I checked that Dr. Maffetone book. Although he cautions a lot about overtraining, the reasons given focus on hormonal imbalances and the effects on physical and mental health. The question of reactive oxygen species (ROS) on longevity were not in there. I have read that the early belief that ROS were destructive to mitochondria is changing in the research. It seems a low level is healthy but an excessive level is not and physical activity (PA) increases longevity and decreases morbidity in older age. Last quote references exercise at 50-70% of VO2 max, this is not a really hard pace, as being conducive to mitochondria. So, I would guess moderate pace long rides are good for health. Personally, I monitor sleep and heart rate variability when doing heavy rando mileage and if in doubt, I take a rest day. YMMV. Who Knows really
ROS is often considered as a toxic metabolic byproduct that causes detrimental damage to multiple cellular components, thereby contributing to the aging process (3, 52). However, as discussed above, mitochondrial ROS is not the major cause of mtDNA mutations, indicating a more complex cellular role. Actions of ROS are pleiotropic. They cause oxidative stress at higher concentrations (pathological) while they act as signaling molecules at lower levels (physiological).
https://www.ncbi.nlm.nih.gov/labs/pm...es/PMC6386233/
It is now widely accepted that the ability to deliver and utilize oxygen by the cardiorespiratory system and skeletal muscles, respectively (e.g., maximal aerobic capacity; VO2
max), is a strong determinant of health and longevity in modern humans [9]. For example, runners have ~45–70% and ~30–50% reduced risk of mortality from cardiovascular disease (CVD) and cancer, respectively, and live 3–10% (2–8 years) longer than non-runners
Aging is characterized by a progressive impairment of all body organs, including those that regulate VO2max and locomotion (e.g., cardiorespiratory, nervous, and musculoskeletal systems), resulting in a ~10% decline in aerobic capacity per decade in both males and females after ~ 30 years of age
((That decline is not assured. Many healthy lifelong aerobic exercisers lose much less. Andrew Coggan and other athletic scientists have shared their aerobic losses and they are much, much less than 10% per decade. ))
Currently, physical activity (PA) and caloric restriction represent the only non-pharmacologic means to enhance health-span and life expectancy by their ability to coordinately rejuvenate the systems that drive the biological aging process [21,22]; however, exercise is the only factor confirmed to lower morbidity and all-cause mortality in epidemiological studies.
Acute contractile activity is a hormetic stress stimulus that temporarily alters intracellular danger signals (ROS, Ca2+
, pH, and hypoxia), lowers cellular energy state (NAD+
/NADH and AMP/ATP), and promotes release of hormones and circulatory factors (‘exerkines’), which synchronously activate signaling pathways that stimulate mitochondrial biogenesis (CaMK II, PGC-1α, SIRT1, and AMPK), antioxidant defense (Nrf2-Keap1, NF-κB, and MAPK), waste recycling (autophagy (ULK1-Beclin1) and 26S proteasome (FOXO3a)), and the immune response (IL-1β, IL-18, IL-6, IL-10, IL-1ra, sTNF-R, etc.) [20,21,128,129,130,131,132,133,134,135,136,137,138,139]. Anabolic GRPs, mainly mediated by Akt-mTOR signaling (e.g., protein synthesis), are activated following exercise concomitant with energy repletion, and may stay elevated for 1–2 days in older adults [140]. Consistent with the concept of hormesis [44,141], repeated exposure to a single-stress stimulus such as exercise improves stress resistance and immunity, rejuvenates mitochondria (increased biogenesis, recycling, and damage removal), and increases the organ functional reserve
The long-term benefits of PA are multi-systemic (muscular, nervous, vascular, endocrine, and immune systems) and culminate in reduced all-cause mortality and enhanced longevity (e.g., ~3–10% in average life expectancy) [10,11]. AET is considered the gold standard to improve mitochondrial biogenesis, insulin sensitivity, and cardiorespiratory fitness across all age groups. In older adults, AET partially reverses mitochondrial dysfunction by augmenting mtDNA copy number, mitochondrial transcript and protein expression, oxidative enzyme function, ATP synthesis, and total mitochondrial volume [142,143,144]. Short et al. demonstrated that the capacity for mitochondrial biogenesis (e.g., PGC-1α, NRF1, and TFAM), mitochondrial gene expression (COX IV and ND4), and Kreb’s cycle/MRC enzyme activities (CS and COX) may be enhanced by AET regardless of age [143]. Indeed, 12 weeks of progressive moderate-intensity AET (50–70% vo2 max) increased total mitochondrial content (mtDNA and cardiolipin), MRC function (NADH oxidase and succinate oxidase), and HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) in older adults
https://www.ncbi.nlm.nih.gov/labs/pm...es/PMC6627948/