the catabolism of slowly turningover proteins of its mitochondrial fraction are thought to be reduced by the emetine treatment.