Effect of bench press exercise intensity on muscle soreness and inflammatory mediators

This study compared four different intensities of a bench press exercise for muscle soreness, creatine kinase activity, interleukin (IL)-1, IL-6, tumor necrosis factor- (TNF-), and prostaglandin E2 (PGE2) concentrations in the blood. Thirty-five male Brazilian Army soldiers were randomly assigned to one of five groups: 50% one-repetition maximum (1-RM), 75% 1-RM, 90% 1-RM, 110% 1-RM, and a control group that did not perform the exercise. The total volume (setsrepetitionsload) of the exercise was matched among the exercise groups. Muscle soreness and plasma creatine kinase activity increased markedly (P0.05) after exercise, with no significant differences among the groups. Serum PGE2 concentration also increased markedly (P0.05) after exercise, with a significantly (P0.05) greater increase in the 110% 1-RM group compared with the other groups. A weak but significant (P0.05) correlation was found between peak muscle soreness and peak PGE2 concentration, but no significant correlation was evident between peak muscle soreness and peak creatine kinase activity, or peak creatine kinase activity and peak PGE2 concentration. All groups showed no changes in IL-1, IL-6 or TNF-. Our results suggest that the intensity of bench press exercise does not affect the magnitude of muscle soreness and blood markers of muscle damage and inflammation.

Exercise intensity optimization for men with high cardiorespiratory fitness

Exercise intensity is a key parameter for exercise prescription but the optimal range for individuals with high cardiorespiratory fitness is unknown. The aims of this study were (1) to determine optimal heart rate ranges for men with high cardiorespiratory fitness based on percentages of maximal oxygen consumption (%VO(2max)) and reserve oxygen consumption (%VO(2reserve)) corresponding to the ventilatory threshold and respiratory compensation point, and ( 2) to verify the effect of advancing age on the exercise intensities. Maximal cardiorespiratory testing was performed on 210 trained men. Linear regression equations were calculated using paired data points between percentage of maximal heart rate (%HR(max)) and %VO(2max) and between percentage of heart rate reserve (%HRR) and %VO(2reserve) attained at each minute during the test. Values of %VO(2max) and %VO(2reserve) at the ventilatory threshold and respiratory compensation point were used to calculate the corresponding values of %HRmax and %HRR, respectively. The ranges of exercise intensity in relation to the ventilatory threshold and respiratory compensation point were achieved at 78-93% of HR(max) and 70-93% of HRR, respectively. Although absolute heart rate decreased with advancing age, there were no age-related differences in %HR(max) and %HRR at the ventilatory thresholds. Thus, in men with high cardiorespiratory fitness, the ranges of exercise intensity based on %HR(max) and %HRR regarding ventilatory threshold were 78-93% and 70-93% respectively, and were not influenced by advancing age.

Exercise Intensity, Inflammatory Signaling, and Insulin Resistance in Obese Rats

DA SILVA, A. S. R., J. R. PAULI, E. R. ROPELLE, A. G. OLIVEIRA, D. E. CINTRA, C. T. DE SOUZA, L. A. VELLOSO, J. B. C. CARVALHEIRA, and M. J. A. SAAD. Exercise Intensity, Inflammatory Signaling, and Insulin Resistance in Obese Rats. Med. Sci. Sports Exerc., Vol. 42, No. 12, pp. 2180-2188, 2010. Purpose: To evaluate the effects of intensity of exercise on insulin resistance and the expression of inflammatory proteins in the skeletal muscle of diet-induced obese (DIO) rats after a single bout of exercise. Methods: In the first exercise protocol, the rats swam for two 3-h bouts, separated by a 45-min rest period (with 6 h in duration-DIO + EXE), and in the second protocol, the rats were exercised with 45 min of swimming at 70% of the maximal lactate steady state-MLSS (DIO + MLSS). Results: Our data demonstrated that both protocols of exercise increased insulin sensitivity and increased insulin-stimulated tyrosine phosphorylation of insulin receptor and insulin receptor substrate 1 and serine phosphorylation of protein kinase B in the muscle of DIO rats by the same magnitude. In parallel, both exercise protocols also reduced protein tyrosine phosphatase 1B activity and insulin receptor substrate 1 serine phosphorylation, with concomitant reduction in c-jun N-terminal kinase and I kappa B kinase activities in the muscle of DIO rats in a similar fashion. Conclusions: Thus, our data demonstrate that either exercise protocols with low intensity and high volume or exercise with moderate intensity and low volume represents different strategies to restore insulin sensitivity with the same efficacy.

Resistance Exercise Intensity Progression in Older Men

Our purpose was to examine possible influences of age on resistance exercise (RE) intensity progression in men. Twenty-four men, divided in young sedentary (YS; n = 10; 25.9 +/- 3.7 years), older sedentary (OS; n = 7; 67.4 +/- 5.2 years), and older runners (OR; n = 7; 71.3 +/- 3.0 years), underwent a 2 times-a-week RE program for 13 weeks. Muscle strength was assessed before and after training by 1-repetition maximum test. RE workloads were recorded for each exercise session, and increases of 5-10% were made whenever adaptation occurred. Muscle strength improved similarly in all groups after RE (P < 0.001). Relative RE intensity progression was not significantly different between YS and OS, except for a greater increase in calf raise relative workload observed in YS (P < 0.05). In contrast, OR displayed greater relative workload increase in 7 and 6 exercises than YS and OS, respectively (P < 0.05). The RE was safe as no injuries or major muscle pain were observed in either group. These results suggest that healthy sedentary older men are capable to exercise and increase RE intensity in the same way as young men, while physically active older men are capable to increase RE intensity in greater way than sedentary young and older men.

AGE DOES NOT AFFECT EXERCISE INTENSITY PROGRESSION AMONG WOMEN

Ciolac, EG, Brech, GC, and Greve, JMD. Age does not affect exercise intensity progression among women. J Strength Cond Res 24(11): 3023-3031, 2010-It has been recommended that the intensity of exercise training (ET) should progress slowly with lower increments in older than in young people. However, scientific evidence supporting this recommendation is lacking. Our aim was to examine possible influences of age on exercise intensity progression in healthy women. Seventeen young (29.1 +/- 5.7 years) and 16 older women (64.5 +/- 4.5 years) underwent 13 weeks of ET consisting of cycle ergometry (CE, 65-75% of reserve heart rate), whole-body resistance exercise (RE, 60% of 1 repetition maximum [1RM]), and stretching. Muscle strength was assessed before and after ET by the 1RM. Cycle ergometry and RE workloads were recorded for each exercise session, and increases of 5-10% were made whenever adaptation occurred. Absolute muscle strength after ET improved (p < 0.001) in both groups, and there were no significant differences between groups. Relative exercise intensity progression was not significantly different between groups for RE (Pearson`s correlation = 0.98 +/- 0.01), but it was greater in older women for CE (p = 0.047). The ET was safe because no injuries or major muscle pain was observed in either group. These results suggest that healthy older women are capable of exercising and increasing exercise intensity in the same way as young women.

Exercise intensity, but not electrolyte reposition, alters plasmatic cortisol and glucose levels of horses submitted to 30 and 60km distance endurance rides

O presente estudo teve como objetivo comparar os níveis plasmáticos de glicose e cortisol de um grupo de eqüinos atletas submetidos ao esforço de longa duração (enduro eqüestre) em distâncias de 30 e 60km, com velocidades médias de 10 e 15km h-1, respectivamente. Os animais foram aleatoriamente separados em dois grupos, sendo que a um deles foi administrada, por via oral, uma pasta eletrolítica hipertônica antes, durante e após as referidas provas. O outro grupo foi usado como controle. Os resultados das concentrações de cortisol revelaram um aumento significativo, no primeiro momento, em que a intensidade do esforço era maior (15km/h), ou com a continuação deste (30km de distância), no segundo momento, para todos os grupos. Os resultados referentes à concentração de glicose permaneceram constantes durante a prova de 30km; entretanto, nos primeiros 20km da prova de 60km, tais resultados revelaram um aumento significativo no grupo controle, retornando a valores basais no momento subseqüente. A reposição eletrolítica tem a sua importância na manutenção do equilíbrio hidroeletrolítico e ácido básico e, no presente estudo, pode ter contribuído para a manutenção da concentração média de glicose plasmática.

Effect of an acute β-adrenergic blockade on exercise intensity corresponding to the lactate minimum

β-Adrenoreceptor blockade is reported to impair endurance, power output and work capacity in healthy subjects and patients with hypertension. The purpose of this study was to investigate the effect in eighth athletic males of an acute β-adrenergic blockade with propranolol on their individual power output corresponding to a defined lactate minimum (LM). Eight fit males (cyclist or triathlete) performed a protocol to determine the power output corresponding to their individual LM (defined from an incremental exercise test after a rapidly induced exercise lactic acidosis). This protocol was performed twice in a double-blind randomized order by each athlete first ingesting propranolol (80mg) and in a second trial a placebo, 120 minutes respectively prior to the test sequence. The blood lactate concentration obtained 7 minutes after anaerobic exercise (a Wingate test) was significantly lower after acute β-adrenergic blockade (8.6 ± 1.6mM) than under the placebo condition (11.7 ± 1.6mM). The work rate at the LM was lowered from 215.0 ± 18.6 to 184.0 ± 18.6 watts and heart rate at the LM was reduced from 165 ± 1.5 to 132 ± 2.2 beats/minute as a result of the blockade. There was a non-significant correlation (r = 0.29) between the power output at the LM with and without acute β-adrenergic blockade. In conclusion, since the intensity corresponding to the LM is related to aerobic performance, the results of the present study, are able to explain in part, the reduction in aerobic power output produced during β-adrenergic blockade.

The effect of prior exercise intensity on oxygen uptake kinetics during high-intensity running exercise in trained subjects

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Manipulation effects of prior exercise intensity feedback by the Borg scale during open-loop cycling

Objective To verify the effects of exercise intensity deception by the Borg scale on the ratings of perceived exertion (RPE), heart rate (HR) and performance responses during a constant power output open-loop exercise. Methods Eight healthy men underwent a maximal incremental test on a cycle ergometer to identify the peak power output (PPO) and heart rate deflection point (HRDP). Subsequently, they performed a constant power output trial to exhaustion set at the HRDP intensity, in deception (DEC) and informed (INF) conditions: DEC-subjects were told that they would be cycling at an intensity corresponding to two categories below the RPE quantified at the HRDP; INF-subjects were told that they would cycle at the exact intensity corresponding to the RPE quantified at the HRDP. Results The PPO and power output at the HRDP obtained in maximal incremental tests were 247.5 +/- 32.1 W and 208.1 +/- 27.1 W, respectively. No significant difference in the time to exhaustion was found between DEC (525 +/- 244 s) or INF (499 +/- 224 s) trials. The slope and the first and second measurements of the RPE and HR parameters showed no significant difference between trials. Conclusions Psychophysiological variables such as RPE and HR as well as performance were not affected when exercise intensity was deceptively manipulated via RPE scores. This may suggest that unaltered RPE during exercise is a regulator of performance in this open-loop exercise.

The adaptive response of humans to exercise: Impact of exercise intensity, fibre-type specific responses and molecular patterns of response

In an attempt to improve the current understanding of the adaptive response to exercise in humans, this dissertation performed a series of studies designed to examine the impact of training intensity and mode on aerobic capacity and performance, fibre-type specific adaptations to training, and individual patterns of response across molecular, morphological and genetic factors. Project #1 determined that training intensity, session dose, baseline VO2max and total training volume do not influence the magnitude of change in VO2max by performing a meta-regression, and meta-analysis of 28 different studies. The intensity of training had no effect on the magnitude of increase in maximal oxygen uptake in young healthy participants, but similar adaptations were achieved with lower training doses following high intensity training. Project # 2 determined the acute molecular response, and training-induced adaptations in aerobic performance, aerobic capacity and muscle phenotype following high-intensity interval training (HIT) or endurance exercise (END). The acute molecular response (fibre recruitment and signal activation) and training-induced adaptations in aerobic capacity, aerobic performance, and muscle phenotype were similar following HIT and END. Project # 3 examined the impact of baseline muscle morphology and molecular characteristics on the training response, and if muscle adaptations are coordinated. The muscle phenotype of individuals who experience the largest improvements (high responders) were lower before training for some muscle characteristics and molecular adaptations were coordinated within individual participants. Project # 4 examined the impact of 2 different intensities of HIT on the expression of nuclear and mitochondrial encoded genes targeted by PGC-1α. A systematic upregulation of nuclear and mitochondrial encoded genes was not present in the early recovery period following acute HIT, but the expression of mitochondrial genes were coordinated at an individual level. Collectively, results from the current dissertation contribute to our understanding of the molecular mechanisms influencing skeletal muscle and whole-body adaptive responses to acute exercise and training in humans.

Plasma cytokine changes in relation to exercise intensity and muscle damage

The purpose of this study was to compare the effects of exercise intensity and exercise-induced muscle damage on changes in anti-inflammatory cytokines and other inflammatory mediators. Nine well-trained male runners completed three different exercise trials on separate occasions: ( 1) level treadmill running at 60% VO2max (moderate-intensity trial) for 60 min; (2) level treadmill running at 85% VO2max (high-intensity trial) for 60 min; (3) downhill treadmill running ( - 10% gradient) at 60% VO2 max (downhill running trial) for 45 min. Blood was sampled before, immediately after and 1 h after exercise. Plasma was analyzed for interleukin-1 receptor antagonist (IL-1ra), IL-4, IL-5, IL-10, IL-12p40, IL-13, monocyte chemotactic protein-1 (MCP-1), prostaglandin E-2, leukotriene B-4 and heat shock protein 70 (HSP70). The plasma concentrations of IL-1ra, IL-12p40, MCP-1 and HSP70 increased significantly (P< 0.05) after all three trials. Plasma prostaglandin E-2 concentration increased significantly after the downhill running and high-intensity trials, while plasma IL-10 concentration increased significantly only after the high-intensity trial. IL-4 and leukotriene B4 did not increase significantly after exercise. Plasma IL-1ra and IL-10 concentrations were significantly higher ( P< 0.05) after the high-intensity trial than after both the moderate-intensity and downhill running trials. Therefore, following exercise up to 1 h duration, exercise intensity appears to have a greater effect on anti-inflammatory cytokine production than exercise-induced muscle damage.