Antioxidants, Oxidative Stress and Mitochondrial Health: How to Time Pre‑Workout Support Without Blunting Gains

Table of Contents

1. Key Highlights:
2. Introduction
3. The paradox of inflammation: why some damage is necessary
4. Oxidative stress, ROS and exercise: a concise primer
5. Timing is everything: pre-workout, intra-workout and post-workout roles
6. Dose matters: more is not better
7. Food-based antioxidants vs. isolated supplements
8. Mitochondria under the hood: why they matter to athletes
9. Nitric oxide, nitrates and the alternative strategy of metabolic efficiency
10. Coenzyme Q10: a familiar mitochondrial ally
11. Emerging compounds: urolithin A and the mitolytic debate
12. PQQ and PGC-1α activation: building new mitochondria
13. A practical framework for athletes: what to take and when
14. Safety, interactions and unanswered questions
15. Implementing changes: sample protocols for different athlete types
16. How to evaluate product labels: what to look for and avoid
17. Reconciling short-term recovery with long-term gains
18. Research perspective: where the field is headed
19. FAQ

Key Highlights:

• Antioxidants can reduce exercise-induced oxidative damage and speed acute recovery, but high doses—especially post-workout—can blunt adaptations and impair long-term gains.
• Timing and dose determine whether antioxidants help or hinder: targeted, lower-dose antioxidants taken pre-workout support performance; chronic high-dose supplementation risks interfering with inflammatory signals needed for muscle growth.
• Mitochondrial-targeted strategies (nitrates/nitric oxide, CoQ10, PQQ, and emerging compounds such as urolithin A) have distinct roles: combine approaches that promote mitochondrial quality and biogenesis rather than relying on a single mitolytic or antioxidant solution.

Introduction

Exercise provokes a controlled assault on muscle tissue. That assault produces reactive oxygen species (ROS) and inflammation—signals that trigger repair and adaptation. The same processes that cause soreness and short-term performance drops also drive the strength, endurance, and metabolic benefits athletes want. Antioxidants blunt oxidative damage, but they also dampen those signals when applied without nuance. The debate among sport scientists and registered dietitians is no longer whether antioxidants can help; it is where, when and how much.

Sports nutrition experts who study pre-workout and recovery strategies emphasize a careful balance. Lower, targeted antioxidant doses and mitochondrial-supporting ingredients in the pre-workout window can reduce unnecessary damage and improve performance. By contrast, indiscriminate, high-dose antioxidant use—especially immediately after training—can impede satellite cell activity, inflammatory signaling, and the remodeling processes that underlie strength and hypertrophy. At the same time, new ingredients that target mitochondria raise both promise and caution: removing dysfunctional mitochondria (mitolysis) without encouraging new mitochondrial formation can be counterproductive.

This article synthesizes expert perspectives, mechanistic science and practical recommendations to guide athletes and coaches who aim to preserve acute performance and recovery while protecting long-term adaptation. It translates complex physiology into actionable strategies for supplement timing, ingredient selection, and training coordination.

The paradox of inflammation: why some damage is necessary

Inflammation and oxidative stress often carry negative connotations. Yet acute inflammation after exercise is a primary driver of adaptation. When muscle fibers experience microtears, immune cells—including neutrophils and macrophages—arrive and produce ROS deliberately. Those reactive species do not simply cause harm; they act as signals that coordinate cleanup, stimulate satellite cells, and initiate remodeling.

Frames help: think of oxidative stress like controlled fire in land management. A managed burn clears dead material and returns nutrients to the soil; unmanaged wildfire destroys. Post-exercise inflammation is the controlled fire that clears damaged proteins and organelles and triggers growth. Completely extinguishing that fire reduces the stimulus that would otherwise prompt muscles to adapt.

Experts point to the timing of that fire. Pre-workout measures that reduce unnecessary oxidative damage during performance can preserve work capacity and delay fatigue. Post-workout suppression of inflammation risks blunting the very cellular responses that generate strength and hypertrophy. That is why registered dietitians and exercise physiologists now caution against blanket, high-dose antioxidant regimens—especially immediately after training.

Real-world example: a strength athlete who floods their system with high-dose vitamin C and vitamin E daily may report reduced soreness but make slower progress over months. Their acute recovery feels better, but markers of muscle protein synthesis and satellite cell activation are muted, slowing long-term gains.

Oxidative stress, ROS and exercise: a concise primer

Reactive oxygen species—molecules such as superoxide, hydrogen peroxide and hydroxyl radicals—arise mainly from mitochondrial electron transport during cellular respiration. Their production increases when ATP demand rises, such as during intense resistance or anaerobic exercise. ROS are chemically reactive and can damage lipids, proteins and DNA when unchecked. That damage is the oxidative stress often referenced in sports nutrition.

But ROS also act as second messengers. They modulate kinase pathways, transcription factors and gene expression that orchestrate adaptation. Key points:

• Source: Mitochondria are the primary source of ROS during aerobic metabolism. Non-mitochondrial sources, like NADPH oxidase in immune cells, also contribute, particularly during inflammation.
• Dose and context: Low to moderate ROS levels stimulate adaptive pathways (hormesis). Excessive ROS cause cellular dysfunction.
• Signaling versus damage: The same molecule that damages a membrane lipid may simultaneously activate transcription factors (e.g., NRF2) that upregulate endogenous antioxidant defenses.

This duality explains why antioxidant interventions produce mixed outcomes. The goal is to control excess oxidative damage that limits performance while preserving the signaling needed for adaptation.

Timing is everything: pre-workout, intra-workout and post-workout roles

Experts recommend placing antioxidants where they reduce unnecessary damage during effort rather than where they blunt repair signaling after exercise. Three windows matter:

• Pre-workout: Antioxidants taken before training can attenuate acute oxidative damage and fatigue. This preserves work capacity, allowing more volume or intensity in a session. When combined with nitric oxide (NO) precursors or nitrates, a pre-workout formulation can improve blood flow and metabolic efficiency, further reducing ROS generation for the same output.
• Intra-workout: For prolonged endurance sessions, moderate antioxidant support can reduce cumulative oxidative stress that impairs performance later in the session. Be cautious about doses and types; whole-food carbohydrate intake and electrolytes remain primary intra-session supports.
• Post-workout: This window requires restraint. Acute inflammation participates in repair, so high-dose antioxidants right after training can interfere with satellite cell recruitment and mitochondrial adaptations. Low-dose or food-based antioxidants that provide baseline nutritional support are acceptable, but megadoses—especially of isolated antioxidant vitamins—carry risk.

Practical application: If an athlete uses a pre-workout product with antioxidants, choose products formulated to provide supportive doses rather than pharmacological amounts. After training, prioritize protein for muscle protein synthesis, carbohydrates to restore glycogen, sleep and overall daily antioxidant intake from fruits and vegetables rather than immediate, high-dose supplementation.

Dose matters: more is not better

The International Society of Sports Nutrition (ISSN) has emphasized a dose-dependent effect of antioxidants: low to moderate intake can support adaptation; high doses can be harmful. The concept is straightforward: antioxidant supplements follow a hormetic curve. At optimal doses they reduce harmful oxidative damage without wiping out physiological signaling. Exceeding that optimal window results in over-suppression of ROS and diminished adaptation.

Evidence from human trials supports this principle. Studies that administered large doses of vitamins C and E found attenuated training adaptations in both endurance and resistance training protocols. Mechanistically, these antioxidants suppressed key signaling molecules and gene expression patterns that drive mitochondrial biogenesis and muscle hypertrophy.

Guiding principles:

• Aim for dietary adequacy first: prioritize fruits and vegetables to supply a spectrum of antioxidants and cofactors.
• Use supplementation to address gaps or targeted needs, not to substitute for a poor diet.
• Avoid chronic, high-dose antioxidant regimens, especially immediately after resistance training sessions aimed at hypertrophy.

Athletic example: A cyclist preparing for an event benefits from targeted antioxidant support during heavy training weeks to reduce accumulated oxidative damage and maintain training quality. However, using high-dose antioxidant pills every day for months may blunt mitochondrial adaptations and reduce endurance gains.

Food-based antioxidants vs. isolated supplements

Whole foods deliver a complex matrix of phytochemicals, fiber and micronutrients that function together. Fruits and vegetables contain vitamin C, carotenoids, polyphenols, flavonoids, and other compounds that modulate oxidative stress in physiologically appropriate ways. Most athletes do not meet recommended intakes of fruits and vegetables, which creates a legitimate role for supplemental support.

Important distinctions:

• Synergy: Compounds like vitamin C interact with polyphenols and carotenoids within a whole-food matrix. That synergy can temper potent effects of isolated high-dose agents.
• Bioavailability: Certain phytochemicals have limited absorption unless paired with fats or other cofactors. A supplement might deliver a high dose but lack the matrix that influences absorption and action.
• Practicality: A concentrated greens powder or food-based multinutrient can help athletes reach baseline antioxidant intake without resorting to pharmacologic dosing.

Example: A daily serving of berries, leafy greens and beets offers vitamin C, polyphenols and nitrates that together improve recovery and vascular function. A pill containing 2,000 mg of vitamin C lacks that spectrum and risks blunting ROS-mediated signals.

Mitochondria under the hood: why they matter to athletes

Mitochondria convert substrates into ATP through oxidative phosphorylation. Higher mitochondrial density and efficiency translate into better endurance and metabolic flexibility. During intense anaerobic efforts, mitochondria still play a central role: the inefficiencies in electron transport increase ROS, which contributes to fatigue.

Key mitochondrial concepts for athletes:

• ATP production capacity sets the ceiling for sustained work output.
• Mitochondrial efficiency influences how much ROS is produced for a given ATP yield.
• Mitochondrial turnover—balancing biogenesis (creation of new mitochondria) with mitophagy (removal of damaged mitochondria)—maintains quality control.

Training stimulates mitochondrial biogenesis via pathways such as PGC-1α. Endurance exercise is especially effective at activating these processes; resistance training also contributes through metabolic stress and localized signaling. Diet and supplements can modulate these pathways, but exercise remains the most consistent and robust stimulus.

Practical point: Improving mitochondrial quality and number enhances both performance and recovery. Strategies that promote biogenesis and simultaneously clear dysfunctional mitochondria are theoretically ideal.

Nitric oxide, nitrates and the alternative strategy of metabolic efficiency

Reducing ROS can be approached indirectly: make ATP production more efficient. Nitrates and nitric oxide (NO) increase blood flow, improve oxygen delivery and can alter electron transport chain efficiency, lowering ROS for a given work output. Beetroot juice, nitrate-rich vegetables and specific NO-boosting ingredients in pre-workout supplements use this route.

Mechanisms:

• Nitrates convert to nitrite and then to nitric oxide, particularly under hypoxic or acidic conditions such as intense exercise.
• NO augments vasodilation, which improves perfusion and oxygen delivery.
• Some evidence shows nitrates can reduce oxygen cost of submaximal exercise, thereby decreasing mitochondrial electron leak and ROS production.

Application: For athletes who need improved work capacity in a session, a pre-workout with nitrates can reduce metabolic cost and ROS accumulation, allowing more effective training without directly suppressing ROS signaling.

Real-world use: Middle-distance runners and cyclists often use beetroot-based supplements before key intervals to improve time-to-fatigue. Because nitrates act primarily by improving metabolic efficiency, they do not carry the same risk of blunting adaptive signaling as large, generic antioxidant doses.

Coenzyme Q10: a familiar mitochondrial ally

Coenzyme Q10 (CoQ10) sits in the inner mitochondrial membrane and facilitates electron transport, with an ancillary role as an antioxidant. It is fat-soluble and often marketed for heart health and mitochondrial support.

Traits and considerations:

• Chronic supplementation of CoQ10 can improve mitochondrial function over time. It may decrease ROS production by stabilizing the electron transport chain.
• CoQ10 is not an immediate performance enhancer in most people; benefits accrue with consistent use.
• Because it is fat-soluble, optimal absorption requires co-ingestion with dietary fats or lipid-based formulations.

Application guidance: CoQ10 is more logical as a daily supplement aimed at long-term mitochondrial health than as a component whose primary utility is immediate pre-workout effects. Athletes who experience palpitations with stimulant-heavy pre-workouts sometimes report CoQ10 helps, but scientific support is modest. Expect gradual improvements in markers of metabolic health rather than sudden boosts in gym performance.

Emerging compounds: urolithin A and the mitolytic debate

Urolithin A has gained attention as a compound that induces mitophagy: the selective removal of dysfunctional mitochondria. It is a metabolite produced by gut microbes metabolizing polyphenols such as ellagitannins, found in pomegranates, walnuts and berries. Supplementation with urolithin A aims to boost mitophagy when endogenous production is low.

Why the controversy:

• Targeted removal of dysfunctional mitochondria sounds beneficial. Defective mitochondria generate excess ROS and reduce efficiency.
• However, removing mitochondria without concurrent stimulation of mitochondrial biogenesis risks creating a temporary deficit in energetic capacity. For athletes who need immediate ATP production—such as before or during training—this could impair performance.
• Experts therefore advise caution: mitolytics should be paired with biogenesis-promoting strategies (exercise, nutrients or molecules that activate PGC-1α).

Combining strategies: For users of urolithin A, timing matters. Consuming it away from the pre-workout window reduces the risk of immediate performance impairment. Pairing chronic urolithin A use with interventions that promote mitochondrial biogenesis—endurance training, PQQ supplementation, or certain nutritional strategies—supports a cycle of removal and renewal.

Safety and evidence: Human trials indicate urolithin A can improve biomarkers of mitochondrial health in older adults, but long-term data in athletic populations is limited. Researchers emphasize the need to evaluate functional outcomes (VO2max, power output) rather than surrogate biomarkers alone.

Practical scenario: An older recreational athlete using urolithin A for mitochondrial quality should ensure their training program includes regular endurance or high-volume metabolic sessions that stimulate mitochondrial biogenesis. They should avoid taking mitolytic supplements immediately before key workouts.

PQQ and PGC-1α activation: building new mitochondria

Pyrroloquinoline quinone (PQQ) and other agents are reported to influence mitochondrial biogenesis pathways, including PGC-1α activation. PGC-1α is a master regulator of mitochondrial gene expression and biogenesis, responding robustly to endurance-type stimuli.

Points to consider:

• Exercise remains the strongest, safest activator of PGC-1α. Endurance training, interval work and volume-based aerobic sessions upregulate mitochondrial biogenesis.
• Nutrients and supplements may augment this response. PQQ has been studied for its potential to stimulate mitochondrial biogenesis and antioxidant defense.
• Pairing biogenesis-promoting strategies with mitophagy-enhancing agents forms a logical cycle: clear the old, build the new.

Example programmatic approach: During a training block focused on mitochondrial improvements, prioritize consistent aerobic work, support it with dietary nitrate and a modest PQQ regimen if appropriate, and reserve mitolytic compounds for off-periods when you can promote rebuilding through training and nutrition.

A practical framework for athletes: what to take and when

Translating physiology into practice requires clarity. Below is a practical framework that aligns with current evidence and expert perspectives.

1. Prioritize whole-food antioxidants daily.

• Aim for a variety of fruits and vegetables across the day. These supplies provide a balanced spectrum of antioxidants and phytochemicals that support baseline health without over-suppressing signaling.
• When whole-food intake is limited due to logistics, use a food-based multinutrient or a greens powder as a baseline.

2. Use targeted antioxidant support pre-workout when necessary.

• Choose pre-workout formulations that include low-to-moderate doses of antioxidant ingredients and nitric oxide precursors or nitrates.
• The goal is to reduce unnecessary oxidative damage during high-intensity bouts and to preserve performance, not to quench all ROS.

3. Avoid high-dose antioxidant megadoses immediately after resistance training.

• Reserve post-workout nutrition for protein, carbohydrates and rehydration. If you supplement with antioxidants post-training, use moderate doses or food-based sources.
• Periodic use of higher antioxidant doses during illness or during unusually heavy training loads may be reasonable, but avoid chronic use that could blunt adaptations.

4. For mitochondrial targeters, adopt a combined approach.

• If using urolithin A, consider taking it outside the pre-workout window and ensure training stimulates mitochondrial biogenesis.
• CoQ10 makes sense as a long-term, daily support for mitochondrial function, but expect benefits over weeks to months rather than acutely.
• Nitrates and NO precursors are best used in the pre-workout window to enhance efficiency and reduce ROS for the same output.

5. Match supplementation to training goals.

• During hypertrophy-focused blocks, minimize interventions that suppress post-exercise inflammatory signaling.
• During high-volume endurance phases or peaking for events, prioritize strategies that maintain training quality (nitrates, moderate antioxidants) and support recovery.

6. Consider individualized testing and monitoring.

• Athletes with specific health conditions, older individuals with mitochondrial decline, or those using medications should consult healthcare professionals before starting mitochondrial-targeted supplements.
• Track performance metrics rather than subjective recovery alone; suppressed soreness is not a reliable proxy for adaptation.

Safety, interactions and unanswered questions

Safety considerations are straightforward but require attention.

• Antioxidant-vitamin interactions: High doses of isolated vitamins can alter drug metabolism and interact with medications. People on anticoagulants or statins should consult clinicians before starting CoQ10 or other agents.
• Long-term outcomes: Many mitochondrial-targeting compounds have limited long-term performance data in athletic populations. Enthusiasm must be balanced by careful, monitored use.
• Individual variance: Gut microbiome composition influences endogenous production of urolithin metabolites. Individuals who lack the necessary microbes may experience different responses to dietary ellagitannins versus direct urolithin supplementation.

Research gaps remain. The optimal dosing windows of many ingredients around real-world training schedules need refinement. Long-term comparative trials that examine performance outcomes, not just biomarkers, are scarce. Interactions between multi-ingredient pre-workouts and chronic supplementation protocols also require clearer delineation.

Implementing changes: sample protocols for different athlete types

Below are evidence-informed, practical protocols tailored to common athlete profiles. These are examples, not prescriptive medical advice.

Recreational strength athlete aiming for hypertrophy:

• Daily: Emphasize whole-food antioxidant intake (berries, greens, citrus), aim for protein spread across meals.
• Pre-workout: Use a stimulant-free NO precursor or low-dose antioxidant formula if it helps session quality. Avoid post-workout megadoses of vitamin C/E.
• Mitochondrial supports: Consider CoQ10 for chronic mitochondrial health; take with a meal containing fat for absorption.

Endurance athlete preparing for a long race:

• Daily: Prioritize beets or nitrate-rich vegetables as part of steady diet; include colorful fruits for polyphenols.
• Pre-key sessions: Use a nitrate-rich pre-workout (beetroot) 2–3 hours before sustained efforts to lower oxygen cost.
• Recovery: Moderate antioxidant intake via foods; avoid chronic high-dose isolated antioxidants during training blocks focused on mitochondrial adaptation.

Older recreational athletes concerned about mitochondrial decline:

• Daily: Integrate consistent aerobic exercise to stimulate PGC-1α; focus on varied diet rich in polyphenols.
• Supplementation: Consider CoQ10 for chronic use and, if exploring urolithin A, stagger timing away from exercise and ensure active training that promotes biogenesis.
• Monitoring: Track functional outcomes (e.g., 6-minute walk, stair-climb power) alongside subjective measures.

Competitive athlete during taper or peaking:

• Taper period reduces training stress; acute antioxidant use to manage illness or travel exposure is reasonable.
• Avoid introducing new mitochondrial-targeted supplements immediately before competition; allow an adaptation period to assess effects.

How to evaluate product labels: what to look for and avoid

When comparing pre-workouts and mitochondrial supplements, decode labels with these criteria:

• Ingredient dosing transparency: Avoid proprietary blends that hide amounts. Known, moderate doses are preferable to undisclosed mega-blends.
• Source and form: CoQ10 ubiquinone vs ubiquinol? Ubiquinol may offer better absorption in some contexts. For nitrates, look for beetroot or standardized nitrate content.
• Synergy vs redundancy: Products that stack multiple antioxidants at high doses increase risk of over-suppression. Favor products that combine nitrates, minimal antioxidant support, and performance ingredients.
• Timing instructions: Products that recommend pre-workout use should have formulas optimized for acute performance. Mitolytic and biogenesis supplements should recommend chronic scheduling rather than immediate pre-workout dosing.

Regulatory note: Dietary supplements are not uniformly regulated. Choose reputable brands that provide third-party testing (e.g., NSF Certified for Sport) and transparent manufacturing practices.

Reconciling short-term recovery with long-term gains

Athletes and coaches face frequent trade-offs: feeling recovered now versus achieving progression over months. The evidence clarifies that faster subjective recovery does not always equal better long-term adaptation. Use the training plan as the primary driver of adaptation; use supplements to support session quality and long-term mitochondrial health without replacing the required physiological stress.

Decision criteria:

• If a supplement helps preserve training intensity and volume without chronically blunting adaptive markers, it is likely useful.
• If a supplement reduces perceived soreness but correlates with plateaued strength or endurance gains, reassess its timing, dose and necessity.

The final arbitrator is measurable performance. Track objective outcomes—strength metrics, power output, race times—alongside subjective recovery to detect whether interventions help or hinder.

Research perspective: where the field is headed

Two domains are attracting attention:

1. Precision supplementation informed by biomarkers and microbiome profiles. Variability in gut microbiota influences endogenous urolithin production. Identifying who benefits most from mitolytic supplementation could improve outcomes.
2. Combined mitophagy/biogenesis strategies. Trials that pair mitolytics with biogenesis stimulators (exercise protocols, PQQ, targeted nutrients) will test whether coordinated cycles of removal and renewal enhance performance and longevity without short-term trade-offs.

Clinicians and sports scientists will refine timing, dosing, and population-specific recommendations as longitudinal data accumulate.

FAQ

Q: Should I take antioxidants before or after a workout? A: Evidence favors moderate antioxidant support before exercise to reduce excess oxidative damage during the session, while avoiding high-dose antioxidants immediately after training when repair and adaptation signals are active. Prioritize whole-food antioxidants daily; use pre-workout products with modest antioxidant content rather than megadoses.

Q: Will vitamin C or E supplementation blunt my muscle gains? A: High, chronic doses of isolated vitamins C and E have been associated with attenuated training adaptations in some studies. Occasional, moderate dosing or obtaining these nutrients through food is less likely to interfere. Avoid routine megadoses, particularly post-exercise.

Q: Is urolithin A beneficial for athletes? A: Urolithin A may improve mitochondrial quality by promoting mitophagy. Benefits appear more relevant to mitochondrial health over time rather than immediate performance enhancement. Avoid taking mitolytic agents immediately before workouts; pair usage with training that stimulates mitochondrial biogenesis to rebuild capacity.

Q: Can nitrates or nitric oxide boosters replace antioxidants? A: No. They represent a complementary strategy. Nitrates increase metabolic efficiency and reduce ROS generation for a given work rate, which helps performance. They do not replace the need for dietary antioxidants that support baseline health.

Q: Should I take CoQ10 as a pre-workout ingredient? A: CoQ10 supports mitochondrial electron transport and functions best as a chronic supplement rather than an acute pre-workout agent. Expect benefits over weeks to months. If you choose CoQ10, take it consistently with a meal containing fat to enhance absorption.

Q: How much fruit and vegetables do I need to avoid taking supplements? A: Optimal intake varies by individual, but many athletes struggle to reach recommended servings. A varied diet supplying multiple fruits and vegetables daily reduces the need for concentrated antioxidant supplements. When dietary patterns fall short due to logistics or appetite, consider food-based supplements to fill gaps.

Q: Can antioxidants help during illness or heavy travel? A: Short-term, higher-dose antioxidant strategies during periods of immune stress or travel can be reasonable to mitigate acute oxidative burden. Use these interventions temporarily and under professional guidance; avoid chronic high-dose protocols.

Q: Are there safety concerns or interactions I should know about? A: Yes. High doses of supplements can interact with medications and affect metabolic pathways. Consult a healthcare professional before starting new supplements, especially if you take prescription medication, have a medical condition, or are pregnant. Choose third-party tested products when available.

Q: How do I know if a supplement is blunting my progress? A: Monitor objective performance measures (strength numbers, time trial results, power output) over weeks and months. If you perceive faster recovery but your performance plateaus or declines, reassess supplementation practices—especially timing and dose of antioxidants.

Q: Can I combine mitolytics with biogenesis supplements safely? A: Theoretically yes, when used thoughtfully. Pair mitolytics like urolithin A with interventions promoting mitochondrial biogenesis (endurance training, PQQ, consistent nutrition). Avoid taking mitolytics immediately before sessions that require maximal mitochondrial output.

Optimizing antioxidant and mitochondrial support around exercise requires tailoring to the athlete’s goals, training phase and baseline diet. Use pre-workout antioxidants and nitrates to preserve session quality. Reserve high-dose antioxidant strategies for short-term needs rather than routine post-workout use. For mitochondrial interventions, prioritize exercise-driven biogenesis and adopt supplements that support cycles of renewal rather than isolated, aggressive mitolysis. Measured, strategic application preserves both acute performance and the long-term adaptations that define athletic progress.