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ATP Production of Muscle Mitochondria after Acute Exercise in Lean and Obese Humans

Kras, Katon A.1; Hoffman, Nyssa1; Roust, Lori R.2; Benjamin, Tonya R.2; De Filippis, Elena A.2; Katsanos, Christos S.1,2

Medicine & Science in Sports & Exercise: October 22, 2018 - Volume Publish Ahead of Print - Issue - p
doi: 10.1249/MSS.0000000000001812
Original Investigation: PDF Only

Introduction Current evidence indicates mitochondrial dysfunction in humans with obesity. Acute exercise appears to enhance mitochondrial function in muscle of non-obese humans, but its effects on mitochondrial function in muscle of humans with obesity are not known. We sought to determine whether acute aerobic exercise stimulates mitochondrial function in subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria in humans with obesity.

Methods We assessed maximal ATP production rate (MAPR) and citrate synthase (CS) activity in isolated SS and IMF mitochondria from subjects with BMI < 27 kg/m2 (median age 25 years, (interquartile range (IQR)) 22-39 years) and subjects with BMI > 32 kg/m2 (median age 29 years, IQR 20-39 years) before and 3 hours after a 45-min cycling exercise at an intensity corresponding to 65% heart rate reserve. SS and IMF mitochondria were isolated from muscle biopsies using differential centrifugation. MAPR and CS activity were determined using luciferase- and spectrophotometric enzyme-based assays, respectively.

Results Exercise increased MAPR in IMF mitochondria in both non-obese subjects and subjects with obesity (P < 0.05), but CS specific activity did not change in either group (P > 0.05). Exercise increased MAPR supported by complex II in SS mitochondria, in both groups (P < 0.05), but MAPR supported by complex I or palmitate did not increase by exercise in the subjects with obesity (P > 0.05). CS specific activity increased in SS mitochondria in response to exercise only in non-obese subjects (P < 0.05).

Conclusions In non-obese humans, acute aerobic exercise increases MAPR in both SS and IMF mitochondria. In humans with obesity, the exercise increases MAPR in IMF mitochondria, but this response is less evident in SS mitochondria.

1Center for Metabolic and Vascular Biology, Arizona State University, Scottsdale, AZ

2College of Medicine, Mayo Clinic in Arizona, Scottsdale, AZ

Corresponding author: Christos S. Katsanos, Ph.D., Center for Metabolic and Vascular Biology, Mayo Clinic Collaborative Resarch Building, 13208 East Shea Boulevard, Scottsdale, AZ 85259. Phone: (480) 301-6015. E-mail:

The study was supported by NIH/NIDDK grant DK094062 (CSK).

Conflict of Interest: The authors have no conflicts of interest to report. The results of the present investigation do not constitute endorsement by ACSM. The authors declare that the results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.

Accepted for publication: October 2018.

© 2019 American College of Sports Medicine