Stay Fit, Stay Young: Mitochondria in Movement: The Role of Exercise in the New Mitochondrial Paradigm

Abstract

Skeletal muscles require the proper production and distribution of energy to sustain their work. To ensure this requirement is met, mitochondria form large networks within skeletal muscle cells, and during exercise, they can enhance their functions. In the present review, we discuss recent findings on exercise-induced mitochondrial adaptations. We emphasize the importance of mitochondrial biogenesis, morphological changes, and increases in respiratory supercomplex formation as mechanisms triggered by exercise that may increase the function of skeletal muscles. Finally, we highlight the possible effects of nutraceutical compounds on mitochondrial performance during exercise and outline the use of exercise as a therapeutic tool in noncommunicable disease prevention. The resulting picture shows that the modulation of mitochondrial activity by exercise is not only fundamental for physical performance but also a key point for whole-organism well-being.

Figure 1

Energy system contribution during exercise. CK: Krebs cycle; I, III, IV: mitochondrial complexes; V: ATP synthase: FADH: reduced flavin adenine dinucleotide; NADH: reduced nicotinamide adenine dinucleotide; ATP: adenosine triphosphate; ADP: adenosine monophosphate.

Figure 2

The creatine kinase/phosphocreatine system. Compartment-specific isoenzymes of creatine kinase (CK) are found in mitochondria (Mt-CK) and cytosol (c-CK). PCr: phosphocreatine, Cr: creatine, ATP: adenosine triphosphate, ADP: adenosine monophosphate.

Figure 3

The energy systems that contribute to sport practice. The phosphagen system (ATP-CP) is used in explosive movements (Immediate energy). Anaerobically created energy overlaps with use of the ATP-CP system to provide energy for activities lasting up to around 3 minutes. Aerobic glycolysis provides energy for longer-distance events by breaking down fat and some carbohydrates.

Figure 4

Exercise-induced mitochondrial signaling and biogenesis in skeletal muscle. ATP: adenosine triphosphate; ADP: adenosine monophosphate; NAD+/NADH: oxidized/reduced nicotinamide adenine dinucleotide; HIF-1α: hypoxia-inducible factors; p38 MAEK: P38 MAPK mitogen-activated protein kinase; CaMK: Ca²⁺/calmodulin-dependent protein kinase: AKT: serine/threonine-specific protein kinase; CREB: cAMP response element-binding protein; ATF2: activating transcription factor 2; MEF2: myocyte enhancer factor-2; AMPK: AMP-activated protein kinase; PGC-1: PPARγ coactivator-1; PPARγ: peroxisome proliferator-activated receptor γ; ROS: reactive oxygen species; SIRT-1: sirtuin 1; TFAM: mitochondrial transcription factor A; TIM: translocase of the inner mitochondrial membrane; TOM; translocase of the outer mitochondrial membrane; AC: acetylated; P: phosphorylated.

Figure 5

Mitochondrial dynamics is affected by/during exercise. PGC-1: PPARγ coactivator-1; ROS: reactive oxygen species; FIS1: mitochondrial fission 1 protein; Drp1: dynamin-related protein 1; OPA1: mitochondrial dynamin like GTPase; MFN1/2: mitofusin 1 and 2 protein.