Biochemical Differences Between the Response to High Intensity versus Moderate Exercise
A range of evidence suggests high intensity exercise to produce different, greater benefits than is the case for more moderate, longer periods of exercise. Researchers here look at the biochemistry of cellular senescence in muscle tissue immediately following exercise, and find the characteristics notably different. The results suggest that high intensity exercise induces more short-term inflammatory cell stress, but removes more of the pre-existing markers of cellular senescence as a result of a greater immune reaction to that stress.
In this study, we asked the question whether the cellular senescence-lowering effect of exercise in human skeletal muscle can occur only at the intensity sufficient to induce DNA damage and inflammation. Biopsied vastus lateralis of 9 sedentary men (age 26.1 ± 2.5 y) were assessed before and after a single bout of moderate steady state exercise (SSE, 60% maximal aerobic power) and high intensity interval exercise (HIIE, 120% maximal aerobic power). Increases in cell infiltration (+1.2 folds), DNA strand break (+1.3 folds), and γ-H2AX+ myofibers (+1.1 folds) occurred immediately after HIIE and returned to baseline in 24 hours. Muscle p16Ink4a mRNA decreased 24 hours after HIIE. SSE had no effect on cell infiltration, p16Ink4a mRNA, and DNA strand break in muscle tissues.
The major findings are as follows: (1) Cellular senescence-lowering effect of aerobic exercise can occur only at high intensity. SSE with similar exercise work failed to lower the p16INK4a mRNA in human skeletal muscle within the 24-h recovery period; (2) HIIE triggered immediate increases in cell infiltration and γ-H2AX+ myofibers, followed by a decreased p16INK4a mRNA in human skeletal muscle 24 hours after recovery; (3) By further examining the individual responses, the senolytic effect of HIIE were contributed solely from those participants with high pre-exercise p16INK4a mRNA in skeletal muscles.
High intensity exercise is known to cause greater levels of lactate production and acidosis than low intensity exercise. Decreased pH has been reported to be a danger signal to activate innate immune response and immune cells are functioned to recognize and clear senescent cells by phagocytosis in humans. Therefore, the acute changes in the microenvironment during and after exercise may be a selection pressure to aged stem cell population resided in the skeletal muscle. Exercise intensity determines the magnitude of cell renewal during a brief period of inflammation.
Taken together, decreased cellular senescence 24 hours after HIIE is best explained by senescent cell clearance following a brief increase of bone marrow cell infiltration into challenged skeletal muscle to participate in the early phagocytic and late regenerative phases of inflammation. DNA damage is a potent stimulator of inflammation. In this study, a fast resolution of DNA damage/repair response 24 hours following HIIE suggests an efficient clearance of senescent cells with DNA damage in human skeletal muscle to resolve the inflammation.
Excellent.
Now is the time to foster increased collaboration and cross-discipline interaction.
Will the interested Kinesiologists and Exercise Scientists please attend your local gerontologist or aging scientist-equivalent to bring in new technology to monitor, assess, recommend, and foster advances in such.
Informing and reaching out to the sympathetic medical professions to push these things forward is crucial.
Very nice detailed study deserving a major follow-up with more and older participants and a longer follow-up period.