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Enhanced whole body maximal aerobic capacity following 12‐weeks of alternating single‐leg knee extension training (706.4)
Author(s) -
Wolff Christopher,
Suer Miranda,
Konopka Adam,
Trappe Todd,
Harber Matthew
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.706.4
Subject(s) - skeletal muscle , aerobic exercise , medicine , vo2 max , leg press , aerobic capacity , exercise physiology , cardiology , endocrinology , muscle strength , heart rate , blood pressure
Maximal aerobic capacity (VO 2 max) is primarily limited by the delivery of oxygen to active tissue, however the role of the peripheral tissues in limiting VO 2 max is unclear. The cardiovascular system and the skeletal muscle both respond favorably to aerobic exercise training, but it is unknown to what extent an improved skeletal muscle phenotype in the absence of altered cardiovascular function enhances VO 2 max. Thus, we employed an alternating single‐leg knee extension exercise training protocol to limit training adaptations to the skeletal muscle and assessed the skeletal muscle phenotype and whole body aerobic capacity. Eight sedentary volunteers (20±1 y; VO 2 max: 2.5±0.3 L . min ‐1 ) completed the 12‐week progressive alternating single‐leg training. Subjects underwent testing to determine whole body VO 2 max, single‐leg peak workload, muscle function and a DXA scan before and after training. Skeletal muscle biopsies were obtained to assess muscle fiber type and fiber size. Following training there were increases (P<0.05) in VO 2 max (9±3%), single‐leg peak workload (43±8%), skeletal muscle size (3±1%) and slow and fast myofiber size (13±4% and 14±4%, respectively) while there was a decrease (P<0.05) in hybrid fiber content (‐33±8%). These data suggest that isolating aerobic training adaptations to the skeletal muscle may improve whole body aerobic capacity independent of altered cardiovascular physiology. Grant Funding Source : Supported by a pilot grant from the National Skeletal Muscle Research Center