Whether left ventricular twist and untwisting rate (LV twist mechanics) respond to localised, peripheral, non-metabolic changes in arterial haemodynamics within an individual's normal afterload-range is presently unknown. Furthermore, previous studies indicate that LV twist mechanics may override the provision of cardiac output, but this hypothesis has not been examined purposefully. Therefore, we acutely altered local peripheral arterial haemodynamics in eleven healthy humans (Women/men: n = 3/8; age: 26±5 years) by bilateral arm heating (BAH). Ultrasonography was used to examine arterial haemodynamics, LV twist mechanics and the twist-to-shortening ratio (TSR). To further determine the arterial function-dependent contribution of LV twist mechanics to cardiac output, partial blood flow restriction to the arms was applied during BAH (BAHBFR). BAH increased arm skin temperatures (Δ+6.4±0.9°C, P<0.0001) but not core temperature (-0.0±0.1°C, P>0.05), concomitant to increases in brachial artery blood flow (Δ 212±77 mL, P<0.0001), cardiac output (Δ 495±487 L min−1, P<0.05), LV twist mechanics (Δ 15.2±5.2 degrees, P<0.05) and TSR (Δ 3.3±1.3, P<0.05) but maintained carotid artery blood flow (Δ 18±147 mL, P>0.05). Subsequently, BAHBFR reduced all parameters to pre-heating levels, except for TSR and heart rate which remained at BAH levels. In conclusion, LV twist mechanics responded to local peripheral arterial haemodynamics within the normal afterload-range in part independent of TSR and heart rate. The findings suggest that LV twist mechanics may be more closely associated with intrinsic sensing of excessive pressure-stress rather than being associated with the delivery of adequate cardiac output.
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