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Dear
Editor-in-chief
Futsal (indoor version of soccer), in the last decade, has gained
popularity all over the world. The game is played 5 - a - side, and during
the competitions unlimited substitutions are permitted. Body movements,
during playing, are characterized by frequent accelerating and stopping,
jumping and tackling (Junge et al., 2004;
Nogueira Ribeiro and Pena Costa, 2006).
Consequently, physical demands are very high (Castagna et al., 2009).
Epidemiological studies report a high incidence of knee and ankle injuries,
owing to playing characteristics and field hard surface (Junge et al.,
2004;
Nogueira Ribeiro and Pena Costa, 2006).
However, to our knowledge, systematic studies on the structural damage
of Patellar (PT) and Achilles (AT) tendons have never been performed.
Aim of this letter is to report the prevalence and incidence of PT and
AT tendinopathies, in the players of a top level futsal team.
Ultrasound (US) examinations were carried out at the beginning and at
the end of the regular season. The diagnosis of tendinopathy and peritendinitis
was performed using strict US criteria (Salini and Abate, 2011).
Neovascularization was estimated by means of Colour Doppler, and graded
as (0), (1+), (2++), (3+++), (4++++), according to the appearance of vessels
inside the tendon (Alfredson and Ohberg, 2005).
Demographic and anthropometric data were registered. By self report, information
about injuries, suffered in the past, or during the season, were collected.
An injury was defined as pain or tendon discomfort regardless of the subsequent
absence from match or training. Players who had tendon damage at US evaluation
were compared with those free from abnormalities.
Data are reported as mean and standard deviation, frequencies and percentage.
Student's t and X 2 tests were used.
At the beginning of the season, 7 players (38.8 %) showed tendon degeneration,
associated with neovascularisation in 7 / 9 tendons (Table
1). Out of them, all asymptomatic when observed, 5 had complained
injuries in the past. The remaining 11 athletes were asymptomatic and
without tendon abnormalities.
At the end of the season, in 3 players, among the ones who did not show
tendon damage at the beginning, US revealed the onset of peritendinitis
with neovascularisation. In most cases, tendinopathy was observed in the
non dominant leg. Therefore, a total of 10 athletes (55.5 %) showed tendon
damage at the end of the season. To sum up, 12 tendons had US signs of
tendinopathy associated with neovascularisation in 10 (Table
1). Among these players, 8 reported tendon discomfort during regular
season, and 4 were forced to stop playing for a short period (~ 10 days).
All the US positive subjects had played for several years and were older
(Table 2).
These results show that PT and AT tendinopathies are very frequent among
futsal players. The high prevalence of tendon lesions, due to acute traumas
and, more frequently, to overuse degeneration, may be explained by the
playing characteristics : the frequent accelerating and stopping, jumping,
tackling, and abrupt jerking movements can indeed cause significant stress
on knee and ankle (Junge et al., 2004,
Nogueira Ribeiro and Pena Costa, 2006).
Moreover, the low heel footwear can expose AT to higher straining and
stretching, and the hard and adherent playing surface, that does not cushion
the blows of the heel, can further stress this tendon (Cain et al., 2007).
The higher prevalence of lesions in the non dominant leg can be explained
by the fact that periods of play are mostly spent in single - leg stance
on this leg, while the dominant foot manipulates the ball (Cain et al.,
2007).
To our knowledge, this is the first US study of tendinopathies in futsal,
and, therefore, every comparison with other sports may be misleading.
For example, Fredberg and Bolvig (Fredberg and Bolvig, 2002)
found, in asymptomatic soccer athletes, at baseline, a percentage of AT
and PT degeneration slightly lower than the one we observed in our group
(34 % vs 38.8 %). At the end of season, in this study (Fredberg and Bolvig,
2002),
US normalization was observed in some athletes, whereas in others, normal
at baseline, signs of degeneration were found. In our group, none of degenerated
tendons improved, while 3 athletes developed signs of tendinopathy. The
comparison, however, is misleading, considering that the main criteria
for the diagnosis of degeneration were tendon thickness in Fredberg's
study (Fredberg and Bolvig, 2002),
and structural abnormalities in our study. Moreover, the discrepancies
can be explained by the playing characteristics, and by the demonstration
that the exercise intensities are higher in futsal than those found in
competitive soccer athletes (Castagna et al., 2009).
In our cohort, the main risk factor related to tendon damage was the number
of years spent in playing futsal; at a lesser extent, the age was found
relevant. Another feature that must be undelined is the frequent observation
of neovessels, found in ten tendons (8 subjects, 2 with bilateral tendinopathy).
Neovessels ingrowth in tendinopathies is dependent by a hypoxic environment,
with subsequent production of Vascular Endothelial Growth Factor (Abate
et al., 2009).
In futsal, the hypoxia contribution may be enhanced. Indeed, the analysis
of activities during the game shows the existence of sprint bouts sequences
(3 - 4 bouts) with very short recovery time (20 - 30 sec of lower intensity),
anaerobic metabolism and high levels of lactate production (Castagna et
al., 2009).
The relevance of asymptomatic tendinopathies in athletes is well known
because, in most cases, tendon ruptures may occur without warning symptoms,
but only when tendinopathic changes are present. When symptoms develop,
the athlete is warned and therefore he should avoid further overload.
In conclusion, this preliminary study shows a high prevalence of tendinopathies
in futsal professional athletes, frequently associated with neovascularisation.
Strengths of this study are the accurate US examination and the homogeneity
of players evaluated. However, the small number of subjects has to be
considered an important limitation and therefore our findings must be
confirmed on larger samples, both in professional and amateur players
of different ages.
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