Novel Resistance Training-Specific Rating of Perceived Exertion Scale Measuring Repetitions in Reserve.

The primary aim of this study was to compare rating of perceived exertion (RPE) values measuring repetitions in reserve (RIR) at particular intensities of 1 repetition maximum (RM) in experienced (ES) and novice squatters (NS). Furthermore, this investigation compared average velocity between ES and NS at the same intensities. Twenty-nine individuals (24.0 ± 3.4 years) performed a 1RM squat followed by a single repetition with loads corresponding to 60, 75, and 90% of 1RM and an 8-repetition set at 70% 1RM. Average velocity was recorded at 60, 75, and 90% 1RM and on the first and last repetitions of the 8-repetition set. Subjects reported an RPE value that corresponded to an RIR value (RPE-10 = 0-RIR, RPE-9 = 1-RIR, and so forth). Subjects were assigned to one of the 2 groups: (a) ES (n = 15, training age: 5.2 ± 3.5 years) and (b) NS (n = 14, training age: 0.4 ± 0.6 years). The mean of the average velocities for ES was slower (p ≤ 0.05) than NS at 100% and 90% 1RM. However, there were no differences (p > 0.05) between groups at 60, 75%, or for the first and eighth repetitions at 70% 1RM. In addition, ES recorded greater RPE at 1RM than NS (p = 0.023). In ES, there was a strong inverse relationship between average velocity and RPE at all percentages (r = -0.88, p < 0.001), and a strong inverse correlation in NS between average velocity and RPE at all intensities (r = -0.77, p = 0.001). Our findings demonstrate an inverse relationship between average velocity and RPE/RIR. Experienced squatter group exhibited slower average velocity and higher RPE at 1RM than NS, signaling greater efficiency at high intensities. The RIR-based RPE scale is a practical method to regulate daily training load and provide feedback during a 1RM test.

The Effect of Time-Equated Concurrent Training Programs in Resistance-Trained Men.

The purpose of this investigation was to compare the effects of three different concurrent training (CT) programs and a resistance training (RT) program. Twenty-three resistance trained men (age: 24 ± 3 years) were randomized into four groups: concurrent RT and high intensity interval cycling (CTH, n = 6), concurrent RT and moderate intensity continuous cycling (CTM, n = 5), RT and barbell circuit training (RTC, n = 6), or RT only (RT, n = 6). Back squat and bench press strength, quadriceps, and pectoralis muscle thickness, VO2peak, and maximum workload (Wmax, Watts) were assessed. Squat strength gains were meaningful in all groups and comparable among CTH (16.88 kg [95% CrI: 11.15, 22.63]), CTM (25.54 kg [95% CrI: 19.24, 31.96]), RTC (17.5 kg [95% CrI: 11.66, 23.39]), and RT (20.36 kg [95% CrI: 15.29, 25.33]) groups. Bench press strength gains were meaningful in all groups and comparable among CTH (11.86 kg [95% CrI: 8.28, 15.47]), CTM (10.3 kg [95% CrI: 6.49, 14.13]), RTC (4.84 kg [95% CrI: 1.31, 8.47]), and RT (10.16 kg [95% CrI: 7.02, 13.22]) groups. Quadriceps hypertrophy was meaningful in all groups and comparable among CTH (2.29 mm [95% CrI: 0.84, 3.76]), CTM (3.41 mm [95% CrI: 1.88, 4.91]), RTC (2.6 mm [95% CrI: 1.17, 4.05]), and RT (2.83 mm [95% CrI: 1.55, 4.12]) groups. Pectoralis hypertrophy was meaningful in CTH (2.29 mm [95% CrI: -0.52, 5.1]), CTM (5.14 mm [95% CrI: 2.1, 8.15]), and RTC (7.19 mm [95% CrI: 4.26, 10.02]) groups, but not in the RT group (1 mm [95% CrI: -1.59, 3.59]); further, between-group contrasts indicated less pectoralis growth in the RT compared to the RTC group. Regarding cardiovascular outcomes, only the RTH and RTM groups experienced meaningful improvements in either measure (VO2peak or Wmax). These data suggest that the interference effect on maximal strength and hypertrophy can be avoided when the aerobic training is moderate intensity cycling, high intensity cycling, or a novel barbell circuit for ~one hour per week and on non-RT days. However, the barbell circuit failed to elicit meaningful cardiovascular adaptations.

The Small GTPase Rab7 Regulates Release of Mitochondria in Extracellular Vesicles in Response to Lysosomal Dysfunction.

Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways that converge on the lysosome. Here, we identified an alternative mechanism to eliminate mitochondria when lysosomal function is compromised. We show that lysosomal inhibition leads to increased secretion of mitochondria in large extracellular vesicles (EVs). The EVs are produced in multivesicular bodies, and their release is independent of autophagy. Deletion of the small GTPase Rab7 in cells or adult mouse heart leads to increased secretion of EVs containing ubiquitinated cargos, including intact mitochondria. The secreted EVs are captured by macrophages without activating inflammation. Hearts from aged mice or Danon disease patients have increased levels of secreted EVs containing mitochondria indicating activation of vesicular release during cardiac pathophysiology. Overall, these findings establish that mitochondria are eliminated in large EVs through the endosomal pathway when lysosomal degradation is inhibited.

Deciphering functional roles and interplay between Beclin1 and Beclin2 in autophagosome formation and mitophagy.

The degradation of macromolecules and organelles by the process of autophagy is critical for cellular homeostasis and is often compromised during aging and disease. Beclin1 and Beclin2 are implicated in autophagy induction, and these homologs share a high degree of amino acid sequence similarity but have divergent N-terminal regions. Here, we investigated the functions of the Beclin homologs in regulating autophagy and mitophagy, a specialized form of autophagy that targets mitochondria. Both Beclin homologs contributed to autophagosome formation, but a mechanism of autophagosome formation independent of either Beclin homolog occurred in response to starvation or mitochondrial damage. Mitophagy was compromised only in Beclin1-deficient HeLa cells and mouse embryonic fibroblasts because of defective autophagosomal engulfment of mitochondria, and the function of Beclin1 in mitophagy required the phosphorylation of the conserved Ser15 residue by the kinase Ulk1. Mitochondria-ER-associated membranes (MAMs) are important sites of autophagosome formation during mitophagy, and Beclin1, but not Beclin2 or a Beclin1 mutant that could not be phosphorylated at Ser15, localized to MAMs during mitophagy. Our findings establish a regulatory role for Beclin1 in selective mitophagy by initiating autophagosome formation adjacent to mitochondria, a function facilitated by Ulk1-mediated phosphorylation of Ser15 in its distinct N-terminal region.

Mitochondria are secreted in extracellular vesicles when lysosomal function is impaired.

Mitochondrial quality control is critical for cardiac homeostasis as these organelles are responsible for generating most of the energy needed to sustain contraction. Dysfunctional mitochondria are normally degraded via intracellular degradation pathways that converge on the lysosome. Here, we identified an alternative mechanism to eliminate mitochondria when lysosomal function is compromised. We show that lysosomal inhibition leads to increased secretion of mitochondria in large extracellular vesicles (EVs). The EVs are produced in multivesicular bodies, and their release is independent of autophagy. Deletion of the small GTPase Rab7 in cells or adult mouse heart leads to increased secretion of EVs containing ubiquitinated cargos, including intact mitochondria. The secreted EVs are captured by macrophages without activating inflammation. Hearts from aged mice or Danon disease patients have increased levels of secreted EVs containing mitochondria indicating activation of vesicular release during cardiac pathophysiology. Overall, these findings establish that mitochondria are eliminated in large EVs through the endosomal pathway when lysosomal degradation is inhibited.

The role of mitochondrial fission in cardiovascular health and disease.

Mitochondria are organelles involved in the regulation of various important cellular processes, ranging from ATP generation to immune activation. A healthy mitochondrial network is essential for cardiovascular function and adaptation to pathological stressors. Mitochondria undergo fission or fusion in response to various environmental cues, and these dynamic changes are vital for mitochondrial function and health. In particular, mitochondrial fission is closely coordinated with the cell cycle and is linked to changes in mitochondrial respiration and membrane permeability. Another key function of fission is the segregation of damaged mitochondrial components for degradation by mitochondrial autophagy (mitophagy). Mitochondrial fission is induced by the large GTPase dynamin-related protein 1 (DRP1) and is subject to sophisticated regulation. Activation requires various post-translational modifications of DRP1, actin polymerization and the involvement of other organelles such as the endoplasmic reticulum, Golgi apparatus and lysosomes. A decrease in mitochondrial fusion can also shift the balance towards mitochondrial fission. Although mitochondrial fission is necessary for cellular homeostasis, this process is often aberrantly activated in cardiovascular disease. Indeed, strong evidence exists that abnormal mitochondrial fission directly contributes to disease development. In this Review, we compare the physiological and pathophysiological roles of mitochondrial fission and discuss the therapeutic potential of preventing excessive mitochondrial fission in the heart and vasculature.

Transgenic Expression of Nrf2 Induces a Pro-Reductive Stress and Adaptive Cardiac Remodeling in the Mouse.

Nuclear factor, erythroid 2 like 2 (Nfe2l2 or Nrf2), is a transcription factor that protects cells by maintaining a homeostatic redox state during stress. The constitutive expression of Nrf2 (CaNrf2-TG) was previously shown to be pathological to the heart over time. We tested a hypothesis that the cardiac-specific expression of full length Nrf2 (mNrf2-TG) would moderately increase the basal antioxidant defense, triggering a pro-reductive environment leading to adaptive cardiac remodeling. Transgenic and non-transgenic (NTG) mice at 7−8 months of age were used to analyze the myocardial transcriptome, structure, and function. Next generation sequencing (NGS) for RNA profiling and qPCR-based validation of the NGS data, myocardial redox levels, and imaging (echocardiography) were performed. Transcriptomic analysis revealed that out of 14,665 identified mRNAs, 680 were differently expressed (DEG) in TG hearts. Of 680 DEGs, 429 were upregulated and 251 were downregulated significantly (FC > 2.0, p < 0.05). Gene set enrichment analysis revealed that the top altered pathways were (a) Nrf2 signaling, (b) glutathione metabolism and (c) ROS scavenging. A comparative analysis of the glutathione redox state in the hearts demonstrated significant differences between pro-reductive vs. hyper-reductive conditions (233 ± 36.7 and 380 ± 68.7 vs. 139 ± 8.6 µM/mg protein in mNrf2-TG and CaNrf2-TG vs. NTG). Genes involved in fetal development, hypertrophy, cytoskeletal rearrangement, histone deacetylases (HDACs), and GATA transcription factors were moderately increased in mNrf2-TG compared to CaNrf2-TG. Non-invasive echocardiography analysis revealed an increase in systolic function (ejection fraction) in mNrf2-TG, suggesting an adaptation, as opposed to pathological remodeling in CaNrf2-TG mice experiencing a hyper-reductive stress, leading to reduced survival (40% at 60 weeks). The effects of excess Nrf2-driven antioxidant transcriptome revealed a pro-reductive condition in the myocardium leading to an adaptive cardiac remodeling. While pre-conditioning the myocardial redox with excess antioxidants (i.e., pro-reductive state) could be beneficial against oxidative stress, a chronic pro-reductive environment in the myocardium might transition the adaptation to pathological remodeling.

Identification of Nrf2-responsive microRNA networks as putative mediators of myocardial reductive stress.

Although recent advances in the treatment of acute coronary heart disease have reduced mortality rates, few therapeutic strategies exist to mitigate the progressive loss of cardiac function that manifests as heart failure. Nuclear factor, erythroid 2 like 2 (Nfe2l2, Nrf2) is a transcriptional regulator that is known to confer transient myocardial cytoprotection following acute ischemic insult; however, its sustained activation paradoxically causes a reductive environment characterized by excessive antioxidant activity. We previously identified a subset of 16 microRNAs (miRNA) significantly diminished in Nrf2-ablated (Nrf2-/-) mouse hearts, leading to the hypothesis that increasing levels of Nrf2 activation augments miRNA induction and post-transcriptional dysregulation. Here, we report the identification of distinct miRNA signatures (i.e. "reductomiRs") associated with Nrf2 overexpression in a cardiac-specific and constitutively active Nrf2 transgenic (caNrf2-Tg) mice expressing low (TgL) and high (TgH) levels. We also found several Nrf2 dose-responsive miRNAs harboring proximal antioxidant response elements (AREs), implicating these "reductomiRs" as putative meditators of Nrf2-dependent post-transcriptional regulation. Analysis of mRNA-sequencing identified a complex network of miRNAs and effector mRNAs encoding known pathological hallmarks of cardiac stress-response. Altogether, these data support Nrf2 as a putative regulator of cardiac miRNA expression and provide novel candidates for future mechanistic investigation to understand the relationship between myocardial reductive stress and cardiac pathophysiology.

Mitochondrial Quality Control and Cellular Proteostasis: Two Sides of the Same Coin.

Mitochondrial dysfunction is a hallmark of cardiac pathophysiology. Defects in mitochondrial performance disrupt contractile function, overwhelm myocytes with reactive oxygen species (ROS), and transform these cellular powerhouses into pro-death organelles. Thus, quality control (QC) pathways aimed at identifying and removing damaged mitochondrial proteins, components, or entire mitochondria are crucial processes in post-mitotic cells such as cardiac myocytes. Almost all of the mitochondrial proteins are encoded by the nuclear genome and the trafficking of these nuclear-encoded proteins necessitates significant cross-talk with the cytosolic protein QC machinery to ensure that only functional proteins are delivered to the mitochondria. Within the organelle, mitochondria contain their own protein QC system consisting of chaperones and proteases. This system represents another level of QC to promote mitochondrial protein folding and prevent aggregation. If this system is overwhelmed, a conserved transcriptional response known as the mitochondrial unfolded protein response is activated to increase the expression of proteins involved in restoring mitochondrial proteostasis. If the mitochondrion is beyond repair, the entire organelle must be removed before it becomes cytotoxic and causes cellular damage. Recent evidence has also uncovered mitochondria as participants in cytosolic protein QC where misfolded cytosolic proteins can be imported and degraded inside mitochondria. However, this process also places increased pressure on mitochondrial QC pathways to ensure that the imported proteins do not cause mitochondrial dysfunction. This review is focused on discussing the pathways involved in regulating mitochondrial QC and their relationship to cellular proteostasis and mitochondrial health in the heart.

Nuclear Parkin Activates the ERRα Transcriptional Program and Drives Widespread Changes in Gene Expression Following Hypoxia.

Parkin is an E3 ubiquitin ligase well-known for facilitating clearance of damaged mitochondria by ubiquitinating proteins on the outer mitochondrial membrane. However, knowledge of Parkin's functions beyond mitophagy is still limited. Here, we demonstrate that Parkin has functions in the nucleus and that Parkinson's disease-associated Parkin mutants, ParkinR42P and ParkinG430D, are selectively excluded from the nucleus. Further, Parkin translocates to the nucleus in response to hypoxia which correlates with increased ubiquitination of nuclear proteins. The serine-threonine kinase PINK1 is responsible for recruiting Parkin to mitochondria, but translocation of Parkin to the nucleus occurs independently of PINK1. Transcriptomic analyses of HeLa cells overexpressing wild type or a nuclear-targeted Parkin revealed that during hypoxia, Parkin contributes to both increased and decreased transcription of genes involved in regulating multiple metabolic pathways. Furthermore, a proteomics screen comparing ubiquitinated proteins in hearts from Parkin-/- and Parkin transgenic mice identified the transcription factor estrogen-related receptor α (ERRα) as a potential Parkin target. Co-immunoprecipitation confirmed that nuclear-targeted Parkin interacts with and ubiquitinates ERRα. Further analysis uncovered that nuclear Parkin increases the transcriptional activity of ERRα. Overall, our study supports diverse roles for Parkin and demonstrates that nuclear Parkin regulates transcription of genes involved in multiple metabolic pathways.

Impact of resistance training program configuration on the circulating brain-derived neurotrophic factor response.

This study examined the acute and resting changes of brain-derived neurotrophic factor (BDNF) and inteleukin-6 (IL-6) and if changes in these biomarkers were correlated during resistance training (RT). Fifteen men with ≥2 years of RT experience (age: 23 ± 3 years, body mass: 84.4 ± 12.3 kg) participated. Subjects performed RT 3×/week for 6 weeks in either a high-repetition (HR; n = 8) or low-repetition (LR; n = 7) group. Protocols during week 1 were HR - Monday: 4 (sets) × 12 (repetitions) at 60% of 1-repetition maximum, Wednesday: 4 × 10 at 65%, Friday: 5 × 8 at 70%; LR - Monday: 8 × 6 at 75%, Wednesday 9 × 4 at 80%, Friday: 10 × 2 at 85%. Total volume was equated for the 6 weeks but not for individual sessions. Greater volume and intensity were performed in LR versus HR (p < 0.01) on Mondays. Plasma was collected immediately before and after exercise of the Monday session. There were no significant interactions or main effects for BDNF (p > 0.05). There was a moderate between-group effect size (0.57) in favor of LR in week 6, suggesting a potentially greater acute increase in BDNF in LR versus HR. For IL-6, a statistically significant main effect was observed for training (p < 0.0001), showing an acute increase in IL-6 in both weeks (p < 0.01); however, no other 3-way or 2-way interactions existed (p > 0.05). A minimum volume threshold of RT may be needed to induce acute elevations in BDNF. Novelty A minimum RT volume threshold may be needed to elicit BDNF. A close proximity to failure may be needed to elicit BDNF. BDNF and IL-6 did not correlate.

Identification of transcriptome signature for myocardial reductive stress.

The nuclear factor erythroid 2 like 2 (Nfe2l2/Nrf2) is a master regulator of antioxidant gene transcription. We recently identified that constitutive activation of Nrf2 (CaNrf2) caused reductive stress (RS) in the myocardium. Here we investigate how chronic Nrf2 activation alters myocardial mRNA transcriptome in the hearts of CaNrf2 transgenic (TG-low and TG-high) mice using an unbiased integrated systems approach and next generation RNA sequencing followed by qRT-PCR methods. A total of 246 and 1031 differentially expressed genes (DEGs) were identified in the heart of TGL and TGH in relation to NTG littermates at ~ 6 months of age. Notably, the expression and validation of the transcripts were gene-dosage dependent and statistically significant. Ingenuity Pathway Analysis identified enriched biological processes and canonical pathways associated with myocardial RS in the CaNrf2-TG mice. In addition, an overrepresentation of xenobiotic metabolic signaling, glutathione-mediated detoxification, unfolded protein response, and protein ubiquitination was observed. Other, non-canonical signaling pathways identified include: eNOS, integrin-linked kinase, glucocorticoid receptor, PI3/AKT, actin cytoskeleton, cardiac hypertrophy, and the endoplasmic reticulum stress response. In conclusion, this mRNA profiling identified a "biosignature" for pro-reductive (TGL) and reductive stress (TGH) that can predict the onset, rate of progression, and clinical outcome of Nrf2-dependent myocardial complications. We anticipate that this global sequencing analysis will illuminate the undesirable effect of chronic Nrf2 signaling leading to RS-mediated pathogenesis besides providing important guidance for the application of Nrf2 activation-based cytoprotective strategies.

Exercise reduced pentraxin 3 levels produced by endotoxin-stimulated human peripheral blood mononuclear cells in obese individuals.

The purpose of this study was to determine whether obesity would reduce the capacity of peripheral blood mononuclear cells (PBMCs) to produce the anti-inflammatory protein pentraxin 3 (PTX3) in response to ex vivo stimulation with lipopolysaccharide (LPS), and if acute aerobic exercise would enhance this PTX3 production capacity. In addition, the inter-relationships of LPS-induced PTX3 with the inflammatory cytokines (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha) were examined. Twenty-one healthy subjects (10 obese and 11 normal-weight) performed an acute bout of aerobic exercise at 75% VO2max. The capacity of PBMCs to produce PTX3 ex vivo following LPS stimulation was the same in obese and normal-weight subjects at rest, and decreased equally in both subject groups following acute aerobic exercise. This is in contrast to plasma PTX3, which is lower in obese subjects at rest and increased equally in both obese and normal-weight subjects following exercise. In addition, ex vivo PTX3 production was positively associated with IL-6 and IL-10 in response to acute aerobic exercise ( r = 0.686, P = 0.020; r = 0.744, P = 0.009, respectively) in normal-weight, but not in obese individuals ( r = 0.429, P = 0.249; r = 0.453, P = 0.189, respectively). These findings indicate that concentrations of PTX3 observed in plasma are relatively independent of those produced by PBMCs ex vivo and the mechanisms associated with PTX3-mediated anti-inflammatory signaling may differ during obesity. Impact statement Our laboratory has previously demonstrated that obese individuals present with lower plasma concentrations of the anti-inflammatory protein pentraxin 3 (PTX3), whereas acute aerobic exercise increases plasma PTX3 levels similarly compared to normal-weight individuals. As a follow-up, the present study demonstrates that PBMCs isolated from obese and normal-weight individuals produce comparable amounts of PTX3 ex vivo in response to lipopolysaccharide (LPS). Furthermore, given that acute aerobic exercise reduced the ex vivo production of PTX3 in both groups, our results clearly indicate that plasma PTX3 levels are relatively independent of those produced by PBMCs ex vivo. In addition, our findings suggest that the mechanisms associated with PTX3-mediated production of the anti-inflammatory cytokine interleukin 10 may be impaired in obese individuals, and thus provides a key finding necessary for the elucidation of PTX3's role in the mediation of anti-inflammatory profiles and the subsequent amelioration of inflammatory disease during obesity.

Volume-equated high- and low-repetition daily undulating programming strategies produce similar hypertrophy and strength adaptations.

The overarching aim of this study was to compare volume-equated high-repetition daily undulating periodization (DUPHR) versus a low-repetition daily undulating periodization (DUPLR) program for muscle performance. Sixteen college-aged (23 ± 3 years) resistance-trained males were counterbalanced into 2 groups: (i) DUPHR (n = 8), with a weekly training order of 12 repetitions (Day 1), 10 repetitions (Day 2), and 8 repetitions (Day 3); and (ii) DUPLR (n = 8), with a weekly training order of 6 repetitions (Day 1), 4 repetitions (Day 2), and 2 repetitions (Day 3). Both groups trained 3 times/week for 8 weeks on nonconsecutive days, with pre- and post-training testing during weeks 1 and 8. Participants performed only squat and bench press exercises each session. Changes in one-repetition maximum (1RM) strength, muscle thickness (MT), and muscular endurance (ME) were assessed. Both groups significantly increased 1RM strength for both squat and bench press (p < 0.01), and no group differences existed (p > 0.05). Similarly, both groups experienced significant increases in chest, lateral quadriceps distal, and anterior quadriceps MT (p < 0.05), but no change was present in either group for lateral quadriceps mid MT (p < 0.05). No group differences were discovered for changes in MT (p > 0.05). ME did not significantly change in the squat or bench press for either group (p > 0.05); however, for squat ME, a moderate effect size was observed for DUPHR (0.57) versus a trivial effect size for DUPLR (0.17). Our findings suggest that in previously trained males, training volume is a significant contributor to strength and hypertrophy adaptations, which occur independently of specific repetition ranges.

[Not Available]. / Eficacia del entrenamiento diario de una repetición de máximo peso en levantadores de pesas bien entrenados: una serie de casos.

Introducción: el propósito de este estudio fue investigar la eficacia del entrenamiento diario de una repetición máxima (1RM) de la sentadilla en fuerza máxima. Material y método: tres levantadores de peso de competición realizaron la sentadilla durante 37 días consecutivos y se reportan como casos individuales. Participante 1 (P1) (masa corporal = 80,5 kg; edad = 28 años) y participante 3 (P3) (masa corporal = 108,8 kg; edad = 34 años) eran levantadores de fuerza; participante 2 (P2) (masa corporal = 64,1 kg; edad = 19 años) fue un levantador de pesas. Cada participante tenía por lo menos 5 años de experiencia con la posición en sentadilla de formación. Durante los días 1-35, los participantes realizaron una sentadilla de 1RM seguida por 5 conjuntos de volumen de 3 repeticiones al 85% o 2 repeticiones al 90% de la 1RM diario. En el día 36, los participantes realizan solo una serie de 1 repetición al 85% de 1RM del día 1; y el día 37 realizaron un 1RM. Resultados: cambios absolutos y porcentaje para P1 del 1 día al 37: + 5 kg/2,3% y desde el primer día al máximo (1RM era el mayor) + 12,5 kg/5,8%. P2 experimentó un aumento de 13,5 kg/10,8% en 1RM del día 1 al 37 y del día 1 al máximo. P3 demostró un aumento de 21 kg/9,5% del día 1 al 37 y del día 1 al máximo. Los tres participantes exhibieron significativa (p < 0,05) las correlaciones entre el tiempo (días) y 1RM (P1: r = 0,65, P2: r = 0,78, P3: r = 0,48). Conclusión: nuestros resultados sugieren que el entrenamiento diario de 1RM había producido efectivamente cambios significativos en la máxima fuerza en los atletas de fuerza competitiva en un periodo relativamente corto de entrenamiento.