Mitochondrial Coupling and Contractile Efficiency in Humans with High and Low V˙O2peaks

Abstract

Introduction: Endurance training elicits tremendous adaptations of the mitochondrial energetic capacity. Yet, the effects of training or physical fitness on mitochondrial efficiency during exercise are still unclear. Accordingly, the purpose of the present study was to examine in vivo the differences in mitochondrial efficiency and ATP cost of contraction during exercise in two groups of adults differing in their aerobic capacity.

Method: We simultaneously assessed the ATP synthesis and O2 fluxes with P-magnetic resonance spectroscopy and pulmonary gas exchange measurements in seven endurance-trained (ET, V˙O2max: 67 ± 8 mL·min⁻¹·kg⁻¹) and seven recreationally active (RA, V˙O2max: 43 ± 7 mL·min⁻¹·kg⁻¹) subjects during 6 min of dynamic moderate-intensity knee extension.

Results: The ATP cost of dynamic contraction was not significantly different between ET and RA (P > 0.05). Similarly, end-exercise O2 consumption was not significantly different between groups (ET: 848 ± 155 mL·min⁻¹ and RA: 760 ± 131 mL·min⁻¹, P > 0.05). During the recovery period, the PCr offset time constant was significantly faster in ET compared with RA (ET: 32 ± 8 s and RA: 43 ± 10 s, P < 0.05), thus indicating an increased mitochondrial capacity for ATP synthesis in the quadriceps of ET. In contrast, the estimated mitochondrial efficiency during exercise was not significantly different (P/O, ET: 2.0 ± 1.0 and RA: 1.8 ± 0.4, P > 0.05). Consequently, the higher mitochondrial capacity for ATP synthesis in ET likely originated from an elevated mitochondrial volume density, mitochondria-specific respiratory capacity, and/or slower postexercise inactivation of oxidative phosphorylation by the parallel activation mechanism.

Conclusion: Together, these findings reveal that 1) mitochondrial and contractile efficiencies are unaltered by several years of endurance training in young adults, and 2) the training-induced improvement in mitochondrial energetic capacity appears to be independent from changes in mitochondrial coupling.

Figure 1

Power output from the MR sampled leg with respect to time throughout the moderate knee-extension exercise in endurance-trained (●) and recreationally active (○) subjects. Values are presented as means ± SD. There was no significant interaction between time and group (P > 0.05).

Figure 2

Changes in pH (A), inorganic phosphate (Pi, B), phosphocreatine (PCr, C) and Adenosine Di-Phosphate (ADP_, D) with respect to time throughout the knee-extension exercise in endurance-trained (●) and recreationally active (○) subjects. Values are presented as means ± SD. There was no significant interaction between time and group for each of the variables (P > 0.05).

Figure 3

Rates of ATP synthesis from glycolysis (A), creatine kinase reaction (B) and oxidative phosphorylation (C) calculated from ³¹P-MR spectroscopy measurements during the last min of knee-extension exercise in endurance-trained and recreationally active subjects. Values are presented as means ± SD. There was no significant difference between groups for each of the variables (P > 0.05).

Figure 4

ATP cost of contraction (A) and estimated in vivo mitochondrial efficiency (P/O ratio, B) during the last min of the knee-extensors in endurance-trained and recreationally active subjects. Data are presented as mean ± SD. There was no significant difference between groups for each of the variables (P > 0.05).

Figure 5

PCr resynthesis with respect to time following exercise in endurance-trained (●) and recreationally active (○) subjects. Data are presented as mean ± SD. The figure insert provides the individual and the mean PCr offset time constant, which was significantly faster in endurance-trained individuals (P < 0.05).