Systematic analysis of adaptations in aerobic capacity and submaximal energy metabolism provides a unique insight into determinants of human aerobic performance

Abstract

It has not been established which physiological processes contribute to endurance training-related changes (Delta) in aerobic performance. For example, the relationship between intramuscular metabolic responses at the intensity used during training and improved human functional capacity has not been examined in a longitudinal study. In the present study we hypothesized that improvements in aerobic capacity (Vo(2max)) and metabolic control would combine equally to explain enhanced aerobic performance. Twenty-four sedentary males (24 +/- 2 yr; 1.81 +/- 0.08 m; 76.6 +/- 11.3 kg) undertook supervised cycling training (45 min at 70% of pretraining Vo(2max)) 4 times/wk for 6 wk. Performance was determined using a 15-min cycling time trial, and muscle biopsies were taken before and after a 10-min cycle at 70% of pretraining Vo(2max) to quantify substrate metabolism. Substantial interindividual variability in training-induced adaptations was observed for most parameters, yet "low responders" for DeltaVo(2max) were not consistently low responders for other variables. While Vo(2max) and time trial performance were related at baseline (r(2) = 0.80, P < 0.001), the change in Vo(2max) was completely unrelated to the change in aerobic performance. The maximal parameters DeltaVe(max) and DeltaVeq(max) (DeltaVe/Vo(2max)) accounted for 64% of the variance in DeltaVo(2max) (P < 0.001), whereas Deltaperformance was related to changes in the submaximal parameters Veq(submax) (r(2) = 0.33; P < 0.01), muscle Deltalactate (r(2) = 0.32; P < 0.01), and Deltaacetyl-carnitine (r(2) = 0.29; P < 0.05). This study demonstrates that improvements in high-intensity aerobic performance in humans are not related to altered maximal oxygen transport capacity. Altered muscle metabolism may provide the link between training stimulus and improved performance, but metabolic parameters do not change in a manner that relates to aerobic capacity changes.

High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats

“…Of particular interest, citrate synthase maximal activity in soleus muscle positively correlated with running performance (r ϭ 0.46, P Ͻ 0.05), whereas the correlation between left ventricular contractile function and running performance was not significant (r ϭ 0.22, P Ͼ 0.12). It is clear that these findings do not guarantee a causal relationship between skeletal muscle aerobic capacity and running performance in our model, but they corroborate previous reports from the literature, demonstrating a strong correlation between skeletal muscle parameters and functional capacity in patients with HF (24) and important relationships between metabolic skeletal muscle adaptations and training and improvements in performance (56). An increased percentage of type I (i.e., oxidative) fibers in soleus and plantaris muscles of both trained groups is further evidence that CMT and HIT enhanced skeletal muscle aerobic metabolism in infarcted rats.…”

Towards the minimal amount of exercise for improving metabolic health: beneficial effects of reduced-exertion high-intensity interval training

“…Alternatively, it could be that our small sample included several non-responders. Previous studies have comprehensively demonstrated that following a period of exercise training part of the population will not adapt for specific parameters (non-responders), and for insulin sensitivity this has been shown to be the case for up to 40% of the population (Boule et al 2005;Vollaard et al 2009;Bouchard and Rankinen 2001). Therefore, further studies with larger sample sizes will be needed to confirm or refute our initial observations.…”

MicroRNAs 29 are involved in the improvement of ventricular compliance promoted by aerobic exercise training in rats

“…These adaptations include hemodynamic, metabolic, and cardiovascular adaptations, such as CH. CH is a physiological increase in left ventricle (LV) mass that contributes to increased ventricular stroke volume and cardiac output (32,38).This CH phenotype is associated with sarcomeres added in series to lengthen the cardiac cell, as well as in parallel. In contrast to pathological CH, physiological CH induced by aerobic training occurs in response to intermittent volume…”

“…These adaptations include hemodynamic, metabolic, and cardiovascular adaptations, such as CH. CH is a physiological increase in left ventricle (LV) mass that contributes to increased ventricular stroke volume and cardiac output (32,38).…”