Training induced adaptation of skeletal muscle and metabolism during submaximal exercise

Abstract

SUMMARY1. Six subjects were trained using a one-leg bicycle exercise for 2 months. The untrained leg served as control. After the training period, muscle oxidative capacity, determined as succinate dehydrogenase activity, was 27 % higher in the trained (as opposed to the control) leg (P < 0.05).2. When the subjects in this situation performed a 1 h two-legged submaximal bicycle exercise bout (150-225 W), determinations of VO, of the single leg (leg blood flow x (A-V)02 difference) revealed that they appeared to choose to work harder with their trained than with their untrained leg, so as to make the relative loads for the two legs the same.3. Determinations of 02 and CO2 on femoral arterial and venous blood demonstrated that the R.Q. was lower in the trained as compared to the untrained leg, 0-91 cf. 0-96 (10 min) and 0-91 cf. 0 94 (50 min) (P < 0.05).4. That metabolism of fat was more pronounced in the trained leg was further supported by the finding of a significant net uptake of free fatty acids in this leg only. Moreover, a lower release of lactate from the trained leg was demonstrated.5. It is suggested that the shift towards a more pronounced metabolism of fat in the trained leg is a function of an increased muscle oxidative capacity.

Skeletal muscle substrate metabolism during exercise: methodological considerations

“…Both studies showed a reduction in CHO utilization. In one of the studies (Henriksson, 1977) this was due to a lower glucose uptake, while in the other study (Kiens et al 1993) it was due to reduced muscle glycogen Saltin & Karlsson, 1971. ) depletion (estimated value; there was no significant difference in muscle glycogen breakdown in the two legs).…”

“…This factor has been highlighted by just three well-controlled studies by experienced researchers. In two of the investigations, the subjects trained one leg and the muscle metabolism was studied in both legs during exercise (Henriksson, 1977;Kiens et al 1993). Both studies showed a reduction in CHO utilization.…”

The Emerging Role of p53 in Exercise Metabolism

“…Acute customary exercise is therefore associated with smaller decreases in adenosine triphosphate (ATP), phosphocreatine and muscle glycogen utilisation, and smaller increases in adenosine diphosphate (ADP), adenosine monophosphate (AMP), inorganic phosphate and muscle lactate [6]. Such adaptations are recognised physiologically by the classic rightward shift of the lactate threshold curve [7], increased utilisation of lipid sources to fuel muscle contraction [8] and an improved ability to complete endurance exercise at higher intensities for a longer period [9].…”

The Rate of Phosphocreatine Hydrolysis and Resynthesis in Exercising Muscle in Humans using 31P-MRS.

“…Consequently, a continuous and highly time-resolved, kinetic evaluation of high energy phosphorus compounds in human muscle during exercise was determined by 31-phosphorus nuclear magnetic resonance spectroscopy ( 31 P-MRS) (Binzoni et al, 1992;Kiessling et al, 1971;Kushmerick and Meyer, 1985;Meyer 1988;Mizuno et al, 1994;Mole et al, 1985;Yoshida and Watari, 1994;Yoshida and Watari, 1997;Yoshida et al, 1996). During exercise, however, both anaerobic and aerobic pathways are activated, making it difficult to measure the ATP production resulting from the more complex pathways of PCr hydrolysis, glycolysis, and oxidative phosphorylation (Gollnick and Hermansen, 1973;Henriksson, 1977;Holloszy, 1973;Saltin and Gollnick, 1983). During recovery, however, the aerobic pathway dominates and ATP production may be easier to analyze because ATP production may arise from PCr resynthesis controlled by aerobic metabolism and mitochondrial oxidative phosphorylation.…”