Dataset Information

The Fuzzy Kinetics Index: an indicator conflating cardiorespiratory kinetics during dynamic exercise.

ABSTRACT:

Purpose

The aim of the present study was to develop a novel index using fuzzy logic procedures conflating cardiorespiratory and pulmonary kinetics during dynamic exercise as a representative indicator for exercise tolerance.

Methods

Overall 69 data sets were re-analyzed: (age: 29 ± 1.2 y [mean ± SEM], height: 179 ± 1.0 cm; body mass: 78 ± 1.4 kg; peak oxygen uptake ([Formula: see text]̇O_2peak): 48 ± 1.1 ml·min^-1·kg^-1), that comprised pseudo random binary sequence work rate (WR) changes between 30 and 80 W on a cycle ergometer, with additional voluntary exhaustion to estimate [Formula: see text]O_2peak. Heart rate (HR), stroke volume (SV) and gas exchange (pulmonary oxygen uptake ([Formula: see text]O_2pulm)) were measured beat-to-beat and breath-by-breath, respectively. For estimation of muscle oxygen uptake ([Formula: see text]O_2musc) kinetics and for the analysis of kinetic responses of the parameters of interest (perfusion ([Formula: see text] = HR·SV), [Formula: see text]O_2pulm, [Formula: see text]O_2musc) the approach of Hoffmann et al. (2013) was applied. For calculation of the Fuzzy Kinetics Index [Formula: see text], [Formula: see text]O_2pulm, and [Formula: see text]O_2musc were used as input variables for the subsequent fuzzy- and defuzzyfication procedures.

Results

For both absolute and relative [Formula: see text]O_2peak a significant correlation has been observed with FKI, whereas the correlation coefficient is higher for relative (r = 0.430; p < 0.001; n = 69) compared to absolute [Formula: see text]O_2peak (r = 0.358; p < 0.01; n = 69). No significant correlations have been found between FKI and age, height or body mass (p > 0.05 each).

Conclusions

The significant correlations between FKI and [Formula: see text]O_2peak represent a physiological connection between the regulatory and the capacitive system and its exercise performance. In turn, the application of FKI can serve as an indicator for healthy participants to assess exercise tolerance and sport performance.

SUBMITTER: Drescher U

PROVIDER: S-EPMC8064983 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Purpose:The present study aimed to determine whether whole-body fat oxidation and muscle deoxygenation kinetics parameters during exercise were related in individuals with different aerobic fitness levels. Methods:Eleven cyclists [peak oxygen uptake ( V.O2?p?e?a?k ): 64.9 ± 3.9 mL?kg-1?min-1] and 11 active individuals ( V.O2?p?e?a?k : 49.1 ± 7.4 mL?kg-1?min-1) performed a maximal incremental cycling test to determine V.O2?p?e?a?k and a submaximal incremental cycling test to assess whole-body fat oxidation using indirect calorimetry and muscle deoxygenation kinetics of the vastus lateralis (VL) using near-infrared spectroscopy (NIRS). A sinusoidal (SIN) model was used to characterize fat oxidation kinetics and to determine the intensity (Fatmax) eliciting maximal fat oxidation (MFO). The muscle deoxygenation response was fitted with a double linear model. The slope of the first parts of the kinetics (a 1) and the breakpoint ([HHb]BP) were determined. Results:MFO (p = 0.01) and absolute fat oxidation rates between 20 and 65% V.O2?p?e?a?k were higher in cyclists than in active participants (p < 0.05), while Fatmax occurred at a higher absolute exercise intensity (p = 0.01). a 1 was lower in cyclists (p = 0.02) and [HHb]BP occurred at a higher absolute intensity (p < 0.001) than in active individuals. V.O2?p?e?a?k was strongly correlated with MFO, Fatmax, and [HHb]BP (r = 0.65-0.88, p ? 0.001). MFO and Fatmax were both correlated with [HHb]BP (r = 0.66, p = 0.01 and r = 0.68, p < 0.001, respectively) and tended to be negatively correlated with a 1 (r = -0.41, p = 0.06 for both). Conclusion:This study showed that whole-body fat oxidation and muscle deoxygenation kinetics were both related to aerobic fitness and that a relationship between the two kinetics exists. Individuals with greater aerobic fitness may have a delayed reliance on glycolytic metabolism at higher exercise intensities because of a longer maintained balance between O2 delivery and consumption supporting higher fat oxidation rates.

Project description:The relationship between the redox state and lactate accumulation in contracting human skeletal muscle was investigated. Ten men performed bicycle exercise for 10 min at 40 and 75% of maximal oxygen uptake [VO2(max.)], and to fatigue (4.8 +/- 0.6 min; mean +/- S.E.M.) at 100% VO2(max.). Biopsies from the quadriceps femoris muscle were analysed for NADH, high-energy phosphates and glycolytic intermediates. Muscle NADH was 0.20 +/- 0.02 mmol/kg dry wt. of muscle at rest, and decreased to 0.12 +/- 0.01 (P less than 0.01) after exercise at 40% VO2(max.), but no change occurred in the [lactate]/[pyruvate] ratio. These data, together with previous results on isolated cyanide-poisoned soleus muscle, where NADH increased while [lactate]/[pyruvate] ratio was unchanged [Sahlin & Katz (1986) Biochem. J. 239, 245-248], suggest that the observed changes in muscle NADH occurred within the mitochondria. After exercise at 75 and 100% VO2(max.), muscle NADH increased above the value at rest to 0.27 +/- 0.03 (P less than 0.05) and 0.32 +/- 0.04 (P less than 0.001) mmol/kg respectively. Muscle lactate was unchanged after exercise at 40% VO2(max.), but increased substantially at the higher work loads. At 40% VO2(max.), phosphocreatine decreased by 11% compared with the values at rest, and decreased further at the higher work loads. The decrease in phosphocreatine reflects increased ADP and Pi. It is concluded that muscle NADH decreases during low-intensity exercise, but increases above the value at rest during high-intensity exercise. The increase in muscle NADH is consistent with the hypothesis that the accelerated lactate production during submaximal exercise is due to a limited availability of O2 in the contracting muscle. It is suggested that the increases in NADH, ADP and Pi are metabolic adaptations, which primarily serve to activate the aerobic ATP production, and that the increased anaerobic energy production (phosphocreatine breakdown and lactate formation) is a consequence of these changes.