This thesis examined thermoregulatory responses in heart failure (HF) patients during exercise at a fixed relative intensity, and at an intensity that elicited a fixed rate of metabolic heat production (Hprod) in a warm environment (30°C). Additionally, the efficacy of a chronic, high-dose (5mg/d for 6wk) pharmacological intervention (folic acid supplementation) as a strategy for improving skin blood flow (SkBF) responses and thus, thermoregulatory control in these patients during exercise was assessed. The findings of three experiments conducted to achieve these aims are presented in this thesis. Experiment #1 was designed to compare thermoregulatory responses in HF and controls (CON) during exercise in the heat. Ten HF (New York Heart Association [NYHA] class I-II), and eight CON were included in the study. Core temperature (Tc), skin temperature (Tsk), and cutaneous vascular conductance (CVC – and index of SkBF) were assessed at rest and during one hour of cycling exercise at 60% of maximal oxygen uptake. Hprod and the evaporative requirements for heat balance (Ereq) were also calculated. Whole-body sweat rate (WBSR) was determined from pre-post nude body mass corrected for fluid intake. While Hprod (HF: 3.9 ± 0.9; CON: 6.4 ± 1.5 W/kg) and Ereq (HF: 3.3 ± 0.9; CON: 5.6 ± 1.4 W/kg) were lower (p < 0.01) for HF compared to CON, both groups demonstrated a similar rise in Tc (HF: 0.9 ± 0.4; CON: 1.0 ± 0.3°C). Despite this similar rise in Tc, Tsk (HF: 1.6 ± 0.7; CON: 2.7 ± 1.2°C), and the elevation in CVC (HF: 1.4 ± 1.0; CON: 3.0 ± 1.2 au/mmHg) were lower (p < 0.05) in HF compared to CON. Additionally, WBSR (HF: 0.36 ± 0.15; CON: 0.81 ± 0.39 L/h) was lower (p = 0.02) in HF compared to CON; however, was similar when corrected for differences in Ereq (p = 0.83). Collectively, these data suggest that patients with HF maybe limited in their ability to manage a thermal load and distribute heat content to the body surface (i.e., skin), secondary to impaired circulation to the periphery. Experiment #2 was designed to examine thermoregulatory responses in HF and CON during exercise at a fixed rate of Hprod, and therefore Ereq, in a 30°C environment. A total of 20 men; 10 HF and 10 CON similar in body size, were included in the study. Rectal temperature (Trec), local sweat rate (LSR), and CVC were measured throughout 60-min of cycle ergometry. WBSR was estimated from pre-post nude body weight corrected for fluid intake. Despite exercising at the same rate of Hprod (HF: 338 ± 43; CON: 323 ± 31 W, p = 0.25), the rise in Trec was greater (p < 0.01) in HF (0.81 ± 0.16°C) than CON (0.49 ± 0.27°C). In keeping with a similar Ereq (HF: 285 ± 40; CON: 274 ± 28 W, p = 0.35), no differences in WBSR (HF: 0.45 ± 0.11; CON: 0.41 ± 0.07 L/h, p = 0.38) or LSR (HF: 0.96 ± 0.17; CON: 0.79 ± 0.15 mg/cm2 /min, p = 0.50) were observed between groups. However, the rise in CVC was lower in HF than CON (HF: 0.83 ± 0.42; CON: 2.10 ± 0.79 au/mmHg, p < 0.01). Additionally, the cumulative body heat storage estimated from partitional calorimetry was similar between groups (HF: 154 ± 106; CON: 196 ± 174 kJ, p = 0.44). Collectively, these findings demonstrate that HF patients exhibit a blunted SkBF response, but no differences in sweating. Given that HF had similar body heat storage to controls at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery. In light of the findings of Experiments #1 and #2, Experiment #3 was subsequently designed to examined the effect of folic acid supplementation (5mg/d for 6wk) on vascular function (brachial artery flow-mediated dilation [FMD]), and SkBF responses (CVC) during 60-min of exercise at a fixed Hprod (300 W) in a 30°C environment in 10 HF (NYHA class I-II) patients and 10 CON. Serum folic acid concentration increased in HF (pre-intervention: 1.4 ± 0.2; post-intervention: 8.9 ± 6.7 ng/ml, p = 0.01) and CON (pre-intervention: 1.3 ± 0.6; post-intervention: 5.2 ± 4.9 ng/ml, p = 0.03). FMD improved by 2.1 ± 1.3% in HF (p < 0.01), but no change was observed in CON postintervention (p = 0.20). During exercise, the external workload performed on the cycle ergometer to attain the fixed level of Hprod for exercise was similar between groups (HF: 60 ± 13; CON: 65 ± 20 W, p = 0.52). Increases in CVC during exercise were similar in HF (pre: 0.89 ± 0.43; post: 0.83 ± 0.45 au/mmHg, p = 0.80) and CON (pre: 2.01 ± 0.79; post: 2.03 ± 0.72 au/mmHg, p = 0.73), although the values were consistently lower in HF for both pre- and post-intervention measurement intervals (p < 0.05). Furthermore, mean arterial pressure was similar in HF (pre: 98 ± 5; post: 94 ± 5 mmHg, p = 0.53) and CON (pre: 102 ± 3; post: 100 ± 3 mmHg, p = 0.65), and no differences were observed between groups during both exercise trials (all p > 0.05). These findings demonstrate that folic acid improves vascular endothelial function in patients with HF, but does not enhance SkBF during exercise at a fixed Hprod in a warm environment. The work presented in this thesis serves to expand our current understanding of the mechanisms responsible for impaired thermoregulatory control, particularly during exercise in the heat, in patients with HF. Furthermore, whilst folic acid did not serve to improve thermoregulatory SkBF during exercise in HF, folic acid improved vascular endothelial function to a greater extent in HF than CON. These data indicate that while folic acid does not alleviate the development of thermal strain during exercise in HF, its utility as a viable treatment option for reducing and/or preventing disease-related changes in vascular endothelial function in these patients warrants further investigation.