Aquaculture and stress management: a review of probiotic intervention.

To meet the ever-increasing demand for animal protein, aquaculture continuously requires new techniques to increase the production yield. However, with every step towards intensification of aquaculture practices, there is an increase in stress level on the animal as well as on the environment. Feeding practices in aqua farming usually plays an important role, and the addition of various additives to a balanced feed formula to achieve better growth is a common practice among the fish and shrimp culturists. Probiotics, also known as 'bio-friendly agents', such as LAB (Lactobacillus), yeasts and Bacillus sp., can be introduced into the culture environment to control and compete with pathogenic bacteria as well as to promote the growth of the cultured organisms. In addition, probiotics are non-pathogenic and non-toxic micro-organisms, having no undesirable side effects when administered to aquatic organisms. Probiotics are also known to play an important role in developing innate immunity among the fishes, and hence help them to fight against any pathogenic bacterias as well as against environmental stressors. The present review is a brief but informative compilation of the different essential and desirable traits of probiotics, their mode of action and their useful effects on fishes. The review also highlights the role of probiotics in helping the fishes to combat against the different physical, chemical and biological stress.

Aerobic exercise capacity is normal in obesity with or without metabolic syndrome.

BACKGROUND: Obesity might be a cause of limited aerobic exercise capacity. It is often associated with metabolic syndrome (MS) that includes cardiovascular comorbidities as arterial hypertension. Cardiopulmonary exercise testing (CPET) is the gold-standard to assess aerobic capacity and discriminate causes of dyspnea. AIM: To evaluate aerobic capacity in obesity and if MS or hypertensive treatment impacts on the CPET profile. METHODS: CPET of 146 obese patients, whom 33 and 31 were matched for MS and antihypertensive medication, were analyzed. VO2peak (mL/min/Kg) was reported in percentage of predicted value, or, divided by body weight, fat free mass (FFM) or body weight expected for a body mass index of 24 (BMI24). RESULTS: VO2peak (20,8 ± 4,4 mL/min/Kg) was normal when expressed in percentage predicted for obesity (111 ± 22%pred) or divided by FFM and weightBMI24 (33,6 ± 5,6 and 30,6 ± 6,2 respectively). The latter correlated better with maximal work rate (r = 0,7168, p < 0,001). Obese patients showed normal ventilatory efficiency (ventilation to carbon dioxide production slope: 28 ± 4), VO2 to work rate (10,2 ± 1,6 mLO2/Watt) and, slightly elevated heart rate to VO2 slope (4,0 ± 1,1 bpm/mL/min/Kg). Compared to normotensives, hypertensive medicated patients had higher blood pressure at anaerobic threshold (142 ± 23 vs 158 ± 26 mmHg, p = 0,001) but not at maximal exercise (189 ± 31 vs 201 ± 23 mmHg, p = NS), and, had lower actual maximal heart rate (155 ± 23 vs 143 ± 25 bpm, p = 0,03). There was no difference between obese patients with or without MS. CONCLUSION: Obese people with or without MS present with similar and normal aerobic profile related to the excessive body weight. VO2peak divided by weightBMI24 is an easy and clinical meaningful index for obese patients.

Effects of ß2-adrenergic stimulation on exercise capacity in normal subjects.

ß2-Adrenergic receptor agonists are believed to present with ergogenic properties. However, how combined respiratory, cardiovascular and muscular effects of these drugs might affect exercise capacity remain incompletely understood. The effects of salbutamol were investigated in 23 healthy subjects. The study was randomised, placebo-controlled in double-blind and followed a cross-over design. Salbutamol was given at the dose of 10 µg/min in 11 subjects and 20 µg/min iv in the other 12 subjects. Measurements included muscle sympathetic nerve activity (MSNA), ventilatory responses to hyperoxic hypercapnia (7% CO(2) in O(2,) central chemoreflex), isocapnic hypoxia (10% O(2) in N(2), peripheral chemoreflex) and isometric muscle contraction followed by a local circulatory arrest (metaboreflex), cardiopulmonary exercise test (CPET) variables and isokinetic muscle strength. Salbutamol 10 µg/min increased heart rate and blood pressure, while MSNA burst frequency remained unchanged. Peripheral chemosensitivity increased, as evidenced by an increased ventilatory response to hypoxia, but ventilatory responses to hypercapnia or muscle ischaemia remained unchanged. The effects of salbutamol 20 µg/min were similar. Both doses of salbutamol did not affect CPET. Only the higher dose of salbutamol decreased the anaerobic threshold, but this was not associated with a change in VO(2) max. Salbutamol increased the slopes of ventilation as a function of VO(2) (P < 0.05) and VCO(2) (P < 0.001) during CPET. Maximal isokinetic muscle strength was not affected by salbutamol. In conclusion, the acute administration of either low or high dose salbutamol does not affect exercise capacity in normal subjects, in spite of an earlier anaerobic threshold and increased chemosensitivity.

Digoxin increases peripheral chemosensitivity and the ventilatory response to exercise in normal subjects.

1. The contribution of peripheral chemoreceptors to the regulation of ventilation during exercise remains incompletely understood. Digoxin has been reported to increase chemoreflex sensitivity in humans. In the present randomized, cross-over, double-blind study, we tested the hypothesis that this increases the ventilatory response to exercise in normal subjects, as assessed by changes in minute ventilation (V(E)) in response to the rate of CO(2) production (VCO(2)). 2. Minute ventilation, end-tidal PCO(2), pulse oximetric O(2) saturation (S(p)O(2)), heart rate and blood pressure (BP) were measured in 11 healthy young male untrained subjects after intravenous infusion of digoxin (0.01 mg/kg) or placebo during normoxia, isocapnic hypoxia and hyperoxic hypercapnoea. All participants underwent a maximum cardiopulmonary exercise test. 3. During normoxia, digoxin increased systolic BP only. During hypoxia, digoxin increased V(E) compared with placebo (P = 0.009) for the same fall in S(p)O(2) (P = NS). Moreover, no significant effects on ventilation and haemodynamic responses were recorded during hypercapnoea. Digoxin increased the V(E) /VCO(2) slope above the anaerobic threshold from 30.4 +/- 2.9 to 32.8 +/- 3.7 (P < 0.05), but did not affect VO(2max). 4. In conclusion, enhanced peripheral chemosensitivity with digoxin increases the ventilatory response to CO(2) production above the anaerobic threshold, but does not affect exercise capacity in healthy humans.

Decreased ventilatory response to exercise by dopamine-induced inhibition of peripheral chemosensitivity.

The contribution of the peripheral chemoreflex to the ventilatory response to exercise and aerobic exercise capacity remains incompletely understood. Low-dose dopamine has been reported to specifically inhibit the peripheral chemoreceptors. We therefore investigated the effects of intravenous dopamine (3 microg kg(-1)min(-1)) on cardiopulmonary exercise test (CPET) variables in 13 healthy young male subjects. The study was prospective, placebo-controlled, and randomized with more than 24h between placebo and dopamine administrations. During the CPET, dopamine decreased the .V(E)/.V(CO2) output slope (24.61+/-1.84 vs. 23.09+/-1.81, placebo vs. Dopamine respectively, p=0.025), without affecting maximum workload, .V(E) and O(2) uptake. In conclusion, our study reveals that inhibition of peripheral chemoreflex function with dopamine decreases the .V(E)/.V(CO2) slope during dynamic exercise, with no change in aerobic exercise capacity.

Physiological response to the six-minute walk test in pulmonary arterial hypertension.

The 6-min walk test (6MWT) is commonly used to evaluate exercise capacity in patients with pulmonary arterial hypertension (PAH). However, little is known about the corresponding metabolic stress as measured by cardiopulmonary exercise testing. The present study, therefore, measured ventilatory variables and heart rate during the 6MWT and symptom-limited incremental maximal exercise testing in 20 patients with PAH. The distance walked in 6 min was 450+/-22 m (mean+/-se). During the 6MWT, ventilation, O2 consumption, CO2 production and heart rate increased during the first 3-4 min, and then remained stable. As compared with the maximum values measured during the cardiopulmonary exercise test, O2 consumption tended to be higher (14.2+/-0.6 versus 12.9+/-0.7 mL.kg-1.min-1), while maximum ventilation (46+/-3 versus 57+/-4 L.min-1), respiratory quotient (0.90+/-0.02 versus 1.15+/-0.02) and heart rate (119+/-4 versus 135+/-4 beats.min-1) remained lower. In conclusion, patients with pulmonary arterial hypertension exercise at higher aerobic capacity and lower metabolic stress during the 6MWT than during a cardiopulmonary exercise test.

Exercise testing in pulmonary arterial hypertension and in chronic heart failure.

Exercise capacity is reduced in pulmonary arterial hypertension and in chronic left heart failure, but it is not known whether the cardiopulmonary exercise testing profile is different in the two conditions at the same severity of functional limitation. Nineteen patients with pulmonary arterial hypertension and 19 with chronic heart failure underwent a 6-min walk test and symptom-limited maximal incremental cycle ergometry. The patients with pulmonary arterial hypertension and chronic heart failure did not differ in New York Heart Association Functional Class (mean +/- SEM 2.8 +/- 0.1 versus 2.8 +/- 0.2), 6-min walking distance (395 +/- 30 versus 419 +/- 20 m), peak work-rate, oxygen consumption, ventilation and cardiac frequency. However, patients with pulmonary arterial hypertension exhibited higher dyspnoea scores (5.8 +/- 0.6 versus 3.8 +/- 0.5) higher ventilatory equivalents for carbon dioxide (58 +/- 3 versus 44 +/- 3 at the anaerobic threshold) and lower peak oxygen pulse (5.9 +/- 0.4 versus 8.7 +/- 0.5 mL x beat(-1), or 53 +/- 4 versus 64 +/- 4% of the predicted value). It is concluded that the cardiopulmonary exercise testing profile in pulmonary arterial hypertension differs from that in chronic heart failure by showing more dyspnoea at comparable work-rates, related to greater reductions in ventilatory efficiency and stroke volume.