Metformin, but not exercise training, increases insulin responsiveness in skeletal muscle of Sprague-Dawley rats

We assessed the effects of combined metformin treatment and exercise training on body composition, on insulin concentration following glucose loading, on insulin-stimulated glucose transport in skeletal muscle, and on muscle glycogen content. Male Sprague-Dawley rats were treated for 35 days with or without metformin (320 mg/kg/day) and/or treadmill exercise training (20 min at 20 m/min, 5 days/wk). Because metformin reduces food intake, pair-fed controls were included. Metformin, training, and pair-feeding all decreased food intake, body weight, and insulin concentration following glucose loading. Metformin and training reduced intra-abdominal fat, but pair feeding did not. In isolated strips derived from soleus, epitrochlearis and extensor carpi ulnaris muscles, metformin increased insulin-stimulated transport of [3H]-2-deoxyglucose by 90%, 89% and 125%, respectively (P < 0.02) and training increased [3H]-2-deoxyglucose transport in the extensor carpi ulnaris muscle only (66%, P < 0.05). Pair-feeding did not alter [3H]-2-deoxyglucose transport. Training increased gastrocnemius muscle glycogen by 100% (P < 0.001). Metformin and pair-feeding did not alter muscle glycogen. We conclude that metformin reverses the maturation-induced impairment of insulin responsiveness in Sprague-Dawley rats by increasing insulin-stimulated glucose transport in skeletal muscle and that this effect is not secondary to reduced food intake. We also conclude that metformin and exercise training may increase insulin sensitivity by different mechanisms, with training causing increased glucose transport only in some muscles and also causing increased muscle glycogen storage.     

Time course of vasodilatory responses in skeletal muscle arterioles: role in hyperemia at onset of exercise

At the onset of dynamic exercise, muscle blood flow increases within 1-2 s. It has been postulated that local vasodilatory agents produced by the vascular endothelium or the muscle itself contribute to this response. We hypothesized that only vasodilators that act directly on the vascular smooth muscle could produce vasodilation of skeletal muscle arterioles in <2 s. To test this hypothesis, we determined the time course of the vasodilatory response of isolated skeletal muscle arterioles to direct application of potassium chloride, adenosine, acetylcholine, and sodium nitroprusside. Soleus and gastrocnemius muscles were dissected from the hindlimbs of male Sprague-Dawley rats. First-order arterioles (100-200 microm) were isolated, cannulated on micropipettes, and pressurized to 60 cmH(2)O in an organ bath. Vasodilatory agents were added directly to the bath, and diameter responses of the arterioles were recorded in real time on a videotape recorder. Frame-by-frame analysis of the diameter responses indicated that none of the vasodilator agents tested produced significant diameter increases in <4 s in either soleus or gastrocnemius muscle arterioles. These results indicate that, although these local vasodilators produce significant vasodilation of skeletal muscle resistance arterioles, these responses are not rapid enough (within 1-2 s) to contribute to the initiation of the exercise hyperemic response at the onset of dynamic exercise.     

Augmented sympathetic tone alters muscle metabolism with exercise: lack of evidence for functional sympatholysis

Shoemaker, J. Kevin, Prasant Pandey, Michael D. Herr, DavidH. Silber, Qing X. Yang, Michael B. Smith, Kristen Gray, and LawrenceI. Sinoway. Augmented sympathetic tone alters muscle metabolismwith exercise: lack of evidence for functional sympatholysis. J. Appl. Physiol. 82(6):1932-1938, 1997.It is unclear whether sympathetic tone opposesdilator influences in exercising skeletal muscle. We examined highlevels of sympathetic tone, evoked by lower body negative pressure(LBNP, 60 mmHg) on intramuscular pH and phosphocreatine (PCr)levels (³¹P-nuclear magnetic resonance spectroscopy) duringgraded rhythmic handgrip (30 contractions/min; ~17, 34, 52 and 69%maximal voluntary contraction). Exercise was performedwith LBNP and without LBNP (Control). At the end of exercise, LBNPcaused lower levels of muscle pH (6.59 ± 0.09) comparedwith Control (6.78 ± 0.05; P < 0.05). PCr recovery, an index of mitochondrial respiration, was lessduring the recovery phase of the LBNP trial. Exercise mean arterialpressure was not altered by LBNP. The protocols were repeated withmeasurements of forearm blood flow velocity and deep venous samples(active forearm) of hemoglobin (Hb) saturation, pH, and lactate. WithLBNP, mean blood velocity was reduced at rest, during exercise, andduring recovery compared with Control (P < 0.05). Also, venous Hbsaturation and pH levels during exercise and recovery were lower withLBNP and lactate was higher compared with Control(P < 0.05). We concludethat LBNP enhanced sympathetic tone and reduced oxygen transport. Athigh workloads, there was a greater reliance on nonoxidativemetabolism. In other words, sympatholysis did not occur.

     

Evidence for a rapid vasodilatory contribution to immediate hyperemia in rest-to-mild and mild-to-moderate forearm exercise transitions in humans.

Controversy exists regarding the contribution of a rapid vasodilatory mechanism(s) to immediate exercise hyperemia. Previous in vivo investigations have exclusively examined rest-to-exercise (R-E) transitions where both the muscle pump and early vasodilator mechanisms may be activated. To isolate vasodilatory onset, the present study investigated the onset of exercise hyperemia in an exercise-to-exercise (E-E) transition, where no further increase in muscle pump contribution would occur. Eleven subjects lay supine and performed a step increase from rest to 3 min of mild (10% maximal voluntary contraction), rhythmic, dynamic forearm handgrip exercise, followed by a further step to moderate exercise (20% maximal voluntary contraction) in each of arm above (condition A) or below (condition B) heart level. Beat-by-beat measures of brachial arterial blood flow (Doppler ultrasound) and blood pressure (arterial tonometry) were performed. We observed an immediate increase in forearm vascular conductance in E-E transitions, and the magnitude of this increase matched that of the R-E transitions within each of the arm positions (condition A: E-E, 52.8 +/- 10.7 vs. R-E, 60.3 +/- 11.7 ml.min(-1).100 mmHg(-1), P = 0.66; condition B: E-E, 43.2 +/- 12.8 vs. R-E, 33.9 +/- 8.2 ml.min(-1).100 mmHg(-1), P = 0.52). Furthermore, changes in forearm vascular conductance were identical between R-E and E-E transitions over the first nine contraction-relaxation cycles in condition A. The immediate and identical increase in forearm vascular conductance in R-E and E-E transitions within arm positions provides strong evidence that rapid vasodilation contributes to immediate exercise hyperemia in humans. Specific vasodilatory mechanisms responsible remain to be determined.     

Smoking impairs muscle protein synthesis and increases the expression of myostatin and MAFbx in muscle

Smoking causes multiple organ dysfunction. The effect of smoking on skeletal muscle protein metabolism is unknown. We hypothesized that the rate of skeletal muscle protein synthesis is depressed in smokers compared with non-smokers. We studied eight smokers (> or =20 cigarettes/day for > or =20 years) and eight non-smokers matched for sex (4 men and 4 women per group), age (65 +/- 3 and 63 +/- 3 yr, respectively; means +/- SEM) and body mass index (25.9 +/- 0.9 and 25.1 +/- 1.2 kg/m(2), respectively). Each subject underwent an intravenous infusion of stable isotope-labeled leucine in conjunction with blood and muscle tissue sampling to measure the mixed muscle protein fractional synthesis rate (FSR) and whole body leucine rate of appearance (Ra) in plasma (an index of whole body proteolysis), the expression of genes involved in the regulation of muscle mass (myostatin, a muscle growth inhibitor, and MAFBx and MuRF-1, which encode E3 ubiquitin ligases in the proteasome proteolytic pathway) and that for the inflammatory cytokine TNF-alpha in muscle, and the concentration of inflammatory markers in plasma (C-reactive protein, TNF-alpha, interleukin-6) which are associated with muscle wasting in other conditions. There were no differences between nonsmokers and smokers in plasma leucine concentration, leucine rate of appearance, and plasma concentrations of inflammatory markers, or TNF-alpha mRNA in muscle, but muscle protein FSR was much less (0.037 +/- 0.005 vs. 0.059 +/- 0.005%/h, respectively, P = 0.004), and myostatin and MAFBx (but not MuRF-1) expression were much greater (by approximately 33 and 45%, respectivley, P < 0.05) in the muscle of smokers than of nonsmokers. We conclude that smoking impairs the muscle protein synthesis process and increases the expression of genes associated with impaired muscle maintenance; smoking therefore likely increases the risk of sarcopenia.     

Heat stress increases muscle glycogen use but reduces the oxidation of ingested carbohydrates during exercise.

The aim of the present study was to test the hypothesis that the oxidation rate of ingested carbohydrate (CHO) is impaired during exercise in the heat compared with a cool environment. Nine trained cyclists (maximal oxygen consumption 65 +/- 1 ml x kg body wt(-1) x min(-1)) exercised on two different occasions for 90 min at 55% maximum power ouptput at an ambient temperature of either 16.4 +/- 0.2 degrees C (cool trial) or 35.4 +/- 0.1 degrees C (heat trial). Subjects received 8% glucose solutions that were enriched with [U-13C]glucose for measurements of exogenous glucose, plasma glucose, liver-derived glucose and muscle glycogen oxidation. Exogenous glucose oxidation during the final 30 min of exercise was significantly (P < 0.05) lower in the heat compared with the cool trial (0.76 +/- 0.06 vs. 0.84 +/- 0.05 g/min). Muscle glycogen oxidation during the final 30 min of exercise was increased by 25% in the heat (2.07 +/- 0.16 vs. 1.66 +/- 0.09 g/min; P < 0.05), and liver-derived glucose oxidation was not different. There was a trend toward a higher total CHO oxidation and a lower plasma glucose oxidation in the heat although this did not reach statistical significance (P = 0.087 and P = 0.082, respectively). These results demonstrate that the oxidation rate of ingested CHO is reduced and muscle glycogen utilization is increased during exercise in the heat compared with a cool environment.     

Daily muscle vibration amelioration of neural impairments of the soleus muscle during 2 weeks of immobilization

V-wave, F wave and H-reflex responses of soleus were used to determine neural adaptations to 2-week immobilization and whether muscle vibration intervention during immobilization would attenuate the negative adaptations induced by immobilization. Thirty subjects were divided into the ankle immobilization group and the immobilization with muscle vibration group. Mechanical vibrations with constant low amplitude (0.3 mm) were applied (12 × 4 min daily) with a constant frequency of 100 Hz on the soleus muscle of the subjects in vibration group during the ankle immobilization period. Soleus maximal M-wave (Mmax) and H-reflex (Hmax) were evoked at rest. F-wave was recorded by supramaximal stimulation delivered at rest and V-wave during maximum voluntary contraction (MVC). The EMG during MVC was represented by its root-mean-square (RMS) value. Each subject was examined before and after 2 weeks of immobilization. Results showed that following 2 weeks of immobilization, Mmax, Hmax and F wave all did not change with immobilization in either group (P > 0.05). After 2 weeks of immobilization, significant reductions in V/Mmax (of 30.78%) (P < 0.01) and EMG RMS (24.82%) (P < 0.001) were found in the immobilization group. However, no significant changes occurred in the immobilization with muscle vibration group. Such findings suggested that 2 weeks of immobilization resulted in neural impairments as evidenced by the reduction in EMG and V wave, and that such decrease was prevented by the intervention of muscle vibration during the immobilization period.     

Populations of rat skeletal muscle mitochondria after exercise and immobilization

We slightly modified an existing procedure (Palmer et al., J. Biol. Chem. 252: 8731-8739, 1977) to isolate two distinct populations of mitochondria from rat skeletal muscle; initial brief Polytron homogenization released the subsarcolemmal mitochondria, and brief exposure of the resultant intact myofibrils to the proteolytic enzyme, Nagarse, extracted the intermyofibrillar mitochondria. The intermyofibrillar mitochondria differed from the subsarcolemmal mitochondr. ia by higher state III respiration measurements and enzymatic activities. These two populations of mitochondria were then isolated from the gastrocnemius muscle that had been induced to perform different amounts of contractile activity. The endurance training program of daily running significantly increased state III respiration and respiratory control index in the subsarcolemmal mitochondria, but the program did not increase these measurements in the intermyofibrillar mitochondria. In addition, 2 days of hindlimb immobilization resulted in a significant decrease in state II respiration and the respiratory control index of the subsarcolemmal mitochondria; however, immobilization did not affect the intermyofibrillar mitochondria. These measurements suggest that the subsarcolemmal mitochondria adapt in response to chronic changes in the level of contractile activity.     

Bimodal distribution of vasodilator responsiveness to adenosine due to difference in nitric oxide contribution: implications for exercise hyperemia.

To gain insight into the role of adenosine (Ado) in exercise hyperemia, we compared forearm vasodilation induced by intra-arterial infusion of three doses of Ado with vasodilation during three workloads of forearm handgrip exercise in 27 human subjects. We measured forearm blood flow (FBF) using Doppler ultrasound and mean arterial pressure (MAP) via brachial artery catheters and calculated forearm vascular conductance (FVC = FBF/MAP) during each infusion dose or workload. We found that about half of the subjects demonstrated robust vasodilator responsiveness to both Ado infusion and exercise, and the other half demonstrated blunted vasodilator responsiveness to Ado infusion compared with exercise. In 15 subjects (identified as "Ado responders"), the change in FVC above baseline was 209 +/- 33, 419 +/- 57, and 603 +/- 75 ml.min(-1).100 mmHg(-1) for the low, medium, and high doses of Ado, respectively, and 221 +/- 35, 413 +/- 54, and 582 +/- 70 ml.min(-1).100 mmHg(-1) for the low, medium, and high exercise workloads, respectively. In the other 12 subjects (identified as "Ado nonresponders"), the change in FVC above baseline was 102 +/- 36, 113 +/- 42, and 151 +/- 54 ml.min(-1).100 mmHg(-1) for the low, medium, and high doses of Ado, respectively (P < 0.05 vs. Ado responders), whereas exercise hyperemia was not different from Ado responders (P > 0.05). Furthermore, infusion of NG-monomethyl-L-arginine (L-NMMA) blunted vasodilator responses to Ado infusion only in Ado responders (P < 0.01 vs. post-L-NMMA) and had no effect on exercise in either group. We also found differences in vasodilator responses to isoproterenol at all doses, but acetylcholine only at one dose, between Ado responders and nonresponders. We conclude that vasodilator responsiveness to Ado exhibits a bimodal distribution among human subjects involving differences in the contribution of nitric oxide to Ado-mediated vasodilation. Finally, our data support the concept that neither Ado nor nitric oxide is obligatory for exercise hyperemia.     

Immediate exercise hyperemia: contributions of the muscle pump vs. rapid vasodilation.

A striking characteristic of the blood flow adaptation at exercise onset is the immediate and substantial increase in the first few (0-5 s) seconds of exercise. The purpose of this mini-review is to put into context the present evidence regarding mechanisms responsible for this phase of exercise hyperemia. One potential mechanism that has received much attention is the mechanical effect of muscle contraction (the muscle pump). The rapid vasodilatory mechanism(s) is another possible mechanism that has recently been shown to exist. This review will provide the reader with 1) an understanding of the basic physics of blood flow and the theories of muscle pump function, 2) a critical examination of evidence both for and against the contribution of the muscle pump or rapid vasodilatory mechanisms, and 3) an awareness of the limitations and impact of experimental models and exercise modes on the contribution of each of these mechanisms to the immediate exercise hyperemia. The inability to measure microvenular pressure continues to limit investigators to indirect assessments of the muscle pump vs. vasodilatory mechanism contributions to immediate exercise hyperemia in vivo. Future research directions should include examination of muscle-contraction-induced resistance vessel distortion as a trigger for rapid smooth muscle relaxation and further investigation into the exercise mode dependency of muscle pump vs. rapid vasodilatory contributions to immediate exercise hyperemia.     

Downhill running: a model of exercise hyperemia in the rat spinotrapezius muscle.

To utilize the rat spinotrapezius muscle as a model to investigate the microcirculatory consequences of exercise training, it is necessary to design an exercise protocol that recruits this muscle. There is evidence that the spinotrapezius is derecruited during standard treadmill exercise protocols performed on the uphill treadmill (i.e., 6 degrees incline). This investigation tested the hypothesis that downhill running would effectively recruit the spinotrapezius muscle as assessed by the presence of an exercise hyperemia response. We used radioactive 15-microm microspheres to determine blood flows in the spinotrapezius and selected hindlimb muscles of female Sprague-Dawley rats at rest and during downhill (i.e., -14 degrees incline; 331 +/- 5 g body wt, n = 7) and level (i.e., 0 degrees incline; 320 +/- 11 g body wt, n = 5) running at 30 m/min. Both level and downhill exercise increased blood flow to all hindlimb muscles (P < 0.01). However, in marked contrast to the absence of a hyperemic response to level running, blood flow to the spinotrapezius muscle increased from 26 +/- 6 ml.min(-1).100 g(-1) at rest to 69 +/- 8 ml.min(-1).100 g(-1) during downhill running (P < 0.01). These findings indicate that downhill running represents an exercise paradigm that recruits the spinotrapezius muscle and thereby constitutes a tenable physiological model for investigating the adaptations induced by exercise training (i.e., the mechanisms of altered microcirculatory control by transmission light microscopy).     

Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise

Saito, Mitsuru, Ryoko Sone, Masao Ikeda, and Tadaaki Mano.Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise. J. Appl.Physiol. 82(4): 1237 - 1243, 1997.Toinvestigate the effects of exercise duration on muscle sympatheticnerve activity (MSNA), heart rate, blood pressure (BP), tympanictemperature, blood lactate concentration, and thigh electromyogram weremeasured in eight volunteers during 30 min of cycling in the sittingposition at an intensity of 40% of maximal oxygen uptake. MSNA burstfrequency increased 18 min after exercise was begun (25 ± 4 bursts/min at baseline and 36 ± 5 bursts/min at 21 min ofexercise), reaching 41 ± 5 bursts/min at the end ofexercise. Heart rate and systolic BP increased during exercise. Twenty minutes after commencement of exercise, however, bothsystolic and diastolic BP values tended to drop compared with theinitial period of exercise. Tympanic temperature increased in atime-dependent manner, and the increment was significant 12 min afterexercise was begun. Blood lactate concentration and integratedelectromyogram showed no significant changes during exercise. Theincreased MSNA during prolonged light-intensity exercise may be asecondary effect of the drop in BP as a result of blood redistributioncaused by thermoregulation rather than by metaboreflex.

     

Age-related changes in conducted vasodilation: effects of exercise training and role in functional hyperemia

Conducted vasodilation may coordinate blood flow in microvascular networks during skeletal muscle contraction. We tested the hypotheses that 1) exercise training enhances conducted vasodilation and 2) age-related changes in the capacity for conduction affect muscle perfusion during contractions. To address hypothesis 1, young (4-5 mo), adult (12-14 mo), and old (19-21 mo) C57BL6 male mice were sedentary or given access to running wheels for 8 wk. Voluntary running distances were significantly different (in km/day): young = 5.8 +/- 0.1, adult = 3.9 +/- 0.1, old = 2.2 +/- 0.1 (P < 0.05). In gluteus maximus muscles, conducted vasodilation was greater in adult than in young or old mice (P < 0.05) and greater in young sedentary than in old sedentary mice but was not affected by exercise training. Citrate synthase activity was greater with exercise training at all ages (P < 0.05). mRNA for endothelial nitric oxide synthase did not differ among ages, but endothelial nitric oxide synthase protein expression was greater in adult and old mice with exercise training (P < 0.05). Connexin 37, connexin 40, and connexin 43 mRNA were not affected by exercise training and did not differ by age. To address hypothesis 2, perfusion of the gluteus maximus muscle during light to severe workloads was assessed by Doppler microprobe at 3-26 mo of age. Maximum perfusion decreased linearly across the lifespan. Perfusion at the highest workload, absolute and relative to maximum, decreased across the lifespan, with a steeper decline beyond approximately 20 mo of age. In this model, 1) exercise training does not alter conducted vasodilation and 2) muscle perfusion is maintained up to near maximum workloads despite age-related changes in conducted vasodilation.     

Chronic maternal feed restriction impairs growth but increases adiposity of the fetal guinea pig

Small size at birth has been associated with an increased risk of central obesity and reduced lean body mass in adult life. This study investigated the time of onset of prenatally induced obesity, which occurs after maternal feed restriction, in the guinea pig, a species that, like the human, develops substantial adipose tissue stores before birth. We examined the effect of maternal feed restriction [70% ad libitum intake from 4 wk before to midpregnancy, then 90% until day 60 gestation (term approximately 69 days)] on fetal growth and body composition in the guinea pig. Maternal feed restriction reduced fetal (-39%) and placental (-30%) weight at 60 days gestation and reduced liver, biceps muscle, spleen, and thymus weights, relative to fetal weight, while relative weights of brain, lungs, and interscapular and retroperitoneal fat pads were increased. In the interscapular depot, maternal feed restriction decreased the volume density of multilocular fat and increased that of unilocular fat, resulting in an increased relative weight of interscapular unilocular fat. Maternal feed restriction did not alter the relative weight of perirenal fat or the volume density of adipocyte populations within the depot but increased unilocular lipid locule size. Maternal feed restriction in the guinea pig is associated with decreased weight of major organs, including liver and skeletal muscle, but increased adiposity of the fetus, with relative sparing of unilocular adipose tissue. If this early-onset obesity persists, it may contribute to the metabolic and cardiovascular dysfunction that these offspring of feed-restricted mothers develop as adults.     

Skeletal muscle and liver glutathione homeostasis in response to training, exercise, and immobilization.

Female beagle dogs were treadmill trained 40 km/day at 5.5-6.8 km/h, 15% upgrade, 5 days/wk for 55 wk. With training, hepatic and red gastrocnemius (RG) total glutathione increased, glutathione peroxidase (GPX) and glutathione reductase (GRD) increased in all the leg muscles studied, and hepatic glutathione S-transferase (GST) activity increased. Joint immobilization (11 wk) did not affect GPX, GRD, and GST of RG, but total glutathione decreased. Male Han Wistar rats were treadmill trained 2 h/day at 2.1 km/h, 5 days/wk for 8 wk. With training, hepatic total glutathione and leg muscle GPX increased but GRD of RG decreased, perhaps because of an increased muscle flavo-protein breakdown during exhaustive training. gamma-Glutamyl transpeptidase was higher in the trained leg muscles. Exhaustive exercise decreased muscle gamma-glutamyl transpeptidase of only control leg muscle, depleted muscle (lesser extent in trained rats) and liver total glutathione of both groups, decreased GRD only in untrained RG, and increased hepatic GST. Endurance training elevated the antioxidant and detoxicant status of muscle and liver, respectively.     

Skeletal muscle protein composition following 5 weeks of ULLS and resistance exercise countermeasures

The effects of 5 weeks of unilateral lower limb suspension (ULLS) and flywheel resistance exercise (RE) on skeletal muscle protein composition were examined in thirty-one subjects (40 +/- 8y), divided into three groups: ULLS, ULLS+RE, and RE. Pre and post biopsy samples were examined for protein concentration, myosin heavy chain (MHC) and actin concentration. VL protein concentration of the three groups did not change. Soleus protein concentration following ULLS decreased (p<0.05). MHC and actin content of the VL and soleus were unaltered. Muscle mass changed from pre to post: ULLS -11% (VL), -11% (soleus), both p<0.05; ULLS+RE +9%, p<0.05; RE +6%, P<0.05. Therefore, the increase or decrease in VL muscle mass over 5 weeks occurred while maintaining protein, MHC and actin. However, soleus muscle atrophy occurred at the expense of other muscle proteins, since MHC and actin were maintained and protein concentrations decreased.     

Plyometric exercise increases serum indices of muscle damage and collagen breakdown

The aim of the present study was to examine the effect of acute plyometric exercise on indices of muscle damage and collagen breakdown. Nine untrained men performed an intense bout of plyometric jumping exercises (experimental group) and nine men remained at rest (control group). Seven days before and 24, 48, and 72 hours after plyometric exercise or rest, several physiological and biochemical indices of muscle damage and two biochemical indices of collagen damage were determined. No significant changes in concentric and eccentric peak torque of knee extensors and flexors or flexion and extension range of motion were found after the plyometric exercise. Delayed-onset muscle soreness increased 48 hours after exercise. Creatine kinase increased 48 and 72 hours post exercise, whereas lactate dehydrogenase increased 24, 48, and 72 hours post exercise. Serum hydroxyproline increased 24 hours post exercise, peaked at 48 hours, and remained elevated up to 72 hours post exercise. Hydroxylysine (which was measured only before exercise and at 48 hours) was found increased 48 hours post exercise. No differences were found in any physiological or biochemical index in the control group. Intense plyometric exercise increased muscle damage, delayed-onset muscle soreness, and serum indices of collagen breakdown without a concomitant decrease in the functional capacity of muscles. Hydroxyproline and hydroxylysine levels in serum seem promising measures for describing exercise-induced collagen degradation. Coaches need to keep in mind that by using plyometric activities, despite the increased muscle damage and collagen turnover that follow, it is not necessarily accompanied by decreases in skeletal muscle capacity.