Abstract
The study objectives were to test the hypothesis that heat stress (HS) during gestational development alters postnatal growth, body composition, and biological response to HS conditions in pigs. To investigate this, 14 first parity crossbred gilts were exposed to one of four environmental treatments (TNTN, TNHS, HSTN, or HSHS) during gestation. TNTN and HSHS dams were exposed to thermal neutral (TN, cyclical 18–22°C) or HS conditions (cyclical 28–34°C) during the entire gestation, respectively. Dams assigned to HSTN and TNHS treatments were heat-stressed for the first or second half of gestation, respectively. Postnatal offspring were exposed to one of two thermal environments for an acute (24 h) or chronic (five weeks) duration in either constant TN (21°C) or HS (35°C) environment. Exposure to chronic HS during their growth phase resulted in decreased longissimus dorsi cross-sectional area (LDA) in offspring from HSHS and HSTN treated dams whereas LDA was larger in offspring from dams in TNTN and TNHS conditions. Irrespective of HS during prepubertal postnatal growth, pigs from dams that experienced HS during the first half of gestation (HSHS and HSTN) had increased (13.9%) subcutaneous fat thickness compared to pigs from dams exposed to TN conditions during the first half of gestation. This metabolic repartitioning towards increased fat deposition in pigs from dams heat-stressed during the first half of gestation was accompanied by elevated blood insulin concentrations (33%; P = 0.01). Together, these results demonstrate HS during the first half of gestation altered metabolic and body composition parameters during future development and in biological responses to a subsequent HS challenge.
Highlights
Heat stress (HS) experienced in utero and during early development alters growth, behavior, learning capacity, body temperature and metabolic function that extend into postgestational life [1,2,3,4]
A gestational by postnatal treatment interaction was detected in skin temperature (P = 0.05, data not shown) whereby gestational treatments exposed to HS during the second half of gestation (TNHS and HSHS) had higher skin temperature (0.5uC) under HS conditions but lower skin temperature under TN conditions (0.3uC) compared to HSTN and TNTN gestational treatments
Heat stress experienced during fetal development can result in physiological anomalies that extend into post-gestational life [1,2,3]
Summary
Heat stress (HS) experienced in utero and during early development alters growth, behavior, learning capacity, body temperature and metabolic function that extend into postgestational life [1,2,3,4]. The mechanisms responsible for HS induced alterations in body composition are not completely understood, it may be partially explained by our recent finding that basal insulin increased in a variety of HS models [15] including pigs [16]. It was recently reported in a rodent model that HS stimulates insulin signaling in skeletal muscle [17]. The increase in insulin (a potent anabolic signal) occurs despite the marked reduction in feed intake and hyper-catabolic hormonal milieu that dominates during HS [1,15]
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