The [High Intensity Interval Training (HIIT)] used during the study was proven effective in enhancing performance and physiological capacities. Power output during HIIT increased from baseline (BL) through light training (LT) and moderate training (MT) (
Figures 1C and 1D). In the phase of excessive training (ET), despite increasing the training load, the improvement in physical performance stagnated, indicating what others have described as accumulating fatigue and maladaptation to the exercise stimuli. After the recovery phase (RE), when the training load was drastically reduced, performance peaked (
Figure 1C).
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The classic cellular response to exercise training is an increase in the amount and respiratory capacity of mitochondria that increases the respiratory capacity of a given unit of muscle. Intrinsic mitochondrial respiration (IMR) is instead the respiratory capacity related to a mitochondrial parameter, often a mitochondrial protein or citrate synthase (CS) activity.
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During the first part of the intervention, from BL to LT and MT, IMR numerically increased (from 13.2 ± 1.8 to 15.7 ± 1.4 pmol·s−1·μg−1) but decreased drastically by 40% (to 9.4 ± 1.1 pmol·s−1·μg−1) during ET compared with MT (
Figure 2A). In RE, intrinsic mitochondrial function seemed to recover numerically but was still 25% lower than that during MT (11.8 ± 1.1 pmol·s−1·μg−1) (
Figure 2A).
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After moderate exercise training, mitochondrial dynamics have been shown to be activated by the promotion of fusion and reduction of fission events.
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We found that Mitofusin 2 (MFN2) (
Figure 5A), which fuses the mitochondrial outer membrane, as well as inner membrane fuser optic atrophy 1 (OPA1) (
Figure 5B) both increased robustly during the first 3 weeks of progressive training load and were most abundant after ET. The activation of mitochondrial fission did not follow a uniform pattern.
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We found that changes in IMR were closely paralleled by changes in glucose tolerance (
Figure 3C).
