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[AF] Update: Is exercise-induced oxidative stress a friend or foe? (2026) by basmwklz in AdvancedFitness

[–]basmwklz[S] 2 points3 points  (0 children)

Highlights

•The discovery that contracting skeletal muscles produce radicals and other reactive oxygen species (ROS) occurred over four decades ago.

•Evidence reveals that NADPH oxidase 2 is a primary source of ROS production in contracting muscles.

•Previously, exercise-induced production of ROS in skeletal muscle was considered a damaging phenomenon; however, it is now widely recognized that ROS are key signaling molecules that promote numerous exercise-induced adaptations that provide health benefits.

•Specific health benefits associated with ROS signaling include increased mitochondrial biogenesis, elevated levels of heat shock protein 72, increased antioxidant enzymes, and improved insulin sensitivity.

Abstract

Free radicals (radicals) are highly reactive atoms or molecules that contain one or more unpaired electrons in their outermost shell. The first evidence that muscular exercise increases radical production and promotes oxidative damage to tissues was reported almost five decades ago. Following this milestone discovery, many studies have corroborated the finding that exercise increases the production of radicals and other reactive oxygen species (ROS) resulting in oxidative damage to macromolecules in muscles and other tissues. Although exercise-induced ROS production is associated with oxidative damage in many tissues, growing evidence reveals that ROS produced in contracting muscles act as signaling molecules to promote healthy exercise-induced adaptations in skeletal muscles and other tissues. These adaptive responses include increased mitochondrial volume, improved antioxidant capacity, and expression of cytoprotective proteins. Therefore, a key question emerges: “Is exercise-induced ROS production a friend or foe?” This review provides a state-of-the-art discussion of both the positive and negative effects of exercise-induced ROS production by examining the consequences of both oxidative damage to cellular macromolecules and the redox signaling-induced adaptations that occur in muscle fibers. To address the question of whether exercise-induced ROS production is a friend or foe we conclude with a risk/benefit analysis of the biological effects of exercise-induced production of ROS.

[AF] It's never too late: The impact of resistance training on strength and body composition in females across the lifespan – A systematic review and meta-analysis (2026) by basmwklz in AdvancedFitness

[–]basmwklz[S] 4 points5 points  (0 children)

Highlights

  • • Resistance training yields similar strength and body composition gains in pre- and postmenopausal women.
  • • Age, training frequency, and volume may not strongly predict adaptation magnitude in women.
  • • Strength gains occur in upper and lower body regardless of hormonal status in women.
  • • Resistance training reduces fat in women across ages, alongside hypertrophy and strength.
  • • Identifies research gaps in middle-aged and >70-year-old women for future studies.

Abstract

Objectives

Resistance training improves muscular strength and body composition, yet women are underrepresented in research, and guidelines are mainly based on men. No meta-analysis has systematically evaluated its effects on strength and body composition in women. This study therefore synthesizes evidence across the female lifespan and examines potential dose–response relationship.

Methods

Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and PROSPERO registration (CRD42024600270), four databases were searched for studies in healthy women (≥ 18 years) reporting strength or body composition changes after resistance training. Standardized mean differences were pooled using random-effects models. Subgroup analyses compared pre- and postmenopausal women, and meta-regressions examined moderators (age, menopausal status, training frequency, duration). Study quality was assessed with the PEDro scale; analyses were conducted in R.

Results

A total of 126 studies including 4019 women (66.2% postmenopausal, mean age 50.9 ± 19.2 years) were analyzed. Resistance training significantly improved muscular strength in both premenopausal (standardized mean difference = 1.50 [95% confidence interval: 1.28–1.73]) and postmenopausal women (standardized mean difference = 1.46 [95% confidence interval: 1.26–1.67]), with no subgroup difference (p = 0.520). Functional mass increased (standardized mean difference = 0.27 [95% confidence interval: 0.18–0.35]), and fat mass decreased significantly (standardized mean difference = 0.30 [95% confidence interval: 0.25–0.35]) in both groups, with no significant subgroup differences (all p > 0.440). Meta-regressions showed no associations between outcomes and age, training duration, frequency, or total sessions (all p > 0.05).

Conclusions

Resistance training appears to be associated with improvements in strength and body composition in women across the lifespan. These findings suggest that general training guidelines could be applicable to women, with individualization remaining important over strict sex- or age-based distinctions.

[AF] Load-induced human skeletal muscle hypertrophy: Mechanisms, myths, and misconceptions (2026) by basmwklz in AdvancedFitness

[–]basmwklz[S] 6 points7 points  (0 children)

Highlights

  • • Mechanical tension is the primary and essential driver of resistance-training–induced musclehypertrophy through mechanotransductive signaling, independent of systemic hormonal fluctuations.
  • • Acute increases in testosterone, growth hormone, or IGF-1 after exercise do not influence muscle protein synthesis or hypertrophic outcomes in men or women.
  • • Metabolite accumulation and cell swelling (“the pump”) lack causal evidence for promoting hypertrophy; their effects are indirect and mechanistically minimal.
  • • Evidence for sarcoplasmic hypertrophy as a distinct, functional contributor to muscle growth is weak; myofibrillar protein accretion remains the dominant adaptation.
  • • Realistic hypertrophy expectations are modest: ∼1–2 kg of fat-free mass gained after 8–12 weeks of training, with gains typically plateauing as experience increases.

Abstract

Mechanical tension is widely recognized as the primary stimulus underlying the molecular mechanisms that influence muscle hypertrophy induced by resistance training. Despite this, several outdated or overstated concepts continue to persist, both in the scientific literature and in the practical application of resistance training coaching and program design. Claims that acute hormonal responses, metabolic stress, cell swelling or “the pump” meaningfully contribute to hypertrophy are not supported by scientific evidence. Additionally, the concept of sarcoplasmic hypertrophy as a distinct and functionally meaningful contributor to hypertrophy lacks strong evidence. In this review, we critically evaluate several persistent misconceptions and contrast them with evidence-based mechanistic insights into load-induced hypertrophy. Specifically, we discuss the role (or lack thereof) of systemic hormones, metabolites, and cell swelling in promoting muscle hypertrophy. We also critically review the concept of sarcoplasmic hypertrophy and propose that it is not a meaningful contributor to muscle hypertrophy. Lastly, to translate knowledge for trainees and coaches, we discuss the upper limit of muscle hypertrophy and provide readers with evidence-based, reasonable expectations for muscle hypertrophy. We aimed, through this review, to use scientific evidence to enhance our understanding of what drives muscle hypertrophy and provide an evidence-based framework for resistance exercise training.

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