Bryce N. Balmain

The impact of an experimentally induced increase in arterial blood pressure on left ventricular twist mechanics

What is the central question of this study? Increases in blood pressure elicited by isometric hand‐grip exercise (IHG) have been shown to impair ventricular twist mechanics. However, the utility of the IHG model is confounded by a concurrent increase in heart rate, which independently influences ventricular mechanics. What is the main finding and its importance? We show that a period of post‐IHG circulatory occlusion isolates the effect of an arterial blood pressure increase from heart rate and magnifies the impairment of left ventricular twist when compared with IHG alone. A protocol using IHG followed by brief circulatory occlusion may serve as a useful tool in examining and understanding the relationships between afterload and cardiac function in various disease states.

Altered thermoregulatory responses in heart failure patients exercising in the heat

Heart failure (HF) patients appear to exhibit impaired thermoregulatory capacity during passive heating, as evidenced by diminished vascular conductance. Although some preliminary studies have described the thermoregulatory response to passive heating in HF, responses during exercise in the heat remain to be described. Therefore, the aim of this study was to compare thermoregulatory responses in HF and controls (CON) during exercise in the heat. Ten HF (NYHA classes I–II) and eight CON were included. Core temperature (Tc), skin temperature (Tsk), and cutaneous vascular conductance (CVC) were assessed at rest and during 1 h of exercise at 60% of maximal oxygen uptake. Metabolic heat production (Hprod) and the evaporative requirements for heat balance (Ereq) were also calculated. Whole‐body sweat rate 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) was lower (P < 0.05) in HF compared to CON. Additionally, whole‐body sweat rate (HF: 0.36 ± 0.15; CON: 0.81 ± 0.39 L/h) was lower (P = 0.02) in HF compared to CON. Patients with HF appear to be 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.

Heart Failure and Thermoregulatory Control: Can Patients With Heart Failure Handle the Heat?

Upon heat exposure, the thermoregulatory system evokes reflex increases in sweating and skin blood flow responses to facilitate heat dissipation and maintain heat balance to prevent the continuing rise in core temperature. These heat dissipating responses are mediated primarily by autonomic and cardiovascular adjustments; which, if attenuated, may compromise thermoregulatory control. In patients with heart failure (HF), the neurohumoral and cardiovascular dysfunction that underpins this condition may potentially impair thermoregulatory responses and, consequently, place these patients at a greater risk of heat-related illness. The aim of this review is to describe thermoregulatory mechanisms and the factors that may increase the risk of heat-related illness in patients with HF. An understanding of the mechanisms responsible for impaired thermoregulatory control in HF patients is of particular importance, given the current and projected increase in frequency and intensity of heat waves, as well as the promotion of regular exercise as a therapeutic modality. Furthermore, novel therapeutic strategies that may improve thermoregulatory control in HF, and the clinical relevance of this work in this population will be discussed.

Thermoeffector Responses at a Fixed Rate of Heat Production in Heart Failure Patients

PurposeHeart failure (HF) patients seem to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq), and/or body size is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF patients and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod and therefore Ereq in a 30°C environment. MethodsRectal temperature, local sweat rate, and cutaneous vascular conductance were measured throughout 60 min of cycle ergometry. Whole-body sweat rate was estimated from pre–post nude body weight corrected for fluid intake. ResultsDespite exercising at the same rate of Hprod (HF, 338 ± 43 W; CON, 323 ± 31 W; P = 0.25), the rise in rectal temperature was greater (P < 0.01) in HF (0.81°C ± 0.16°C) than in CON (0.49°C ± 0.27°C). In keeping with a similar Ereq (HF, 285 ± 40 W; CON, 274 ± 28 W; P = 0.35), no differences in whole-body sweat rate (HF, 0.45 ± 0.11 L·h−1; CON, 0.41 ± 0.07 L·h−1; P = 0.38) or local sweat rate (HF, 0.96 ± 0.17 mg·cm−2·min−1; CON, 0.79 ± 0.15 mg·cm−2·min−1; P = 0.50) were observed between groups. However, the rise in cutaneous vascular conductance was lower in HF than in CON (HF, 0.83 ± 0.42 au·mm Hg−1; CON, 2.10 ± 0.79 au·mm Hg−1; P < 0.01). In addition, the cumulative body heat storage estimated from partitional calorimetry was similar between groups (HF, 154 ± 106 kJ; CON, 196 ± 174 kJ; P = 0.44). ConclusionsCollectively, these findings demonstrate that HF patients exhibit a blunted skin blood flow response, but no differences in sweating. Given that HF patients had similar body heat storage to that of CON 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.

Relating exercise-induced desaturation and gas-exchange in pulmonary artery hypertension

We measured pulmonary gas exchange during six minute walk test (6MWT) in patients with idiopathic (IPAH) and congenital heart disease-related pulmonary hypertension (CHDPH), and determined the relationship between the degree of desaturation and changes in minute ventilation to carbon dioxide production V˙EV˙CO2 and end-tidal partial pressure for carbon dioxide (PetCO2) in both groups. Fifty-two patients (IPAH, n = 28; CHDPH, n = 24) completed 6MWT with simultaneous pulmonary gas exchange. Whilst no significant difference in six minute walk distance was observed between groups (IPAH: 529 ± 89; CHDPH: 476 ± 119 m, p = 0.10), oxygen uptake, carbon dioxide production, and minute ventilation were higher in IPAH than CHDPH (p < 0.01). In addition, CHDPH desaturated to a greater extent than IPAH with a lower post-6MWT SPO2 (IPAH: 92.3 ± 7.9; CHDPH: 73.3 ± 14.9%, p < 0.01). The change in SpO2 correlated to the change in V˙E/V˙CO2 (r=-0.44, p = 0.02) and PetCO2 (r = 0.49, p < 0.01) for CHDPH, but not IPAH. The exercise-induced hypoxic stimulus during 6MWT in CHDPH may be associated with an enhanced ventilatory response.

Aging and Thermoregulatory Control: The Clinical Implications of Exercising under Heat Stress in Older Individuals

Climate change is predicted to bring about a greater variability in weather patterns with an increase in extreme weather events such as sustained heat waves. This change may have a direct impact on population health since heat waves can exceed the physiological limit of compensability of vulnerable individuals. Indeed, many clinical reports suggest that individuals over the age of 60 years are consistently the most vulnerable, experiencing significantly greater adverse heat-related health outcomes than any other age cohort during environmental heat exposure. There is now evidence that aging is associated with an attenuated physiological ability to dissipate heat and that the risk of heat-related illness in these individuals is elevated, particularly when performing physical activity in the heat. The purpose of this review is to discuss mechanisms of thermoregulatory control and the factors that may increase the risk of heat-related illness in older individuals. An understanding of the mechanisms responsible for impaired thermoregulation in this population is of particular importance, given the current and projected increase in frequency and intensity of heat waves, as well as the promotion of regular exercise as a means of improving health-related quality of life and morbidity and mortality. As such, the clinical implications of this work in this population will be discussed.

Folic acid supplementation improves vascular endothelial function, yet not skin blood flow during exercise in the heat, in patients with heart failure

Heart failure (HF) patients are susceptible to heat strain during exercise, secondary to blunted skin blood flow (SkBF) responses, which may be explained by impaired nitric oxide (NO)-dependent vasodilation. Folic acid improves vascular endothelial function and SkBF through NO-dependent mechanisms in healthy older individuals and patients with cardiovascular disease. We examined the effect of folic acid supplementation (5 mg/day for 6 wk) on vascular function [brachial artery flow-mediated dilation (FMD)] and SkBF responses [cutaneous vascular conductance (CVC)] during 60 min of exercise at a fixed metabolic heat production (300 ẆHprod) in a 30°C environment in 10 patients with HF (New York Heart Association Class I-II) and 10 healthy controls (CON). Serum folic acid concentration increased in HF [preintervention (pre): 1.4 ± 0.2; postintervention (post): 8.9 ± 6.7 ng/ml, P = 0.01] and CON (pre: 1.3 ± 0.6; post: 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 heat production for exercise was similar between groups (HF: 60 ± 13; CON: 65 ± 20 external workload, 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 postintervention measurement intervals ( 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 metabolic heat production in a warm environment.