Premium
Low intensity exercise in humans accelerates mitochondrial ATP production and pulmonary oxygen kinetics during subsequent more intense exercise
Author(s) -
CampbellO'Sullivan Síun P.,
ConstantinTeodosiu Dumitru,
Peirce Nicholas,
Greenhaff Paul L.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2001.013238
Subject(s) - exercise intensity , intensity (physics) , phosphocreatine , medicine , exercise physiology , physical exercise , endocrinology , vastus lateralis muscle , chemistry , anaerobic exercise , vo2 max , endurance training , incremental exercise , heart rate , physical therapy , skeletal muscle , energy metabolism , blood pressure , physics , quantum mechanics
We undertook this study to determine whether low intensity exercise (55 % V̇ O2 ,max ) would significantly alter the metabolic and ventilatory responses observed during 10 min of subsequent moderate intensity exercise (75 % V̇ O2 ,max ). By executing this work, we hoped to further our understanding of the mechanisms that limit mitochondrial ATP production at the onset of exercise. Seven healthy human subjects performed 10 min of moderate intensity exercise in the presence and absence of 10 min of low intensity exercise, which preceded the moderate intensity exercise by 3 min. Muscle biopsy samples were obtained from the vastus lateralis at pre‐determined time points and oxygen consumption kinetics were determined at rest and during low and moderate intensity exercise. Following low intensity exercise and 3 min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal levels, but V̇ O2 had returned to the resting rate. When moderate intensity exercise was preceded by low intensity exercise, there was a significant sparing of phosphocreatine (PCr, ∼25 %, P < 0.05) and reductions in glucose 6‐phosphate (G‐6‐P, ∼50 %, P < 0.05) and lactate (∼50 %, P < 0.05) accumulation during the first minute of moderate intensity exercise. No differences were observed after 10 min of moderate intensity exercise. The V̇ O2 on‐kinetic response over the first minute of moderate intensity exercise was accelerated when preceded by low intensity exercise. Collectively, our results suggest the lag in the oxidative ATP delivery at the onset of moderate intensity exercise can be overcome by prior low intensity exercise. Furthermore, our findings support the view that this lag is at least in part attributable to a limitation in acetyl group delivery/availability at the onset of exercise, rather than delayed oxygen supply.