Author(s): JESKANEN, T., YLINEN, V., VALTONEN, R., STENBÄCK, V., MÄKELÄ, K., NÄPÄNKANGAS, J., KERKÄLÄ, R., PÖLLÄNEN, N., PIRINEN, E., HEINZ, K.H., TULPPO, M., Institution: UNIVERSITY OF OULU, Country: FINLAND, Abstract-ID: 883

INTRODUCTION:
Exaggerated blood pressure (BP) and heart rate (HR) responses to incremental exercise are associated with the development of hypertension and future cardiovascular events. We hypothesized that skeletal muscle mitochondrial function is associated with cardiac workload, quantified as Rate Pressure Product (RPP), during exercise in normotensive individuals.
METHODS:
Healthy adults (n = 18; 9 females; age 25 ± 4 years, Vo2max 42±5 and 46±6 ml/kg/min for female and male, respectively) performed a maximal exercise test on a cycle ergometer. The test began at 0 W and followed an incremental protocol starting at 40 W, with load increases every 2 minutes until exhaustion. Breath-by-breath gas exchange was measured to determine peak oxygen uptake (VO2peak) and the respiratory compensatory point (RCP). HR and systolic BP were recorded at each load to calculate RPP. The cardiac workload response to exercise was defined as the change in RPP from 0 W to the intensity corresponding to RCP (ΔRPP). Muscle biopsies from the vastus lateralis were collected on separate days to assess mitochondrial respiration as a readout of mitochondrial function.
RESULTS:
ΔRPP from 0 W to RCP intensity was 18181±2147 mmHg·bpm (range: 14644–23597) and Complex I mediated respiration was 31.9±13.7 pmol·mg⁻¹·s⁻¹ (range: 9.7–57.2). ΔRPP was correlated only with Complex I (r=-0.69, p=0.002) and sex (r=0.50, p=0.035). In a forward stepwise linear regression analysis with ΔRPP as the dependent variable and baseline RPP, sex, and complex I mediated respiration as predictors, complex I mediated respiration was the only variable significantly associated with ΔRPP (adjusted R2=0.44; unstandardized β=−107; 95% CI:−167 to−47; p=0.002).
CONCLUSION:
The cardiac workload response to exercise is strongly associated with skeletal muscle mitochondrial function in young normotensive individuals.