Christopher Lee
Research Subjects
Research Interests
Christopher Lee has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Mark S. Miller
Department of Kinesiology University of Massachusetts Amherst Massachusetts USA
3 shared publications - Amanda E. Paluch
Department of Kinesiology and Institute for Applied Life Sciences, University of Massachusetts Amherst, Amherst, MA, USA
2 shared publications - Philip C. Woods
School of Public Health and Health Sciences, University of Massachusetts 1 Department of Kinesiology Amherst, MA
2 shared publications Aurora D. Foster
University of Massachusetts
1 shared publication- Chad R. Straight
Combat Capabilities Development Command Soldier Center Natick Massachusetts USA
1 shared publication - Edward P. Debold
Department of Kinesiology, University of Massachusetts, Amherst, MA 01003
1 shared publication
Latest Publications
- 1 April 2025
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 328 (4) , C1220-C1233
Cellular and molecular contractile function in aged human skeletal muscle is altered by phosphate and acidosis and partially reversed with an ATP analog
Skeletal muscle fatigue is caused, in part, by increased production of phosphate and hydrogen ions, resulting in decreased force generation. We found that reduced force in fibers from older adults was due to altered function of myosin and actin, including slower protein interactions and reduced force per myosin head. Additionally, an ATP analog, dATP, partially reversed contractile dysfunction induced by increased phosphate and hydrogen, improving force production and altering myosin-actin interactions dependent upon fiber type.
- 1 April 2025
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 328 (4) , C1220-C1233
Cellular and molecular contractile function in aged human skeletal muscle is altered by phosphate and acidosis and partially reversed with an ATP analog
Skeletal muscle fatigue is caused, in part, by increased production of phosphate and hydrogen ions, resulting in decreased force generation. We found that reduced force in fibers from older adults was due to altered function of myosin and actin, including slower protein interactions and reduced force per myosin head. Additionally, an ATP analog, dATP, partially reversed contractile dysfunction induced by increased phosphate and hydrogen, improving force production and altering myosin-actin interactions dependent upon fiber type.
- 1 December 2024
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 327 (6) , C1400-C1415
Effects of age on human skeletal muscle: a systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size, and distribution
Human studies examining the cellular mechanisms behind sarcopenia, or age-related loss of skeletal muscle mass and function, have produced inconsistent results. A systematic review and meta-analysis were performed to determine the aging effects on protein expression, size, and distribution of fibers with various myosin heavy chain (MyHC) isoforms. Study eligibility included MyHC comparisons between young (18–49 yr) and older (≥60 yr) adults, with 27 studies identified. Relative protein expression was higher with age for the slow-contracting MyHC I fibers, with correspondingly lower fast-contracting MyHC II and IIA values. Fiber sizes were similar with age for MyHC I, but smaller for MyHC II and IIA. Fiber distributions were similar with age. When separated by sex, the few studies that examined females showed atrophy of MyHC II and IIA fibers with age, but no change in MyHC protein expression. Additional analyses by measurement technique, physical activity, and muscle biopsies provided important insights. In summary, age-related atrophy in fast-contracting fibers lead to more of the slow-contracting, lower force-producing isoform in older male muscles, which helps explain their age-related loss in whole muscle force, velocity, and power. Exercise or pharmacological interventions that shift MyHC expression toward faster isoforms and/or increase fast-contracting fiber size should decrease the prevalence of sarcopenia. Our findings also indicate that future studies need to include or focus solely on females, measure MyHC IIA and IIX isoforms separately, examine fiber type distribution, sample additional muscles to the vastus lateralis (VL), and incorporate an objective measurement of physical activity.
- 1 December 2024
- Published by American Physiological Society in American Journal of Physiology-Cell Physiology
- Vol. 327 (6) , C1400-C1415
Effects of age on human skeletal muscle: a systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size, and distribution
Human studies examining the cellular mechanisms behind sarcopenia, or age-related loss of skeletal muscle mass and function, have produced inconsistent results. A systematic review and meta-analysis were performed to determine the aging effects on protein expression, size, and distribution of fibers with various myosin heavy chain (MyHC) isoforms. Study eligibility included MyHC comparisons between young (18–49 yr) and older (≥60 yr) adults, with 27 studies identified. Relative protein expression was higher with age for the slow-contracting MyHC I fibers, with correspondingly lower fast-contracting MyHC II and IIA values. Fiber sizes were similar with age for MyHC I, but smaller for MyHC II and IIA. Fiber distributions were similar with age. When separated by sex, the few studies that examined females showed atrophy of MyHC II and IIA fibers with age, but no change in MyHC protein expression. Additional analyses by measurement technique, physical activity, and muscle biopsies provided important insights. In summary, age-related atrophy in fast-contracting fibers lead to more of the slow-contracting, lower force-producing isoform in older male muscles, which helps explain their age-related loss in whole muscle force, velocity, and power. Exercise or pharmacological interventions that shift MyHC expression toward faster isoforms and/or increase fast-contracting fiber size should decrease the prevalence of sarcopenia. Our findings also indicate that future studies need to include or focus solely on females, measure MyHC IIA and IIX isoforms separately, examine fiber type distribution, sample additional muscles to the vastus lateralis (VL), and incorporate an objective measurement of physical activity.
- 27 June 2024
- Published by International Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY)
Effects of age on human skeletal muscle: A systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size and distribution
INPLASY202460109 Effects of age on human skeletal muscle: A systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size and distribution Keywords: aging, sarcop…
- 27 June 2024
- Published by International Platform of Registered Systematic Review and Meta-analysis Protocols (INPLASY)
Effects of age on human skeletal muscle: A systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size and distribution
INPLASY202460109 Effects of age on human skeletal muscle: A systematic review and meta-analysis of myosin heavy chain isoform protein expression, fiber size and distribution Keywords: aging, sarcop…