Veronica Vleck - Triathlon training, illness & injury by Triatlon Slovenije - PSS

‘Triathlon Training, Illness & Injury.’ 1 Veronica

Vleck, Ph.D.

FCT Research Fellow. CIPER. Faculdade de Motricidade Humana, Universidade Tecnica de Lisboa. Estrada da Costa 1499-002 1499 002 Cruz Quebrada- Dafundo, Portugal. Email: vvleck@fmh.utl.pt

Participation rates

• 24 M households watched Sydney Games • 2.3 M did at least 1 tri in USA in 2010, (55%  over 2009) • 1.9 M of which on-road (64%  over 2009, 148%  over 2007) • P Participation ti i ti 1993 1993-2000 2000 b butt h has  similarly i il l every yr since 1st Games 2

Potential new OG formats both “sprint distance”

• Already most popular event distance • USAT 2008: 78% sprint, 58% Olympic distance, 29% half Ironman (1/2 IM) IM), 17% Ironman (IM) • Rio 2016 will likely  media profile •  popularity among (majority population of) non –elites elites likely to be sustained 3

Availability of support

• Age-groupers, esp less experienced ones less likely to get coaching support •

(Dolan, 2011)

Only 26% “don’t want or need a coach” but 46% without a precise training plan (USAT TMOT, 2009)

BUT • Although tri is not the sum of its parts (Millet, Vleck & Bentley, 2009), little littl research h exists i t th thatt can h help l athletes thl t putt one together. • Tri training is inadequately quantified. • Links between training, inj & illness unclear. • Little examination of what can be used to predict maladaptation & attempt to avoid inj maladaptation, inj, illness or  perf

Training for different formats • 1 comparative calc of means of lit – (Vleck, 2003) • Data agreed with the 1 comparative research study for Olympic distance (OD) vs Ironman (IR) from 1993 (Vleck) • No published evaluation of extent to which this is changing over time

• OD athletes may spend less overall time per week than long distance (LD i.e. half Ironman (1/2 IM) & Ironman (IM)) athletes doing longer, low intensity, ‘long run’ (p<0 05 for both genders) & ‘long (p<0.05 long bike’ bike sessions (p<0 (p<0.05, 05 for females only). • Length of individual such sessions is likely less in OD than LD athletes (p<0.05). •

Superior OD athletes also do  speed work cycle and  long run sessions per week (both p<0.05). Inferior OD athletes do  back to back cycle-run transition (T2) t i i th training than LD athletes thl t (p<0.05) ( <0 05)

• (Vleck, (Vleck data from 1993)

Intensity distribution

• Very few prospective longitudinal studies

(Millet et al., 2002;

Vleck, 2010; Neal et al., 2012)

• IM ( 6 months pre-race): 69 ± 9%, 25 ± 8%, and 6 ± 2%, low, mid, high intensity • OD (1994), similar results

Average wkly rate of change in % time in each intensity Increasingly greater for bike & run as the athletes progresse progressed through the season Toward the competitive period

Very little published publishe info about how elites train (lots of variability, variability participation in altitude altitu training)

Competition demand (rough): • Simulated sprint: 85-90 % VO2peak (Taylor et l., l 2012)

• Non-drafting OD: 81-85 % VO2peak (Delextrat et al., 2005; Gonzalez-Haro et al., 2005

• Elite OD: course dependant, some multiple short term high intensity efforts • ½ IM: 68-70 % VO2peak • IM : 80% HRmax

(Gillum et al., 2006)

(Laursen et al al., 2005) 10

Level of dehydration/ risk for heat illness

• Not fully established for sprint/OD • IM: total BW turnover of 16 L/ 1.33 l.h-1 reported • BW loss can be 3-8% (double half-IM) in males, NS in females but may  in hyponatremics • Latter rare in races <4h, more >8h

Potential effects • Notwithstanding the lack of available training detail, triathletes suggested to undergo “extreme extreme amounts of exercise” • ? associated w DNA modulation,  risk of cardiovascular events (Neubauer, 2009), &/ or  immune status. • Cumulative oxidative ([O]) stress (Shah et al., 2011),  [o] of plasma lipoproteins & potential contribution to atherosclerosis may offset +ve effects of tri training? • U- & S- shaped relationships betw ex (load) & health may exist in age-groupers age groupers (Poulsen et al al., 1999) & Elites, Elites respectively.

Immunological response over the tr year • Horn et al. (2010)- 10 yr retrospective AIS athlete study : – Lower white blood cell (WBC) & neutrophil counts than other sports. – 65% neutropenia, 5% monocytopenia But a 4 yr prospective study in Spanish Elites (Diaz et al., 2010) within normal limits both in pre-comp & comp • Infection risk may  w  run I training (Robson Ansley et al., 2007) • Host protection to novel pathogens may be compromised during periods of heavy training and in the recovery from arduous d competition i i (Cosgrove et al., 2012) • Southern hemisphere athletes:  infection risk in early spring, summer, & late autumn/winter (Broadbent et al., 2011) 13

Although competition reported not to pose any acute health risks to well prepared & well supplied healthy athletes ((Gastmann et al.,, 1998), ), immune suppression pp has been demonstrated post-race

• OD triathlon may  level of lgA mediated immune protection at the mucosal surface. Exposure to water bourne micro-organisms may incur  risk of at least upper respiratory tract infection (URTI) • As for IM triathlon: – neutrophil death seen immediately post. – Significant changes in [0] stress & immunological markers k seen 20 min i postt

BUT! • O OD induced immune system alterations, muscle damage & metabolic changes  rapidly (Lopez et al., 2011; Shinkai et al., 1993)

• IM related [O] stress markers normal 5d post

(Neubauer,

2009; Wagner, 2011)

• Extent to which postulated “infection infection window” window exists or persists ∞ existence of +ve adaptive mechanisms (such as the up-regulation of repair mechanisms &  activity of the endogenous antioxidative system), themselves dependant on training & performance status 16

Is there an immune dose:response relationship? • Sig diffs in magnitude of [O] stress markers (Medina et al., y exist betw yyounger g vs. older;; poorly p y trained vs. well2012)) may trained athletes; athletes with a lower vs. a higher antioxidant status; or at different periods of the training year • Even minor differences in training status in same athlete group  diff changes in markers of lipid peroxidation • Better training levels might confer  protection against [O] stress (Brites et al al., 2006; Margaritis et al al., 1997) • Data for half-IM and IM athletes, & controls (Knez et al., 2007) suggestt dose-response d relationship l ti hi b betw t [O] enzyme adaptation & the ex response, but as yet unclear how tri training or race duration intensity / freq affects propensity for DNA damage (Wagner et al., 2011). 17

Other training/racing illness/ inj related issues • Platelet & coagulation activation, & other cardiovascular system related changes g • Changes to bone health

(Claessens et al., 1999a, b; 2000, 2001; Whyte et al., l 2000 2000; K Knez ett al., l 2008 2008; D Douglas l ett al., l 1988 1988; S Scharf h f ett al., l 2010 2010; Sh Shave ett al., l 2004; Gratze et al., 2005; Haykowsky et al., 2001; Leetma et al., 2008),

• Changes Ch tto b body d weight i ht

(Walsh et al., 2012)

• Platelet activation ((hypothesised yp to  risk of thromboembolytic y events) &  plasmin formation may occur during comp > 2 hrs (Hanke et al., 2010, Bartsch et al., 1994, Mockel et al., 2001).

• ? triggered by run induced mechanical stress on thrombocytes &/ or inflammation (Hanke et al., 2010). 18

Competition & cardiac function

• OD – NS –ve effects on left ventricular (LV) function or myocardial tissue (Leetma et al., 2008).

–  abnormal changes to LV function (La Gerche et al., 2012) that may occur with  race distance (Haykowsky et al., 2001; Whyte et al., 2000) appear to disappear within 24h (Haykowsky et al., al 2001) 2001).

– No effect on blood [[B-naturietic p peptide] p ] ((a marker of cardiac failure) in regularly trained.

What about Ironman? •  troponin & B-type naturetic peptide 45 min after ½ IM & IM, IM both of which ∞ w  right ventricular (RV) ejection fraction, but levels normal 1 wk post (La Gerche et al., 2008, 2012)

• IM competition p often results in p persistently y  cardiac troponin T levels ((Tulloh et al.., 2006; Rifai et al., 1999). Associated  in troponin levels ∞ w ECG evidence of abnormal left ventricular (LV) function. This may be ∞ occurrence of pulmonary oedema (Boggio-Alarco et al., 2006; Millet et al al., 2010) 2010).

• However, even when short term RV recovery appears complete… 20

Long term training may:

•  Possible myocardial fibrosis & remodelling in a small, genetically ti ll susceptible, tibl % (Claessens (Cl ett al., l 1999 a,b, b 2000 2000, 2001 2001; O’Keefe, 2012).

• This theoretically might ∞ atrial & ventricular arrhythmias & cardiovascular risk, esp in older triathletes •  RV remodeling in well-trained endurance athletes w longer hi t history off competitive titi experience i (La Gerche G et al., 2011)2011) ? Cumulative effect of repetitive endurance ex on RV change & fibrosis? • Long g term sequelae q of structural or other changes g that occur to the triathlete heart unclear 21

•  ventricular p premature beats after max ex test in well trained triathletes than controls

(Claessens et al., 1999, 2000, 2001,

O’Keefe, 2012)

• But not the best triathletes w the best results who had the most characteristics of eccentric & concentric LV hypertrophy • Nor did the triathletes w the greatest training volumes p exhibit the most extensive heart adaptations

Nonetheless • The triathlete who displays the first indications of evolution to a pathological hypertrophic and dilated cardiac myopathy (i.e. VPB) & and other specific electrocardiographic and echocardiographic findings is a candidate for 'sudden cardiac death.’ • Acute changes in baseline hemodynamics and autonomic regulation w IM comp may make such athletes vulnerable to post-race orthostatic challenges.

What else? • Little known re extent to which bone mineral density (BMD) & tendency to skeletal probs ∞ by tr induced changes in circulating hormones (Lucia et al., 1996; Maimoun et ) al.,, 2004).

• Knee cartilage thickness (Mulhbauer et al., 2000), abnormal b l MRI fifindings di (Shellock et al., 2003) & BMD McClanahan et al., 2002) not sig diff from controls. • Susceptibility to disordered eating (de Bates et al., 2002; Blaydon and Lindner, 2002), anorexia i nervosa (Kiraly et al., 2003), bulimia nervosa (Clark, 1993), or other female athlete triad characteristics (Hoch et al., 2007; Voss et al., 1997; Bennell et al., 24 1996) may affect illness/injury susceptibility.

Illness: to what extent does it occur? • Minimal prospective data

(Vleck, 2010, Spence et al., 2007; Main et al., 2010, 2012;

available il bl tto lilink k with ith th the immunological/ [O] stress related data

Broadbent, 2011; Jeans and Schwellnuss, 1994)

e.g. (Vleck, 2010, 26 wks) 40.9, 36.4, 11.4, 9.1 and 2.3 % of 247 illnesses were 'virus’-, 'heavy legs/ delayed onset muscle soreness (DOMS)-', 'sleep-, & 'appetite'- related. • Most commonly observed symptoms in order DOMS> heavy l legged> d> lloss off appetite tit > virus i related. l t d Coincided C i id d w perff  on 15 % occasions. • No further details of aetiology.

Caused by? • Unclear to what extent upper respiratory tract infection (URTI) may be due to infection or other inflammatory symptoms that mimic it

(Walsh et al., 2011).

• Of 25 cases of URTI symptoms (Spence et al., 2007) in 63 t i thl t / cyclists, triathletes/ li t 28% each hd due tto rhinovirus hi i & influenzae (A & B), 16% to parainfluenzae, 8% each to streptococcus peneumonia & coronovirus coronovirus, & 4% each to Epstein Barr virus reactivation & metapenumovirus.

• Some UTRI symptoms may be of a non-infectious non infectious inflammatory nature, due more to: – local drying y g out of the mucosal surfaces and increased exposure to air bourne pathogens (Cox et al., 2004))

– bronchial hyper-reactivity (incidence of which in Elites is 195-286 faster than normal rate for asthma development (Knopfli et al., 2007; Ali et al., 2012; Friman et al., 2000; Spence et al., 2007; Bougault et al., 2009);

– muscle damage induced migration of inflammatory cytokines (Walsh et al., 2011). • URTI incidence in Broadbent’s study (2011) < international yearly average (of 2). 27

Tri specific issues •

Unclear to what extent training/racing induced imunological changes affect overall disease susceptibility

• swimming conditions may  risk for specific conditions e.g. A Acanthamoeba th b kkeratitis titi (Tabin et al., 2001), & uncommon diseases e.g. schistosomiasis (Jeans and Schwellnus, 2004; Holtzhausen, p p 2010)) & leptospirosis • Clinical presentation of leptospirosis varies markedly & may include nonspecific symptoms easily mistaken for common febrile illnesses such as flue.

!•

Before outbreak awareness established, 0 athletes who sought ht medical di l care suspected t d off h having i lleptospirosis t i i (Morgan et al., 2001).

• P Potential i l problem bl off misdiagnosed i di d ill illness, w attendant d risk of inappropriate management strategy (Mucallef-Stafrace et al., 2010).

• Viral myocarditis = reason behind sudden cardiac death in 5-22% 5 22% of athletes <35 yrs • Important p to take subtle discomforts seriously y & initiate further evaluation when viral infection is strongly suspected, esp. in spring & summer • Overall outcomes of triathlete illness in terms of economic cost, cost training time loss & or perf unknown unknown, only some indirect clues. Same is true for injury

Injury: what’s new ? • Extent to which injj & illness impact p on each other (e.g.  leptospirosis risk w wounds; [o] stress & acute lung injury) & on perf unclear

• Little new tri specific injury research since last review (Vleck, 2010)- still next to zero comparative data for kids/ para specific older age age-groups/ groups/

• Some new swim/cycle/run specific case study data that may possibly have implications for race guidelines e.g. g overly y tight g wetsuit   spontaneous p recurrent pneumomediastimum/ pulmonary oedema, Propellor injury New & unexpected issues constantly arise…

What specific aspects may injury risk? Thermal stress/ sudden cardiac death related activity p aspects p of tri may y but little examination of what specific injury risk e.g. Harris et al. (2010) 1.5/100,000)- drowning was reported cause of death for the 13/14 swim fatalities but drowning lacks the accurate risk exposure data that are req to establish aetiology. 8/9 athletes who were autopsied had cardiac abnormalities. What else is new?

Temporal injury prevalence/ incidence •

(Rimmer & Coniglione, 2010),

non-elites. IM, ½ IM

• 72% ½ IM inj within hrs 6-7 (78/1000 starters) •  rate of severe inj in IM w longer treatment • -ve skew of inj. severity with  finishing time •  med support req. in later stages of comp? • Follow-up req. Necessitates consensus statement (esp re def of recurring inj) & active governing body support for the implementation of a longitudinal prospective database 33

Optimising performance • Little published investigation (Paton and Hopkins, 2005). of extent t which to hi h perff mustt  for f it to t be b competitively titi l significant i ifi t • Th Theoretical ti l iissues w calculation l l ti off summated t d ttraining i i load across >1 sport • Some studies using Banister model / binary logistic regression / linear mixed modelling (Millet et al., al 2002 2002, 2005; 2005 Vleck, Vleck 2010; Main et al., 2010, 2012; Barnett 2012)

Training logs Major, method by which majority monitor training, injury & g one than a heart illness ((Vleck,, 2010).) ((Dolan,, 2011)) >2x using rate monitor. Monitoring heart rate variability (HRV) may only prove realistic in a few. Scores on: DALDA (Robson-Ansley (R b A l ett al., l 2003) REST-Q sport (Barnett et al., 2012, Kellman and Kallus, 2001); Athlete Burnout Questionnaire (ABQ) & MultiComponent Training distress Scale (MTDS) (Main et al., 2009; 2012)

Profile P fil off Mood M d St States-C t C (POMS (POMS-C) C) & various i signs i and d symptoms of illness and injury (SAS) (Vleck, 2010) have potential to highlight athletes under excessive stress. 35

Key points: â&#x20AC;˘ Critical that signs & causes of training stress syndromes more clearly mapped, such that most appropriate management strategy employed â&#x20AC;˘ Standardised level of detail for post post-race race medical reports, with adequate statistical analysis and feed back into ITU based preparticipation evaluation/ injury prevention framework, recommended.