Chronic Resistance Exercise Research Articles

A 9-month Progressive Resistance Training Program Attenuates Acute Exercise-Induced Lipid Peroxidation in Healthy Men and Women

PURPOSE: To determine the impact of a progressive resistance training (RT) program on acute exercise-induced oxidative stress and antioxidant responses in young adults. METHODS: Recreationally active men and women (N = 13F/11M; 23.1 ± 3.9 y) participated in a supervised, whole-body RT program for 9 months (3x/wk). Prior to (T0) and following the RT program (T9), subjects completed an acute resistance exercise bout (ARET) at the same relative intensity which consisted of 6 sets of 10 repetitions of back squats with 2 min of rest between sets. Blood was collected pre-exercise, immediately post, and 15, 30, and 60 min after completion of the ARET. Plasma biomarkers of oxidative stress and antioxidants were measured via HPLC. RESULTS: At T0, the ARET increased (p<0.05) plasma oxidized glutathione, malondialdehyde (MDA), uric acid, glutathione, and α- and γ-tocopherol, without affecting plasma vitamin C concentrations (p=0.43). Following 9-months of RT, plasma antioxidants, including vitamin C, increased following the ARET. Compared to T0, RT significantly attenuated MDA responses induced by acute exercise (T0AUC=131.1 vs. T9AUC=118.3 μM × min, p=0.013) and specific differences were observed immediately post-exercise and at 15 and 30 min (p<0.01) with a trend for a reduction at 60 min (p=0.063). CONCLUSIONS: These preliminary findings indicate that chronic resistance exercise reduces acute exercise-induced lipid peroxidation by increasing antioxidant defenses. Additional work is underway to better define how acute exercise increases circulating antioxidants.

Cumulative responses of muscle protein synthesis are augmented with chronic resistance exercise training

The purpose of this study was to determine the anabolic response of a single bout of high intensity resistance exercise (RE) following 5 weeks of RE training. To complete these studies, Sprague-Dawley rats were assigned by body mass to RE, exercise control (EC), or sedentary cage control (CC) groups and studied over 36 h after 5 weeks of RE (squat-like) training. Cumulative (final 36 h) fractional rates of muscle protein synthesis (FSR) were determined by ²H₂O, and acute (16 h post-RE) rates of muscle protein synthesis (RPS) were determined by flooding with l-[2,3,4,5,6-³H]phenylalanine. Regulators of peptide-chain initiation, 4E-BP1, eIF4E and the association of the two were determined by Western blotting and immunoprecipitation respectively. No differences were observed with acute measures of RPS obtained 16 h following the final exercise bout in the plantaris or soleus muscles (P > 0.05). Consistent with this observation, 4E-BP1 was similarly phosphorylated and bound to eIF4E among all groups. However, upon determination of the cumulative response, FSR was significantly increased in the plantaris of RE vs. EC and CC (0.929±0.094, 0.384±0.039, 0.300±0.022% h(-1) respectively; P<0.001), but not the soleus. With the advantage of determining cumulative FSR, the present study demonstrates that anabolic responses to RE are still evident after chronic RE training, primarily in muscle composed of fast-twitch fibres.

A Limited Role for PI(3,4,5)P3 Regulation in Controlling Skeletal Muscle Mass in Response to Resistance Exercise

BackgroundSince activation of the PI3K/(protein kinase B; PKB/akt) pathway has been shown to alter muscle mass and growth, the aim of this study was to determine whether resistance exercise increased insulin like growth factor (IGF) I/phosphoinositide 3-kinase (PI3K) signalling and whether altering PI(3,4,5)P3 metabolism genetically would increase load induced muscle growth.Methodology/Principal FindingsAcute and chronic resistance exercise in wild type and muscle specific PTEN knockout mice were used to address the role of PI(3,4,5)P3 regulation in the development of skeletal muscle hypertrophy. Acute resistance exercise did not increase either IGF-1 receptor phosphorylation or IRS1/2 associated p85. Since insulin/IGF signalling to PI3K was unchanged, we next sought to determine whether inactivation of PTEN played a role in load-induced muscle growth. Muscle specific knockout of PTEN resulted in small but significant increases in heart (PTEN+/+ = 5.00±0.02 mg/g, PTEN−/− = 5.50±0.09 mg/g), and TA (PTEN+/+ = 1.74±0.04 mg/g, PTEN−/− = 1.89 ±0.03) muscle mass, while the GTN, SOL, EDL and PLN remain unchanged. Following ablation, hypertrophy of the PLN, SOL or EDL muscles was similar between PTEN−/− and PTEN+/+ animals. Even though there were some changes in overload-induced PKB and S6K1 phosphorylation, 1 hr following acute resistance exercise there was no difference in the phosphorylation state of S6K1 Thr389 between genotypes.Conclusions/SignificanceThese data suggest that physiological loading does not lead to the enhanced activation of the PI3K/PKB/mTORC1 axis and that neither PI3K activation nor PTEN, and by extension PI(3,4,5)P3 levels, play a significant role in adult skeletal muscle growth.

Fibrinogen, D-dimer and tPA Antigen Concentrations Following Acute and Chronic Blood Flow Restricted Resistance Exercise

Fibrinogen, D-dimer and tPA Antigen Concentrations Following Acute and Chronic Blood Flow Restricted Resistance Exercise

The assessment of in vivo protein synthesis following chronic resistance exercise using 2 H 2 O

The assessment of in vivo protein synthesis following chronic resistance exercise using ² H ₂ O

Changes of central haemodynamic parameters during mental stress and acute bouts of static and dynamic exercise

Chronic dynamic (aerobic) exercise decreases central arterial stiffness, whereas chronic resistance exercise evokes the opposite effect. Nevertheless, there is little information available on the effects of acute bouts of exercise. Also, there is limited data showing an increase of central arterial stiffness during acute mental stress. This study aimed to determine the effect of acute mental and physical (static and dynamic exercise) stress on indices of central arterial stiffness. Fifteen young healthy volunteers were studied. The following paradigms were performed: (1) 2 min of mental arithmetic, (2) short bouts (20 s) of static handgrip at 20 and 70% of maximal voluntary contraction (MVC), (3) fatiguing handgrip at 40% MVC and (4) incremental dynamic knee extensor exercise. Central aortic waveforms were assessed using SphygmoCor software. As compared to baseline, pulse wave transit time decreased significantly for all four interventions indicating that central arterial stiffness increased. During fatiguing handgrip there was a fall in the ratio of peripheral to central pulse pressure from 1.69+/-0.02 at baseline to 1.56+/-0.05 (P<0.05). In the knee extensor protocol a non-significant trend for the opposite effect was noted. The augmentation index increased significantly during the arithmetic, short static and fatiguing handgrip protocols, whereas there was no change in the knee extensor protocol. We conclude that (1) during all types of acute stress tested in this study (including dynamic exercise) estimated central stiffness increased, (2) during static exercise the workload posed on the left ventricle (expressed as change in central pulse pressure) is relatively higher than that posed during dynamic exercise (given the same pulse pressure change in the periphery).

Growth Hormone Release During and Following Acute Resistance Exercise Includes Disulfide-linked Aggregates

Growth hormone (GH) exists as a family of nearly 100 different molecular variants, which can include oligomers linked via non-covalent or covalent (disulfide) bonds. Previous data (Hymer, et al., 2001) have demonstrated that chemically reducing post exercise serum [via glutathione (GSH)] results in elevated GH concentrations, indicating the presence of disulfide-linked aggregates. PURPOSE: To provide a further characterization of GH aggregates in the exercise-induced hormonal milieu before and after 8 wks of chronic exercise training. METHODS: Thirteen males (27.5 ± 1.4 yr) underwent two different 8-wk resistance training programs designed to improve military performance. Prior to and following the training programs, subjects performed an acute exercise test (AET; 6 sets of 10 repetition maximum squat with 2-min inter-set rest periods), and had venous blood drawn before (Pre), during (Mid), and post AET (0, 15, and 30 min post exercise). Plasma GH concentrations were determined in the non-reduced (−GSH) and reduced (+GSH; [1 0mM GSH] for 18 h) states using a commercially available IRMA assay. Data were analyzed using repeated measures ANOVA with a LSD post-hoc test. RESUITS: No differences were observed in the GH responses of the 2 training programs; therefore, training group data were collapsed for analysis. Significant main effects were observed for GSH reduction (p<0.01), suggesting that +GSH increased the GH signal (+GSH: 1.7 ±0.3 vs. -GSH: 1.4 ±0.3 ?g/L), and time (p<0.01), indicating that GH concentrations increased during the AET (Pre: 0.1 ± 0.0 <Mid: 1.3 ± 0.4 < Post: 2.9 ± 0.6 ?g/L) and declined in recovery (15-minpost: 2.2 ± 0.4 > 30-min post: 1.4 ± 0.4 ?g/L). A significant reduction × time interaction effect indicated that serum contained disulfide-linked GH aggregates at Mid, 0, 15 and 30 min post (p<0.01). For integrated GH AUC concentrations, a reduction main effect suggested that total GH released contained disulfide-linked molecular variants (+GSH: 7.7 ± 1.4 vs. -GSH: 6.4 ± 1.3 min*μg/L; p<0.01). No effects of chronic resistance exercise on the GH response were observed. CONCLUSIONS: Disulfide-linked GH aggregates, which may sustain the biological half-life of GH, are released during and following acute exercise; however, this response does not appear to be altered with chronic training.

PERSONAL DIGITAL VIDEO: A METHOD TO MONITOR DRUG REGIMEN ADHERENCE DURING HUMAN CLINICAL INVESTIGATIONS

1. Maintaining patient adherence to a drug regimen has proven to be difficult. Missed doses can impact drug efficacy and disease control, leading to increased health-care costs. 2. During clinical drug trials, poor adherence could lead to false conclusions regarding drug efficacy. Therefore, the purpose of the present study was to determine the feasibility of using personal digital video cameras to monitor adherence to a medication regimen during a clinical investigation. 3. Older men and women (60-78 years) participated in a double-blind, placebo-controlled trial to determine the effect of ibuprofen or paracetamol on skeletal muscle adaptations to chronic resistance exercise training. Patients took three daily doses of either a placebo or the maximal daily over-the-counter dose of ibuprofen (1.2 g/day) or paracetamol (4.0 g/day) for 12 weeks. Prior to beginning the study, subjects were trained to use a personal digital video camera to record their drug consumption. 4. Subjects correctly recorded 4,956 of 5,375 doses, resulting in an average camera compliance rate of 92% (71-100%). 5. We describe a method of monitoring adherence to a prescribed drug regimen during a clinical investigation. Camera compliance rates, which directly confirm drug consumption, were higher than what is typically obtained with other methods of monitoring adherence. This camera compliance method provides the investigator with a simple and convenient means to generate direct evidence of drug consumption.

Chronic resistance training in women potentiates growth hormone in vivo bioactivity: characterization of molecular mass variants

This investigation determined the influence of acute and chronic resistance exercise on responses of growth hormone (GH) molecular variants in women. Seventy-four healthy young women (23 +/- 3 yr, 167 +/- 7 cm, 63.8 +/- 9.3 kg, 26.3 +/- 4.0% body fat) performed an acute bout of resistance exercise (6 sets of 10 repetition maximum squat). Blood samples were obtained pre- and postexercise. Resulting plasma was fractionated by molecular mass (fraction A, >60 kDa; fraction B, 30-60 kDa; and fraction C, <30 kDa) using chromatography. Fractionated and unfractionated (UF) plasma was then assayed for GH using three different detection systems (monoclonal immunoassay, polyclonal immunoassay, and rat tibial line in vivo bioassay). Subjects were then matched and randomly placed into one of four resistance exercise training groups or a control group for 24 wk. All experimental procedures were repeated on completion of the 24-wk resistance training programs. After acute exercise, immunoassays showed consistent increases in UF GH samples and fractions B and C; increases in fraction A using immunoassay were seen only in the monoclonal assay. No consistent changes in bioactive GH were found following acute exercise. Conversely, chronic exercise induced no consistent changes in immunoassayable GH of various molecular masses, whereas, in general, bioassayable GH increased. In summary, although acute exercise increased only immunoactive GH, chronic physical training increased the biological activity of circulating GH molecular variants. Increased bioactive GH was observed across all fractions and training regimens, suggesting that chronic resistance exercise increased a spectrum of GH molecules that may be necessary for the multitude of somatogenic and metabolic actions of GH.

Acute insulin is not necessary for post exercise elevations of muscle protein synthesis after 5 weeks of resistance exercise training

In rats, insulin elevates rates of muscle protein synthesis (RPS) following resistance exercise (RE), and the acute effect of insulin on RPS persists after 4 weeks of training. The purpose of this study was to determine if administration of insulin elevates RPS after acute or chronic RE in human skeletal muscle. Eight men performed unilateral RE (knee extensions; 4 sets of 7 repetitions, 2 or 3 days/week), while the other leg served as a non-exercised control. The RE leg was familiarized (3 sessions) prior to training. The initial experiment studied the effect of familiarization on RPS following the first bout of exercise. For this and the secondary experiment, both legs engaged in a single bout of RE 16 h prior to taking a muscle biopsy from the m. vastus lateralis of each leg. Individual muscle bundles were placed in specially designed clips to maintain length and assessed for RPS, with and without insulin, in vitro. Results demonstrated that the post exercise elevation of RPS after the first bout of RE only occurs in the presence of insulin, regardless of familiarization. However, after 5 weeks of RE, RPS was elevated in the trained leg, with or without insulin, but only in the presence of insulin in the untrained leg. These results suggest that insulin may be important for enhancing skeletal muscle RPS at the onset of exercise, but the importance of available insulin for post exercise elevations of RPS dissipates with training.

Chronic Resistance Exercise Training Improves Natural Killer Cell Activity in Older Women

Regular exercise has been reported to slow the age-associated declines in natural killer cell activity (NKCA). To evaluate this response, we recruited older, postmenopausal women (65-85 years old) to fill one of two groups: training (10 weeks of resistance exercise; TR) or control. Blood samples were collected from an arm vein in the TR group at rest (PRE), immediately following (POST), and 2 hours (2H) following an acute bout of resistance exercise both before (BEFORE) and after (AFTER) training. Leukocytes and NKCA were determined by flow cytometry and a whole blood (51)Cr release assay, respectively. Acute exercise increased total leukocyte (p < .05), CD8 (p < .05), CD4 (p < .05), and CD56 counts (p < .05), but there was no effect of training. NKCA was greater TR-AFTER-PRE (136%), -POST (80%), and -2H (127%) compared to similar values from TR-BEFORE (p < .05). Increased resting NKCA after chronic resistance training suggests that immunity has been improved.

Designing Resistance Training Programmes to Enhance Muscular Fitness

The popularity of resistance training has grown immensely over the past 25 years, with extensive research demonstrating that not only is resistance training an effective method to improve neuromuscular function, it can also be equally effective in maintaining or improving individual health status. However, designing a resistance training programme is a complex process that incorporates several acute programme variables and key training principles. The effectiveness of a resistance training programme to achieve a specific training outcome (i.e. muscular endurance, hypertrophy, maximal strength, or power) depends on manipulation of the acute programme variables, these include: (i) muscle action; (ii) loading and volume; (iii) exercise selection and order; (iv) rest periods; (v) repetition velocity; and (vi) frequency. Ultimately, it is the acute programme variables, all of which affect the degree of the resistance training stimuli, that determine the magnitude to which the neuromuscular, neuroendocrine and musculoskeletal systems adapt to both acute and chronic resistance exercise. This article reviews the available research that has examined the application of the acute programme variables and their influence on exercise performance and training adaptations. The concepts presented in this article represent an important approach to effective programme design. Therefore, it is essential for those involved with the prescription of resistance exercise (i.e. strength coaches, rehabilitation specialists, exercise physiologists) to acquire a fundamental understanding of the acute programme variables and the importance of their practical application in programme design.

TLR4 Is Lower in Resistance-Trained Older Women and Related to Inflammatory Cytokines

Regular exercise may offset age-associated increases in inflammatory cytokines and reduce the risk of developing diseases with an inflammatory etiology by exerting "anti-inflammatory" effects. Toll-like receptor 4 (TLR4) signaling stimulates inflammatory cytokine production, and may explain the "anti-inflammatory" effect attributed to regular exercise. Therefore, the purpose of the present study was to compare the effect of acute (3 sets, 9 exercises, 10 repetitions at 80% of the 1-repetition maximum) and chronic resistance exercise on TLR4 and inflammatory cytokines. Venous blood samples were collected from trained (TR, N = 10) and untrained (UT, N = 10) older (65-80 yr) postmenopausal women: before (PRE), immediately post (POST), and 2 h (2H), 6 h (6H), and 24 h (24H) after completion of exercise. Cell-surface expression of TLR4 (two-color immunofluorescent cytometry), LPS (25 microg x mL(-1))-stimulated cytokine production (ELISA), plasma cytokines (ELISA), and mRNA expression of TLR4 and cytokines (RT-PCR) were determined for each sample. TR had 124% less cell-surface TLR4 expression than UT (P < 0.05). A significant time effect was found for LPS-stimulated IL-6, IL-1beta, and TNF-alpha, where 6H was significantly greater than all other samples. No significant effects were found for plasma (IL-6 and TNF-alpha) or mRNA expression (IL-6, TNF-alpha, and IL-1beta) of inflammatory cytokines. When subjects were grouped according to cell-surface TLR4 expression (HI and LO), LPS-stimulated TNF-alpha (302%), IL-1beta (209%), and IL-6 (167%) production was greater for HI than LO (P < 0.05). Regularly exercising older women expressed less cell-surface TLR4 but did not have lower plasma levels or produce less LPS-stimulated inflammatory cytokines at rest or in response to a single bout of resistance exercise. TLR4 changes may explain the "anti-inflammatory" effect that has recently been attributed to chronic (2x wk for previous 24 months) resistance exercise training.

CD14+ Cell-Surface Expression of Toll-like Receptor 4 is Lower in Exercise Trained Older Women

1054 PURPOSE: Inflammatory cytokines are associated with an increased risk of cardiovascular disease, diabetes mellitus, cachexia, and osteoporosis and are often increased in age-advanced persons. Toll-like receptor 4 (TLR4) is the primary signaling receptor for lipopolysaccharide (LPS) and TLR4 signaling stimulates inflammatory cytokine production. Thus, TLR4 may explain lower LPS-stimulated cytokine expression we have observed in older, trained persons. The purpose of the present study was to compare the effect of both acute (3 sets of 8 reps for 9 exercises at 80% of the 1RM) and chronic resistance exercise on CD14+ cell-surface expression of TLR4. METHODS: Blood samples were collected from trained (TR, n = 10, > 6 months of resistance exercise) or untrained (UT, n = 10), older (65–80 yrs) post-menopausal women before, immediately after, 2-h, 6-h, and 24-h after exercise. Cell-surface expression of TLR4 was determined by two-color immunocytometry. LPS-stimulated (LPS, 25 μg.ml−1) whole-blood production of IL-6, IL-1β, and TNF-α were determined by ELISA. Plasma IL-6 and TNF-α were analyzed by ELISA. After cell-surface TLR4 analysis, subjects were placed into groups of high and low TLR4 “expressers” (HI and LO) and group comparisons for IL-6, TNF-α, and IL-1β were made. RESULTS: There was 124% lower TLR4 cell-surface expression in TR than UT, but no significant effects were found for plasma (IL-6 & TNF-α) or mRNA expression (IL-6, TNF-α, & IL-1β) of inflammatory cytokines. A significant time effect was found for LPSstimulated IL-6, IL-1β, and TNF-α, where 6-h was significantly greater than all other samples. HI produced more LPS-stimulated TNF-α (302%), IL-1β (209%), and IL-6(167%) than LO. CONCLUSION: Acute exercise did not alter TLR4 expression; but TR expressed 2.3-fold less TLR4 than UT, suggesting that chronic exercise alters TLR4. Despite a difference in cell-surface TLR4, plasma, mRNA, and LPS-stimulated inflammatory cytokine were not different between groups. High TLR4 expressers produced significantly more LPS-stimulated IL-6, TNF-α, and IL-1β than low TLR4 expressers.

Protein metabolism and age: influence of insulin and resistance exercise.

Skeletal muscle proteins are constantly being synthesized and degraded, and the net balance between synthesis and degradation determines the resultant muscle mass. Biochemical pathways that control protein synthesis are complex, and the following must be considered: gene transcription, mRNA splicing, and transport to the cytoplasm; specific amino acyl-tRNA, messenger (mRNA), ribosomal (rRNA) availability; amino acid availability within the cell; the hormonal milieu; rates of mRNA translation; packaging in vesicles for some types of proteins; and post-translational processing such as glycation and phosphorylation/dephosphorylation. Each of these processes is responsive to the need for greater or lesser production of new proteins, and many states such as sepsis, uncontrolled diabetes, prolonged bed-rest, aging, chronic alcohol treatment, and starvation cause marked reductions in rates of skeletal muscle protein synthesis. In contrast, acute and chronic resistance exercise cause elevations in rates of muscle protein synthesis above rates found in non-diseased rested organisms, which are normally fed. Resistance exercise may be unique in this capacity. This chapter focuses on studies that have used exercise to elucidate mechanisms that explain elevations in rates of protein synthesis. Very few studies have investigated the effects of aging on these mechanisms; however, the literature that is available is reviewed.

Muscle protein metabolism in the elderly: influence of exercise and nutrition.

Although the causes of sarcopenia are multi-factorial, at least some, such as poor nutrition and inactivity, may be preventable. Changes in muscle mass must be a result of net muscle protein breakdown over that particular time period. Stable isotope methodology has been used to examine the metabolic basis of muscle loss. Net muscle protein breakdown may occur due to a decrease in the basal level of muscle protein synthesis. However, changes of this type would likely be of small magnitude and undetectable by current methodology. Hormonal mediators may also be important, especially in association with forced inactivity. Net muscle protein breakdown may be also attributed to alterations in the periods of net muscle protein synthesis and breakdown each day. Reduced activity, combined with ineffectual nutrient intake, could lead to decreased net muscle protein balance. Chronic resistance exercise training clearly is an effective means of increasing muscle mass and strength in elderly individuals. Although sometimes limited, acute metabolic studies provide valuable information for maintenance of muscle mass with age.

Hypertrophy of skeletal muscle in diabetic rats in response to chronic resistance exercise.

This study had the following objectives: 1) to determine whether diabetic rats could increase muscle mass due to a physiological manipulation (chronic resistance exercise), 2) to determine whether exercise training status modifies the effect of the last bout of exercise on elevations in rates of protein synthesis, and 3) to determine whether chronic resistance exercise alters basal glycemia. Groups consisted of diabetic or nondiabetic rats that performed progressive resistance exercise for 8 wk, performed acute resistance exercise, or remained sedentary. Arterial plasma insulin in diabetic groups was reduced by about one-half (P < 0.05) compared with nondiabetic groups. Soleus and gastrocnemius-plantaris complex muscle wet weights were lower because of diabetes, but in response to chronic exercise these muscles hypertrophied in diabetic (0.028 +/- 0.003 vs. 0.032 +/- 0.0015 g/cm for sedentary vs. exercised soleus and 0.42 +/- 0.068 vs. 0.53 +/- 0.041 g/cm for sedentary vs. exercised gastrocnemius-plantaris, both P < 0.05) but not in nondiabetic (0.041 +/- 0.0026 vs. 0.042 +/- 0.003 g/cm for sedentary vs. exercised soleus and 0.72 +/- 0.015 vs. 0.69 +/- 0.013 g/cm for sedentary vs. exercised gastrocnemius-plantaris) rats when muscle weight was expressed relative to tibial length or body weight (data not shown). Another group of diabetic rats that lifted heavier weights showed muscle hypertrophy. Rates of protein synthesis were higher in red gastrocnemius in chronically exercised than in sedentary rats: 155 +/- 11 and 170 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in exercised diabetic and nondiabetic rats vs. 110 +/- 14 and 143 +/- 7 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in sedentary diabetic and nondiabetic rats. These elevations, however, were lower than in acutely exercised (but untrained) rats: 176 +/- 15 and 193 +/- 8 nmol phenylalanine incorporated x g muscle(-1) x h(-1) in diabetic and nondiabetic rats. Finally, chronic exercise training in diabetic rats was associated with reductions in basal glycemia, and such reductions did not occur in sedentary diabetic groups. These data demonstrate that, despite lower circulating insulin concentrations, diabetic rats can increase muscle mass in response to a physiological stimulus.

Resistance exercise overtraining and overreaching. Neuroendocrine responses.

Overtraining is defined as an increase in training volume and/or intensity of exercise resulting in performance decrements. Recovery from this condition often requires many weeks or months. A shorter or less severe variation of overtraining is referred to as overreaching, which is easily recovered from in just a few days. Many structured training programmes utilise phases of overreaching to provide variety of the training stimulus. Much of the scientific literature on overtraining is based on aerobic activities, despite the fact that resistance exercise is a large component of many exercise programmes. Chronic resistance exercise can result in differential responses to overtraining depending on whether either training volume or training intensity is excessive. The neuroendocrine system is a complex physiological entity that can influence many other systems. Neuroendocrine responses to high volume resistance exercise overtraining appear to be somewhat similar to overtraining for aerobic activities. On the other hand, excessive resistance training intensity produces a distinctly different neuroendocrine profile. As a result, some of the neuroendocrine characteristics often suggested as markers of overtraining may not be applicable to some overtraining scenarios. Further research will permit elucidation of the interactions between the neuroendocrine system and other physiological systems in the aetiology of performance decrements from overtraining.