Efecto de la densidad larvaria y secuencial alimentaria en el cultivo larvario de corvina (Argyrosomus regius Asso, 1801) durante el primer mes de vida

Effect of larval density and feeding sequence on meagre (Argyrosomus regius Asso, 1801) larval rearing during the first month of life. In the present work two comparative studies of the effect of larval density and feeding sequence were performed. For such, two initial larval densities, 50 larvae.l-1 and 100 larvae.l-1 were established. In each density three feeding sequences were tested, applying different combinations of rotifers (Brachionus sp.) and Artemia sp. at different larval ages. After 30dah, standard length, dry weight and final survival were determined. Final survival was affected by initial larval density and feeding sequence. Lower density promotes better growth in dry weight and standard length for all the feeding sequences tested. In addition, feeding sequences affects larval growth and survival. Best result in survival (62,81±4,77%) were obtained with high larval density and T2 feeding sequence.

Reductions in systemic and skeletal muscle blood flow and oxygen delivery limit maximal aerobic capacity in humans

[EN] BACKGROUND: A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (VO2max) in humans. Severe heat stress drastically reduces VO2max, but the mechanisms have never been studied. METHODS AND RESULTS: To determine the main contributing factor that limits VO2max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (+10 degrees C and +1 degrees C). Heat stress reduced VO2max, 2-legged VO2, and time to fatigue by 0.4+/-0.1 L/min (8%), 0.5+/-0.2 L/min (11%), and 2.2+/-0.4 minutes (28%), respectively (all P<0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O2 delivery declined significantly (all 5% to 11%, P<0.05), yet arterial O2 content and leg vascular conductance remained unchanged. Despite increasing leg O2 extraction, leg VO2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. CONCLUSIONS: These results demonstrate that in trained humans, severe heat stress reduces VO2max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O2 delivery, and O2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O2 delivery to locomotive muscle.