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

Katon A. Kras, Nyssa Hoffman, Lori R. Roust, Tonya R. Benjamin, Elena A. De Filippis, Christos Katsanos

Research output: Contribution to journalArticle

Abstract

Introduction Current evidence indicates mitochondrial dysfunction in humans with obesity. Acute exercise appears to enhance mitochondrial function in the muscle of nonobese 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 adenosine triphosphate production rate (MAPR) and citrate synthase (CS) activity in isolated SS and IMF mitochondria from subjects with body mass index < 27 kg·m -2 (median age, 25 yr; interquartile range, 22-39 yr) and subjects with body mass index > 32 kg·m -2 (median age, 29 yr; interquartile range, 20-39 yr) before and 3 h after a 45-min cycling exercise at an intensity corresponding to 65% HR reserve. The SS and IMF mitochondria were isolated from muscle biopsies using differential centrifugation. Maximal adenosine triphosphate production rate and CS activities were determined using luciferase-based and spectrophotometric enzyme-based assays, respectively. Results Exercise increased MAPR in IMF mitochondria in both nonobese 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). Citrate synthase-specific activity increased in SS mitochondria in response to exercise only in nonobese subjects (P < 0.05). Conclusions In nonobese 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.

Original languageEnglish (US)
Pages (from-to)445-453
Number of pages9
JournalMedicine and science in sports and exercise
Volume51
Issue number3
DOIs
StatePublished - Mar 1 2019

Fingerprint

Muscle Mitochondrion
Mitochondria
Adenosine Triphosphate
Exercise
Obesity
Citrate (si)-Synthase
Muscles
Body Mass Index
Enzyme Assays
Luciferases
Centrifugation
Biopsy

Keywords

  • ADIPOSITY
  • CITRATE SYNTHASE
  • INTERMYOFIBRILLAR MITOCHONDRIA
  • SUBSARCOLEMMAL MITOCHONDRIA

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Adenosine Triphosphate Production of Muscle Mitochondria after Acute Exercise in Lean and Obese Humans. / Kras, Katon A.; Hoffman, Nyssa; Roust, Lori R.; Benjamin, Tonya R.; De Filippis, Elena A.; Katsanos, Christos.

In: Medicine and science in sports and exercise, Vol. 51, No. 3, 01.03.2019, p. 445-453.

Research output: Contribution to journalArticle

Kras, Katon A. ; Hoffman, Nyssa ; Roust, Lori R. ; Benjamin, Tonya R. ; De Filippis, Elena A. ; Katsanos, Christos. / Adenosine Triphosphate Production of Muscle Mitochondria after Acute Exercise in Lean and Obese Humans. In: Medicine and science in sports and exercise. 2019 ; Vol. 51, No. 3. pp. 445-453.
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abstract = "Introduction Current evidence indicates mitochondrial dysfunction in humans with obesity. Acute exercise appears to enhance mitochondrial function in the muscle of nonobese 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 adenosine triphosphate production rate (MAPR) and citrate synthase (CS) activity in isolated SS and IMF mitochondria from subjects with body mass index < 27 kg·m -2 (median age, 25 yr; interquartile range, 22-39 yr) and subjects with body mass index > 32 kg·m -2 (median age, 29 yr; interquartile range, 20-39 yr) before and 3 h after a 45-min cycling exercise at an intensity corresponding to 65{\%} HR reserve. The SS and IMF mitochondria were isolated from muscle biopsies using differential centrifugation. Maximal adenosine triphosphate production rate and CS activities were determined using luciferase-based and spectrophotometric enzyme-based assays, respectively. Results Exercise increased MAPR in IMF mitochondria in both nonobese 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). Citrate synthase-specific activity increased in SS mitochondria in response to exercise only in nonobese subjects (P < 0.05). Conclusions In nonobese 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.",
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T1 - Adenosine Triphosphate Production of Muscle Mitochondria after Acute Exercise in Lean and Obese Humans

AU - Kras, Katon A.

AU - Hoffman, Nyssa

AU - Roust, Lori R.

AU - Benjamin, Tonya R.

AU - De Filippis, Elena A.

AU - Katsanos, Christos

PY - 2019/3/1

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N2 - Introduction Current evidence indicates mitochondrial dysfunction in humans with obesity. Acute exercise appears to enhance mitochondrial function in the muscle of nonobese 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 adenosine triphosphate production rate (MAPR) and citrate synthase (CS) activity in isolated SS and IMF mitochondria from subjects with body mass index < 27 kg·m -2 (median age, 25 yr; interquartile range, 22-39 yr) and subjects with body mass index > 32 kg·m -2 (median age, 29 yr; interquartile range, 20-39 yr) before and 3 h after a 45-min cycling exercise at an intensity corresponding to 65% HR reserve. The SS and IMF mitochondria were isolated from muscle biopsies using differential centrifugation. Maximal adenosine triphosphate production rate and CS activities were determined using luciferase-based and spectrophotometric enzyme-based assays, respectively. Results Exercise increased MAPR in IMF mitochondria in both nonobese 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). Citrate synthase-specific activity increased in SS mitochondria in response to exercise only in nonobese subjects (P < 0.05). Conclusions In nonobese 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.

AB - Introduction Current evidence indicates mitochondrial dysfunction in humans with obesity. Acute exercise appears to enhance mitochondrial function in the muscle of nonobese 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 adenosine triphosphate production rate (MAPR) and citrate synthase (CS) activity in isolated SS and IMF mitochondria from subjects with body mass index < 27 kg·m -2 (median age, 25 yr; interquartile range, 22-39 yr) and subjects with body mass index > 32 kg·m -2 (median age, 29 yr; interquartile range, 20-39 yr) before and 3 h after a 45-min cycling exercise at an intensity corresponding to 65% HR reserve. The SS and IMF mitochondria were isolated from muscle biopsies using differential centrifugation. Maximal adenosine triphosphate production rate and CS activities were determined using luciferase-based and spectrophotometric enzyme-based assays, respectively. Results Exercise increased MAPR in IMF mitochondria in both nonobese 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). Citrate synthase-specific activity increased in SS mitochondria in response to exercise only in nonobese subjects (P < 0.05). Conclusions In nonobese 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.

KW - ADIPOSITY

KW - CITRATE SYNTHASE

KW - INTERMYOFIBRILLAR MITOCHONDRIA

KW - SUBSARCOLEMMAL MITOCHONDRIA

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