Acute lower‐limb heating improves exercise performance in individuals with heart failure with reduced ejection fraction

Introduction

Exercise‐based cardiac rehabilitation in individuals with heart failure with reduced ejection fraction (HFrEF) elicits clinically meaningful improvements in exercise capacity and quality of life while reducing hospital readmissions. ¹ Training dose is an important determinant of the response to cardiac rehabilitation, where both the volume and intensity of exercise performed are critical to the magnitude of adaptation. ² Achieving more work (intensity, or duration) within a given session likely leads to greater adaptive responses and may improve clinical outcomes following exercise‐based rehabilitation. ³ Ergogenic aids that facilitate an ability to perform more work during each rehabilitation session may therefore be of clinical importance. An acute bout of passive heating increases core, skin and tissue temperatures, augmenting blood flow and shear stress and subsequent oxygen delivery. ⁴ Therefore, we aimed to assess whether acute lower‐limb heating increases femoral artery blood flow and lower‐limb tissue oxygenation, that translates to increased post‐heating exercise performance in individuals with HFrEF.

Methods

Twenty‐two adults aged 50–80 years with a diagnosis of HFrEF volunteered and provided written informed consent for this double‐blind randomized crossover trial (HREC/2020/QPCH/66725). All participants were medically stable with no exacerbations within 3 months of participation. All testing was conducted at Griffith University, Gold Coast, Australia, or The Prince Charles Hospital, Brisbane, Australia.

Individuals who consented to participate completed an incremental shuttle walk test (ISWT) and were familiarized with the endurance shuttle walk test (ESWT). Walk speed of the ESWT was determined as 85% of the final velocity achieved in the ISWT. On separate days, participants completed two randomized 45‐min lower‐limb (knee‐down) immersion protocols in a circulated water bath maintained to either 42°C (hot) or 30°C (control). Participants then completed the ESWT in accordance with standardized procedures ⁵ within 5 min of being removed from the lower‐limb immersion bath. Briefly, participants walked back‐and‐forth along a 10‐m track (marked with cones) at the pre‐determined speed until volitional fatigue. The assessor for the ESWT was blinded to the lower‐limb immersion condition. Heart rate and pulse oximetry were recorded throughout immersion and the ESWT, while blood pressure (mean arterial pressure [MAP], brachial artery oscillometry) was recorded during immersion. Femoral artery blood flow (Doppler ultrasound) was measured at baseline resting, and at 15‐min intervals during water immersion in a subset of eight participants. Muscle oxygenation was measured immediately following water immersion, and continuously throughout each ESWT using near‐infrared spectroscopy, to estimate tissue saturation index (TSI) of the medial head of the gastrocnemius. Rating of perceived exertion (RPE; modified Borg scale, 0–10) was recorded at the completion of the ESWT.

The primary outcome measure of interest was the change in ESWT distance. Data were analysed using linear mixed‐effects models (α = 0.05) in Jamovi (v.2.3.28).

Results

Twenty‐two participants (one woman, median [interquartile] age 71 [67–74] years, 1.7 [1.7–1.8] m, 78 [67–93] kg, left ventricular ejection fraction 37 [32–44] %, New York Heart Association functional class I [I–II]) completed both trial conditions. End‐exercise ISWT was 6.1 [5.5–6.6] km·h⁻¹. MAP was not different during baseline rest (hot: 86 [81–96] vs. control: 86 [82–98] mmHg, p = 0.31), or at the completion of the water immersion protocol (hot: 86 [81–96] vs. control: 88 [81–93] mmHg, p = 0.73). Femoral artery blood flow was higher following lower‐limb heating (hot: 547 [410–875] vs. control: 208 [121–275] ml·min⁻¹, p = 0.02). ESWT distance was 696 [545–1170] m following hot and 544 [402–986] m following the control water immersion (mean increase of 201 [95% confidence interval 96–307] m, p < 0.001) (Figure  1A ). There was a time by condition interaction effect for the change in TSI from pre‐to‐post ESWT (p = 0.004) (Figure  1B ). TSI at the start of the ESWT was higher following hot compared to control water immersion (hot: 60.3 [56.8–63.3] % vs. control: 53.5 [49.3–58.7] %, p < 0.001), however, TSI was not different between hot and control conditions at the end of the ESWT (hot: 50.7 [46.5–54.0] % vs. control: 48.8 [46.2–52.6] %, p = 0.16). Pre‐ (hot: 69 [60–81] vs. control: 68 [62–83] beats·min⁻¹, p = 0.72) and end‐ (hot: 120 [105–131] vs. control: 114 [98–124] beats·min⁻¹, p = 0.18) ESWT heart rate, pulse oximetry (pre‐ hot: 96 [95–99] % vs. control: 98 [96–99] %, p = 0.06) and end‐ (hot: 97 [92–98] % vs. control: 96 [91–98] %, p = 0.50) and RPE were not different between hot (6 [5–7] AU) and control (5 [4–7] AU) conditions (p = 0.44).

Figure 1.

(A) Mean (standard deviation) endurance shuttle walk test (ESWT) distance following immersion of the lower limbs in either 30°C or 42°C water for 45 min. (B) Change in tissue saturation index during the ESWT following immersion of the lower limbs in either 30°C or 42°C water for 45 min.

Discussion

Our data provide preliminary evidence as to the potential of an acute, 45‐min bout of lower‐limb heating to increase submaximal exercise endurance in individuals with HFrEF. These findings are in support of previous work which show that warm water immersion (neck deep, ~34°C) increases cardiac output and stroke volume in individuals with chronic heart failure, ⁶ and that lower‐limb heating (knee down, ~42°C) increases arterial blood flow and 6‐min walk distance in individuals with peripheral artery disease. ⁷ Together, highlighting the potential of acute passive heating to elicit pronounced central and peripheral haemodynamic changes in individuals with cardiovascular disease. ⁴ While vasodilatation in the cutaneous vasculature is thought to be the primary mechanism behind these changes, increased skeletal muscle blood flow likely contributes as well. ⁴ Therefore, it remains unclear whether the observed TSI increases in the current investigation primarily reflect increased muscle oxygenation or are also reflective of increased skin blood flow following passive heating. ⁸ This presents as a limitation of the current findings and an important area for future research. Nevertheless, it stands to reason that increased arterial blood flow at the end of passive heating likely translates to enhanced oxygen availability to the working muscle, subsequently enhancing exercise endurance. However, other factors such as psychological, ⁷ and autonomic effects of passive heating ⁴ cannot be discounted.

Whether the observed increase in acute exercise performance translates into an ability to repeatedly perform more work during exercise training sessions, and thus provides a greater adaptive stimulus during cardiac rehabilitation remains untested. Despite this, our data highlight the potential of this intervention as a non‐pharmacological ergogenic aid to improve acute exercise performance in individuals living with HFrEF. Further trials are needed to ascertain the efficacy of lower‐limb heating to promote greater work, and greater adaptive stimulus following training interventions.

Funding

The Prince Charles Hospital Foundation, Innovation Grant, Griffith University.

Conflict of interest: none declared.