Biological aging refers to the cumulative functional decline that can occur even when chronological age is similar across individuals. In some older athletes, performance appears to be preserved or even optimized relative to peers, prompting the phrase “aging like wine.” From a medical perspective, this phenomenon is not magic; it reflects measurable differences in cellular senescence, inflammation, endocrine signaling, neuromuscular integrity, and metabolic regulation.
At the cellular level, aging accelerates when cells undergo replicative exhaustion and stress-induced senescence. Senescent cells adopt a pro-inflammatory secretory phenotype (SASP), releasing cytokines and chemokines that can impair tissue repair and increase systemic inflammation. However, regular endurance and resistance training can modulate these pathways: exercise improves antioxidant capacity, reduces oxidative stress burden, and can lower chronic low-grade inflammation. The net effect is a slower decline in physiological reserve, which may help explain why some septuagenarians (and select late-30s athletes) maintain high performance.
Metabolic resilience is another cornerstone. Aging is associated with mitochondrial dysfunction, reduced oxidative phosphorylation efficiency, and impaired metabolic flexibility. Aerobic training enhances mitochondrial biogenesis through signaling pathways such as PGC-1α, improving ATP production and endurance capacity. Resistance training increases muscle fiber cross-sectional area and improves insulin sensitivity, mediated in part by enhanced glucose transporter activity and improved signaling through insulin receptor pathways. Improved insulin sensitivity reduces risk of sarcopenic obesity, a condition in which declining muscle mass is accompanied by increased fat mass.
Sarcopenia and neuromuscular decline typically limit athletic performance with age. Clinically, sarcopenia involves loss of skeletal muscle mass, strength, and/or physical performance. Resistance training counteracts muscle loss by promoting hypertrophy and motor unit recruitment efficiency. Importantly, the nervous system also ages: reaction time, coordination, and motor learning can decline. Yet skilled athletes often exhibit preserved or compensatory neuromuscular strategies through extensive practice. Training-induced neuroplasticity supports continued motor performance via synaptic adaptation and improved recruitment patterns.
Endocrine changes play an additional role. With age, testosterone and growth hormone axis activity often decline, potentially reducing anabolic signaling. Nevertheless, athletes who maintain training intensity, body composition, and sleep may preserve functional anabolic responsiveness, including androgen receptor sensitivity and favorable body composition–related hormone profiles. Cortisol regulation also matters; chronic stress elevates cortisol, which can promote catabolism and impair recovery. Adequate recovery, including sleep and nutrition, normalizes hypothalamic-pituitary-adrenal axis activity and allows training adaptations rather than cumulative fatigue.
Inflammation and immune aging—sometimes termed immunosenescence—affect physical recovery and injury risk. Older individuals often exhibit altered immune cell phenotypes and diminished vaccine responses, along with persistent low-grade inflammation (inflammaging). Exercise can re-balance immune function by enhancing anti-inflammatory cytokine profiles and improving macrophage polarization toward tissue-repair states. This may reduce recovery time and support consistent performance.
Cardiometabolic health is another mechanism underpinning “performance longevity.” Vascular aging increases arterial stiffness and impairs oxygen delivery. Regular aerobic activity improves endothelial function via nitric oxide bioavailability and reduces atherogenic risk factors. Improved cardiovascular efficiency translates into better oxygen uptake, which is crucial for high-intensity sports demands.
Injury prevention and musculoskeletal maintenance are clinically relevant. Aging cartilage shows altered extracellular matrix turnover, and tendons may become less resilient. Strength training, neuromuscular conditioning, and progressive loading stimulate remodeling, increasing tendon stiffness in an adaptive range and improving joint stability. Adequate vitamin D status, sufficient protein intake, and omega-3 fatty acid consumption can support collagen turnover and muscle recovery, though individualized assessment is important.
Finally, biological aging is influenced by lifestyle and genetics. Epigenetic clocks—biomarker models based on DNA methylation patterns—can indicate faster or slower biological aging relative to chronological age. Factors such as smoking cessation, weight management, sleep duration and quality, physical activity consistency, and stress reduction tend to correlate with more favorable epigenetic aging trajectories.
Therefore, when an older athlete demonstrates exceptional performance, the most plausible medical explanation is that training has preserved physiological function by mitigating senescence-related inflammation, sustaining mitochondrial and metabolic efficiency, maintaining muscle and neuromuscular performance, and supporting cardiometabolic and recovery systems. “Aging like wine” reflects a favorable balance between biological wear-and-tear and adaptive capacity rather than an absence of aging.
Source: @FutureCanes
Alex Ohári 🔴⚫️: Jordan Staal (37) was the oldest player to ever score in each of the first 3 games of a Stanley Cup final. You can make it 4. One of his best ever seasons at age 37. Aging like wine.. #breaking
— @FutureCanes May 1, 2026
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