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Training intensity-dependent and tissue-specific increases in lactate uptake and MCT-1 in heart and muscle
Author(s) -
Steven K. Baker,
Karl J. A. McCullagh,
Arend Bonen
Publication year - 1998
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/jappl.1998.84.3.987
Subject(s) - medicine , endocrinology , skeletal muscle , chemistry , lactate threshold , treadmill , heart rate , blood lactate , blood pressure
We investigated the effects of 3 wk of moderate- (21 m/min, 8% grade) and highintensity treadmill training (31 m/min, 15% grade) on 1) monocarboxylate transporter 1 (MCT-1) content in rat hindlimb muscles and the heart and 2) lactate uptake in isolated soleus (Sol) muscles and perfused hearts. In the moderately trained group MCT-1 was not increased in any of the muscles [Sol, extensor digitorum longus (EDL), and red (RG) and white gastrocnemius (WG)] (P > 0.05). Similarly, lactate uptake in Sol strips was also not increased (P > 0.05). In contrast, in the heart, MCT-1 (+36%, P < 0.05) and lactate uptake (+72%, P < 0.05) were increased with moderate training. In the highly trained group, MCT-1 (+70%, P < 0.05) and lactate uptake (+79%, P < 0.05) were increased in Sol. MCT-1 was also increased in RG (+94%, P < 0.05) but not in WG and EDL (P > 0.05). In the highly trained group, heart MCT-1 (+44%, P < 0.05) and lactate uptake (+173%, P < 0.05) were increased. In conclusion, it has been shown that 1) in both heart and skeletal muscle lactate uptake is increased only when MCT-1 is increased; 2) training-induced increases in MCT-1 occurred at a lower training intensity in the heart than in skeletal muscle; 3) in the heart, lactate uptake was increased much more after high-intensity training than after moderate-intensity training, despite similar increases in heart MCT-1 with these two training intensities; and 4) the increases in MCT-1 occurred independently of any changes in the heart's oxidative capacity (as measured by citrate synthase activity).

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