Table 2.
Possible molecular modifications responsible for the phenotypic adaptations of heat acclimation.
| Heat Acclimation Adaptation | Molecular Modification | Evidence Source |
|---|---|---|
| CORE TEMPERATURE | ||
| Lower resting core temp | Altered genes related to metabolic efficiency, | rat gene studies (31:211–12) |
| Altered mitochondrial biogenesis | reptiles (31:213) | |
| Hypothalamic neurogenesis and cell type | rat brain (31:205–8) | |
| Altered norepinephrine/angiotensin II receptor | ||
| densities and sensitivity | rats (31:206) | |
| Lowered CNS thresholds | Genes encoding ion channels, ion pumps, | rat gene studies (31:208) |
| and hypothalamic receptors | rats (31:206) | |
| Increased heat loss sensitivity | Genes encoding hormone/transmitter receptors | rat gene studies (31:205) |
| BLOOD FLOW RESPONSE | ||
| Lower vasodilatory threshold | Altered hypothalamic CNS thresholds | rats (31:205–208) |
| Increased vasodilatory sensitivity | Attenuated adrenergic response | rats (31:203) |
| Altered baroreceptor function | rats (32:437) | |
| Altered nitric oxide receptors | rats (31:216) | |
| Vascular remodeling | humans (31:203) | |
| VEGF up-regulation | rats (31:212) | |
| Increased splanchnic blood flow | Less vasoconstriction related to increased nitric oxide | rats (31:203) |
| and reduced adrenergic response | ||
| EVAPORATIVE COOLING RESPONSE | ||
| Lower saliva production threshold | CNS effects | rats (31:205–208) |
| Increased sweating sensitivity | Sweat gland receptor sensitivity | human sweat glands (31:203) |
| Reduced evaporative electrolyte loss | Altered ion transport and fluid conservation | rats (31:214) |
| ALTERED BODY FLUIDS | ||
| Increased plasma volume | Altered aquaporine genes | rats (31:212) |
| Plasma volume conservation | Maintain intravascular protein mass | rats, humans (31:214–215) |
| LOWER HEART RATE | ||
| Altered sympathetic response | Reduced autonomic drive | rats (31:214) |
| Intrinsic changes in cardiac pacer cells | Altered Ca2+ transport | rats (31:217) |
| Increased myocardial distensibility | Cardiac remodeling | rats (31:216–217) |
| Increased plasma volume | Maintain intravascular protein mass | rats, humans (31:214–215) |
| GREATER MUSCULAR ENDURANCE | ||
| Attenuated drop in power | Intrinsic signaling adjustment | rats (31:219) |
| Altered lipid metabolism | rats (31:219) | |
| THERMOTOLERANCE AND CRYOPROTECTION | ||
| Increased critical body temp | HSP pathway upregulation | rats, mice, humans (31:208–209) |
| Increased anti-oxidative pathways | ROS scavenger genes | rat gene, mice (31:208,213) |
| Increased anti-apoptosis pathways | Bcl-xL and pro-apoptotic death promoter Bad | rat heart cells (31:208,213) |
| Increased anti-inflammatory pathways | HSP-induced resistance to TNF-α and IL-1 | rodents, tumor cells (32:435) |
| Decreased inflammatory responses | TNF-α and IL-1 | human macrophages (32:435) |
| Activate cellular immune responses | Formation of specific immune complexes | human monocytes (32:435) |
| Increased resistance to ischemic damage | HSP and HIF effects on brain and heart | nematodes, rats (31:211) |
| Increased epithelial integrity | HSP effect on intestinal permeability | humans, human cells (32:439) |
References where a discussion of the evidence for the molecular adaptation listed in column 2, are shown in the last column as (reference number: page numbers).