ABSTRACT Physiological plasticity of early developmental stages is a key way by which organisms can survive and adapt to environmental change. We investigated developmental plasticity of aspects of the cardio-respiratory physiology of encapsulated embryos of a marine gastropod, Littorina obtusata , surviving exposure to moderate hypoxia ( P O 2 =8 kPa) and compared the development of these survivors with that of individuals that died before hatching. Individuals surviving hypoxia exhibited a slower rate of development and altered ontogeny of cardio-respiratory structure and function compared with normoxic controls ( P O 2 >20 kPa). The onset and development of the larval and adult hearts were delayed in chronological time in hypoxia, but both organs appeared earlier in developmental time and cardiac activity rates were greater. The velum, a transient, ‘larval’ organ thought to play a role in gas exchange, was larger in hypoxia but developed more slowly (in chronological time), and velar cilia-driven, rotational activity was lower. Despite these effects of hypoxia, 38% of individuals survived to hatching. Compared with those embryos that died during development, these surviving embryos had advanced expression of adult structures, i.e. a significantly earlier occurrence and greater activity of their adult heart and larger shells. In contrast, embryos that died retained larval cardio-respiratory features (the velum and larval heart) for longer in chronological time. Surviving embryos came from eggs with significantly higher albumen provisioning than those that died, suggesting an energetic component for advanced development of adult traits.

SUMMARY Hypothermic incubation reduces the ability of the late-stage chicken embryo to mount endothermic heat production. This study investigates whether blood O 2 transport is similarly limited by cooler incubation temperatures. Two populations of chicken embryos were incubated at 38°C and 35°C. At Hamilton–Hamburger (HH) developmental stage 41–42, hypothermic incubation had no significant effect on hematocrit(∼26%) or [Hb] (7 g%). However, in the final stages of incubation (stage 43–44), hypothermic incubation reduced hematocrit from ∼31% at 38°C to ∼27.5% at 35°C. Hypothermic incubation similarly caused a reduced [Hb] from 8.5 g% (38°C) to 6.25 g% (35°C), indicating a reduction in blood O 2 -carrying capacity in embryos. Incubation temperature had a strong effect on blood–O 2 affinity in late development (stage 43–44), with P 50 at 38°C falling significantly from ∼6 kPa in 38°C embyros to ∼4 kPa in 35°C embryos. P O 2 values in chorioallantoic arterial blood at HH 41–42 were 4.3 kPa at pH 7.46 (38°C) and 3.4 kPa at pH 7.39 (35°C). In chorioallantoic venous blood these values were 9.1 kPa at pH 7.34 (38°C) and 8.1 kPa at pH 7.42 (35°C). With further development to HH 43–44, chorioallantoic arterial blood oxygenation fell to 2.4 kPa at pH 7.54 (38°C) and 2.8 kPa at pH 7.52 (35°C). Similarly, P O 2 in chorioallantoic venous blood fell slightly to 7.7 kPa at pH 7.42 (38°C) and 7.4 kPa at pH 7.48 (35°C). Collectively, these data reveal that beyond HH 41–42, 35°C embryos experience retarded hematological development, and the findings that support the observed delayed metabolic response to acute temperature changes.

SUMMARY Chronic exposure to a low incubation temperature clearly slows the development of poikilothemic chicken embryos (or any other poikilotherms), but little is known about the more subtle developmental effects of temperature,especially on physiological regulatory systems. Consequently, two populations of chicken embryos were incubated at 38°C and 35°C. When compared at the same development stage, incubation temperature had no significant impact on embryonic survival or growth. Moreover, the relative timing of major developmental landmarks (e.g. internal pipping), expressed as a percentage of development, was unaffected by temperature. The ability to maintain the rate of oxygen consumption( V̇ O 2 ) during an acute drop in ambient temperature ( T a ) improved from Hamburger–Hamilton (HH) stages 39–40 to 43–44 in the 38°C but not the 35°C populations. Late stage (HH43–44) embryos incubated at 38°C could maintain V̇ O 2 (approximately 27–33 μl g –1 min –1 )during an acute drop in T a to approximately 30°C. However, at the same stage 35°C embryos acutely measured at 38°C were unable to similarly maintain their V̇ O 2 , which fell as soon as T a reached 36°C. Thus, while hypothermic incubation does not affect gross development (other than would be predicted from a simple effect of Q 10 ), there is a significant delay in the relative timing of the onset of thermoregulatory ability induced by hypothermic incubation.