J D MacDougall’s research while affiliated with McMaster University and other places

This study investigated the effects of 7 weeks of sprint training on changes in electrolyte concentrations and acid‐base status in arterial and femoral venous blood, during and following maximal exercise for 30 s on an isokinetic cycle ergometer. Six healthy males performed maximal exercise, before and after training. Blood samples were drawn simultaneously from brachial arterial and femoral venous catheters, at rest, during the final 10 s of exercise and during 10 min of recovery, and analysed for whole blood and plasma ions and acid‐base variables. Maximal exercise performance was enhanced after training, with a 13% increase in total work output and a 14% less decline in power output during maximal cycling. The acute changes in plasma volume, ions and acid‐base variables during maximal exercise were similar to previous observations. Sprint training did not influence the decline in plasma volume during or following maximal exercise. After training, maximal exercise was accompanied by lower arterial and femoral venous plasma [K ⁺ ] and [Na ⁺ ] across all measurement times ( P < 0.05 ). Arterial plasma lactate concentration ([Lac ⁻ ]) was greater ( P < 0.05 ), but femoral venous plasma [Lac ⁻ ] was unchanged by training. Net release into, or uptake of ions from plasma passing through the exercising muscle was assessed by arteriovenous concentration differences, corrected for fluid movements. K ⁺ release into plasma during exercise, and a small net K ⁺ uptake from plasma 1 min post‐exercise ( P < 0.05 ), were unchanged by training. A net Na ⁺ loss from plasma during exercise ( P < 0.05 ) tended to be reduced after training ( P < 0.06 ). Release of Lac ⁻ into plasma during and after exercise ( P < 0.05 ) was unchanged by training. Arterial and venous plasma strong ion difference ([SID]; [SID] =[Na ⁺ ]+[K ⁺ ]–[Lac ⁻ ]–[Cl ⁻ ]) were lower after training (mean differences) by 2.7 and 1.8 mmol l ⁻¹ , respectively ( P < 0.05 ). Arterial and femoral venous C0 2 tensions and arterial plasma [HCO 3 ⁻ ] were lower after training (mean differences) by 1.7mmHg, 4.5mmHg and 1.2mmol l ⁻¹ , respectively ( P < 0.05 ), with arterial plasma [H ⁺ ] being greater after training by 2.2 nmol 1 ⁻¹ ( P < 0.05 ). The acute changes in whole blood volume and ion concentrations during maximal exercise were similar to previous observations. Arterial and femoral whole blood [K ⁺ ] and [Cl ⁻ ] were increased, whilst [Na ⁺ ] was lower, across all observation times after training ( P < 0.05 ). Net uptake or release of ions by exercising muscle was assessed by arteriovenous whole blood concentration differences, corrected for fluid movements. A net K ⁺ uptake by muscle occurred at all times, including exercise, but this was not significantly different after training. An increased net Na ⁺ uptake by muscle occurred during exercise ( P < 0.05 ) with greater Na ⁺ uptake after training ( P < 0.05 ). Net muscle Lac ⁻ release and Cl ⁻ uptake occurred at all times ( P < 0.05 ) and were unchanged by training. Sprint training improved muscle ion regulation, associated with increased intense exercise performance, at the expense of a greater systemic acidosis. Increased muscle Na ⁺ and K ⁺ uptake by muscle during the final seconds of exercise after training are consistent with a greater activation of the muscle Na ⁺ ‐K ⁺ pump, reduced cellular K ⁺ loss and the observed lesser rate of fatigue. The greater plasma acidosis found after sprint training was caused by a lower arterial plasma [SID] due to lower plasma [K ⁺ ] and [Na ⁺ ], and higher plasma [Lac ⁻ ].

This study investigated the effects of 7 weeks of sprint training on gas exchange across the lungs and active skeletal muscle during and following maximal cycling exercise in eight healthy males. Pulmonary oxygen uptake (V̇O 2 ) and carbon dioxide output (V̇CO 2 ) were measured before and after training during incremental exercise ( n = 8 ) and during and in recovery from a maximal 30 s sprint exercise bout by breath‐by‐breath analysis ( n = 6 ). To determine gas exchange by the exercising leg muscles, brachial arterial and femoral venous blood O 2 and CO 2 contents and lactate concentration were measured at rest, during the final 10 s of exercise and during 10 min of recovery. Training increased ( P < 0.05 ) the maximal incremental exercise values of ventilation (V̇ E , by 15.7 ± 7.1%), V̇CO 2 (by 9.3 ± 2.1%) and V̇O 2 (by 15.0 ± 4.2%). Sprint exercise peak power (3.9 ± 1.0% increase) and cumulative 30 s work (11.7 ± 2.8% increase) were increased and fatigue index was reduced (by −9.2 ± 1.5%) after training ( P < 0.05 ). The highest V̇ E , V̇CO 2 and V̇O 2 values attained during sprint exercise were not significantly changed after training, but a significant ( P < 0.05 ) training effect indicated increased V̇ E (by 19.2 ± 7.9%), V̇CO 2 (by 9.3 ± 2.1%) and V̇O 2 (by 12.7 ± 6.5%), primarily reflecting elevated post‐exercise values after training. Arterial O 2 and CO 2 contents were lower after training, by respective mean differences of 3.4 and 21.9 ml l ⁻¹ ( P < 0.05 ), whereas the arteriovenous O 2 and CO 2 content differences and the respiratory exchange ratio across the leg were unchanged by training. Arterial whole blood lactate concentration and the net lactate release by exercising muscle were unchanged by training. The greater peak pulmonary V̇O 2 and V̇CO 2 with sprint exercise, the increased maximal incremental values, unchanged arterial blood lactate concentration and greater sprint performance all point strongly towards enhanced gas exchange across the lungs and in active muscles after sprint training. Enhanced aerobic metabolism after sprint training may contribute to reduced fatigability during maximal exercise, whilst greater pulmonary CO 2 output may improve acid‐base control after training.

To examine the effect of fibre type on potentiation and fatigue. Young men (n = 4 per group) with a predominance of type I [61.4 +/- 6.9% (SD), group I (GI)] or type II [71.8 +/- 9.2%, group II (GII)] fibres in vastus lateralis, performed a fatigue protocol of sixteen 5-s maximal voluntary isometric contractions (MVCs) of the right knee extensors. Maximal twitches and corresponding muscle action potentials (M-waves) were evoked before the first MVC, during the 3-s rest period after each MVC and at intervals during the 5-min recovery period after the last MVC. Group II [49.3 +/- 2.6% (SE)] had a greater decrease in MVC force than GI (22.8 +/- 6.2%) during the fatigue protocol. Group II (126.4 +/- 13.6%) showed greater twitch force potentiation early in the fatigue protocol than GI (38.2 +/- 2.3%), but greater depression at the end (33.7 +/- 13.7% vs.17.4 +/- 3.4%). Twitch time-to-peak torque (TPT) and half relaxation time (HRT) initially decreased but then increased as the fatigue protocol progressed; GII had a greater increase in HRT. During a 5-min recovery period twitch force increased above the prefatigue level and remained so until the end of the recovery period; the pattern was similar in GI and GII. Twitch TPT and HRT remained elevated during recovery. M-wave area increased throughout the fatigue protocol and the first part of recovery before returning to baseline values in GII, whereas there were no significant changes in GI. The interaction between potentiation and fatigue was amplified in GII early in the fatigue protocol with concurrently greater twitch and M-wave potentiation, and greater MVC force decrease and HRT increase. Late in the protocol, GII had a greater decrease in twitch and MVC force combined with greater M-wave potentiation. It is concluded that fibre type distribution influences potentiation and fatigue of the twitch, and potentiation of the M-wave during fatiguing exercise.

In this study, we employed single-leg submaximal cycle training, conducted over a 10-wk period, to investigate adaptations in sarcoplasmic reticulum (SR) Ca(2+)-regulatory proteins and processes of the vastus lateralis. During the final weeks, the untrained volunteers (age 21.4 +/- 0.3 yr; means +/- SE, n = 10) were exercising 5 times/wk and for 60 min/session. Analyses were performed on tissue extracted by needle biopsy approximately 4 days after the last training session. Compared with the control leg, the trained leg displayed a 19% reduction (P < 0.05) in homogenate maximal Ca(2+)-ATPase activity (192 +/- 11 vs. 156 +/- 18 micromol. g protein(-1). min(-1)), a 4.3% increase (P < 0.05) in pCa(50), defined as the Ca(2+) concentration at half-maximal activity (6.01 +/- 0.05 vs. 6.26 +/- 0.07), and no change in the Hill coefficient (1.75 +/- 0.15 vs. 1.76 +/- 0.21). Western blot analysis using monoclonal antibodies (7E6 and A52) revealed a 13% lower (P < 0.05) sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) 1 in trained vs. control in the absence of differences in SERCA2a. Training also resulted in an 18% lower (P < 0.05) SR Ca(2+) uptake and a 26% lower (P < 0.05) Ca(2+) release. It is concluded that a downregulation in SR Ca(2+) cycling in vastus lateralis occurs with aerobic-based training, which at least in the case of Ca(2+) uptake can be explained by reduction in Ca(2+)-ATPase activity and SERCA1 protein levels.

Recent evidence from our laboratory and others have suggested that the mechanism for a decrease in resting blood pressure after an acute bout of exercise is a centrally mediated decrease in total peripheral resistance. This study examined the effect of the central serotonergic system on post exercise hypotension (PEH) in 11 borderline hypertensive individuals (nine male, two female) aged 24.5 +/- 5.1 years. Each subject completed two, 30-min cycling bouts at 70% of VO2peak while under placebo or a selective serotonin re-uptake inhibitor (SSRI) treatment. Blood pressure was recorded directly from the radial artery, and treatments were randomised, double blinded and separated by at least 14 days. Baseline blood pressure was 145/72 mm Hg for systolic (SBP) and diastolic (DBP) respectively. Peripheral measures of serotonin (5-HT) were lower under SSRI treatment, whereas the major 5-HT metabolite, 5-hydroxyindoleacetic acid, was not significantly changed, indicating elevated central 5-HT levels. There was no difference in any of the haemodynamic variables between trials. Despite an increased heart rate for the initial 75 min post exercise, SBP was decreased as much as 23 mm Hg during the initial 60 min post exercise, after which it had returned to normal. DBP was unchanged after exercise. Circulating adrenaline (0.60 +/- 0.14 ng/mL to 1.3 +/- 1.6 ng/ml) and noradrenaline (0.27 +/- 0.31 ng/ml to 4.5 +/- 2.1 ng/ml) were significantly elevated during exercise. Both returned to pre-exercise levels within 15 min post exercise. Unexpectedly, oxygen uptake was slightly (5%), but significantly increased over the entire duration of the SSRI trial. We conclude that the central serotonergic system is not responsible for PEH in our borderline hypertensive population.

Our purpose was to examine whether the transient suppression of blood pressure that occurs during the hours following acute exercise (termed post exercise hypotension) persists throughout an active period of subsequent mild exercise and simulated activities of daily living (ADL) using direct measurements of arterial pressure. Eight recreationally active participants, with low borderline systolic hypertension completed 30 min of cycle ergometry at 70% VO(2Peak) and 30 min of quiet seated rest on separate days (randomised order). Following exercise and rest, subjects completed a 70-min protocol of mild exercise and simulated ADL. Blood pressure was monitored throughout by catheterisation of the radial artery. Exercise resulted in lower systolic (SBP), diastolic (DBP) and mean arterial pressure (MAP) throughout the post exercise ADL period compared to control measurements taken without prior exercise. The maximal difference in SBP, DBP and MAP between trials was 26, 7 and 13 mm Hg respectively. Average differences in SBP, DBP and MAP between trials were 16, 5 and 8 mm Hg respectively. This relative hypotension occurred in spite of higher heart rates during the ADL measurement period following the prior exercise. Furthermore, many of the blood pressure measurements during the post exercise period were significantly lower than the pre-exercise values during the same trial. We conclude that post exercise hypotension persists during mild exercise and simulated ADL. Although the duration of this relative hypotension needs to be determined, acute exercise may serve as a non-pharmacological aid in the treatment of hypertension.

The purpose of this study was to assess strength performance after an acute bout of maximally tolerable passive stretch (PS(max)) in human subjects. Ten young adults (6 men and 4 women) underwent 30 min of cyclical PS(max) (13 stretches of 135 s each over 33 min) and a similar control period (Con) of no stretch of the ankle plantarflexors. Measures of isometric strength (maximal voluntary contraction), with twitch interpolation and electromyography, and twitch characteristics were assessed before (Pre), immediately after (Post), and at 5, 15, 30, 45, and 60 min after PS(max) or Con. Compared with Pre, maximal voluntary contraction was decreased at Post (28%) and at 5 (21%), 15 (13%), 30 (12%), 45 (10%), and 60 (9%) min after PS(max) (P < 0.05). Motor unit activation and electromyogram were significantly depressed after PS(max) but had recovered by 15 min. An additional testing trial confirmed that the torque-joint angle relation may have been temporarily altered, but at Post only. These data indicate that prolonged stretching of a single muscle decreases voluntary strength for up to 1 h after the stretch as a result of impaired activation and contractile force in the early phase of deficit and by impaired contractile force throughout the entire period of deficit.

We have previously quantified the extent of myofibrillar disruption which occurs following an acute bout of resistance exercise in untrained men, however the response of well-trained subjects is not known. We therefore recruited six strength-trained men, who ceased training for 5 days and then performed 8 sets of 8 uni-lateral repetitions, using a load equivalent to 80% of their concentric (Con) 1-repetition maximum. One arm performed only Con actions by lifting the weight and the other arm performed only eccentric actions (Ecc) by lowering it. Needle biopsy samples were obtained from biceps brachii of each arm approximately 21 h following exercise, and at baseline (i.e., after 5 days without training), and subsequently analyzed using electron microscopy to quantify myofibrillar disruption. A greater (P < or = 0.05) proportion of disrupted fibres was found in the Ecc arm (45 +/- 11%) compared with baseline values (4 +/- 2%), whereas fibre disruption in the Con arm (27 +/- 4%) was not different (P > 0.05) from baseline values. The proportion of disrupted fibres and the magnitude of disruption (quantified by sarcomere counting) was considerably less severe than previously observed in untrained subjects after an identical exercise bout. Mixed muscle protein synthesis, assessed from approximately 21-29 h post-exercise, was not different between the Con- and Ecc-exercised arms. We conclude that the Ecc phase of resistance exercise is most disruptive to skeletal muscle and that training attenuates the severity of this effect. Moreover, it appears that fibre disruption induced by habitual weightlifting exercise is essentially repaired after 5 days of inactivity in trained men.

In small mammals, muscles with shorter twitch contraction times and a predominance of fast-twitch, type II fibers exhibit greater posttetanic twitch force potentiation than muscles with longer twitch contraction times and a predominance of slow-twitch, type I fibers. In humans, the correlation between potentiation and fiber-type distribution has not been found consistently. In the present study, postactivation potentiation (PAP) was induced in the knee extensors of 20 young men by a 10-s maximum voluntary isometric contraction (MVC). Maximal twitch contractions of the knee extensors were evoked before and after the MVC. A negative correlation (r = -0. 73, P < 0.001) was found between PAP and pre-MVC twitch time to peak torque (TPT). The four men with the highest (HPAP, 104 +/- 11%) and lowest (LPAP, 43 +/- 7%) PAP values (P < 0.0001) underwent needle biopsies of vastus lateralis. HPAP had a greater percentage of type II fibers (72 +/- 9 vs. 39 +/- 7%, P < 0.001) and shorter pre-MVC twitch TPT (61 +/- 12 vs. 86 +/- 7 ms, P < 0.05) than LPAP. These data indicate that, similar to the muscles of small mammals, human muscles with shorter twitch contraction times and a higher percentage of type II fibers exhibit greater PAP.

Nine recreationally active, borderline hypertensive subjects completed 30 min of arm ergometry (ARM) at 65% VO2 peak and 30 min of leg ergometry (LEG) at 70% VO2 Peak (randomised order). Blood pressure was monitored before and for 1 h after exercise using the Finapres method. Systolic, diastolic and mean blood pressures were significantly reduced for the entire 1 h post exercise. This reduction was independent of exercise modality, but there was an indication for the duration of the effect to be prolonged following the leg exercise. We conclude that the mass of the working muscle does not directly effect the magnitude of post-exercise hypotension (PEH) but may influence the duration of the response. These results suggest that a central mechanism or decreased vascular responsiveness is responsible for PEH.