Mitochondrial Net Oxidative Capacity, but Not Oxygen Delivery, Determines Mechanical Net Efficiency for High-Intensity Exercise

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Background: Mechanical net efficiency ( η net) has proven to be mainly dependent on skeletal muscle mitochondria density. Due to the difficulty of estimating energy expenditure for high-intensity exercise, ηnet was only evaluated for intensities below the lactate (La - ) threshold. Therefore, the aim of this study was to estimate ηnet at high-intensity exercise, to find its main determinants and to compare them to those of moderate-intensity ηnet. Considering the relevance of oxygen delivery and extraction during near-maximal effort, we hypothesized that stroke volume (SV), cardiac output (Q) and net oxidative phosphorylation could be the three main factors influencing the η net for high-intensity exercise. Methodology: On the first day, 14 healthy participants (9 males, 5 females; age 24 ± 3 years) performed an incremental exercise test on a semi-recumbent ergometer to determine the peak oxygen uptake (VO 2max ) and power output (PPO). On the second day, the subjects performed a sub-maximal graded exercise test on the same ergometer with two 6-minute steps at 25% (moderate intensity) and 75% (high intensity) of the PPO. VO 2 and heart rate (HR) were monitored continuously and La - was collected at the end of each step. SV was assessed using cardiac ultrasound during exercise and Q was derived from SV and HR. We considered the last 30 s of each step. η net was calculated as the ratio of mechanical work (converted to kcal·min −1 ) to energy expenditure above the resting metabolism (also converted to kcal·min −1 ). Net expenditure was calculated from the VO2 values. For each step with more than 4.0 mmol·L −1 of La - , the glycolytic contribution was added to aerobic metabolism and estimated considering 3.0 mL·kg −1 of VO 2 for each 1 mmol·L −1 of La - accumulation. On the last day, the subject underwent a muscle biopsy of vastus lateralis to measure the net oxidative phosphorylation capacity (P-L net OX ). Summary of Results: The subject reached a mean PPO of 291±71 W and a VO 2max of 3.65±0.95L·min −1 . η net 25 was 21.7±5.3%, while η net 75 was 17.9±2.9%. HR 25 and SV 25 were 103.8±15.0bpm and 97.1±21.6mL, while HR 75 and SV 75 were 173.2±9.2bpm and 116.4±45.9mL, with the resulting Q 25 and Q 75 of 10.1±2.0 and 22.0±5.1L·min −1 , respectively. P-L net OX was 75.8±22.8pmol·s -1 ·mg -1 . The analyses do not show a correlation between central hemodynamics parameters and η net for either 25% (SV 25 : r = 0.224 and Q 25 : r = 0.220) and 75% of PPO (SV 75 : r = -0.280 and Q 75 : r = 0.390), despite the HR is lower for higher efficiency at 25% of PPO (HR 25 : r =-0.630, p=0.016*; HR 75 : r=-0.280). Conversely, P-L net OX correlates positively with η net 75 (r=0.600; p=0.023*), but not with η net 25 (r=-0.130). Conclusions: Contrary to our hypothesis, these results indicate that central hemodynamics parameters do not influence η net at high exercise intensity. However, mitochondria oxidative capacity positively correlates with high intensity η net. Therefore, high intensity η net is likely a product of peripheral factors related to mitochondria oxidative capacity rather than a consequence of central hemodynamic response. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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