Hormonal Responses to Resistance and Endurance Exercise

Hormonal responses to exercise are a cornerstone of how the body translates mechanical stress into physiological adaptation. When we lift a heavy barbell or log miles on a bike, we are not merely moving muscles; we are triggering a cascade of endocrine signals that orchestrate substrate mobilization, tissue remodeling, and systemic homeostasis. Understanding these signals—what they are, when they appear, how they differ between resistance and endurance modalities, and how training variables shape them—provides athletes, coaches, and clinicians with a powerful toolkit for optimizing performance, recovery, and long‑term health.

Acute Hormonal Landscape: The First Hours After Exercise

Catecholamines: Epinephrine and Norepinephrine

Both resistance and endurance bouts provoke a rapid surge in epinephrine (adrenaline) and norepinephrine (noradrenaline) from the adrenal medulla. These catecholamines act within seconds to minutes, preparing the body for “fight‑or‑flight” by:

• Increasing heart rate and cardiac output – delivering oxygen and nutrients to active tissues.
• Stimulating glycogenolysis in liver and skeletal muscle, raising blood glucose.
• Promoting lipolysis in adipose tissue, liberating free fatty acids (FFAs) for oxidation.

The magnitude of the catecholamine response scales with exercise intensity and the proportion of fast‑twitch motor unit recruitment. High‑intensity resistance sets (e.g., 6‑8 RM) and vigorous interval endurance work both elicit pronounced spikes, whereas low‑intensity steady‑state cardio produces a more modest rise.

Cortisol: The Stress Hormone

Cortisol, secreted by the adrenal cortex, follows a biphasic pattern. An initial rise appears within 15–30 minutes of exercise onset, peaking around 30–60 minutes post‑exercise, then gradually returning to baseline over several hours. Its primary actions include:

• Gluconeogenesis – converting amino acids and glycerol into glucose.
• Protein catabolism – providing amino acids for hepatic glucose production.
• Anti‑inflammatory effects – modulating immune cell activity.

In resistance training, cortisol peaks are typically lower than in prolonged endurance sessions, reflecting the shorter duration and intermittent nature of the stimulus. However, very high training volumes or insufficient recovery can lead to chronically elevated cortisol, which may blunt anabolic signaling and impair adaptation.

Growth Hormone (GH) and Insulin‑Like Growth Factor‑1 (IGF‑1)

Growth hormone is released from the anterior pituitary in a pulsatile fashion, with exercise acting as a potent stimulus. Acute GH spikes are most robust when:

• Exercise intensity exceeds ~70 % of VO₂max (for endurance) or loads exceed 60 % of 1RM (for resistance).
• Rest intervals are short, creating metabolic stress.
• Total training volume is high, especially when combined with moderate‑to‑high intensity.

GH promotes lipolysis and stimulates hepatic production of IGF‑1, which then circulates bound to IGF‑binding proteins (IGFBPs). IGF‑1 exerts anabolic effects on skeletal muscle by activating the PI3K‑Akt‑mTOR pathway, enhancing protein synthesis and satellite cell proliferation. Notably, the GH response is more pronounced after resistance sessions that incorporate large muscle mass and short rest periods, whereas endurance exercise elicits a modest but still meaningful GH elevation, particularly after high‑intensity interval work.

Testosterone

Testosterone, the primary androgen in males and a significant anabolic hormone in females, rises acutely after resistance training, especially when:

• Large muscle groups are engaged (e.g., squats, deadlifts).
• Training intensity is high (≥ 85 % 1RM) and volume is moderate (3–5 sets per exercise).
• Rest intervals are brief (≤ 90 seconds).

Endurance exercise can cause a transient dip in testosterone immediately post‑exercise, likely mediated by elevated cortisol and catecholamines. However, chronic endurance training does not necessarily depress basal testosterone levels in well‑trained individuals; the acute dip is typically short‑lived and rebounds within a few hours.

Insulin and Glucagon

Exercise induces a complex interplay between insulin (an anabolic, glucose‑lowering hormone) and glucagon (a catabolic, glucose‑raising hormone). During both resistance and endurance bouts:

• Insulin secretion falls due to sympathetic activation and reduced plasma glucose.
• Glucagon rises, stimulating hepatic glycogenolysis and gluconeogenesis.

Post‑exercise, especially after resistance training, insulin sensitivity is markedly enhanced for up to 48 hours, facilitating rapid glycogen replenishment and protein synthesis when nutrients are consumed. Endurance exercise also improves insulin sensitivity, but the magnitude and duration are generally lower than after high‑intensity resistance work.

Myokines and Cytokines: IL‑6, IL‑15, and Beyond

Skeletal muscle functions as an endocrine organ, releasing myokines in response to contraction. Interleukin‑6 (IL‑6) is the most studied; it spikes dramatically during prolonged endurance exercise (up to 100‑fold) and modestly during high‑intensity resistance sets. IL‑6 serves several purposes:

• Mobilizing substrates – stimulating lipolysis and hepatic glucose output.
• Anti‑inflammatory signaling – inducing production of IL‑10 and IL‑1ra.
• Promoting muscle repair – acting on satellite cells.

Other myokines such as IL‑15 (linked to muscle hypertrophy) and brain‑derived neurotrophic factor (BDNF) are more responsive to resistance training, especially when mechanical tension is high.

Chronic Hormonal Adaptations: Training Over Weeks and Months

The Anabolic‑Catabolic Balance

Repeated exposure to the acute hormonal milieu described above leads to a shift in the body’s anabolic‑catabolic equilibrium. Over time:

• Resting testosterone levels may increase modestly in response to progressive overload resistance training, particularly in previously untrained individuals.
• Basal GH and IGF‑1 concentrations can rise, supporting long‑term muscle hypertrophy and bone health.
• Cortisol responsiveness may attenuate, reflecting improved stress tolerance and more efficient recovery mechanisms.

Endurance training, especially when performed at high volumes, can lead to a slight reduction in basal testosterone and a modest increase in resting cortisol, but these changes are typically within physiological ranges and are offset by cardiovascular and metabolic benefits.

Hormone Receptor Sensitivity

Beyond circulating concentrations, chronic training modulates receptor density and signaling efficiency:

• Androgen receptor (AR) up‑regulation in skeletal muscle after sustained resistance training enhances the tissue’s responsiveness to testosterone.
• Insulin receptor (IR) density and post‑receptor signaling improve markedly after both resistance and endurance training, underpinning the well‑documented increase in insulin sensitivity.
• β‑adrenergic receptor sensitivity can be blunted after prolonged high‑intensity endurance work, a protective adaptation to prevent excessive catecholamine‑driven catabolism.

Hormonal Crosstalk and the mTOR Pathway

The mammalian target of rapamycin (mTOR) integrates signals from nutrients, growth factors, and mechanical load. Resistance training activates mTOR primarily through:

• Mechanical tension → phosphatidic acid production → mTOR activation.
• GH/IGF‑1 signaling → PI3K‑Akt cascade → mTOR.
• Amino acid availability, especially leucine, which synergizes with the above pathways.

Endurance training, conversely, can activate AMP‑activated protein kinase (AMPK), which phosphorylates and inhibits mTOR, favoring oxidative adaptations over hypertrophy. The balance between AMPK and mTOR activity is a key determinant of whether an athlete’s phenotype leans toward endurance capacity or muscular size.

Modulating Hormonal Responses Through Training Variables

Sex Differences in Hormonal Responses

• Testosterone: Men possess 10‑20× higher circulating testosterone, leading to a more pronounced anabolic response to resistance training. Women experience modest increases in free testosterone post‑exercise, which still contribute to muscle protein synthesis.
• Estrogen: In women, estrogen exerts protective effects on muscle membrane integrity and may attenuate cortisol‑induced catabolism. Training during the follicular phase (low estrogen) often yields slightly higher strength gains, whereas the luteal phase (high estrogen) may favor endurance adaptations.
• Growth Hormone: Both sexes display similar GH spikes relative to body mass, but women may experience a slightly prolonged GH elevation due to lower IGF‑binding protein concentrations.
• Insulin Sensitivity: Women generally exhibit higher baseline insulin sensitivity, which can be further enhanced by both resistance and endurance training.

Understanding these nuances enables individualized programming that respects hormonal milieu while targeting specific performance goals.

Practical Applications for Athletes and Practitioners

1. Periodize Load and Volume to Harness Anabolic Hormones
• Strength phases (4–6 weeks) with heavy loads, moderate volume, and short rests maximize testosterone, GH, and IGF‑1.
• Hypertrophy phases (6–8 weeks) with moderate loads, higher volume, and 60–90 s rests sustain anabolic hormone exposure while limiting cortisol.

2. Integrate High‑Intensity Interval Endurance Sessions Sparingly
• Use 1–2 interval sessions per week to exploit catecholamine and GH surges without chronically elevating cortisol.
• Pair intervals with resistance training on separate days or with sufficient recovery (≥ 48 h) to avoid hormonal interference.

3. Nutrient Timing to Leverage Hormonal Windows
• Post‑resistance: Consume a protein‑rich (≈ 0.3 g/kg) and carbohydrate‑moderate (≈ 0.5 g/kg) meal within 30–60 minutes to capitalize on heightened insulin sensitivity and GH/IGF‑1 activity.
• Post‑endurance: Prioritize carbohydrate replenishment (≈ 1.0–1.2 g/kg) to restore glycogen and blunt prolonged cortisol elevation; add protein (≈ 0.2 g/kg) if muscle repair is a priority.

4. Monitor Hormonal Markers for Overtraining Prevention
• Regularly assess resting morning cortisol, testosterone (or free testosterone), and HRV (as an indirect autonomic marker).
• Persistent elevation of cortisol coupled with depressed testosterone and reduced HRV may signal inadequate recovery.

5. Consider Supplementation Wisely
• Creatine monohydrate can augment phosphocreatine stores, indirectly supporting higher training intensity and thus greater anabolic hormone release.
• Vitamin D and omega‑3 fatty acids have been shown to modulate inflammatory cytokine responses, potentially attenuating excessive cortisol spikes.

Future Directions and Emerging Research

• Myokine Profiling: Advances in proteomics are revealing a broader spectrum of muscle‑derived hormones (e.g., irisin, myostatin, follistatin) that may fine‑tune the anabolic‑catabolic balance. Understanding how specific training modalities modulate these factors could lead to more precise prescription of exercise for muscle health.
• Hormone‑Based Periodization: Some elite programs are experimenting with “hormone‑guided” training cycles, adjusting load and volume based on weekly hormonal assessments rather than solely on performance metrics.
• Sex‑Specific Protocols: Ongoing investigations aim to delineate optimal training windows across the menstrual cycle, leveraging natural hormonal fluctuations to maximize strength or endurance adaptations.
• Aging and Hormonal Plasticity: While the present article avoids the “age” scope, emerging data suggest that resistance training can partially restore age‑related declines in anabolic hormone signaling, opening avenues for longevity‑focused exercise prescriptions.

Concluding Thoughts

Hormonal responses are the invisible architects that translate the mechanical and metabolic stresses of resistance and endurance exercise into lasting physiological change. Acute spikes in catecholamines, cortisol, growth hormone, testosterone, and insulin set the stage for substrate mobilization and tissue signaling. Repeated exposure reshapes hormone concentrations, receptor sensitivities, and intracellular pathways, ultimately dictating whether an athlete becomes stronger, more endurance‑capable, or both.

By appreciating the distinct hormonal signatures of resistance versus endurance work—and by deliberately manipulating training variables, nutrition, and recovery—practitioners can steer the endocrine environment toward desired outcomes. This endocrine‑centric perspective not only enriches our scientific understanding of exercise adaptation but also equips coaches and athletes with actionable strategies to train smarter, recover better, and sustain performance across the lifespan.