Abstract

Early studies postulated that oxygen uptake (VO2) and heart rate (HR) keep linearity during progressive exercise. Nevertheless, other works showed a breakpoint on the HR temporal response, associated probably, to the anaerobic threshold (AT). PURPOSE: to analyze the relationship between the HR and VO2 time responses during progressive and maximal exercise. METHODS: Twenty-four healthy male soccer players (22±5yr, 74±7kg, 177±7cm) performed a progressive and maximal running test. Pulmonary gas exchange was analyzed breath-by-breath, and the HR was recorded each R-R period. Blood lactate concentration (BLC) was analyzed on the end of each stage. The AT was expressed by the gas exchange (ventilatory threshold - VT and respiratory compensation - RC) and the BLC (lactate threshold - LT). The values of VO2, HR and BLC, after cubic interpolation for phase alignment, were filtered (zero crossing moving average). Sequentially, HR was fitted for all possible divisions into 3 contiguous lines, and the array yielding the least-pooled residual sum of squares was chosen as representing the best fit, and further two breakpoints (HR1 and HR2) were obtained. The coefficients for each HR segment were compared to that of VO2 using t-paired Student' test (?=0.05), and the relation between breakpoints and the AT was expressed by Pearson coefficient RESULTS: Maximal VO2 (VO2max), HR and BLC averaged 62.9±6.1 ml.kg-1.min−1, 189±8bpm and 16.8±3.5mM respectively. The HR breakpoints averaged 43.9±5.9 and 89.7±7.5% of the VO2max, which resulted, on average, in weak correlation with VT (r=0.23; ns), RC (r=0.42;p<0.05) and LT (r=0.77; p<0.05). The HR and VO2 were strongly correlated (r=0.99; p<0.01) until HR1, decaying to 0.85 (p<0.05) until HR2. On the other hand, at intensities higher than that point, HR increase rate presented a drop, resulting in 57% of the explained variance of VO2 (r=0.75; p<0.05). Furthermore, calculating the difference between the expected (extrapolation of the 2nd segment) and measured HR values for the 3rd segment, we found a chronotropic deficit of 25.24±22.07beats, which was correlated to the LT (r=0.46; p<0.05). Additionally, we hypothesized that HR1, when the HR increase rate tends to rise, may be related to stroke volume (SV) time response. Literature shows that a drop on the SV increase rate occurs at approximately 40% of the VO2max, and here, we found a change in the HR response at 43.9% of the VO2max. CONCLUSION: given the two HR breakpoints, two main findings must be presented here: (1) the first breakpoint can be related to the S V time response; and (2) the second breakpoint represents a chronotropic deficit, which is related to the AT.

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