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A low-frequency to a high-frequency component ratio (LF/HF) in heart rate variability (HRV) may not accurately reflect sympathetic nervous activity during exercise. Thus, a valid HRV-based index of sympathetic nervous activity is needed. Therefore, the heart rate to LF ratio (Heart rate/LF) was evaluated as sympathetic nervous activity index which is reflected by catecholamine levels during incremental exercise. In this study, 15 healthy adults performed an incremental exercise test using a cycle ergometer. HRV was derived from electrocardiography and HRV components related to the autonomic nervous system were obtained using frequency analysis. Heart rate/LF was calculated using the heart rate and LF component produced by HRV analysis. Catecholamine, blood lactate levels and respiratory gas were also measured throughout the exercise test. While LF/HF did not increase with increasing exercise intensity, Heart rate/LF non-linearly increased during the incremental exercise test, as did noradrenaline and blood lactate. Interestingly, Heart rate/LF values were positively correlated with noradrenaline (ρ = 0.788, p < 0.05) and blood lactate (ρ = 0.802, p < 0.05) levels and carbon dioxide production (ρ = 0.903, p < 0.05) from at rest through the exercise stages. Heart rate/LF reflects sympathetic nervous activity and metabolic responses during incremental cycling exercise and has potential as an HRV index of sympathetic nervous activity during exercise. Trial registration: UMIN Japan identifier: UMIN000039639. [ABSTRACT FROM AUTHOR]

Purpose: Cognitive performance appears to be impaired during high-intensity exercise, and this occurs concurrently with a reduction in cerebral blood flow (CBF). However, it is unclear whether cognitive impairment during high-intensity exercise is associated with reduced CBF. We tested the hypothesis that a reduction in CBF is responsible for impaired cognitive performance during high-intensity exercise. Methods: Using a randomized crossover design 17 healthy males performed spatial delayed response and Go/No-Go tasks in three conditions (exercise [EX], exercise+CO2 [EX+CO2], and a nonexercising control [CON]). In the EX and EX+CO2, they performed cognitive tasks at rest and during 8 min of moderate and high-intensity exercise. Exercise intensity corresponded to ~50% (moderate) and ~80% (high) of peak oxygen uptake. In the EX+CO2, the participants inspired hypercapnic gas (2% CO2) during high-intensity exercise. In the CON, they performed the cognitive tasks without exercise. Results: Middle cerebral artery mean velocity increased during high-intensity exercise in the EX+CO2 relative to the EX (69.4 [10.6] cm·s−1, vs 57.2 [7.7] cm·s−1, P < 0.001). Accuracy of the cognitive tasks was impaired during high-intensity exercise in the EX (84.1% [13.3%], P < 0.05) and the EX+ CO2 (85.7 [11.6%], P < 0.05) relative to rest (EX: 95.1% [5.3%], EX+CO2: 95.1 [5.3%]). However, no differences between the EX and the EX+CO2 were observed (P > 0.10). These results demonstrate that restored CBF did not prevent cognitive impairment during high-intensity exercise. Conclusions: We conclude that a reduction in CBF is not responsible for impaired cognitive performance during high-intensity exercise. [ABSTRACT FROM AUTHOR]