Aerobic conditioning

Aerobic conditioning is the use of continuous, rhythmic movement of large muscle groups to strengthen the heart and lungs (cardiovascular system),[1] as well as changes to the skeletal muscles.[2] Improvement in aerobic conditioning occurs when athletes expose themselves to an increase in oxygen uptake and metabolism, but to keep this level of aerobic conditioning, the athletes must keep or progressively increase their training to increase their aerobic conditioning.

Aerobic conditioning is usually achieved through aerobic exercise such as running, swimming, rowing machine, elliptical, treadmill, cycling,[3] etc. A stronger heart does not pump more blood by beating faster but by beating more efficiently, primarily via increased stroke volume and left ventricular mass.[4] Trained endurance athletes can have resting heart rates as low as a reported 28 beats per minute (Miguel Indurain) or 32 beats per minute (Lance Armstrong),[5] both of whom were professional cyclists at the highest level.

Aerobic conditioning makes the heart and lungs pump blood more efficiently, delivering more oxygen to muscles and organs.[6] Skeletal muscles also become aerobically conditioned, as regular aerobic exercise produces a shift in muscle fibres from more type II (fast twitch/glycolytic) into more type I (slow-twitch/oxidative).[2] Type I muscle fibres have far more mitochondria than type II, making type I fibres the producers of adenosine triphosphate (ATP) primarily through oxidative phosphorylation rather than anaerobic glycolysis.

Some neuromuscular diseases recommend regular aerobic exercise (of varying intensities depending on the disease) in order for the skeletal muscles to become aerobically conditioned, providing symptom relief or slowing the course of the disease, for example metabolic myopathies, Duchenne muscular dystrophy, and idiopathic inflammatory myopathies (IIM).[7][8][9]

  1. ^ "AAOS - OrthoInfo". orthoinfo.aaos.org. Retrieved 2016-05-17.
  2. ^ a b Widmann, Manuel; Nieß, Andreas M.; Munz, Barbara (April 2019). "Physical Exercise and Epigenetic Modifications in Skeletal Muscle". Sports Medicine (Auckland, N.Z.). 49 (4): 509–523. doi:10.1007/s40279-019-01070-4. ISSN 1179-2035. PMID 30778851. S2CID 73481438.
  3. ^ ("Aerobic Exercise,"2023).
  4. ^ Stone, Nicholas M.; Kilding, Andrew E. (2009). "Aerobic Conditioning for Team Sport Athletes". Sports Medicine. 39 (8): 615–642. doi:10.2165/00007256-200939080-00002. ISSN 0112-1642. PMID 19769413. S2CID 23256471.
  5. ^ The Lance Armstrong Performance Program ISBN 1-57954-270-0
  6. ^ "Effects of Exercise on the Heart". Boundless. 2016-01-04. Archived from the original on 2016-10-12.
  7. ^ Urtizberea, Jon Andoni; Severa, Gianmarco; Malfatti, Edoardo (May 2023). "Metabolic Myopathies in the Era of Next-Generation Sequencing". Genes. 14 (5): 954. doi:10.3390/genes14050954. ISSN 2073-4425. PMC 10217901. PMID 37239314.
  8. ^ Heydemann, Ahlke (2018-06-20). "Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies". Nutrients. 10 (6): 796. doi:10.3390/nu10060796. ISSN 2072-6643. PMC 6024668. PMID 29925809.
  9. ^ Alemo Munters, Li; Dastmalchi, Maryam; Katz, Abram; Esbjörnsson, Mona; Loell, Ingela; Hanna, Balsam; Lidén, Maria; Westerblad, Håkan; Lundberg, Ingrid E.; Alexanderson, Helene (2013-08-13). "Improved exercise performance and increased aerobic capacity after endurance training of patients with stable polymyositis and dermatomyositis". Arthritis Research & Therapy. 15 (4): R83. doi:10.1186/ar4263. ISSN 1478-6362. PMC 3978470. PMID 23941324.