Gerhard Smekal

A physiological profile of tennis match play

PURPOSE The aim of this investigation was to examine physiological demands of single match play in tennis. METHODS 20 players performed 10 matches of 50 min. Respiratory gas exchange measures (RGEM) and heart rates (HR) were measured using two portable systems. Lactate concentration was determined after each game. The average oxygen uptake (VO2) of 270 games was 29.1 +/- 5.6 mL.kg-1.min-1 (51.1 +/- 10.9% of VO2max). Average VO2 for a game ranged from 10.4 to 47.8 mL.kg-1.min-1 (20.4 and 86.8% of VO2max). Average lactate concentration (LA) was 2.07 +/- 0.9 mmol.L-1 (ranging from 0.7 to 5.2 mmol.L-1). Furthermore, we monitored the duration of rallies (DR), the effective playing time (EPT), and the stroke frequency (SF). The average values of 270 games were DR: 6.4 +/- 4.1 s, EPT: 29.3 +/- 12.1%, SF: 42.6 +/- 9.6 shots.min-1. RESULTS Multiple regression revealed that the DR was the most promising variable for the determination of VO2 in match play (r = 0.54). The body surface area (BSA) and EPT were also entered into the calculation model. In games of two defensive players, VO2 was significantly higher than in games with at least one offensive player. CONCLUSION Our results suggest that energy demands of tennis matches are significantly influenced by DR. The highest average VO2 of a game of 47.8 mL.kg-1.min-1 may be regarded as a guide to assess endurance capacity required to sustain high-intensity periods of tennis matches compared with average VO2 of 29.1 mL.kg-1.min-1 for the 270 games. Our results suggest that proper conditioning is advisable especially for players who prefer to play from the baseline.

Impaired Mitochondrial Function and Insulin Resistance of Skeletal Muscle in Mitochondrial Diabetes

OBJECTIVE Impaired muscular mitochondrial function is related to common insulin resistance in type 2 diabetes. Mitochondrial diseases frequently lead to diabetes, which is mostly attributed to defective β-cell mitochondria and secretion. RESEARCH DESIGN AND METHODS We assessed muscular mitochondrial function and lipid deposition in liver (hepatocellular lipids [HCLs]) and muscle (intramyocellular lipids [IMCLs]) using 31P/1H magnetic resonance spectroscopy and insulin sensitivity and endogenous glucose production (EGP) using hyperinsulinemic-euglycemic clamps combined with isotopic tracer dilution in one female patient suffering from MELAS (myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome and in six control subjects. RESULTS The MELAS patient showed impaired insulin sensitivity (4.3 vs. 8.6 ± 0.5 mg · kg−1 · min−1) and suppression of EGP (69 vs. 94 ± 1%), and her baseline and insulin-stimulated ATP synthesis were reduced (7.3 and 8.9 vs. 10.6 ± 1.0 and 12.8 ± 1.3 μmol · l−1 · min−1) compared with those of the control subjects. HCLs and IMCLs were comparable between the MELAS patient and control subjects. CONCLUSIONS Impairment of muscle mitochondrial fitness promotes insulin resistance and could thereby contribute to the development of diabetes in some patients with the MELAS syndrome.

Short-Term Exercise Training Does Not Stimulate Skeletal Muscle ATP Synthesis in Relatives of Humans With Type 2 Diabetes

OBJECTIVE We tested the hypothesis that short-term exercise training improves hereditary insulin resistance by stimulating ATP synthesis and investigated associations with gene polymorphisms. RESEARCH DESIGN AND METHODS We studied 24 nonobese first-degree relatives of type 2 diabetic patients and 12 control subjects at rest and 48 h after three bouts of exercise. In addition to measurements of oxygen uptake and insulin sensitivity (oral glucose tolerance test), ectopic lipids and mitochondrial ATP synthesis were assessed using1H and31P magnetic resonance spectroscopy, respectively. They were genotyped for polymorphisms in genes regulating mitochondrial function, PPARGC1A (rs8192678) and NDUFB6 (rs540467). RESULTS Relatives had slightly lower (P = 0.012) insulin sensitivity than control subjects. In control subjects, ATP synthase flux rose by 18% (P = 0.0001), being 23% higher (P = 0.002) than that in relatives after exercise training. Relatives responding to exercise training with increased ATP synthesis (+19%, P = 0.009) showed improved insulin sensitivity (P = 0.009) compared with those whose insulin sensitivity did not improve. A polymorphism in the NDUFB6 gene from respiratory chain complex I related to ATP synthesis (P = 0.02) and insulin sensitivity response to exercise training (P = 0.05). ATP synthase flux correlated with O2uptake and insulin sensitivity. CONCLUSIONS The ability of short-term exercise to stimulate ATP production distinguished individuals with improved insulin sensitivity from those whose insulin sensitivity did not improve. In addition, the NDUFB6 gene polymorphism appeared to modulate this adaptation. This finding suggests that genes involved in mitochondrial function contribute to the response of ATP synthesis to exercise training.

The heart rate performance curve and left ventricular function during exercise in patients after myocardial infarction

PURPOSE The aim of the study was to investigate the heart rate turn point (HRTP) in the time course of the heart rate performance curve (HRPC) in patients after myocardial infarction, and the relationship between the HRTP, the left ventricular function, and the second lactate turn point (LTP2). METHODS We studied the degree and the direction of the HRPC and the left ventricular ejection fraction (LVEF) in 49 male patients 57 +/- 8 d after their first posterior wall infarction (MI). An incremental cycle ergometer test was performed and three phases of energy supply were defined (I: aerobic; II: aerobic-anaerobic transition; III: anaerobic) via blood lactate LA concentration. HRTP and LVEF-turn points (LVEFTP) were assessed by linear turn point analysis. The degree and direction of the deflection of HRPC were described as factor k (k > 0.1: downward deflection; -0.1 < k < 0.1: linear time curse; k < -0.1: upward deflection). The LVEF was determined by RNA. The difference between Pmax and LTP2 was calculated for LVEF (delta LVEF). RESULTS An HRTP could be found in 44 and a LVEFTP in 47 cases. The HRTP occurred at 85 +/- 17 Watt (W), which correlated (r = 0.95; P < 0.001) with the LTP2 (84 +/- 17 W) and the LVEFTP (84 +/- 17 W, r = 0.93; P < 0.001). From LTP2 to Pmax a significant decrease in LVEF was found. There was a correlation between the percentage of HRmax at the HRTP and k (r = 0.70), as well as delta LVEF (r = 0.56). CONCLUSIONS To prevent myocardial overloading, it seems to be useful to determine the HRTP, which indicate the workload where LVEF decreases.

Left ventricular function in response to the transition from aerobic to anaerobic metabolism

The purpose of this investigation was to study myocardial function at rest, during three phases of energy supply, and during recovery. Radionuclide angiography was performed during the aerobic phase (phase I, rest-first lactate increase), the aerobic-anaerobic transition phase (phase II, first lactate increase-second lactate increase), the anaerobic phase (phase III, second lactate increase-maximal work performance (Pmax)), and during recovery. Thirty-eight male patients (59 +/- 7 d after myocardial infarction) were compared with 19 healthy control subjects and 21 sport students of comparable age. Left ventricular ejection fraction (LVEF) increased from rest to phase I and from phase I to phase II in sports students and control subjects. During phase III, LVEF did not change significantly in sports students, but it decreased significantly in control subjects. This is in contrast to the patients, who showed an increase of LVEF from resting values (47 +/- 3%) to phase I (50 +/- 1%), no change during phase II (51 +/- 2%), and a decrease to resting values (45 +/- 2) during phase III. All subjects showed an increase in stroke volume (SV) during phase I and II, reaching a maximum at phase II. This was evidenced by an improvement of the systolic function with a constant left ventricular end-diastolic volume (EDV) in control subjects and sports students. In contrast, an improved SV in patients was achieved through an increase in EDV and a less distinct increase in the left ventricular end-systolic volume (ESV). Maximal LVEF values were measured during the first 90 s of recovery in all subjects. Values during recovery are not representative of load dependent myocardial function. This increase in LVEF does not cause an increase in cardiac output but is a consequence of changes in the EDV and ESV, which decrease again immediately after the end of exercise performance.

Oral magnesium therapy, exercise heart rate, exercise tolerance, and myocardial function in coronary artery disease patients

Background: Previous studies have demonstrated that in patients with coronary artery disease (CAD) upward deflection of the heart rate (HR) performance curve can be observed and that this upward deflection and the degree of the deflection are correlated with a diminished stress dependent left ventricular function. Magnesium supplementation improves endothelial function, exercise tolerance, and exercise induced chest pain in patients with CAD. Purpose: We studied the effects of oral magnesium therapy on exercise dependent HR as related to exercise tolerance and resting myocardial function in patients with CAD. Methods: In a double blind controlled trial, 53 male patients with stable CAD were randomised to either oral magnesium 15 mmol twice daily (n = 28, age 61±9 years, height 171±7 cm, body weight 79±10 kg, previous myocardial infarction, n = 7) or placebo (n = 25, age 58±10 years, height 172±6 cm, body weight 79±10 kg, previous myocardial infarction, n = 6) for 6 months. Maximal oxygen uptake (VO2max), the degree and direction of the deflection of the HR performance curve described as factor k<0 (upward deflection), and the left ventricular ejection fraction (LVEF) were the outcomes measured. Results: Magnesium therapy for 6 months significantly increased intracellular magnesium levels (32.7±2.5 v 35.6±2.1 mEq/l, p<0.001) compared to placebo (33.1±3.1.9 v 33.8±2.0 mEq/l, NS), VO2max (28.3±6.2 v 30.6±7.1 ml/kg/min, p<0.001; 29.3±5.4 v 29.6±5.2 ml/kg/min, NS), factor k (−0.298±0.242 v −0.208±0.260, p<0.05; −0.269±0.336 v −0.272±0.335, NS), and LVEF (58±11 v 67±10%, p<0.001; 55±11 v 54±12%, NS). Conclusion: The present study supports the intake of oral magnesium and its favourable effects on exercise tolerance and left ventricular function during rest and exercise in stable CAD patients.

Effect of high-volume and -intensity endurance training in heart transplant recipients.

BACKGROUND A recommended component of heart transplant recipients (HTR) is endurance-oriented exercise therapy. However, the trainability of HTR after transplantation is vague. We examined the effect of high-volume and -intensity exercise training on exercise performance in HTR, compared with HTR undergoing regular rehabilitation training, and sedentary healthy subjects (SHS). METHODS We studied four groups of individuals; of those, three groups were HTR. Subjects were a regularly trained HTR group of denervated (HTR-D; N = 15), reinnervated (HTR-R; N = 26) hearts, a high-volume and -intensity endurance-training group (training time 7-20 h.wk(-1); HTR-ET; N = 12), and a group of sedentary healthy subjects (SHS; N = 21). All participants performed cardiopulmonary exercise testing. RESULTS The HTR-ET achieved a significantly higher performance (255 +/- 47 W, VO(2max) of 45.2 +/- 6.9 mL.kg(-1).min(-1)) in contrast to all other groups (HTR-D: 119 +/- 17 W, VO(2max) of 17.4 +/- 4.5 mL.kg(-1).min(-1); HTR-R: 119 +/- 17 W, VO(2max) of 16.9 +/- 3.7 mL.kg(-1).min(-1); SHS: 184 +/- 19 W, VO(2max) of 35.0 +/- 6.9 mL.kg(-1).min(-1)). The HR at maximal power output in the HTR-ET was 169 +/- 17 bpm and similar to SHS (164 +/- 17 bpm), but significantly higher than HTR-D (125 +/- 16) and HTR-R (142 +/- 10). Maximal lactate concentration (LAmax) of HTR-ET was 9.9 +/- 2.2 mmol.L(-1), comparable to SHS (9.2 +/- 2.1 mmol.L(-1)), and significantly higher than HTR-D (5.5 +/- 1.5 mmol.L(-1)) and HTR-R (5.1 +/- 1.0 mmol.L(-1)). CONCLUSIONS Data suggest that HTR can perform high-volume and -intensity exercise training, reaching exercise performance comparable to or even exceeding values of sedentary or moderately trained healthy subjects.

Parasympathetic receptor blockade and the heart rate performance curve

Parasympathetic receptor blockade and the heart rate performance curve. Med. Sci Sports Sci., Vol. 30. No. 2, pp. 229-233, 1998. The aim of the present study was to investigate the influence of parasympathetic receptor blockade on the heart rate performance curve (HRPC). Twenty healthy male subjects performed a first cycle ergometer test (F), showing a HRPC deflection of varying degree and direction. Subjects then in random order performed two additional cycle ergometer tests, one with atropine (A) and the other with placebo (P). Two lactate turn points (LTP1, and LTP2) were determined by means of linear regression turn point analysis. The degree and direction of the deflection of the HRPC was calculated mathematically as factor kHR (kHR>0 = downsloping of HPRC; kHR<0 = upsloping of HRPC). In comparison with that in F and P, HR in A was significantly higher at rest, LTP1, LTP2, and during recovery, but not at Power(max). An upsloping deflection of the HRPC was seen in only five cases in F and P, whereas in A 10 cases were observed (P < 0.05). In A, kHR was significantly lower than in F and P. A significant correlation for kHR was found among F, P, and A. Independent from parasympathetic receptor blockade and the HR at Power(max), the HR at LTP2 was lower in cases with negative kHR (upsloping). In A as well as in P a significant correlation was observed between kHR and HR at LTP2. The individual time course of HRPC is reproducible and may be independent of parasympathetic activity.

A Single Nucleotide Polymorphism Associates With the Response of Muscle ATP Synthesis to Long-Term Exercise Training in Relatives of Type 2 Diabetic Humans

OBJECTIVE Myocellular ATP synthesis (fATP) associates with insulin sensitivity in first-degree relatives of subjects with type 2 diabetes. Short-term endurance training can modify their fATP and insulin sensitivity. This study examines the effects of moderate long-term exercise using endurance or resistance training in this cohort. RESEARCH DESIGN AND METHODS A randomized, parallel-group trial tested 16 glucose-tolerant nonobese relatives (8 subjects in the endurance training group and 8 subjects in the resistance training group) before and after 26 weeks of endurance or resistance training. Exercise performance was assessed from power output and oxygen uptake (Vo2) during incremental tests and from maximal torque of knee flexors (MaxTflex) and extensors (MaxText) using isokinetic dynamometry. fATP and ectopic lipids were measured with 1H/31P magnetic resonance spectroscopy. RESULTS Endurance training increased power output and Vo2 by 44 and 30%, respectively (both P < 0.001), whereas resistance training increased MaxText and MaxTflex by 23 and 40%, respectively (both P < 0.001). Across all groups, insulin sensitivity (382 ± 90 vs. 389 ± 40 mL ⋅ min−1 ⋅ m−2) and ectopic lipid contents were comparable after exercise training. However, 8 of 16 relatives had 26% greater fATP, increasing from 9.5 ± 2.3 to 11.9 ± 2.4 μmol ⋅ mL−1 ⋅ m−1 (P < 0.05). Six of eight responders were carriers of the G/G single nucleotide polymorphism rs540467 of the NDUFB6 gene (P = 0.019), which encodes a subunit of mitochondrial complex I. CONCLUSIONS Moderate exercise training for 6 months does not necessarily improve insulin sensitivity but may increase ATP synthase flux. Genetic predisposition can modify the individual response of the ATP synthase flux independently of insulin sensitivity.

Respiratory gas exchange and lactate measures during competitive orienteering.

PURPOSE In the past, orienteering sports analyses were based on heart rate (HR) and lactate (LA) measures. This study assessed additional respiratory gas exchange measures (RGEM) to provide further information regarding the physiological requirements of orienteering competitions (OTC). METHODS Eleven elite male athletes performed simulated OTC. RGEM were performed using a portable system. LA was determined after each section (total of six) of OTC. Athletes were also subjected to treadmill testing (TT). RESULTS Average values for the entire OTC were [OV0312]O(2OTC): 56.4 +/- 4.5 mL.kg-1.min-1 (83.0 +/- 3.8% of [OV0312]O(2max) of TT), HR(OTC): 172 +/- 11 bpm, and LA(OTC): 5.16 +/- 1.5 mmol.L-1. The highest measured [OV0312]O(2OTC) of an athlete in this study was 64.4 +/- 2.9 mL.kg-1.min-1. [OV0312]O(2OTC) was 94.6 +/- 5.2% of [OV0312]O(2IAT) (IAT= individual anaerobic threshold), HR(OTC) was 98.0 +/- 2.9% of HR(IAT), respiratory exchange ratio was 97 +/- 3.8% and LA(OTC) was 143.9 +/- 24.2% of LA(IAT). In contrast to [OV0312]O(2) and LA, average HR were similar in all sections of OTC despite topographical differences of the course. No correlations were found between running time of OTC and variables of endurance performance. Running time correlated with running distance (P < 0.001; r = 0.83) and running speed (r = 0.98; P < 0.001). CONCLUSION 1) Energy requirements during OTC were derived predominately via aerobic metabolism. 2) The highest [OV0312]O(2OTC) value of 64.4 mL.kg-1.min-1 may be regarded as the reference for intensities of OTC. 3) During OTC, most athletes avoid high-intensity periods of long duration. 4) Performance in OTC was essentially influenced by technical abilities. 5) Using only LA for evaluation may lead to overestimation of energy demands during OTC. 6) HR measures were not sufficiently sensitive to ascertain energy requirements of the OTC. Therefore, RGEM provided additional information regarding energy expenditure of OTC compared with LA and HR measures alone.