This study investigated the relationship between depressive symptom response during tryptophan (TRP) depletion and a functional polymorphism of the promoter region of the serotonin (5-HT) transporter gene (SLC6A4). 1 Forty-three subjects in remission from a major depressive episode who underwent TRP depletion were genotyped. DNA was extracted from blood lymphocytes or from cheek cells. 2 The two common alleles are designated long (l) and short (s). Depressive symptoms were measured with the 25-item Hamilton Depression Rating Scale (HDRS). 3 There was a significant association between the l homozygous genotype and the depressive response to TRP depletion, with a significant main effect of time (F = 8.763, df = 3, 38, P = Ͻ0.001), and time × l homozygous allele interaction (F = 3.676, df = 3, 38, P = 0.02). Individuals whose genotype predicted increased 5-HT transporter activity may be more susceptible to depressive changes in response to transient 5-HT perturbations. The use of endophenotypic markers for affective disorders such as the mood response to TRP depletion may facilitate studies of complex genetic traits such as depression by decreasing its heterogeneity. Molecular Psychiatry ( Although the TRP-free amino acid drink utilized in this project rapidly and consistently depletes plasma levels of this 5-HT precursor, 4,5 reduces 5-HT synthesis, 6,7 and lowers cerebrospinal fluid levels of the 5-HT metabolite 5HIAA, 8,9 the behavioral responses observed in subjects with similar clinical and treatment history vary dramatically. Delgado et al 10 reported that individuals recently achieving remission from major depression during treatment with a serotonin reuptake inhibitor experienced a transient return of depressive symptoms, but not all subjects experienced a similarly dramatic response. Others have replicated these findings, also noticing differing rates of mood response. 11,12 Benkelfat et al 13 and Klaassen et al 14 showed that healthy subjects with a family history of affective disorders were more likely than healthy controls to experience mood changes in response to TRP depletion. Although the effect for group was statistically significant, the degree of mood response within each group was also varied. Smith et al 15 and Moreno et al 5 reported that medication-free remitted depressed patients also experience transient depressive changes in response to TRP depletion. In these studies, the response was also varied with about two thirds of the subjects accounting for most of the mood changes observed. Furthermore, Leyton et al, 16 while studying a similar population, reported that only a small portion of their subjects experienced mood response during TRP depletion. An important and unanswered question remains: What determines which subjects will experience a mood response to TRP depletion and which ones will not?A number of potential explanations have been proposed including the possibility that individuals having depressive mood responses to TRP depletion are doing so because their brain 5-HT has depleted ...
Critical power (CP) delineates the heavy and severe exercise intensity domains, and sustained work rates above CP result in an inexorable progression of oxygen uptake to a maximal value and, subsequently, the limit of exercise tolerance. The finite work capacity above CP, W′, is defined by the curvature constant of the power-duration relationship. Heavy or severe exercise in a hot environment generates additional challenges related to the rise in body core temperature (Tc) that may impact CP and W′. The purpose of this study was to determine the effect of elevated Tc on CP and W′. CP and W′ were estimated by end-test power (EP; mean of final 30s) and work above end-test power (WEP), respectively, from 3-min "all-out" tests performed on a cycle ergometer. Volunteers (n = 8, 4 female) performed the 3-min tests during a familiarization visit and two experimental visits (Thermoneutral vs Hot, randomized crossover design). Before experimental 3-min tests, subjects were immersed in water (Thermoneutral: 36°C for 30 min; Hot: 40.5°C until Tc was ≥ 38.5°C). Mean Tc was significantly greater in Hot compared to Thermoneutral (38.5±0.0°C vs. 37.4±0.2°C; mean±SD, P<0.01). All 3-min tests were performed in an environmental chamber (Thermoneutral: 18°C, 45% RH; Hot: 38°C, 40% RH). EP was similar between Thermoneutral (239 ± 57W) and Hot (234 ± 66W; P = 0.55). WEP was similar between Thermoneutral (10.9 ± 3.0 kJ) and Hot (9.3 ± 3.6; P = 0.19). These results suggest that elevated Tc has no significant impact on EP or WEP.
INTRODUCTION Hypertension remains among the most prevalent cardiovascular disease risk factors world‐wide. Aerobic exercise training is the current gold‐standard non‐pharmacological intervention for lowering blood pressure, yet passive heat therapy is an effective alternative means of reducing blood pressure and improving cardiovascular health for individuals that are unable or unwilling to engage in traditional exercise training. However, the effectiveness of heat therapy versus exercise training has not been compared in adults with untreated hypertension. Therefore, the purpose of this ongoing clinical trial is to compare the effectiveness of hot water immersion (HWI) versus aerobic exercise training (EX) in lowering blood pressure and improving cardiovascular function. Data presented are preliminary (mid‐point) comparisons following 15 sessions of either HWI or EX. HYPOTHESIS It was hypothesized that hot water immersion would be more effective than traditional aerobic exercise training in reducing blood pressure and improving cardiovascular function in adults with untreated hypertension. METHODS Prior to randomization, all subjects (n=6, 1F) completed resting vascular function testing, including measurements of blood pressure (automated sphygmomanometer), cardiac output (acetylene wash‐in method), and carotid‐femoral pulse wave velocity (PWV). Systemic vascular conductance (SVC) was calculated as cardiac output/mean arterial pressure (MAP). Following pre‐testing (PRE), subjects were randomized into either HWI (n=4, 1F) or EX (n=2). During HWI, subjects were immersed to the level of the sternum in 40.5°C water for 45 minutes. EX consisted of upright cycling at 60% of heart rate reserve (HRR) for 40 min, with 5 min each for warm‐up and cool‐down at 30% of HRR. Participants completed 15 sessions of either HWI or EX prior to mid‐point (MID) testing. Combined data are presented as the change from PRE as mean ± SD and were analyzed using a paired‐samples t test. Group mean data for HWI versus EX are presented as the change from PRE as means ± SD and were analyzed using an unpaired two sample t‐test. RESULTS Following 15 sessions of either HWI or EX, systolic blood pressure tended to be reduced (‐5±4 mmHg; p=0.10). The change in systolic blood pressure (SBP) was directionally similar between HWI and EX (∆ from PRE, HWI vs. EX; ‐3±5 vs. ‐7±7 mmHg; p=0.59), whereas the change in diastolic blood pressure (DBP) was divergent between HWI and EX (‐3±8 vs. +5±10 mmHg; p=0.43). Accordingly, changes in MAP were disparate between HWI and EX (‐3±7 vs. +2±9 mmHg; p=0.61). Cardiac output was similar between HWI and EX (‐0.09±0.71 vs. ‐0.76±1.07 L/min; p=0.53), as were changes in SVC (‐0.3±6.6 vs. ‐7.6±15.9 mL•min‐1•mmHg‐1; p=0.63). Overall, PWV was reduced by both interventions (‐0.6±0.3 m/s; p=0.01) and changes in PWV were similar between HWI and EX (‐0.6±0.4 vs. ‐0.5±0.4 m/s; p=0.72). CONCLUSIONS Preliminary data from this ongoing clinical trial suggest both hot water immersion and exercise are similarly effective in lowering s...
One of the physiological changes following moderate intensity aerobic exercise is a transient reduction in blood pressure, termed post‐exercise hypotension (PEH), which is exercise intensity and duration dependent. This short‐term reduction in blood pressure is dependent upon skeletal muscle histamine production and release, which causes increased conductance via local activation of histamine H1 and H2 receptors. PEH is abolished when antihistamines are consumed prior to exercise. Additionally, histamine‐receptor antagonism during a single bout of exercise modifies expression of the transcriptome related to inflammation, angiogenesis, and metabolism. Due to the large role histamine plays in post‐exercise recovery, the scope of histamine receptor activation in adaptations to aerobic exercise training needs to be determined. Therefore, the purpose of this study was to examine histamine’s role in promoting adaptation to exercise. It is hypothesized that blocking histamine’s actions will attenuate adaptations that occur from aerobic exercise training. 16 young, healthy, recreationally active individuals (5M, 11F) volunteered for this study. All volunteers completed 6 weeks of exercise training (3–4 times a week), for a total of 21 exercise sessions. Exercise training combined 18 sessions of continuous exercise (1 hour at 60% VO2peak) and 3 sessions of high intensity interval training (30 min between 30 and 90% VO2peak). Volunteers were randomly placed into a placebo or histamine antagonism (540 mg fexofenadine; a H1‐receptor antagonist, and 300 mg of ranitidine; a H2‐receptor antagonist) group, and consumed medication 1 hour prior to each exercise session. Data was collected 4 times throughout the study with pre and post exercise training measures, as well as after every 2 weeks of exercise training. Measurements of VO2peak and cycle ergometry work rate were obtained. Exercise training resulted in increased absolute VO2peak of all subjects (9.4±1.5%; P<0.01); however, no difference was seen between groups (10.9±1.8% control vs 7.9±2.4% blockade; P=0.35). Additionally, exercise training resulted in increased cycle ergometry work rate of all subjects (11.2±1.6%; P<0.01); however, there was a trend for blunted improvement with blockade (7.7±2.4%) vs control (14.6±2.8%; P=0.08). In conclusion, blocking histamine’s actions had no effect on VO2 adaptations to exercise training. Additional information about factors related to O2 delivery and consumption are needed to understand the relationship between histamine and cardiovascular adaptation to exercise training. Support or Funding Information Support provided by: The Eugene & Clarissa Evonuk Memorial Graduate Fellowship
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