Muscle Metaboreflex Modulation of Biventricular Function During Exercise

In supine resting conditions muscle metaboreflex activation (MMA) elicits an increase in blood pressure through sympathetic-mediated vasoconstriction, while direct cardiac augmentation is masked by vagal activity. We tested the hypothesis that biventricular function would be augmented by superimposing MMA during exercise (EX) where vagal activity is markedly reduced. While undergoing cardiac magnetic resonance imaging (2.89T, Siemens Prisma), 12 participants (mean±SD; 26±4 yrs, 9 females, BMI=22.1±2.3 kg/m 2 ) performed step ergometry EX at 50 W for 5 min. This was followed by 2 min of isometric handgrip (right hand) at 40% maximal voluntary contraction during uninterrupted EX. Ten seconds before termination of handgrip, circulatory occlusion in the exercising arm was achieved by inflating a brachial cuff at 220 mmHg (MMA). EX continued with superimposed MMA (EX+MMA) for an additional 5 min. Imaging was performed to attain comprehensive cardiac coverage, utilizing a contiguous series of 23 short-axis slices (8 mm each) and 15 horizontal long-axis slices (8 mm each). Acquisition included 50-75 temporal frames (36 ms/frame) and employed a validated free-breathing technique. Images were acquired in the last 2-min of EX and EX+MMA. Right (RV) and left ventricular (LV) end-diastolic (EDV) and end-systolic (ESV) endocardial borders were measured at end-expiration, with stroke volume calculated as the average of LV and RV stroke volume to account for respiratory variation. Data were analyzed with two-way repeated measures ANOVA with Sidak multiple comparisons tests and t-tests. Resting cardiac values were as follows: RVEDV=203±51 ml, RVESV=88±24 ml, LVEDV=201±36 ml, LVESV=81±16 ml, stroke volume=116±28 ml, heart rate=70±10 bpm, cardiac output=8.1±2.3 l/min. Simultaneously determined pulmonary oxygen uptake was similar from EX (0.97±13 l/min) to EX+MMA (1.00±15 l/min, p = 0.1524), suggesting comparable metabolic requirements for both conditions. There was no effect of exercise condition on RVEDV (EX: 199±49 ml to EX+MMA: 193±46 ml) and LVEDV (EX: 204±38 ml to EX+MMA: 203±37 ml, interaction: p = 0.1817). There was a significant ventricle by exercise condition interaction (p=0.0065) for ESV where RVESV (EX: 76±23 to EX+MMA: 64±18 ml, p < 0.0001) and LVESV (EX: 76±17 to EX+MMA: 72±15 ml, p = 0.0424) decreased during EX+MMA. The magnitude in ESV reduction was greater in the RV (-12±12 ml) compared to the LV (-4±7 ml, p = 0.0065). Stroke volume increased 4±6 ml from EX (126±25 ml) to MMA+EX (130±28 ml, p = 0.0399). There was a non-significant increase in heart rate from EX (106±11 bpm) to EX+MMA (109±13 bpm, p = 0.1782). Consequently, cardiac output increased from EX (13.3±2.6 l/min) to EX+MMA (14.1±3.1 l/min, p = 0.0546). Together, the data demonstrate that while MMA induced greater reductions in RVESV compared to LVESV, the overall impact on SV was modest. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.