Endurance training decreases the non‐linearity in the oxygen uptake–power output relationship in humans

Abstract

In this study, we hypothesized that 5 weeks of cycling endurance training can decrease the magnitude of the non-proportional increase in oxygen uptake (˙ V O 2) to power output relationship (˙ V O 2 'excess') at exercise intensities exceeding the lactate threshold (LT). Ten untrained, physically active men performed a bout of incremental cycling exercise until exhaustion before and after training. The mitochondrial DNA copy number, myosin heavy chain composition and content of uncoupling protein 3 and sarcoplasmic reticulum Ca 2+-ATPases (SERCAs) were analysed in muscle biopsies taken from vastus lateralis before and after training. The training resulted in an enhancement of the power-generating capabilities at maximal oxygen uptake (˙ V O 2 max) by ∼7% (P = 0.002) despite there being no changes in ˙ V O 2 max (P = 0.49). This effect was due to a considerable reduction in the magnitude of the ˙ V O 2 'excess' (P < 0.05) above the LT. A decrease in plasma ammonia concentration was found during exercise after training (P < 0.05). A downregulation of SERCA2 in vastus lateralis (P = 0.006) was observed after training. No changes in myosin heavy chain composition, selected electron transport chain proteins, uncoupling protein 3 or the mitochondrial DNA copy number (P > 0.05) were found after training. We conclude that the training-induced increase in power-generating capabilities at ˙ V O 2 max was due to attenuation of the ˙ V O 2 'excess' above the LT. This adaptive response seems to be related to the improvement of muscle metabolic stability, as judged by a lowering of plasma ammonia concentration. The enhancement of muscle metabolic stability after training could be caused by a decrease in ATP usage at a given power output owing to downregulation of SERCA2 pumps. The oxygen cost of cycling above the lactate threshold (LT) can be decreased after a few weeks of endurance training, as expressed by the lowering of the magnitude of the slow component of oxygen uptake (˙ V O 2) kinetics (Casaburi et al. 1987; Womack et al. 1995; Carter et al. 2000). However, the mechanism responsible for this effect remains unclear. There is a growing body of evidence to suggest that the increase in the oxygen cost of work during heavy-intensity exercise is caused by fatigue of the active muscle fibres (Zoladz et al. 2008; Hepple et al. 2010; Cannon et al. 2011) and, in particular, by a disturbance in the concentrations of muscle metabolites, i.e. a decrease in muscle phosphocreatine and a rise in free ADP, free AMP, free inosine monophosphate, creatine, inorganic phosphate and H + , potent to decrease muscle mechanical efficiency (Woledge, 1998; Zoladz et al. 2006). It is well known that endurance training can enhance muscle metabolic stability, i.e. lead to reduced changes in the concentrations of the above-mentioned muscle metabolites for a given ATP turnover (approximately

Running Performance at High Running Velocities Is Impaired but V′O2max and Peripheral Endothelial Function Are Preserved in IL-6−/− Mice

“…In order to understand the physiological background of this mechanism, we measured some muscle proteins expression/activities involved in oxygen cost of work including sarcoplasmic reticulum Ca 2+ -ATPase1 (SERCA1), uncoupling protein-3 (UCP-3) as well as COX and CS activities (for overview see [24]–[26]). We have found lower expression of SERCA1 in soleus muscle in IL-6 −/− than in WT mice (Figure 5A).…”

“…We have found lower expression of SERCA1 in soleus muscle in IL-6 −/− than in WT mice (Figure 5A). This could at least partly explain the lower oxygen cost of running at sub-maximal running velocities in the IL-6 −/− mice (for overview see [24]–[26]). Lower oxygen cost of the run in the IL-6 −/− mice could be also due to lower expression of UCP-3 in their locomotor muscles and lower energy dissipation during exercise (see e.g.…”

Coronary and muscle blood flow during physical exercise in humans; heterogenic alliance

“…Therefore, an increase in power 60 output in this exercise domain by 50 W requires an increase ofVO 2 61 by $500 mL O 2 min À1 . Exercise of higher intensities (above the 62 lactate threshold [LT]) requires about 20% more oxygen uptake per 63 W of generated power output than below the LT [5,[9][10][11][12]. Accord- 64 ingly, an increase in power output above the LT by 50 W requires 65 an increase ofVO 2 by $600 mL O 2 min À1 .…”

“…A schematic presentation of the relationship between oxygen uptake (VO 2 ) and power output during the incremental exercise test in humans (an increase of power output by 30 W every 3 min) -based on data from Zoladz et al [9]. See also [5,[10][11][12]. Note the difference in the slope in VȮ 2 -the power output relationship below and above the PO at the LT (the power output at the lactate threshold), resulting in about 20% difference between the power output observed at theVO 2max (Obs.…”

“…about 3.6 mL O 2 kg body mass À1 min À1 ), 55 also called MET (being defined as a multiple of the resting 56 metabolic rate) [8]. Increased exercise intensity enhances pulmo-57 nary oxygen uptake, which during moderate-intensity cycling 58 exercise increases linearly with power output at the rate of about 59 10 ml O 2 per W (''gain'') [5,[9][10][11][12]. Therefore, an increase in power 60 output in this exercise domain by 50 W requires an increase ofVO 2 61 by $500 mL O 2 min À1 .…”