Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

Abstract

Combined heat acclimation (AC) and exercise training (EX) enhance exercise performance in the heat while meeting thermoregulatory demands. We tested the hypothesis that different stress-specific adaptations evoked by each stressor individually trigger similar cardiac alterations, but when combined, overriding/trade-off interactions take place. We used echocardiography, isolated cardiomyocyte imaging and cDNA microarray techniques to assay in situ cardiac performance, excitationcontraction (EC) coupling features, and transcriptional programs associated with cardiac contractility. Rat groups studied were controls (sedentary 24°C); AC (sedentary, 34°C, 1 mo); normothermic EX (treadmill at 24°C, 1 mo); and heat-acclimated, exercise-trained (EXAC; treadmill at 34°C, 1 mo). Prolonged heat exposure decreased heart rate and contractile velocity and increased end ventricular diastolic diameter. Compared with controls, AC/EXAC cardiomyocytes demonstrated lower L-type Ca 2ϩ current (ICaL) amplitude, higher Ca 2ϩ transient (Ca 2ϩ T), and a greater Ca 2ϩ T-to-ICaL ratio; EX alone enhanced I CaL and Ca 2ϩ T, whereas aerobic training in general induced cardiac hypertrophy and action potential elongation in EX/ EXAC animals. At the genomic level, the transcriptome profile indicated that the interaction between AC and EX yields an EXACspecific molecular program. Genes affected by chronic heat were linked with the EC coupling cascade, whereas aerobic training upregulated genes involved with Ca 2ϩ turnover via an adrenergic/ metabolic-driven positive inotropic response. In the EXAC cardiac phenotype, the impact of chronic heat overrides that of EX on EC coupling components and heart rate, whereas EX regulates cardiac morphometry. We suggest that concerted adjustments induced by AC and EX lead to enhanced metabolic and mechanical performance of the EXAC heart. echocardiography; isolated cardiomyocytes; Ca 2ϩ signaling; genomic responses HEAT ACCLIMATION (AC) and exercise training (EX) are powerful stressors, causing structural cardiac remodeling and improving mechanical performance. Each stressor has its own adaptive requirements, e.g., increased peripheral blood flow to enhance heat dissipation, required for AC, or increased muscle blood flow to augment the oxygen supply and muscle power output needed during bouts of exercise. Evidence derived from isolated rat heart preparations prompted the hypothesis that different stress-specific adaptive signaling mechanisms trigger the similar cardiac alterations evoked by each stressor alone. Upon AC, an increase in left cardiac ventricular compliance and systolic pressure with a concomitant decrease in oxygen consumption suggests enhanced cardiac efficiency (25-26). At the cellular level, greater Ca 2ϩ transient amplitude compensates for decreased myofilament Ca 2ϩ responsiveness and plays a major role in greater force development (4). Myosin isoform redistribution from the predominantly fast myosin isoform (V1) to slow myosin isoform (V3) predominance and the altered expression of Ca 2ϩ r...

Two years of combined high-intensity physical training and heat acclimatization affect lymphocyte and serum HSP70 in purebred military working dogs

“…Thus the results of the second and third PPTs, conducted at the end of the summer when ambient temperatures peak, specifically reflect the impact of heat acclimation superimposed on exercise training. Similar interpretations have been made in studies of heat acclimation of human subjects (22,25,26,33).…”

Heat Acclimation, Epigenetics, and Cytoprotection Memory

“…11) and taken together suggest that in sedentary acclimated animals increased cardiac compliance is a physiological/biochemical cardiac adjustment to increase stroke volume (111). Active acclimation, in contrast, induced cardiac hypertrophy (92,111).…”

“…The weighted adaptations required to cope with the dual stress have rarely been dissected in an integrative manner. Recent data on cardiac and skeletal muscle (110,111) performance in animals subjected to combined heat acclimation/exercise training versus acclimation to each of these stressors alone allows assessment of the contribution of each stressor to the cross-adapted phenotype.…”

“…11) and taken together suggest that in sedentary acclimated animals increased cardiac compliance is a physiological/biochemical cardiac adjustment to increase stroke volume (111). Active acclimation, in contrast, induced cardiac hypertrophy (92,111). Decreased end systolic diameter with no change in end diastolic diameter, imply increased stroke volume in these hearts due to the increased contractile response; the outcome of increased muscle mass (111) rather than enhanced compliance.…”

“…The genes encoding membrane and cytosolic components associated with membrane potential, Ca 2+ trafficking and turnover are acclimatory targets (34,111).…”