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

¹Translational Biomedicine, School of Engineering and Physical Sciences, Heriot-Watt University Edinburgh; ²Centre for Integrated Systems Biology and Medicine, University Medical School, Nottingham, United Kingdom; ³CLINTECH Department, Section of Anesthesiology and Intensive Care, Karolinska University Hospital, Huddinge; ⁴Department of Laboratory Medicine, Division of Clinical Physiology, Karolinska Institutet, Karolinska University Hospital, Stockholm; ⁵The Wenner-Gren Institute, Arrhenius Laboratories, Stockholm University; and ⁶Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden

Submitted 6 November 2008 ; accepted in final form 2 February 2009

It has not been established which physiological processes contribute to endurance training-related changes () 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 (O_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 O_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 O_2max to quantify substrate metabolism. Substantial interindividual variability in training-induced adaptations was observed for most parameters, yet "low responders" for O_2max were not consistently low responders for other variables. While O_2max and time trial performance were related at baseline (r² = 0.80, P < 0.001), the change in O_2max was completely unrelated to the change in aerobic performance. The maximal parameters E_max and Veq_max (E/O_2max) accounted for 64% of the variance in O_2max (P < 0.001), whereas performance was related to changes in the submaximal parameters Veq_submax (r² = 0.33; P < 0.01), muscle lactate (r² = 0.32; P < 0.01), and acetyl-carnitine (r² = 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.

phosphocreatine; maximal oxygen uptake capacity; lactate; low responder