Acute Heavy Resistance Exercise Protocol Research Articles

Acute Heavy Resistance Exercise Protocol Induces Significant Physiological Stress Elevating Extracellular Heat Shock Protein

Acute Heavy Resistance Exercise Protocol Induces Significant Physiological Stress Elevating Extracellular Heat Shock Protein

Physiological Effects of Nucleotide Supplementation on Resistance Exercise Stress in Men and Women

Nucleotide supplementation can reduce postexercise immunosuppression and hypothalamic-pituitary axis (HPA) axis activation in endurance exercise models. Nucleotide supplementation may aid recovery from other exercise modalities, such as heavy resistance exercise. Thus, the purpose of this investigation was to investigate the effects of nucleotide supplementation on the acute cortisol and immune responses to heavy resistance exercise and its effects on recovery. A double-blinded, crossover, mixed methods design with 10 men and 10 women was used. Each performed an acute heavy resistance exercise protocol (AHREP) after a loading period with a nucleotide or placebo supplement. Before and after the AHREP, and at 24, 48, and 72 hours post, blood samples were analyzed for cortisol, myeloperoxidase (MPO), and absolute neutrophil, lymphocyte, and monocyte counts. Creatine kinase (CK) was analyzed before and 24, 48, and 72 hours after the AHREP. Performance measures, including peak back squat isometric force and peak countermovement jump power were also analyzed. Nucleotide supplementation resulted in significant (p ≤ 0.05) decreases in cortisol and MPO immediately after the AHREP, and significantly lower CK values 24 hours later. The AHREP significantly affected leukocyte counts; however, no treatment effects were observed. Greater isometric force was observed immediately after AHREP and at 24 hours and 48 hours with nucleotide supplementation. Nucleotide supplementation seems to attenuate muscle damage, HPA axis and immune system activation, and performance decrements after heavy resistance exercise.

Higher chronic psychological stress is associated with blunted affective responses to strenuous resistance exercise: RPE, pleasure, pain

The aim of this study was to determine whether mental stress moderates perceptions of muscular pain, exertion, pleasure and arousal during a bout of strenuous resistance exercise. Two hundred and ten undergraduate students recruited from resistance exercise classes were screened with the Perceived Stress Scale (PSS). Fifty-seven individuals (age = 20.1 ± 1.2 y) were invited to complete the Undergraduate Stress Questionnaire (USQ), a measure of life event stress, and fitness testing. They later performed a two-phase, acute heavy-resistance exercise protocol: first phase: 10-repetition maximum (RM) leg press test; second phase: six sets at 80–100% of 10-RM. During exercise, participants responded to the Feeling Scale (pleasure), Felt Arousal Scale, Omni-RPE and the Pain Intensity Scale. Affective responses and heart rate were analyzed with a hierarchical linear modeling (HLM) growth curve analysis. USQ moderated the trajectories of affective responses and heart rate during exercise. Higher stress (USQ) levels were significantly related to lower rise in RPE (time2, p = .002; time3, p < .001) and heart rate (time2, p < .001; time3, p < .001). USQ had a main effect on pleasure and arousal (p values < .001), in which higher levels of stress were related to less affect. Models using the PSS scale produced similar results. PSS, but not USQ, interacted with time to predict pain (time2, p = .048; time3, p = .024). Relationships held even after adjusting for covariates, such as depression. Future research should determine if differential responses to exercise by stress have implications for behavioral interventions and mental health outcomes.

TNF-α and TNFR1 responses to recovery therapies following acute resistance exercise.

The purpose of this investigation was to compare the effect of two commonly used therapeutic modalities (a) neuromuscular electrical stimulation (NMES) and (b) cold water immersion (CWI) on circulating tumor necrosis factor alpha (TNF-α) and monocyte TNF-α receptor (TNFR1) expression following intense acute resistance exercise and subsequent recovery. Thirty (n = 30) resistance trained men (22.5 ± 2.7 y) performed an acute heavy resistance exercise protocol on three consecutive days followed by one of three recovery methods (CON, NMES, and CWI). Circulating TNF-α levels were assayed and TNFR1 expression on CD14+ monocytes was measured by flow cytometry measured PRE, immediately post (IP), 30-min post (30M), 24 h post (24H), and 48 h post (48H) exercise. Circulating TNF-α was elevated at IP (p = 0.001) and 30M (p = 0.005) and decreased at 24H and 48H recovery from IP in CON (p = 0.015) and CWI (p = 0.011). TNF-α did not significantly decrease from IP during recovery in NMES. TNFR1 expression was elevated (p < 0.001) at 30M compared to PRE and all other time points. No significant differences between groups were observed in TNFR1 expression. During recovery (24H, 48H) from muscle damaging exercise, NMES treatment appears to prevent the decline in circulating TNF-α observed during recovery in those receiving no treatment or CWI.

Effects of β-Hydroxy-β-methylbutyrate Free Acid Ingestion and Resistance Exercise on the Acute Endocrine Response.

Objective. To examine the endocrine response to a bout of heavy resistance exercise following acute β-hydroxy-β-methylbutyrate free acid (HMB-FA) ingestion. Design. Twenty resistance trained men were randomized and consumed either 1 g of HMB-FA (BetaTor) or placebo (PL) 30 min prior to performing an acute heavy resistance exercise protocol. Blood was obtained before (PRE), immediately after (IP), and 30 min after exercise (30P). Circulating concentrations of testosterone, growth hormone (GH), insulin-like growth factor (IGF-1), and insulin were assayed. Data were analyzed with a repeated measures ANOVA and area under the curve (AUC) was analyzed by the trapezoidal rule. Results. The resistance exercise protocol resulted in significant elevations from PRE in testosterone (P < 0.01), GH (P < 0.01), and insulin (P = 0.05) at IP, with GH (P < 0.01) and insulin (P < 0.01) remaining elevated at 30P. A significant interaction was noted between groups in the plasma GH response at IP, which was significantly higher following HMB-FA compared to PL (P < 0.01). AUC analysis revealed an elevated GH and IGF-1 response in the HMB-FA group compared to PL. Conclusion. HMB-FA prior to resistance exercise augments the GH response to high volume resistance exercise compared to PL. These findings provide further support for the potential anabolic benefits associated with HMB supplementation.

Sex differences in creatine kinase after acute heavy resistance exercise on circulating granulocyte estradiol receptors

Previous research has shown reduced tissue disruption and inflammatory responses in women as compared to men following acute strenuous exercise. While the mechanism of this action is not known, estrogen may reduce the inflammatory response through its interaction with granulocytes. The purpose of this study was to determine if estrogen receptor β expression on granulocytes is related to sex differences in tissue disruption in response to an acute heavy resistance exercise protocol. Seven healthy, resistance-trained, eumenorrheic women (23 ± 3 years, 169 ± 9.1 cm, 66.4 ± 10.5 kg) and 8 healthy, resistance-trained men (25 ± 5 years, 178 ± 6.7 cm, 82.3 ± 9.33 kg) volunteered to participate in the study. Subjects performed an acute resistance exercise test consisting of six sets of five squats at 90% of the subject's one repetition maximum. Blood samples were obtained pre-, mid-, post-, and 1-, 6-, and 24-h postexercise. Blood samples were analyzed for 17-β-estradiol by ELISA, creatine kinase by colorimetric enzyme immunoassay, and estradiol receptors on circulating granulocytes through flow cytometry. Men had higher CK concentrations than women at baseline/control. Men had significantly higher CK concentrations at 24-h postexercise than women. No significant changes in estradiol β receptors were expressed on granulocytes after exercise or between sexes. While sex differences occur in CK activity in response to strenuous eccentric exercise, they may not be related to estradiol receptor β expression on granulocytes. Thus, although there are sex differences in CK expression following acute resistance exercise, the differences may not be attributable to estrogen receptor β expression on granulocytes.

Leukocyte β2-Adrenergic Receptor Expression in Response to Resistance Exercise

Epinephrine and norepinephrine mediate interactions between the neuroendocrine and the immune systems to alter immune cell activity. Although both systems respond to exercise stress, less is known about how they interact in response to such stress. The purpose of this investigation was to examine β2-adrenergic receptor (β2-ADR) expression on circulating leukocytes to an acute bout of resistance exercise in men and women. Resistance-trained men (n = 8; mean ± SD age = 24.63 ± 5.07 yr, body mass index = 26.09 ± 2.21 kg·m(-2)) and women (n = 7; age = 22.13 ± 3.09 yr, body mass index = 22.63 ± 2.03 kg·m(-2)) performed an acute resistance exercise protocol (six sets of five-repetition maximum heavy squats) and a control test (i.e., identical conditions with no exercise) in a balanced, randomized order. Using a within-subject design, β2-ADR expressions on circulating leukocytes were evaluated with flow cytometry, and plasma epinephrine and norepinephrine were evaluated with high-performance liquid chromatography. Plasma epinephrine and norepinephrine increased during the exercise bout and returned to baseline during recovery. β2-ADR expression on monocytes was elevated in anticipation of the exercise protocol. β2-ADR expression on monocytes and granulocytes decreased during the exercise. β2-ADR expression on lymphocytes was elevated during the recovery time points. In conclusion, β2-ADR expression on leukocyte subpopulations changes in response to acute heavy resistance exercise protocol. The present findings provide insights into the potential temporal interactions between the neuroendocrine and the immune systems in response to the physiological stress of acute heavy resistance exercise in men and women.

B2-Adrenergic Receptor Expression on Human Leukocytes in Response to Acute Heavy Resistance Exercise

Epinephrine and norepinephrine mediate interactions between the neuro-endocrine and the immune systems, to alter immune cell activity. While both systems respond to exercise stress, less in known about how they interact in response to such stress. PURPOSE: To examine B2-Adrenergic receptor (B2-ADR) expression on circulating leukocytes to an acute bout of resistance exercise in men and women. METHODS: Resistance trained men (mean ± SD (n=8) age: 23.28 ± 4.26 y; body mass index: 24.51 ± 2.61 kg/m2) and women ((n=7) age: 22.13 ± 3.09 y; body mass index: 22.63 ± 2.03 kg/m2) performed an acute resistance exercise protocol (6 sets of 5 RM heavy squats) and a control test (i.e., identical conditions with no exercise) in a balanced, randomized order. Using a within subject design, B2-Adrenergic receptor (B2-ADR) expression on circulating leukocytes were evaluated with flow cytometry and plasma epinephrine and norepinephrine were evaluated with high performance liquid chromatography. RESULTS: Plasma epinephrine and norepinephrine increased during the exercise bout and returned to baseline during recovery (p<0.05). B2-ADR expression on monocytes was elevated in anticipation of the exercise protocol (p<0.05). B2-ADR expression on monocytes and granulocytes decreased during the exercise (p<0.05). B2-ADR expression on lymphocytes was elevated during the recovery time points (p<0.05). CONCLUSION: B2-ADR expression on leukocyte subpopulations changes in response to acute heavy resistance exercise protocol. Present findings provide insights into the temporal interactions between the neuro-endocrine and the immune systems in response to the physiological stress of acute heavy resistance exercise in men and women.

Changes in power curve shapes as an indicator of fatigue during dynamic contractions

The purpose of this study was to analyze exercise-induced leg fatigue during a dynamic fatiguing task by examining the shapes of power vs. time curves through the combined use of several statistical methods: B-spline smoothing, functional principal components and (supervised and unsupervised) classification. In addition, granulometric size distributions were also computed to allow for comparison of curves coming from different subjects. Twelve physically active men participated in one acute heavy-resistance exercise protocol which consisted of five sets of 10 repetition maximum leg press with 120s of rest between sets. To obtain a smooth and accurate representation of the data, a basis of 180 B-splines was used. Functional principal component (FPC) analysis was used to find the dominant modes of variation in the curves. A multivariate cluster over the FPC scores and a k-nearest neighbor classification led to three interpretable groups corresponding to different levels of fatigue. Fatigue-induced changes in the shapes of the power curves were evident, in which curves progressively flatten and develop a second power peak. In a practical setting FPC analysis greatly reduces dimensionality and the use of granulometries allows for comparison of the curve shapes without distorting the time scale.In contrast to the present methodology, which considers each curve as a datum, classical statistical approaches using summary parameters of time series may lead to limited information about the impact of dynamic fatiguing protocols on kinematic and kinetic time-course changes in curve shapes.

Anticipatory responses of catecholamines on muscle force production

Few data exist on the temporal relationship between catecholamines and muscle force production in vivo. The purpose of this study was to examine the influence of preexercise arousal on sympathoadrenal neurohormones on muscular force expression during resistance exercise. Ten resistance-trained men completed two experimental conditions separated by 7 days: 1) acute heavy resistance exercise protocol (AHREP; 6 x 10 repetitions parallel squats, 80% 1 repetition maximum) and 2) control (Cont; rest). Peak force (F(peak)) was recorded during a maximal isometric squat preceding each set and mean force (F(mean)) was measured during each set. Serial venous blood samples were collected before the AHREP and immediately preceding each set. Blood collection times were matched during Cont. Preexercise epinephrine (Epi), norepinephrine (NE), and dopamine (DA) increased (P <or= 0.05) above Cont by 270, 255, and 164%, respectively. During exercise, Epi, NE, and DA continued to increase by 512, 271, and 38%, respectively, above preexercise values. F(peak) and F(mean) decreased by approximately 20-25% over the course of the AHREP. Post hoc data analysis revealed that five subjects (F(maintainers)) showed no decline (P >or= 0.05) in muscular performance (F(peak), F(mean)) during AHREP and that five subjects (F(reducers)) had significant reductions in F(peak) and F(mean). Integrated area under the curve for Epi, NE, and F(peak) were greater (P < 0.02) for F(maintainers) than F(reducers). In conclusion, an anticipatory rise in catecholamines existed, which may be essential for optimal force production at the onset of exercise.

Influence Of Catecholamines On Muscle Force Production Capabilities

Catecholamines are implicated in the body's ability to generate muscular force, yet few studies have examined how transient changes in catecholamine concentrations regulate the expression of muscular force during exercise. PURPOSE The purpose of this study was to examine the role of sympathoadrenal neurohormones in the expression of muscular force/power during whole-body resistance-exercise. METHODS Ten resistance-trained men (22.6±2.1yrs; 89.09±9.9kg; 179.1±6.6cm) completed two experimental conditions separated by 7 days: i) acute heavy resistance exercise protocol (AHREP; 6 sets × 10 repetitions of parallel barbell squats, 80% 1RM), and ii) control (CONT; rest in controlled environment). Peak force (Fpeak) was recorded during a maximal isometric squat preceding each set in the AHREP. Mean force (Fmean) and mean power output (Pmean) were measured during each AHREP set. Serial venous blood samples were collected prior to (−60, −30, −15, −10, and −5 minutes) the AHREP, and immediately preceding each set during the AHREP. Blood collection times were matched for CONT. RESULTS Peak pre-exercise epinephrine (EPI), norepinephrine (NE), and dopamine (DA) concentrations increased (P ≤ 0.05) above CONT values 270%, 255%, and 164%, respectively. During exercise, EPI, NE, and DA increased (P ≤ 0.05) 512%, 271%, and 38% above pre-exercise values. Fpeak, Fmean, and Pmean decreased ∼20–25% (P ≤ 0.05) over the course of the AHREP. Post-hoc data analysis revealed five subjects had significant (P ≤ 0.05) reductions in Fpeak, Fmean, and Pmean and were classified as 'force reducers' (Freducers). The remaining subjects (Fmaintainers, N=5) showed no decline in muscular performance (Fpeak, Fmean, Pmean) during the AHREP. During exercise, the integrated area under the curve (AUC) for EPI, NE, and Fpeak were different (p < 0.02) between Fmaintainers and Freducers. In Fmaintainers, pre-exercise AUC for EPI, NE, and DA was correlated with Fpeak, and Fmean and Pmean achieved during the first set. Exercise-induced AUC for EPI was correlated (r2 = 0.80, P = 0.01) with Fpeak AUC in Fmaintainers only. The percent change (%Δ) in EPI and %Δ NE was correlated (EPI, r2 = 0.69; NE, r2 = 0.91) with %Δ Fpeak in Fmaintainers only. CONCLUSIONS Muscular force/power expression is closely associated with the magnitude of change above basal catecholamine concentrations prior to and during high-intensity resistance exercise. The relationship between sympathoadrenal neurohormones and the expression of muscular force therefore appears dependent upon individual responses.

Influence Of Catecholamines On Muscle Force Production Capabilities

Catecholamines are implicated in the body's ability to generate muscular force, yet few studies have examined how transient changes in catecholamine concentrations regulate the expression of muscular force during exercise. PURPOSE The purpose of this study was to examine the role of sympathoadrenal neurohormones in the expression of muscular force/power during whole-body resistance-exercise. METHODS Ten resistance-trained men (22.6±2.1yrs; 89.09±9.9kg; 179.1±6.6cm) completed two experimental conditions separated by 7 days: i) acute heavy resistance exercise protocol (AHREP; 6 sets × 10 repetitions of parallel barbell squats, 80% 1RM), and ii) control (CONT; rest in controlled environment). Peak force (Fpeak) was recorded during a maximal isometric squat preceding each set in the AHREP. Mean force (Fmean) and mean power output (Pmean) were measured during each AHREP set. Serial venous blood samples were collected prior to (−60, −30, −15, −10, and −5 minutes) the AHREP, and immediately preceding each set during the AHREP. Blood collection times were matched for CONT. RESULTS Peak pre-exercise epinephrine (EPI), norepinephrine (NE), and dopamine (DA) concentrations increased (P ≤ 0.05) above CONT values 270%, 255%, and 164%, respectively. During exercise, EPI, NE, and DA increased (P ≤ 0.05) 512%, 271%, and 38% above pre-exercise values. Fpeak, Fmean, and Pmean decreased ∼20–25% (P ≤ 0.05) over the course of the AHREP. Post-hoc data analysis revealed five subjects had significant (P ≤ 0.05) reductions in Fpeak, Fmean, and Pmean and were classified as 'force reducers' (Freducers). The remaining subjects (Fmaintainers, N=5) showed no decline in muscular performance (Fpeak, Fmean, Pmean) during the AHREP. During exercise, the integrated area under the curve (AUC) for EPI, NE, and Fpeak were different (p < 0.02) between Fmaintainers and Freducers. In Fmaintainers, pre-exercise AUC for EPI, NE, and DA was correlated with Fpeak, and Fmean and Pmean achieved during the first set. Exercise-induced AUC for EPI was correlated (r2 = 0.80, P = 0.01) with Fpeak AUC in Fmaintainers only. The percent change (%Δ) in EPI and %Δ NE was correlated (EPI, r2 = 0.69; NE, r2 = 0.91) with %Δ Fpeak in Fmaintainers only. CONCLUSIONS Muscular force/power expression is closely associated with the magnitude of change above basal catecholamine concentrations prior to and during high-intensity resistance exercise. The relationship between sympathoadrenal neurohormones and the expression of muscular force therefore appears dependent upon individual responses.

High-Affinity Growth Hormone Binding Protein and Acute Heavy Resistance Exercise

The purpose of this investigation was to examine the influence of resistance training on circulating concentrations of growth hormone binding protein (GHBP) in response to acute heavy resistance exercise. Using a cross-sectional experimental design, a group of resistance-trained men (RT, N=9, 7.9+/-1.3 yr resistance training experience) and a group of untrained men (UT, N=10) performed an acute heavy resistance exercise protocol (AHREP) consisting of 6 sets of 10 repetition maximum parallel squats. Blood samples were obtained 72 h before exercise, immediately before exercise, and 0, 15, 30, 45, and 60 min after exercise. Significant increases (P<0.05) in GHBP, immunoreactive growth hormone (iGH), and IGF-1 were observed in both subject groups after AHREP. There were no differences (P>0.05) between groups in GHBP at rest or after AHREP. However, RT exhibited a significantly greater iGH response to AHREP than UT subjects, and significantly higher IGF-1 values at rest and after exercise. Significant positive correlations were found between GHBP and BMI, body fat, and leptin in both groups. A significant positive correlation also was observed between resting leptin and GHBP values in UT but not RT subjects. In summary, these data indicate that resistance training does not increase blood GHBP. Nevertheless, the increases observed with IGF-1 concentrations in the resistance-trained subjects do suggest an apparent adaptation with the regulation of this hormone. If there was in fact an increase in GH sensitivity and GH receptor expression at the liver that was not detected by blood GHBP in this study, it may be possible that factors contributing to the circulating concentration of GHBP other than hepatocytes (e.g., leptin and adipocytes) may serve to mask training-induced increases in circulating GHBP of a hepatic origin, thus masking any detectable increase in GH receptor expression.

Response of High-Affinity Growth Hormone Binding Protein to Acute Heavy Resistance Exercise

1664 PURPOSE: The purpose of this investigation was to examine the effects of acute and chronic heavy resistance exercise on circulating concentrations of growth hormone binding protein (GHBP). METHODS: Using a cross-sectional experimental design, a group of resistance-trained men (N = 9) with at least five years of resistance training N = experience (mean ± SE years experience: 7.94 ± 1.31) and a group of untrained men (N = 10) performed an acute heavy resistance exercise protocol (6 sets of 10 repetition N = maximum parallel squats). Blood samples were obtained 72-hours prior to exercise, immediately prior to exercise, as well as 0, 15, 30, 45, and 60 minutes post-exercise. RESULTS: Significant (P: <0.05) resistance-exercise induced increases in GHBP, immunoreactive growth hormone, and IGF-1 were observed in both subject groups. No significant differences in GHBP were observed between groups either at rest or post-exercise. Resistance-trained men exhibited a significantly greater iGH response to acute resistance exercise than untrained subjects. Resistance-trained men exhibited significantly higher IGF-1 than untrained subjects at rest and post-exercise. Significant positive correlations were observed between GHBP and BMI, body fat, and leptin. A significant positive correlation was also observed between resting leptin and GHBP in the untrained subjects, whereas this relationship was not observed in the trained subjects. CONCLUSIONS: These data indicate that resistance training does not increase blood GHBP, thus indicating no change in GH receptor expression after training despite increases in IGF-1, which may indicate greater hepatic GH sensitivity. However, other factors that strongly influence blood GHBP, including leptin and adipose cells, may mask training-induced increases in circulating GHBP.

Leptin concentrations experience a delayed reduction after resistance exercise in men.

Leptin is an important metabolic hormone providing the brain with information concerning energy balance. Most studies have reported that circulating leptin concentrations are unaltered by acute, moderate exercise. We hypothesized that these studies have been limited by short sampling schemes (<4 h) postexercise and may have missed a time-delayed reduction in circulating leptin concentrations. Ten men (age = 21 +/- 1 yr, height = 177 +/- 2 cm, body mass = 79 +/- 3 kg, body fat = 11 +/- 1%BF, .VO(2max) = 51 +/- 1 mL.kg-1.min-1) completed an acute heavy-resistance exercise protocol (AHREP) (50 total sets comprised of the squat, bench press, leg press, and lat pull-down) from 1500 to 1700 h. Blood was sampled hourly postexercise until 0600 h the next morning and also during a time-matched control period. Leptin concentrations were measured by an immunoradiometric assay. Resting energy expenditure (REE) was measured via indirect calorimetry using a ventilated hood beginning approximately 0600 h after both overnight conditions. The estimated caloric expenditure from the AHREP was 856 +/- 114 kcal. No significant differences (P > 0.05) between the control and exercise conditions were observed for serum leptin concentrations until 9 h postexercise. Significant interaction effects (P < 0.05) indicated lower serum leptin concentrations postexercise at hours 9 (2.9 vs 2.2 ng.mL-1), 10 (2.7 vs 2.0 ng.mL-1), 12 (2.5 vs 1.8 ng.mL-1), and 13 (2.6 vs 1.8 ng.mL-1). This delayed reduction was accompanied by a 12% elevation (P < 0.05) in morning-after REE (0.25 +/- 0.02 vs 0.28 +/- 0.02 L.min-1). Leptin concentrations experience a delayed ( approximately 9 h) reduction in the systemic circulation after acute resistance exercise. This decline is likely associated with the disruption in metabolic homeostasis created by the high-intensity, long-duration, energy expenditure and subsequent excess post oxygen consumption from the AHREP and is not due to losses in fat mass.